Home Posts tagged "Rugged Magazine"

The Rugged Kitchen: Installment 4

By: Eric Cressey

Normally, we have qualified individuals like Christina Jenkins and Ko Attleberry put together The Rugged Kitchen for us. However, with qualified individuals come recipes that actually require thought and a passion for cooking. As a overworked grad student who really couldn't care less about making his food look pretty, I tend to rely on healthy recipes that I can make in just a few minutes, thus allowing me to get out of the kitchen as quickly as possible. Normally, I just cook in bulk every 4-5 days and then work off of plastic bags in the fridge, but there are a few "recipes" that I actually follow, so I figured I'd share them with all you readers that can sympathize with me. You'll notice that I don't include quantities; it's because I don't measure anything out. Yes, I really am that lazy. Remember, the KISS (keep it simple, stupid) strategy works just as well in the kitchen as it does in the gym.

Bean and Egg Burrito What you need:

- Egg whites (the carton kind or regular eggs that you crack yourself) - Black Beans - Salsa - Hot Sauce - Fat Free Cheddar Cheese - Any veggies you like (I use spinach; you may want onions, peppers, etc.) - Whole Wheat Tortilla (optional) - Chili Powder (optional)

This makes a great protein and carb meal. Basically, you just make a round omelet (use non-stick cooking spray) with the veggies mixed into the egg whites; don't add the cheese yet, though. Once it's done, lay it out on a plate and toss on the cheese (it'll melt; don't worry), beans, salsa, hot sauce, and chili powder (if desired). Roll it up and eat it. If you wish to add more carbs, you can wrap the whole wheat tortilla around the egg layer. This whole process should take about four minutes. Chocolate Slop If you were a little porker as a youngster like me, when Mom made brownies and offered to let you lick out the mixing bowl, you salivated like Homer Simpson on a tour of the Duff Beer production plant. This little piece of heaven is the closest thing to brownie mix that can actually be considered healthy; give it a shot. What you need:

- Calcium Caseinate or Milk Protein Isolate Powder* - Whey Powder (isolate, concentrate, or a mixture of the two)* - Psyllium Husk Powder

*Note: Biotest Low-Carb Metabolic Drive powder works perfectly for this recipe, as it's a blend of the two different categories.

Put some water in a bowl, and then add your protein powder (ideally in a 2:1 caseinate/MPL:whey ratio) and a tablespoon or two of psyllium husk powder. Be sure to mix as you add. Add as much water as you want; you can make it like pudding or the thicker brownie mix that I like. I like to have it with almonds before I hit the sack; it makes a great, high fiber, slow-digesting protein and fat meal before bed. Lazy Man's Calico Beans This is a recipe that's really popular at our family gatherings. Unfortunately, the original recipe isn't all that healthy; it includes ketchup, pork 'n beans, cooked bacon, and regular ground beef (note: beef is great, just not in protein and carb meals). I just changed things up to make it healthier and appropriate for a protein and carb meal. What you'll need:

- 1 lb. Lean Ground Turkey (cook it separately before adding it to the mix) - 1 Can Pinto Beans - 1 Can Black Beans - 1 Can Kidney Beans - Apple Cider Vinegar - Spicy Mustard - ½ Bag Onion Soup Mix

Toss all of this into a crock-pot and let it cook for a few hours on low. Eat it. Enjoy it. Beef Jerky If loving beef jerky is wrong, I don't want to be right; this stuff might be my favorite food in the world. The store-bought kind is a convenient protein source that you can take anywhere, but nothing tops the homemade version on taste and tenderness. When you use lean red meat, it's also very healthy. The only trade-off is that unless you have a load of preservatives in your kitchen cabinet, you'll have to keep this stuff refrigerated and eat it within a few days of cooking it. What you'll need:

- 1 eye of round or top or bottom round roast - Whatever type of flavoring you desire (soy, teriyaki, Tabasco, or barbecue sauce) - Spices (salt and pepper are sufficient, but you may want some chili powder, etc.)

Slice the roast into small strips about three inches long, one inch wide, and ¼ inch thick. If you use an eye of round roast, be sure to slice it lengthwise to keep it reasonably tender. Use a fork to poke some holes in the meat; it'll keep it tender and allow it to soak up the marinade better. Marinade the strips in the flavoring of your choice (I like Tabasco and pepper) overnight. The next day, set the strips directly on the oven rack; you'll probably want to use a pan underneath to keep all the drippings off of the bottom of your oven. Set the oven on the lowest possible setting (150°, or the "Warm" setting will do fine), and leave the strips alone for at least five hours to "dry out." Basically, the tougher you like your jerky, the longer you should leave them in. That concludes this installment of the "Rugged Kitchen."  For more information on some great healthy recipes, I highly recommend John Berardi and John K. Williams' fantastic Gourmet Nutrition e-book or, even better, JB's entire Precision Nutrition package, which includes the recipe book and a whole lot more at a great deal.

Now, shouldn't you be stuffing your face?

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The Strongmen Speak

An Interview with Brad Cardoza and John Sullivan By Eric Cressey

Walk into any gym and you'll encounter some really big guys. Heck, you might even find a few who can move some reasonably impressive weight on the bench. Rarely, you'll see people who actually deadlifts. And, once in a millennium, you might encounter someone who smokes a crisp 400-lb. butt-to-heels squat that brings a tear to your eye. I can guarantee you, however, that you've probably never encountered someone who can do what Brad Cardoza and John Sullivan do regularly in their training. That's not to say, however, that you should simply discount what these guys have to offer; chances are that some Strongman training methods could take your performance and physique to all new levels. You'll probably learn a few new ways to frighten the old ladies in your gym, too! EC: Tell me about yourselves to set the stage, fellas. Please omit anything related to your criminal records, favorite colors, and Sully's weird rash. BC: I've pretty much run the gamut in terms of participation in strength sports. I lifted in high school and threw the discus (some school and conference records), then went on to have a successful career at Division III UMASS-Dartmouth, where I was ranked #1 in the country in the hammer throw and held the UMASS-Dartmouth school record in the 35# weight throw. As a result, UMASS-Amherst offered me a D-I athletic scholarship, so I gladly accepted the opportunity to be involved with a program that had good coaching and a solid strength and conditioning program. I wound up going to D-I Nationals and still hold the UMASS school record in the hammer throw. I got away from competing for a few years after college, as I was busy trying to start a career www.pinnaclestrengthandfitness.com as a personal trainer in Boston. While working at Boston Sports Clubs for two years, I met quite a few people, most notably Sully. It took a little while, but he finally convinced me to give Strongman a try. Needless to say, I'm very happy he did; it has become the most important part of my life these days. This is one thing people have a hard time understanding about me: when I am involved in a sport that I love, it comes before everything else in my life besides loved ones. At UMASS, track came before classes, and now strongman comes before work, sometimes even my health. This attitude has lead to a lot of improvement, as I earned my pro card in the International Federation of Strength Athletes (IFSA); had some success in powerlifting during 2003 (575 squat, 375 bench, and 650 deadlift without much specific preparation); and received sponsorship from AtLarge Nutrition www.atlargenutrition.com and APT Pro Wrist Wraps www.prowristwraps.com. Then again, my approach has led to some frustration at times as well; I'm now dealing with my third major injury in only two months (a record for me); this time I'm going to need surgery (Editor's Note: at publication time, Brad has not only had the surgery, he's back in the gym already!).

JS: When I originally started becoming more focused on strength sports, I was interested in powerlifting. I began to learn more and more about the Westside system of powerlifting, and began to use their methods in my training. In 2002, I met the owners of Total Performance Sports in Everett, Mass., who were running the Mass. State Strongman Championships. They convinced me to come down to their place and give it a try. I did, and loved it. I wasn't sure I was going to enter the contest, but after about a month of training there, they basically said, "you're entered". I was kind of nervous, but in retrospect it was the best decision that was ever made for me. I won my division, and I was hooked after that. Later that same year I started working for Art McDermott, training clients at Highland Strength & Fitness in Andover, MA. I have trained there for all of my subsequent Strongman competitions. My last competition was NASS Nationals, where I placed 5th in the 200 lb. class. I've also been involved in Olympic lifting of late. EC: Those answers once again reaffirm my belief that lifting heavy stuff is more addictive than any drug – even Viagra on a trip to the Playboy mansion. Anyway, what does a typical week of training look like to you? BC: When I am healthy and preparing for a competition, my typical week would look something like this:

Monday - Max effort overhead pressing day (maybe a little thick bar bench or something to keep the bodybuilder in me happy!) Tuesday - Max effort leg day. This would include squat and deadlift variations as well as my single leg support stuff (my favorite) Wednesday or Thursday - There are usually two event days per week when preparing for a competition. This would usually be one of them; the other falls on Saturday. Usually, you are training for 5-6 events, so I prefer to do three of them on Wednesday/Thursday and three of them on Saturday. Friday - Upper body pull day. This includes all of my back work as well as any direct arm or grip stuff that I might need. Saturday - Event day #2

I should also mention that I usually mix in some Olympic movement at least once a week. Sometimes, I'll do it on a day off, or possibly just throw it in wherever I feel it fits best. JS: A typical training week is a little tough, since the nature of the events in a Strongman contest can vary so widely. That said, here is a template similar to the one I used to prepare for the 2004 X-Treme Strongman Showdown, where I placed second. Keep in mind that this template reflects my personal strengths and weaknesses, and may not necessarily be optimal for someone else.

Monday: A) Heavy Pull/Good Morning (DL or DL variation once every 14-21 days) B) Harness Front Squat or Olympic Squat C1) Lunge Variation C2) Core Work Tuesday: A) Jerk Variation B1) T-Bar Row B2) Close grip Bench C) External Rotation Work Thursday: A) Power Clean B) Box Squat C) Core Work Saturday: Events

I don't do much overhead or grip work because I tend to do very well in those types of events. I focus on exercises that will bring up exercises like stones, which are a weakness for me.

EC: As sweet as training Strongman-style to prepare for Strongman competitions is, it stands to reason that the overwhelming majority of our readers have other goals. How can the ordinary fitness enthusiasts integrate Strongman training into their programs? Bodybuilders? Powerlifters? Other athletes? Regular weekend warriors? BC: What people have to realize is that Strongman training means nothing more than integrating explosive, compound movements into your workouts. I am actually quite impressed with how many guys at my gym have taken my advice and started doing a lot more squat and deadlift work. I even see guys attempting 1-leg reverse hypers, pull-throughs, etc. It all comes down to wanting to be athletic and strong - not just big or buff. I will admit that when I first arrived at UMASS and my coach told me that I wouldn’t be bench pressing again during my collegiate career, I was heartbroken! No more than two years later, when it was time for max day and everyone on the team was doing benches, squats, and cleans, I was no where to be found. I maxed on front squats, snatches, and behind the neck push presses! At this point, I was convinced that these were the lifts that were turning me into a successful hammer thrower, so "missing out" on the others was of absolutely no frustration. As far as strongman events are concerned, there are usually a limited number of things you can do at a traditional commercial gym. One the most beneficial and rewarding events is the farmer's walk. These were tough to do at the gym until I realized I had two of these guys at my disposal: Throw some tape in the middle of the handle to make it a little bit thicker, and it is probably the best farmer's simulation you will get without the real implements.

Besides farmer's, there aren’t too many events you can replicate in the gym, and this is when you have to use the imagination a little bit. Zercher holds (Conan's wheel), stiff leg pull-throughs (stones)…there are lots of things you can do that will be great for you and maybe even amp you up enough to try a competition sometime! Grip is the only other thing about which you ought to worry if you're thinking about competing. Sully covered that one pretty well in his article last month, though, didn't he? All that you have to remember is that most people's grips suck; I know mine did. The more heavy pulling you do on a weekly basis, the more rapidly your grip will improve. Certainly, it doesn’t hurt to add the grip-specific stuff as well. JS: I think certain athletes can benefit greatly from Strongman training. Strength athletes like powerlifters can expect greater hip, back, and abdominal stability, strength, and power from using Strongman equipment like the super yoke, stones, tries, kegs, and sandbags. Bodybuilders can fill the sandbags with chicken breasts to make sure they get their 1200 grams of protein a day, and use the kegs to stock up on posing oil! For combat athletes, I think it can also be extremely beneficial. Lifting oddly shaped, uneven objects will tax your body in a way you don't normally encounter in the weight room. On top of that, strongman medleys are an unbelievably effective conditioning method. Summarily, I've had great utilizing these methods with my football, hockey, wrestling, and baseball clients (just to name a few). EC: Any tips on improvising home versions of various Strongman implements? I've heard that the Strongmen are the closest thing to a freaky big and strong Bob Villa that one can imagine! BC: This depends! If you live with Art McDermott at Highland Strength and Fitness (www.highlandstrength.com), then yeah - just bring the stones into the driveway, pull out all the tires, and get to it after warming-up with a keg for height in the back yard! Most people don’t have these luxuries, so it really depends on what you have at your fingertips. If someone was really interested in training Strongman without spending any money, I would probably tell him to get the following Kegs – There are a lot of things you can do with a keg, and many of them you will see in competitions. First, it's ideal to get as many as you can so that you can have a variety of different weights. You will have to fill each keg with different stuff like water, sand, lead, and shot. Once you have all the kegs you can do the following:

1. Overhead presses- (strict, or clean and press) 2. Carries- (much like a Husafell stone) Try doing sprints while holding a 200 lb keg. 3. Loading – If you have platforms, you can load kegs just as you would load stones. A little bit more awkward, but it gets the job done. 4. Keg throw for height – This may be my favorite. It feels very similar to a snatch to me, and will build explosive power like you can only imagine!

Tires – Many people assume that tires are just for flipping, but different size tires can actually come in handy with:

1. Tire flip- Okay, so this one is pretty self-explanatory. This might be one of the most beneficial exercises I have ever done - inside the gym or training events.

2. Tire throw for distance – If you have ever seen someone throw the discus, this one might make sense to you. Start with a tire from a smaller car, something like Sully’s Sentra. If you can throw your flipping tire, give me a call. This would mean that we need to bring you straight to the Olympic training center to start throwing the discus. 3. Drags – If you don’t have a sled, tie some tires together and drag those. This might be a pain, but it works, and dragging on grass will make it much tougher

Odd-shaped stones – Once again, not too many people have Atlas Stones or Husafell stones on hand, but if you have a quarry of any kind or even a cheap or generous mason in the area, you’re in luck. Your options with this implement include:

1. Loading – This is just like the Atlas stones you have seen; if you have a platform or even a keg onto which to load them, you’re all set. These may hurt and be a little bit more awkward than it real Atlas stones, but it does the job. 2. Throwing – Instead of throwing the stone like a discus, you would throw either for distance like a shot, or for height over a bar. 3. Carrying: Nothing beats a true Husafell stone carry. If you are lucky, you might be able to find a somewhat triangular piece of granite or something similar. As long as it sits in your arms comfortably, this could be on of the best free training implements of all.

You'll notice the similarities between the odd-shaped stone and keg exercises; this just underscores the importance of variety! Anything heavy on which you can get you hands – Last but not least comes everything else. You name it: blocks of wood; cars or trucks for pushing and pulling; sledgehammer swings; etc. If you are familiar with the events you will be able to pull it off. Just remember that it takes a very special (read: crazy!) person to be able to go out into the cold and be excited about running around holding onto kegs and rocks. Once you start seeing results from integrating workouts like this into your weekly routine, you will be hooked, I promise. Just have fun and if you feel like your isolating a muscle, stop immediately (just kidding). All that I ask is that you stop doing day purely for arms! EC: Whoa, Brad covered a lot. Say what you want, Sully, and then we'll make up the difference with a photo of you picking up a car. JS: Personally, I feel that for most of this stuff, you need to find the actual implements. As Brad mentioned, however, kegs, tires, and sandbag aren't too difficult to come by. You can also probably find a quarry or construction site and "borrow" some heavy stones. Or, you can just pick up cars.

EC: Okay, time to play the "glass is half empty" game. What are the downsides of competing as a Strongman? BC: My top four answers would have to be:

1. Injuries - I have had more injuries in the eighteen months than I have had in my entire life. There's been a hernia, broken foot, pulled hamstring, disk problems, and pec tear… and the list is still growing! 2. Convenience - I have to drive a total of three hours just to get proper equipment and training partners. 3. Getting beat – This is pretty much applicable to any sport, but I hate it when I don't win. 4. Nuisances in the Gym – Specifically, I'm referring to all of the attention that "strong guys " pay to you at the gym. Ever since I started competing and word got around, I constantly have guys lifting next to me and trying to show me up. At times, it gets ridiculous and I have to say something.

JS: It really tests your mettle, both mentally and physically. Plus, it's lots of fun to train and compete. There really is a great camaraderie in the sport. EC: Okay, now that you jerks have depressed our readers and killed the enthusiasm we'd built beforehand, let's finish on a positive note and highlight why being a Strongman competitor rules. That is, unless, of course, you'd like to club some baby seals, set a kitten on fire, or make fun of the handicapped. Got any good party tricks or cool stories? BC: How about another list?

1. Personal satisfaction - I have never been more excited with my accomplishments and training than I have been over the past 1.5 years. I am doing things that I thought (assumed) I would never be able to do. That keeps me going. 2. Being called one of the strongest small people in the country isn't half bad either. 3. The people – The individuals involved in Strongman competitions are some of the friendliest, most helpful people I have ever known. Ever since Sully introduced me to the sport, I am constantly amazed at how cool all of these people are. 4. When it comes down to it, I am just happy to have a successful career in the best sport in the world. People can try to argue this if they so choose, but I have never seen more talented athletes in my life. I am constantly amazed at some of the feats of strength and athleticism I see on a regular basis. 5. I wish I could say party tricks, but there's not much I can pull out my sleeve in that regard. Actually, I take that back. When I was in Vegas for Olympia this year, I spent a bunch of time doing overhead presses with a couple of girls in the hot tub. First they asked me to pose, so I figured I would go with the second option so that Sully wouldn't give me a hard time for acting like a bodybuilder. I guess that could be considered a party trick. I also like to throw things far at parties; I used to do this a lot in college, but not so much anymore. Usually, "things" consists of kegs, people, or whatever else is lying around.

JS: My family and friends automatically assume that I want to help them move, since I compete. Also, people look at the cuts and scars on your arms from doing stones and think you have some kind of weird rash. And, by far the worst, people ask, "Oh, you compete in bodybuilding?" Crushing full cans of soda and ripping phone books are always good times, too. EC: Way to try to explain that rash, Sully. Unfortunately, it isn't on your forearms… On that sickening note, it's time to wrap this up. Thanks very much for your time, guys, and best of luck.

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Maximum Muscularity II

by Eric Cressey and Tim Skwiat In Part 1, Tim and Eric set forth the dietary framework for Maximum Muscularity. Now, training and supplementation take center stage. * Add Fuel to the Fire...On non-lifting days, we highly recommended that you perform high-intensity interval training (HIIT) in place of the resistance training. The fact that HIIT is most heavily reliant on muscle glycogen during exercise does not mean that it is an inefficient method of exercise for fat loss. On the contrary, HIIT is a much more efficient means of achieving fat loss than steady-state aerobics. Otherwise, you wouldn't see so many non-spandex deserving aerobics instructors with greater than 30% body fat! When the post-exercise period is factored in and excess post-exercise oxygen consumption (EPOC) is taken into account, the total amount of fat and calories burned as a result of the HIIT is actually greater than with its lower intensity counterparts (20-22). And, let's not forget that in given the right work: rest ratio, you'll almost always perform more total work with HIIT than steady-state aerobics. Tremblay et al. found that subjects who performed a HIIT program showed a ninefold greater decrease in the sum of six subcutaneous skinfolds relative to a group of subjects that performed an endurance training program (23). Additionally, interval training is considered to be superior to steady-state, submaximal cardiovascular activity in improving VO2max (24). We know what you're thinking: "Why should I worry about VO2max? I lift weights; VO2max is only important for spandex-clad cyclists!" Well, even if being a more functional lifter (or athlete, if that's your cup o' tea) isn't reason enough to value VO2max improvements, you will still be interested to know that a greater VO2max value has been associated with increased thermic effect of food (25). That's right - jack up the VO2max, and the dozen Krispy Kremes that "accidentally" vanish in your presence are less likely to be stored as body fat. As if all these benefits weren't enough, let's consider the explosive nature of HIIT work. Typically, your ball-busting work periods are in the 10-30 second range, a timeframe that closely approximates the duration of most strength training sets. In other words, you'll be training the same energy systems (ATP-PC and fast glycolysis) as in strength training (13). And, less scientifically, picture yourself digging deep to propel yourself forward during a sprint. Now, think of the last time your hip and knee extensors kicked in as fired out of "the hole" during a set of squats. You can bet that training your explosiveness will carry over to such performances. Finally, when you notice how insanely sore your hams, glutes, quads, calves, obliques, and lower back are after your first sprinting session, you'll be convinced of how effective HIIT can be in promoting muscle growth. Okay, now that you understand why HIIT beats steady-state aerobics like a redheaded stepchild, let's consider the mode and structure of your HIIT sessions. There are plenty of options available: cycling, elliptical trainers (preferably with arm motion included), rowing, jumping rope, and boxing. However, ask any HIIT-aficionado, and he'll tell you that sprints are king! That said, the table below summarizes some HIIT guidelines to adhere to regardless of your mode of choice. Note: Because we are using interval training for physique enhancement rather than purely for performance improvement, these selections depart from traditional interval training protocols. At the very least, they represent the shortest end of the spectrum in terms of rest intervals, as total recovery should not be reached before the onset of the next work interval.
Work Period Rest Period Work: Rest Ratio Repetitions Duration
10s 50s 1:5 15 15:00
15s 45s 1:3 15 15:00
20s 40s 1:2 15 15:00
30s 60s 1:2 10 15:00
These guidelines are, however, very general; you'll need to modify them slightly based on your fitness level. With that in mind, suppose you do three HIIT sessions per week. You might opt to do all three at a 1:5 work: rest ratio the first week, and then switch to a 1:2 ratio for the second week. Or, you could add another interval each week. Finally, you could perform each session for the week at a different intensity. That's one of the beauties of Maximum Muscularity: flexibility. Just be sure to change your protocol of choice every few weeks. Following the bout of HIIT, a brief (i.e. 5-15 minutes) session of low-intensity aerobics might work to enhance fat loss. It appears that inadequate blood flow to adipose tissue during high-intensity exercise is the culprit behind reduced fat oxidation (26). As a result, immediately upon cessation of high-intensity exercise, there is a marked increase in the concentration of plasma free fatty acids (2). By exercising at an intensity that relies primarily on the use of plasma fatty acids (i.e. less than 60% of heart rate reserve), you will maximize adipose tissue lipolysis and fat oxidation. On HIIT days, the same schedule (i.e. time of training) need not be followed, but the same diet plan should be preserved. Again, it?s important to remember that high-intensity aerobic exercise (i.e. HIIT) is very heavily glycogen-dependent and can be much more depleting that resistance training. Significant glycogen depletion can occur with a mere 15-30 minutes of exercise performed at very high intensities (i.e. 90-130% of VO2max), which is similar to the protocol that is followed in HIIT-style training (12). Therefore, you should not be at all leery about maintaining your carbohydrate intake after HIIT sessions. We recommend one complete day of rest from exercise per week. On this activity-free day, you should focus on consuming mostly meals of protein, fats, and fibrous veggies, as described above. That said, on this day, a breakfast of protein and carbs is warranted in most cases, particularly for those who are focusing on gaining muscle mass. Lastly, if your primary goal is muscle growth, you may choose to limit the frequency of HIIT to 1-2 sessions per week. Additionally, for these same individuals, the frequency of the lower intensity aerobic sessions may be reduced or the sessions themselves shortened. With HIIT completing the training mix, here's what your sample split might look like:
Upon Rising HIIT Weight training*
Monday: 20-45 minutes --- Late Afternoon
Tuesday: 20-45 minutes --- Late Afternoon
Wednesday: --- Sprints ---
Thursday: 20-45 minutes --- Late Afternoon
Friday: 20-45 minutes --- Late Afternoon
Saturday: --- Sprints ---
Sunday: Relax. Kill, cook and eat furry woodland creatures.
*Note: Weight training sessions may be followed by 5-15 minutes of low-intensity aerobics. *Topping off the Tank...Some individuals may find that after a period of time following these guidelines that glycogen stores are not adequately topped off. Increasing the carbohydrate content of the protein and carb meals and/or increasing overall caloric intake can circumvent this dilemma. However, these increases are not feasible for some, particularly those in a hypoenergetic state who are using this plan as a vehicle for fat loss. That said, many individuals might find that a day of higher carbohydrate intake is needed once every 6-12 days. Obviously, this is a very broad range due to individual differences, so it may take some trial and error (start with every twelfth day). As a rule of thumb, the leaner you are, the more frequently you should carb up. Rather than engaging in an uncontrolled overfeed (consisting of refined, processed, sugary carbs), simply increase the number of protein and carb meals. These meals should be very similar in composition to those that you utilize on a daily basis (healthy carb sources). We encourage you to implement this day of reglycogenation following a weight training session; ideally, the training session would be performed early in the day (i.e. after one protein and fat meal) and be followed by 3-5 protein and carb meals containing 60-100g of carbohydrate each. Total carbohydrate intake will vary based on frequency of reglycogenation periods (i.e. degree of depletion) and activity level on that particular day. To maximize glycogen restoration, a carbohydrate intake of 3-5g/kg of lean body mass is a good starting point; more or less may be optimal. All in all, you'll need to pay close attention to your response to varying levels of carbohydrate intake, as well as varying frequencies of high-carb days. You will, however, still see comparable results if you opt to incorporate the increased carb intake on a rest day (breakfast should be the largest meal, and carb should slowly be tapered off as the day progresses). This higher carb day will prove beneficial in that it will be very anti-catabolic and will fill up muscle glycogen stores. More importantly for some, it will help to quell any possible mental cravings. Implementing the reglycogenation strategy in a relatively glycogen-depleted state will actually make possible more glycogen storage than if glycogen is restored on a daily basis (27). More glycogen = more energy. More energy = harder training. Harder training = more muscle and less fat. *Supplements...Although the Maximum Muscularity plan does not require extensive supplementation, several supplements will increase its efficacy. With that in mind, we recommend: 1) BCAAs: These anti-catabolic amino acids will definitely prove valuable in the morning before the fasted-state activity and during your regular HIIT sessions. Xtreme Formulations' ICE is an excellent choice in this regard, as it also offers an appreciable dose of glutamine. 2) Nootropic: Marc McDougal outlined various nootropic supplements recently in his article, "This is Your Brain on Drugs". It goes without saying that many of these agents will enhance focus throughout the day ? especially during training sessions - and will help to create the vision of Maximum Muscularity that will keep you going! 3) Glucose disposal agents, particularly R-ALA: These are excellent complements to the protein and carb meals following training as well as the periodic high-carb days. We highly recommend R-lipoic acid (R-ALA) at a dosage of 100mg per 50g carbohydrates consumed in a meal. The capsules should be taken 20-30 minutes prior to the meal. In general, the brands of regular old-school ALA are racemic mixture products; they include both the R+ (naturally occurring form) and S- (synthetic form) isomers. R-ALA has proven more effective than its synthetic counterpart in promoting appropriate glucose disposal in skeletal muscle (28-30). This natural form is, however, pricier, so if cost is an issue or you just happen to have some old stuff kicking around, rest assured that the racemic (traditional) mixtures of ALA will still prove valuable (28,31,32). In short, with improved glucose disposal and enhanced insulin sensitivity, you'll be storing more carbs as glycogen and promoting anabolism. 4) Yohimbine: Increasing circulating catecholamines via supplementation or exercise results in elevated thermogenesis. Unfortunately, circulating norepinephrine (NEP) is not selective in the receptors to which it binds. While NEP binding to beta receptors stimulates thermogenesis, bindings to alpha 2 receptors trigger a negative feedback response that inhibits further NEP release. Because alpha 2 receptors are activated at low catecholamine levels (32), this phenomenon is most applicable at rest. Therefore, full-force thermogenesis may never be in effect! One way to overcome the alpha-inhibition of lipolysis is to ingest ephedrine and/or caffeine to increase circulating catecholamines, although this potential solution only reduces alpha-induced inhibition of lipolysis to a moderate degree (33). Yohimbine, as a selective alpha 2 receptor antagonist, is the key to maximizing lipolysis (34). By binding and antagonizing alpha 2 receptors, yohimbine inhibits the NEP negative feedback loop. Therefore, by maximizing circulating catecholamines, you also maximize thermogenesis and lipolysis. An added benefit of yohimbine is increased peripheral blood flow (35,36). Blood flow to adipose tissue is necessary to transport free fatty acids in the bloodstream (after the breakdown of triglycerides in adipose tissue) to tissues for oxidation in the mitochondria. Activation of the alpha receptors (via NEP) causes vasoconstriction, and, consequently, less blood flow, to peripheral tissues (37,38). In this respect, yohimbine's ability to inhibit the activation of alpha receptors provides maximal peripheral blood flow. Note: We are speaking of the yohimbine alkaloid from the yohimbe herb (similar to ephedrine being the active alkaloid in ephedra). Therefore, we recommended that you choose the hydrochloride version (i.e. Yohimbine HCl) over the herbal yohimbe in order to ensure purity and avoid unknown side effects of other alkaloids in the same family. If you choose the to go the herbal route, be sure to verify that you are dealing with a reputable company that lists the standardization for yohimbine on the label. The appropriate dosage for Yohimbine HCl is 0.2mg/kg (35,36), with smaller dosages providing less favorable results. A final word of caution: insulin completely blunts the lipolytic actions of yohimbine. Therefore, you should only ingest it before the low-intensity aerobic sessions and at times well separated from carbohydrate-containing meals. 5) Green Tea: This tasty beverage not only gives you a versatile option from water, but it also offers several other benefits of which you can take advantage. Green tea is now being recognized for a plethora of health benefits including those as an anti-oxidant, cholesterol lowering, antidepressant, capillary-strengthening and lipolysis-enhancing agent. As mentioned above, it may also act as a glycemic modifier in that it slows carbohydrate absorption. However, there?s even more exciting benefits than that. Recent research demonstrated that subjects who supplemented with a green tea extract containing 90 mg epigallocatechin gallate (EGCG) and 50mg caffeine three times daily resulted in a 4% greater energy expenditure and significantly lower respiratory quotient (i.e. greater fat oxidation) compared to subjects that consumed 50mg of caffeine alone or subjects that received a placebo (39). The fact that the subjects receiving the green tea extract experienced these benefits and the caffeine group did not clearly illustrates the inherent benefits of the EGCG, which is thought to be the most pharmacologically active catechin polyphenol in green tea. In light of this data, we recommend drinking 5-10 cups of green tea daily, either decaffeinated or caffeinated depending on the timing of ingestion. Obviously, these supplements should serve as an addendum to your everyday supplements: multivitamin, antioxidants, protein powder, EFAs, and creatine. Beyond these specific recommendations, feel free to include other supplements as your budget allows. Conclusion The physique enhancement strategies set forth in the Maximum Muscularity plan are based on thorough evaluation scientific literature and anecdotal evidence. You'll be optimizing the hormonal milieu to control catabolism and anabolism, manipulating macronutrient and caloric intake for various activities, and paying close attention to nutrient timing as it relates to substrate utilization and storage. Beyond just offering an avenue to aesthetic improvements, Maximum Muscularity is a long-term perspective that enables you to achieve and maintain optimal health status regardless of the short-term goal. Rejoice, Rugged-Brethren! The old-school days of uncomfortable overfeeding followed by painstaking underfeeding are over! The stratagem to getting Huge and Ripped is now reality more than ever. All you have to provide is the determination and effort. References 1. Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, & Wolfe RR. Regulation of fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol 1993 Sep;265(3 Pt 1):E380-91. 2. Rasmussen BB, Holmback UC, Volpi E, Morio-Liondore B, Paddon-Jones D, Wolfe RR. Malonyl coenzyme A and the regulation of functional carnitine palmitoyltransferase-1 activity and fat oxidation in human skeletal muscle. J Clin Invest 2002 Dec;110(11):1687-93. 3. Sweetman, SC (ed). Martindale: The Complete Drug Reference. Pharmaceutical Press: London, 2002. 4. Dulloo AG, Geissler CA, Horton T, Collins A, & Miller DS. Normal caffeine consumption: influence on thermogenesis and daily energy expenditure in lean and postobese human volunteers. Am J Clin Nutr. 1989 Jan;49(1):44-50. 5. Horowitz, JF, Mora-Rodriguez R, Byerley LO, Coyle EF. Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. Am J Physiol 1997 Oct;273(4 Pt 1):E768-75. 6. Montain SJ, Hppoer MK, Coggan AR, Coyle EF. Exercise metabolism at different time intervals after a meal. J Appl Physiol. 1991 Feb;70(2):882-8. 7. Nair KS, Halliday D, & Garrow JS. Thermic response to isoenergetic protein, carbohydrate or fat meals in lean and obese subjects. Clin Sci (Lond). 1983 Sep;65(3):307-12. 8. Day JL, et al. (1978). Factors governing insulin and glucagon responses during normal meals. Clin Endocrinol (Oxf). 1978 Nov;9(5):443-54. 9. Schade DS, & Eaton RP. Modulation of fatty acid metabolism by glucagon in man. I. Effects in normal subjects. Diabetes. 1975 May;24(5):502-9. 10. Dorgan J, et al. Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. Am J Clin Nutr 64(6): 850-855. 1996. 11. Howarth, NC, E Saltzman, SB Roberts. Dietary fiber and weight regulation. Nutr Rev. 2001 May;59(5):129-39. Review. 12. Lowery, L. Temporal Nutrition, Part 1. Testosterone Magazine. 21 Mar 2003. http://www.t-mag.com/nation_articles/253temp.jsp. 13. Baechle, TR, & Earle, RW. Essentials of Strength and Conditioning: 2nd Edition. Human Kinetics, 2000. 14. Essen-Gustavsson B, & Tesch PA. Glycogen and triglyceride utilization in relation to muscle metabolic characteristics in men performing heavy-resistance exercise. Eur J Appl Physiol Occup Physiol. 1990;61(1-2):5-10. 15. Keizer HA, et al. Influence of liquid and solid meals on muscle glycogen resynthesis, plasma fuel hormone response, and maximal physical working capacity. Int J Sports Med. 1987 Apr;8(2):99-104. 16. Bourghouts LB, & Keizer HA. Exercise and insulin sensitivity: a review. Int J Sports Med. 2000 Jan;21(1):1-12. Review. 17. Zhang J, & Kashket S. Inhibition of salivary amylase by black and green teas and their effects on the intraoral hydrolysis of starch. Caries Res. 1998;32(3):233-8. 18. Lee YS. The effects of various intensities and durations of exercise with and without glucose in milk ingestion on postexercise oxygen consumption. J Sports Med Phys Fitness. 1999 Dec;39(4):341-7. 19. Parker DC, & Rossman LG. Human growth hormone release in sleep: nonsuppression by acute hyperglycemia. J Clin Endocrinol Metab. 1971 Jan;32(1):65-9. 20. Phelain, JF, Reinke E, Harris MA, & Melby CL. Postexercise energy expenditure and substrate oxidation in young women resulting from exercise bouts of different intensity. J Am Coll Nutr. 1997 Apr;16(2):140-6. 21. Bahr R, & Sejersted OM. Effect of intensity of exercise on excess postexercise O2 consumption. Metabolism. 1991 Aug;40(8):836-41. 22. Smith J, & McNaughton L. The effects of intensity of exercise on excess postexercise oxygen consumption and energy expenditure in moderately trained men and women. Eur J Appl Physiol Occup Physiol. 1993;67(5):420-5. 23. Tremblay A, Simoneau JA, & Bouchard C. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism. 1994 Jul;43(7):814-8. 24. Gorostiaga, EM, Walter CB, Foster C, & Hickson RC. Uniqueness of interval training at the same maintained exercise intensity. Eur. J. Appl. Physiol. 1991;63:(2)101?107. 25. Hill JO, Heymsfield SB, McMannus C 3rd, & DiGirolamo M. Meal size and thermic response to food in male subjects as a function of maximum aerobic capacity. Metabolism 1984 Aug;33(8):743-9. 26. Samra JS, et al. Effects of epinephrine infusion on adipose tissue: interactions between blood flow and lipid metabolism. Am J Physiol. 1996 Nov;271(5 Pt 1):E834-9. 27. Goforth HW Jr, Arnall DA, Bennett BL, & Law PG. Persistence of supercompensated muscle glycogen in trained subjects after carbohydrate loading. J Appl Physiol. 1997 Jan;82(1):342-7. 28. Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, & Tritschler HJ. Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Am J Physiol 1997 Jul;273(1 Pt 1):E185-91. 29. Saengsirisuwan V, Kinnick TR, Schmit MB, & Henriksen EJ. Interactions of exercise training and lipoic acid on skeletal muscle glucose transport in obese Zucker rats. J Appl Physiol 2001 Jul;91(1):145-53. 30. Moini H, Tirosh O, Park YC, Cho KJ, & Packer L. R-alpha-lipoic acid action on cell redox status, the insulin receptor, and glucose uptake in 3T3-L1 adipocytes. Arch Biochem Biophys 2002 Jan 15;397(2):384-91. 31. Jacob S, Henriksen EJ, Schiemann AL, Simon I, Clancy DE, Tritschler HJ, Jung WI, Augustin HJ, & Dietze GJ. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung. 1995 Aug;45(8):872-4. 32. Jacob S, Henriksen EJ, Tritschler HJ, Augustin HJ, & Dietze GJ. Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid. Exp Clin Endocrinol Diabetes. 1996;104(3):284-8. 33. Arner P, Kriegholm E, et al. Adrenergic regulation of lipolysis in situ at rest and during exercise. J Clin Invest. 1990 Mar;85(3):893-8. 34. Goldberg MR, & Robertson D. Yohimbine: a pharmacological probe for study of the alpha 2-adrenoreceptor. Pharmacol Rev. 1983 Sep;35(3):143-80. Review. 35. Berlan M, Galitzky J, Riviere D, et al (1991). Plasma catecholamine levels and lipid mobilization induced by yohimbine in obese and non-obese women. Int J Obes. 1991 May;15(5):305-15. 36. Galitzky J, Taouis M, Berlan M, Riviere D, et al. Alpha 2-antagonist compounds and lipid mobilization: evidence for a lipid mobilizing effect of oral yohimbine in healthy male volunteers. Eur J Clin Invest. 1988 Dec;18(6):587-94. 37. Millet L, Barbe M, Lafontan M, Berlan M, Galitzky J. Catecholamine effects on lipolysis and blood flow in human abdominal and femoral adipose tissue. J Appl Physiol. 1998 Jul;85(1):181-8. 38. Ruffolo RR, Bondinell W, Hieble JP. Alpha- and beta-adrenoceptors: from the gene to the clinic. 2. Structure-activity relationships and therapeutic applications. J Med Chem. 1995 Sep 15;38(19):3681-716. Review. 39. Dulloo, AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Chantre P, & Vandermander J. Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans. Am J Clin Nutr. 1999 Dec;70(6):1040-5.
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Maximum Muscularity

By Tim Skwiat and Eric Cressey Typically, whenever a trainee aspiring to improve his physique utters, "I want to gain muscle and lose fat...", he is immediately greeted by eager critics from opposite ends of the spectrum. First, there are those experts that pounce on the opportunity to suppress such a bold quest. They proclaim that such a task is doomed for failure, and simply respond with an unscientific, "You can't. Choose one or the other." In contrast, there are those that say that such a mission is rather simple. While the former cynics are just downright ignorant, the latter faction is just as useless, offering no other advice than one must train hard and eat right. Uh, duh! With that in mind, we'd like to introduce a plan that we feel will lead to what many call the Holy Grail of Bodybuilding: Maximum Muscularity. The term "Maximum Muscularity" elicits a beautiful vision of the classic physique of someone like Arnold or Serge Nubret. Maximum Muscularity isn't just about being ripped...yet of beanpole proportions, nor is it just about being huge--yet uncomfortably rotund. Rather, Maximum Muscularity is fusion of the two: being Ripped and Huge; it's about becoming a walking, super-sized anatomy chart. It's about pushing the envelope of one's capabilities to add muscle and lose fat. In a broad sense, the ultimate goal of Maximum Muscularity is to gain muscle mass and lose fat mass. However, the principles of Maximum Muscularity also apply to gaining muscle while keeping bodyfat constant OR to losing fat while maintaining all hard-earned muscle--both scenarios involve a drop in percent body fat. The context in which you view the aforementioned goals is paramount to the realization of these favorable scenarios. Rather than asking "How do I gain muscle and lose fat at the same time?", we ask you to ponder, "How do I gain muscle and lose fat in the same training period?" Our reasoning is very simple; at any given moment in time, the body is either in a state of anabolism (i.e. tissue-synthesizing: muscle or fat gain) or catabolism (tissue-destroying: breakdown of triglyceride, glycogen or protein stores). This is not to say, however, that one cannot control the shift from anabolism to catabolism or vice versa at various times throughout the day. With the Maximum Muscularity protocol, you will do just that. This approach departs from the traditional Bulk and Cut scheme to which so many trainees adhere. This plan is especially well suited to those individuals who tend to store fat easily and gain more fat than muscle during traditional bulking cycles; it can and should be applied year-round and for long-term purposes. In short, there is absolutely no need to deviate from the Maximum Muscularity plan, as it is easily adapted to suit any physique goal and provides great versatility. Gaining muscle and losing fat in the same training period is the culmination of diligent training and dietary practices. Paramount to achieving this lofty goal is the creation of a superior anabolic state and enhanced insulin sensitivity through various dietary and training measures. From a nutritional standpoint, you'll be paying specific attention to nutrient timing and energy intake to capitalize on and manage your body's hormonal milieu in order to promote muscle gain and fat loss. Likewise, your training protocol is of paramount importance to providing the anabolic and metabolic stimuli necessary to accomplish such a mythical feat. That said, here is a summary of the Maximum Muscularity principles: *(Optional) Kickstart your day with some low to moderate activity (i.e. aerobics) before your first meal of the day. You're going to watch SportsCenter anyway, right? Why not jump on a treadmill or bike for 20-45 minutes while taking in the "Plays of the Week?" On the other hand, if infomercials and cooking shows suit your fancy, then we recommend you shell out five payments of $49.95 for "Saggy Man Breasts for Dummies;" you probably aren't cut out for Maximum Muscularity. This activity is, of course, optional and by no means needs to be done indoors. Intensity should be kept at 40-60% of heart rate reserve. At this low intensity, the majority of energy will be derived from plasma fatty acids (i.e. broken down from adipose tissue) (1) and will give your metabolism a brief kick in the pants without sacrificing precious lean body mass (1). Prior to these low-intensity sessions, one can utilize stimulants (i.e. caffeine and ephedrine) and other fat mobilizers (i.e. yohimbine). These implements will enable you to maximize adipose tissue lipolysis without worrying about any unfavorable consequences in terms of insulin sensitivity and glucose disposal, as these sessions will not be followed immediately by carbohydrate-laden meals. The half-life of caffeine is broadly defined as 3-7 hours, depending on dosage and activity (exercise decreases this time period) (3). Assuming that you are leaving adequate time (i.e. 5 hours) between your morning java wave and any carbohydrate-containing meal, consumption of caffeine in the morning should not be problematic. Also of note, researchers have noted a 3-4% increase in metabolic rate in the 2.5 hours following ingestion of 100mg caffeine (4). We don't know about you, but we're all for maximizing our metabolic rates during the time of day where lipolysis is highest! *Stoking the Fat-Burning Inferno...Consume protein and fat meals (a small amount of carbs from fibrous, low-calorie vegetables is encouraged with these meals) in the hours leading up to training. The caloric value of these meals should be at or slightly below what you would be eating at these times during a traditional maintenance phase. This allows you to keep insulin at bay and blood glucose stable, thus permitting an optimal environment for lipolysis. Ingesting a substantial amount of carbs, and the resulting insulin response, inhibits lipolysis both at rest (4) and during exercise (5,6). This same elevation in insulin will also suppress release of growth hormone (GH)), another critical player in our quest for Maximum Muscularity. Since most of you work jobs that demand little high-intensity activity, your energy needs will be most efficiently met by the metabolism of fat. Because fat can provide 2 ? times as much energy as carbohydrate per gram, it is the optimal substrate at low levels of oxygen consumption (e.g. napping at work or during class). Protein and fat meals with very few carbs are beneficial in several other regards in these low-energy expenditure scenarios. First, such meals keep blood glucose and insulin levels stable, thus ensuring that you avoid episodes of hormonal hunger and dulled mental acuity that are associated with unstable blood glucose, insulin, and serotonin concentrations. In addition, the thermic effect?the amount of calories burned in order to process foodstuffs--of protein is about twice that of carbohydrate and more than three times that of fat (7); thus, by eating more protein, you'll be burning more calories! Also, protein and fat meals stimulate the release of glucagon (8), which ensures that fatty acids are released into the bloodstream for oxidation (9). Furthermore, protein and fat meals--along with ample amounts of fiber from low-carb, fibrous veggies that accompany these meals--slow digestion and offer far more satiety per gram than carbohydrates. By setting fat intake at a minimum of 0.5g/lb LBM, you'll be supporting endogenous testosterone levels and all the good stuff (e.g. libido, strength) that goes along with them (10). Assuming that you're balancing out your mono/poly/saturate intake, you'll also be deriving some cardiovascular health benefits (among others). While you're probably at least somewhat cognizant of the myriad of benefits of polyunsaturated fats--namely omega-3s--it is critical that you do not overlook the formidable cardioprotective benefits of monounsaturated fats (i.e. olive oil, mixed nuts, etc.). Be sure to get plenty of fibrous veggies (e.g. broccoli, cauliflower, spinach) with these meals for fiber and other important nutrients. Howarth et al. recently demonstrated a decrease of 10% in daily caloric intake and a loss of 4.2 pounds in subjects that consumed an additional 15g of fiber daily over a period of four months! (11) We encourage you to emphasize whole-foods whenever possible to maximize satiety and the thermic effect of your feedings. We want to reiterate the fact that Maximum Muscularity emphasizes maximizing nutrient intake via whole-food sources. * Maximum Muscularity and Density...There are countless solid training programs to suit your goals; there's no excuse for not having the aforementioned anabolic stimulus for impressive size and strength gains. When choosing a program, however, recall that some styles of training are less suitable for improving glucose tolerance and insulin sensitivity. Specifically, the aforementioned carbohydrate metabolism factors are negatively affected by training that focuses on heavy negatives/long eccentrics (12). In light of the fact that we're constantly striving to maximize these critical factors and use them to our advantage, you'll definitely want to adapt your training accordingly (i.e. lowering carbohydrate intake during training periods that emphasize eccentrics, if you choose to include them at all). Ideally, you should be in the gym for 3-5 sessions per week. An added bonus of training in the late afternoon is that you increase the likelihood of maintaining constantly high testosterone levels throughout the day. Testosterone levels are typically highest in the morning and gradually decrease as the day progresses; by interrupting this decline with exercise-induced increases, you may be able to overcome this aspect your body's natural hormonal milieu (13). The importance of the resistance-training component of the plan cannot be overemphasized. However, it's beyond the scope of such a comprehensive article to prescribe a new routine or training program. Rather, we direct you to consider the works of Charles Poliquin, Ian King, Don Alessi, Brian Haycock, Charles Staley, Dave Tate, Christian Thibaudeau, Chad Waterbury, Joel Marion, and John Romaniello. * You may find it advantageous to follow up your resistance training session with 5-15 minutes of low- to moderate-intensity aerobic exercise, preferably a full-body mode (i.e. Elliptical trainer or jogging). The purpose of this aerobic session is to gorge those muscles that were just trained with blood. This massive blood flow will assist recovery by: 1) removing waste products from the muscles, 2) transporting nutrients and oxygen to the muscles, and 3) shuttling metabolic by-products (i.e. lactic acid) from the muscle to the liver for recycling (i.e. gluconeogenesis). Two added benefits: more energy expenditure and glycogen utilization, which creates a greater glucose economy, allows for more carbohydrate to be eaten in the recovery period, and enhances glucose uptake and skeletal muscle insulin sensitivity- critical factors for improvement in body composition. Be forewarned, though, that even at low and moderate intensities, if the aerobic components cause the exercise sessions to carry on too long (i.e. greater than 75 minutes), they may very well do more harm than good over an extended period of time. As such, it's important to keep you resistance training sessions to 60 minutes or less. Several factors, however, are contraindications (in most cases) to performing post-training aerobic activity; most notable among these factors are excellent pre-existing insulin sensitivity and high volume strength-training programs. * The High-Octane Refuel- Resistance training can be heavily reliant on muscle glycogen and carbohydrate for fuel (14), while intense interval training can be even more taxing on the body's carbohydrate reserves (15). Therefore, during and after the training bouts are the most opportune times to capitalize on excellent insulin sensitivity and enhanced glucose uptake where you desire it most: skeletal muscles (16). Here's where individual differences strongly come into play; this portion of the plan needs to be altered according to one's training and physique goals, as carbohydrate recommendations are going to be vital to achieve optimal results. Most individuals either handle carbs well or poorly. Likewise, most individuals are primarily geared toward fat loss or muscle gain. With respect to the latter case, we have stated that the primary goal of this plan is to accomplish both. Nonetheless, choose from the following recommendations relative to your primary training goals and carbohydrate tolerance. For those individuals with poor insulin sensitivity and a predisposition to easy fat storage, a single meal of protein and carbs should be consumed following training. While it is well established that liquid nutrition (e.g. Relentless, Vendetta) is an excellent choice as a post-training recovery meal, this meal can be either whole-food (i.e. solid) or liquid (i.e. Relentless). Due to the fact that carbohydrate is restricted to a single meal, one may opt for a food source over a liquid source. In the event that the whole-food route is chosen, one should consume BCAAs and glutamine (i.e. ICE) during training. This meal should contain approximately 50g of carbohydrate (about 0.6-0.7g/kg lean body mass) and adequate protein to meet daily needs. Alternatively, if you are looking primarily to pack on slabs of ripped muscle and/or handle carbs very well, then we recommend you approach the mid/post-training window more aggressively. It goes without saying that nutrition during and immediately after training is optimal for building muscle. With this in mind, we recommend that you consume a serving of Vendetta or 1/2 serving of Relentess during and another one-half serving of Relentless immediately after training. You lean folk have already established outstanding insulin sensitivity and are in the quest of the optimal anabolic/anti-catabolic environment. Therefore, approximately one hour after the post-training liquid meal, we recommend an additional protein and carb meal. This meal is not for the timid or carbophobics; rather, the carbohydrate content of this meal should range from 1.0-2.5g/kg of lean body mass. This is a rather large range, but our recommendation is to push the envelope; if you are hesitant to utilize such a carb intake, begin with the lower end of the range and gradually add over a few weeks if fat gain is not apparent. The protein content of this meal should be 0.5-1.25g/kg of lean body mass. The carb sources in all of the whole-food protein and carb meals (either one or two) should be comprised of low to moderate GI/II sources (i.e. oats, yams, whole-grain/mixed-grain bread, beans, fruits, etc). Also of benefit to lower the glycemic and insulinemic response to the carbohydrate would be to include extra fiber (i.e. veggies) and a high quality vinegar or lemon juice. Consume plenty of water with your high-carb meals?as well as throughout the day?because for every 1g of glycogen stored in the muscle, 2.7g of water are stored along with it. We advise you to drink at least 24 oz. of water/fluid with each meal. Adding lemon juice to your H20 is also a good idea, as doing so will not only offer flavor without calories, but also because it may act as glycemic modifier (i.e. lower glycemic response). Drinking decaf green tea may also help to slow down carbohydrate absorption (17), as well as provide other excellent benefits (see below). We offer further advice in the supplement section as to how you might be able to further increase muscle glucose uptake and improve the insulin response to the meal. * You should consume protein and fat meals following the last protein and carb meal and continue them until the next training session. Make sure that at least two hours have elapsed after your last protein and carb meal before resuming protein and fat meals. However, there is no problem in ending the day with a protein and carb meal. These carbs will not interfere with fat loss (18) and will actually decrease recovery time. Contrary to popular belief, there seems to be NO inhibition of sleep-induced growth hormone release with acute hyperglycemia (19). Nevertheless, if you are still concerned over the issue of growth hormone release and insulin, then allowing about 90 minutes after eating the meal to go to sleep should be adequate to calm your nerves. To these individuals who train later and consume the protein and carb meals as their last (i.e. going without a meal for 90 minutes before sleeping), we strongly recommend a serving of Ultra Peptide upon awakening in the middle of the night. There's no need to set an alarm, though. Just drink an extra liter of water before you hit the sack and you-ll wake up on your own. With these recommendations in mind, a sample day's diet might look something like this: Breakfast: Eggs/Egg whites with Salad, olive/flaxseed oil, fish oil, vinegar, lemon juice Mid Morning: Turkey, broccoli, nuts, vinegar, lemon juice Lunch: Tuna, spinach, olive/flaxseed oil, vinegar, lemon juice Mid-Afternoon: Steak, green beans, fish oil Train: Appropriate pre/mid/post training drink (e.g. ICE, Vendetta, Relentless) Dinner:
For those prioritizing growth and those with good carb tolerance: Chicken, Yams, Salad, vinegar, lemon juice or For those prioritizing fat loss and those with poor carb tolerance: Steak, salad, olive/flaxseed oil, vinegar, lemon juice
Before Bed: Cottage Cheese, Xtreme Ultra Peptide, Natural Peanut Butter 2AM trip to the can (optional): Xtreme Ultra Peptide *Note: Protein intake should be set at 4.0-4.5g/kg of lean body mass In Part 2, Tim and Eric will discuss how to integrate training into the dietary considerations outlined above. References 1. Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, & Wolfe RR. Regulation of fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol 1993 Sep;265(3 Pt 1):E380-91. 2. Rasmussen BB, Holmback UC, Volpi E, Morio-Liondore B, Paddon-Jones D, Wolfe RR. Malonyl coenzyme A and the regulation of functional carnitine palmitoyltransferase-1 activity and fat oxidation in human skeletal muscle. J Clin Invest 2002 Dec;110(11):1687-93. 3. Sweetman, SC (ed). Martindale: The Complete Drug Reference. Pharmaceutical Press: London, 2002. 4. Dulloo AG, Geissler CA, Horton T, Collins A, & Miller DS. Normal caffeine consumption: influence on thermogenesis and daily energy expenditure in lean and postobese human volunteers. Am J Clin Nutr. 1989 Jan;49(1):44-50. 5. Horowitz, JF, Mora-Rodriguez R, Byerley LO, Coyle EF. Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. Am J Physiol 1997 Oct;273(4 Pt 1):E768-75. 6. Montain SJ, Hppoer MK, Coggan AR, Coyle EF. Exercise metabolism at different time intervals after a meal. J Appl Physiol. 1991 Feb;70(2):882-8. 7. Nair KS, Halliday D, & Garrow JS. Thermic response to isoenergetic protein, carbohydrate or fat meals in lean and obese subjects. Clin Sci (Lond). 1983 Sep;65(3):307-12. 8. Day JL, et al. (1978). Factors governing insulin and glucagon responses during normal meals. Clin Endocrinol (Oxf). 1978 Nov;9(5):443-54. 9. Schade DS, & Eaton RP. Modulation of fatty acid metabolism by glucagon in man. I. Effects in normal subjects. Diabetes. 1975 May;24(5):502-9. 10. Dorgan J, et al. Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. Am J Clin Nutr 64(6): 850-855. 1996. 11. Howarth, NC, E Saltzman, SB Roberts. Dietary fiber and weight regulation. Nutr Rev. 2001 May;59(5):129-39. Review. 12. Lowery, L. Temporal Nutrition, Part 1. Testosterone Magazine. 21 Mar 2003. http://www.t-mag.com/nation_articles/253temp.jsp. 13. Baechle, TR, & Earle, RW. Essentials of Strength and Conditioning: 2nd Edition. Human Kinetics, 2000. 14. Essen-Gustavsson B, & Tesch PA. Glycogen and triglyceride utilization in relation to muscle metabolic characteristics in men performing heavy-resistance exercise. Eur J Appl Physiol Occup Physiol. 1990;61(1-2):5-10. 15. Keizer HA, et al. Influence of liquid and solid meals on muscle glycogen resynthesis, plasma fuel hormone response, and maximal physical working capacity. Int J Sports Med. 1987 Apr;8(2):99-104. 16. Bourghouts LB, & Keizer HA. Exercise and insulin sensitivity: a review. Int J Sports Med. 2000 Jan;21(1):1-12. Review. 17. Zhang J, & Kashket S. Inhibition of salivary amylase by black and green teas and their effects on the intraoral hydrolysis of starch. Caries Res. 1998;32(3):233-8. 18. Lee YS. The effects of various intensities and durations of exercise with and without glucose in milk ingestion on postexercise oxygen consumption. J Sports Med Phys Fitness. 1999 Dec;39(4):341-7. 19. Parker DC, & Rossman LG. Human growth hormone release in sleep: nonsuppression by acute hyperglycemia. J Clin Endocrinol Metab. 1971 Jan;32(1):65-9.
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Fishy Advice, Part II

By Eric Cressey

It's time to pick up where I left off last month in Part I.  To "reset" the stage, I'll just say that fish oil is good because it helps with:

Crohn's Disease:

  • Belluzzi et al (1996) found that 2.7 g of fish oil per day for one-year significantly reduced the incidence of relapse in Crohn's patients in remission. Thirty-nine of the patients received the fish oil, while 39 others received a placebo; the relapse rate was 41% lower in the former group. Regression analysis indicated that the positive effects of fish oil were independent of patient age, sex, previous surgery history, disease duration, and smoking status (34).

Ulcerative Colitis:

  • Barbosa et al (2003) hypothesized that omega-3 fatty acids from fish oil tend to exert their anti-inflammatory effects in ulcerative colitis via decreases in plasma oxidative stress, acting as free radical scavengers (35).
  • In a study of eighteen patients with active ulcerative colitis (characterized by diarrhea and rectal inflammation; ain't that a pretty picture?), four months of 5.4 g combined EPA and DHA supplementation (vs. placebo) led to significantly "reductions in rectal dialysate leukotriene B4 levels, improvements in histologic findings, and weight gain (36)." English translation: their rectums looked, felt, and performed better.


  • Nagakura et al (2000) found that ten months of EPA and DHA supplementation lessened asthma symptoms and acetylcholine sensitivity in 29 children with severe bronchial asthma (in collaboration with a controlled environment and diet) (37).
  • Three weeks of 5.4 g combined EPA and DHA markedly blunted exercise-induced asthma in ten elite athletes and improved post-exercise pulmonary function significantly (38).

Cystic Fibrosis:

  • In a study of thirty cystic fibrosis patients that received EPA and DHA supplementation as 1.3% of their total calories for eight months, researchers noted significant decreases in markers of inflammation. Subtle improvements in forced expiratory volume (a measure of pulmonary function) were noted as well. Furthermore, in comparison with the previous eight-month period, the patients (collectively) required much fewer days (392 vs. 721) of antibiotic therapy during the eight months on EPA and DHA (39).

Chronic Obstructive Pulmonary Disease (COPD):

  • Shahar et al (1994) examined the relationship between dietary omega-3 fatty acid intake and COPD in 8,960 smokers, finding that combined EPA and DHA intake was "inversely related to the risk of COPD in a quantity-dependent fashion (40)." In other words, if you're going to smoke, you might as well complement that metallic cough with some fish breath; it'll probably protect you from COPD down the road.
  • Romieu and Trenga (2001) observed that "data also suggest that omega-3 fatty acids may have a potentially protective effect against airway hyperreactivity and lung function decrements" in both children and adults (41).

Sickle Cell Anemia:

  • In patients with sickle cell disease, omega-3 fatty acid supplementation at 0.1 g/kg per day "reduced the frequency of pain episodes requiring presentation to the hospital from 7.8 events during the preceding year to 3.8 events/year." Conversely, subjects receiving dietary olive oil (the control group) experienced 7.1 pain events/year, only slightly less than the 7.6 event average from the previous year. This reduction in pain episodes was likely attributable to the effects of EPA and DHA on reducing prothrombotic activity (42).
  • A study of Nigerian children found that omega-3 fatty acid concentrations were 40-50% lower in the phospholipid membranes of children with sickle cell disease than in those of healthy children. The researchers noted that "the phospholipids of the children with SCD are less fluid relative to those of their healthy counterparts. (43)"

Menstrual Symptoms:

  • In a Danish study, low intakes of omega-3 fatty acids were correlated with more severe menstrual symptoms. Dysmenorrhea correlations were also observed in low omega-3: omega-6 ratios and vitamin B12 deficiencies. The body utilizes omega-3s to create type-3 prostaglandins that are less "aggressive" than those formed from other fatty acids. The net result of utilizing omega-3s as raw materials appears to be milder symptoms. Prostaglandins act like hormones, controlling uterine contractions and pains (44).

Vision/Eye problems (glaucoma):

  • Ninety days of DHA with vitamins E and B significantly improved computerized visual field (CVF) and retinal contrast sensitivity in thirty chronic glaucoma patients. The researchers concluded that such a supplement merits inclusion in an intervention to prevent the progression of glaucoma-related damage (45).

Multiple Sclerosis:

  • Cunnane et al (1989) found that in comparison with their healthy counterparts, MS patients had lower omega-3 fatty acids in their plasma (46).
  • As a follow-up, Gallai and colleagues (1995) found that omega-3 supplementation in MS patients led to decreases in proinflammatory eicosanoids, indicating potential for fish oil in modulating some immune function decrements associated with MS (47).

Prenatal and postpartum support:

  • Supplementation with DHA between the 24th and 28th week of pregnancy significantly increased (by roughly six days on average) the duration of gestation. Birth weight, length, and head circumference all increased slightly as well (48).
  • A study of Norwegian children found that "use of cod liver oil in the first year of life was associated with a significantly lower risk of type 1 diabetes." Regression analysis implied that this effect was independent of the oil's vitamin D content, and was likely due to the omega-3 fatty acids in the oil (49).
  • Malcolm et al (2003) noted an association between "the DHA status of infants at term and early postnatal development of the pattern-reversal VEP [visual evoked potential], indicating that DHA status itself may influence maturation of the central visual pathways" in infants. These assertions were based on results seen in a trial of one hundred women that received either fish oil capsules or a placebo (50).
  • Uauy and colleagues (2003) found not only that long chain polyunsaturated fatty acid supplementation in newborns improved visual acuity at four months, but also there was "a significant relation between the total DHA equivalents provided and effectiveness (51)." In other words, more was better (to a certain point, of course). This effect is likely due to effects on physical properties of the membranes, neurotransmitters, and modulation of gene expression in the retina and brain (52).
  • Because of the crucial role of essential fatty acids as structural components of all cell membranes, profound implications can be seen at the "brain, retina and other neural tissues are particularly rich in long-chain polyunsaturated fatty acids (LC-PUFA) (52)."
  • Uauy et al (2001) asserted that "light sensitivity of retinal rod photoreceptors is significantly reduced in newborns with n-3 fatty acid deficiency, and that docosahexaenoic acid (DHA) significantly enhances visual acuity maturation and cognitive functions (52)." Furthermore, "DHA also has significant effects on photoreceptor membranes and neurotransmitters involved in the signal transduction process; rhodopsin activation, rod and cone development, neuronal dendritic connectivity, and functional maturation of the central nervous system (52)." It beats feeding potato chips to your kids, doesn't it?
  • Data from Dunstan et al (2003) suggests that there may be a role for omega-3 fatty acids in the prevention of allergic disease. In a study of 83 atopic pregnant women receiving fish oil or placebo, the researchers noted that infants from the fish oil group had significantly less severe atopic dermatitis at age one, although no difference in the frequency of the disease was apparent between groups (53).
  • Williams and colleagues (1995) described preeclampsia (affecting pregnant women) as "a systemic disease characterized by diffuse endothelial dysfunction, increased peripheral vascular resistance, coagulation abnormalities, antioxidant deficiency, persistent elevations of maternal leukocyte-derived cytokines, and hyperlipidemia (54)." These researchers conducted a study to examine the relationship between omega-3 fatty acid intake and preeclampsia. Women with the lowest omega-3 levels were 7.6 times more likely than those with the highest levels to have preeclampsia-related complications during their pregnancies. Moreover, "a 15% increase in the ratio of omega-3 to omega-6 fatty acids was associated with a 46% reduction in risk of preeclampsia (54)."


  • Psoriatic lesions are characterized by increased concentrations of arachidonic acid. EPA exerts an anti-inflammatory effect that likely works to counteract the pro-inflammatory effects of arachidonic acid and its metabolites. In a study of 83 patients with chronic plaque-type psoriasis, researchers found that omega-3 fatty acid infusions were superior to omega-6 infusions (the placebo) "with respect to change in severity of psoriasis per body area, change in overall erythema, overall scaling and overall infiltration, as well as change in overall assessment by the investigator and self-assessment by the patient (55)."
  • Grimminger et al (1993) observed that high dose intravenous omega-3 fatty acid supplementation exerted a rapid beneficial effect on inflammatory skin lesions in twenty patients hospitalized with acute guttate psoriasis. These effects were most likely mediated through eicosanoid metabolism regulation (56).


  • Hydroa vacciniforme ?also known as photosensitivity ? is a serious skin disorder characterized by blistering (especially on the face) after even the slightest amount of sun exposure; it affects primarily children. In a small study, Rhodes and White reported that three months of fish oil supplementation reduced erythemal sensitivity to UVA and UVB (two types of ultraviolet radiation), and yielded modest improvements in overall symptoms (57).

Diabetes/Insulin Resistance:

  • Increased oxidative stress is a hallmark of type 2 diabetes. Jain et al (2002) sought to determine the effects of very low dose omega-3 fatty acid supplementation (0.6 g combined EPA and DHA) on type 2 diabetics. Even at such a low dose, they found that the patients in the omega-3 group exhibited significantly greater improvements in glycemic status, blood pressure, lipid profiles, and reductions in markers of oxidative stress as compared to a placebo group of type 2 diabetics (58).
  • It's well established that the various types of fatty acids are clearly involved in the onset of chronic conditions (such as insulin resistance and obesity) characterized by inflammation. In overweight subjects, higher concentrations of saturated fats and omega-6 and lower concentrations of omega-3 fatty acids are significantly associated with higher concentrations of circulating interleukin-6 (IL-6), a marker of inflammation. Interestingly, though, these associations are not apparent in lean subjects (59).
  • In a 14-year study of 84,204 female nurses ages 34-59, the risk of type 2 diabetes was significantly positively associated with high consumptions of trans fatty acids and cholesterol, whereas the condition was negatively associated with omega-3 and omega-6 polyunsaturated fatty acids. The investigators estimated that "replacing 2% of energy from trans fatty acids isoenergetically with polyunsaturated fat would lead to a 40% lower risk" of type 2 diabetes (60). I guess it's time to replace the doughnuts in the nurses' lounge with canned salmon. Or, you could contact Krispy Kreme about introducing the chocolate frosted sardine filled doughnut!
  • Chicco et al (1996) found that low-dose fish oil supplementation in rats led to significant reductions in blood lipids and plasma insulin levels without changes in glucose tolerance. The investigators hypothesized that because no changes in pancreatic insulin content were apparent, the lower insulin levels may have been due to improvements in peripheral insulin sensitivity (61).
  • Unfortunately, studies attempting to demonstrate these effects in humans have been less impressive (62-64). In spite of the fact that omega-3 consumption in the form of fish increased HDL cholesterol and improved overall dyslipidemia in overweight patients, Mori et al (1999) found no independent effect of fish consumption on glucose or insulin (62). Others have come to similar conclusions with actual fish oil supplementation (63,64).

Resting Metabolic Rate:

  • Eric Noreen has done extensive work examining the effect of fish oil on resting metabolic rate (RMR). At the 2003 American College of Sports Medicine Annual Conference, Noreen presented the results of a study that compared RMR in subjects supplemented with 9g of safflower oil (predominately omega-6), 3, 6, or 9g of 60% concentrated fish oil. The fish oil groups saw daily RMR increases of 141 to 448 calories, whereas the safflower group's RMR actually decreased. As an added bonus, the fish oil group also lost a little bit of fat mass while gaining some lean body mass. (65)

Body Composition Regulation and Leptin:

  • Leptin is a hormone released by adipocytes that has a great impact on body fat levels. In simple terms, the amount of leptin present in one's body serves as feedback to the brain about whether one is okay as far as nutritional status is concerned. As you get leaner, leptin levels drop; as you get pudgier, they go up. These are important responses, as high leptin concentrations are associated with decreased hunger and food intake and increased energy expenditure, all of which are important factors in getting and staying lean.
  • Unfortunately, as you get leaner, leptin levels drop as your body essentially senses starvation-like conditions; this decrease makes it difficult to get and stay lean. Fish oil may be able to help with this problem, as rats fed high omega-3 diets demonstrate up-regulation in plasma leptin concentrations significantly above what is predicted based on body fat levels (66,67).
  • In an overfeeding study of rats with 42% of their energy intakes as fish oil, safflower oil, olive oil, or beef tallow, the fish oil group had the greater lean body mass gains and the lowest fat mass gains (68). In other words, if you're going to stuff yourself, be sure to include some fish oil in the feast.

Psychological Disorders:

  • Maes et al (1999) observed that there is a significant deficiency in omega-3 fatty acids serum phospholipids and red blood cell membranes in major depression. Furthermore, the deficiency is likely a result of abnormal omega-3 metabolism in depressed patients and may continue in spite of treatment with antidepressants (69). As such, fish oil treatment may serve as an important adjunct to ? or even a replacement for - traditional antidepressant therapy
  • Hibbeln and Salem (1995) proposed that low concentrations of polyunsaturated fatty acids may be related to increased risks of suicide, depression, alcoholism, and post-partum depression (70).
  • Four out of five trials of EPA in the treatment of schizophrenia have demonstrated significant reduction in patient episodes of severe mania and depression following supplementation (71).
  • In an eight-week study of 28 clinically depressed patients receiving either 9.6 g omega-3 fatty acids per day or a placebo, there were significant decreases in scores on the Hamilton Rating Scale for Depression, an evaluative tool on which high scores indicate more severe feelings of depression (72).
  • Zanarini and Frankenburg (2003) studied the effects of 1 g/day ethyl-EPA (or placebo) on thirty females with borderline personality disorder. The ethyl-EPA supplement proved "to be superior to placebo in diminishing aggression as well as the severity of depressive symptoms (73)."
  • Attention-deficit/hyperactivity disorder (ADHD) may be related to an abnormality in polyunsaturated fatty acid metabolism. As such, both Richardson and Puri (2000) and Kidd (2000) have proposed that omega-3 fatty acid supplementation may have merits in the treatment of this condition, although more research is warranted in this regard (74,75).

The Response to Stress:

  • Here's one for the Type A folks out there. Delarue et al (2003) studied seven subjects on two occasions separated by three weeks. In the first session, these seven individuals were subjected to mental stress in the form of mental arithmetic and the Stroop task, and measures of sympathoadrenal activation (plasma cortisol, catecholamines, energy expenditure, and adipose tissue lipolysis) were taken thirty minutes after the stress. After this mental stress challenge, each subject supplemented with 7.2 g fish oil/day for three weeks, at which point they took the battery of tests again. In this second session, plasma epinephrine, cortisol, energy expenditure, and plasma non-esterified fatty acids concentrations, were all significantly lower than in the initial session. The investigators therefore concluded that omega-3 fatty acid supplementation "inhibits the adrenal activation elicited by a mental stress, presumably through effects exerted at the level of the central nervous system (76)." It appears that omega-3 fatty acids are able to partially inhibit the pro-inflammatory response to psychological stress (77). Ever get a racing heart or high blood pressure before a test, presentation, or job interview? Fish oil may be just what you need to get mellow!

Migraine Headaches:

  • In a study of 27 adolescents with chronic migraines, supplementation with fish oil led to reductions of 87% in headache frequency, 74% in headache duration, and 78% in headache severity compared to a period prior to the study. Interestingly, olive oil (the placebo) produced similar results, although they were not quite as favorable (78).


  • Many anticonvulsant medications for epileptics have highly undesirable side effects. In light of the profound roles of omega-3 fatty acids in immune and nervous system activities, Rabinovitz and colleagues (2004) compared the effects of carbamazepine (CBZ) and SR-3, a compound with a 1:4 omega-3: omega-6 ratio, on seizure control efficiency, and protection against cognitive impairment and cortisol elevation in rats. While the two treatments were equally effective in controlling seizures, SR-3 proved to be superior on the latter two measures (79). Treating epilepsy with omega-3 compounds is certainly a new frontier, so more research is warranted (especially in human subjects) to determine its true efficacy.

Chronic Fatigue Syndrome (CFS):

  • The exact cause of CFS remains to be determined, but there is speculation that it could involve abnormalities at the immune, neuroendocrine, and autonomic levels. Because fish oil inhibits the production of certain pro-inflammatory substances, many experts believe that it holds great potential in the treatment of CFS. Research is ongoing (80).


  • Several experts predict a role for omega-3 fatty acids in the treatment of fibromyalgia; anecdotal evidence supports this assertion, and further research is certainly warranted on this front (81).


  • In chronic liver disease, widespread inflammation can cause the liver to become fibrotic. In light of the known anti-inflammatory benefits of omega-3 fatty acids, Hayashi et al (1999) studied the effect of EPA and DHA supplementation on four patients with hepatitis B infection, one with hepatitis C virus cirrhosis, and one with alcohol-related cirrhosis. Subtle reductions were observed in globulin (a marker of liver pathology) with simultaneous increases in HDL cholesterol and various apolipoproteins (protective agents against hepatitis-related liver disease) (82).

Closing Thoughts

If you aren't taking fish oil, you're an idiot. Seriously. Okay, I'll leave you with a bit more practical wisdom instead. The typical fish oil capsule you'll encounter is 1000 mg fish oil; we, however, are more concerned with the EPA and DHA content of that 1000 mg. In most cases, you'll find 180 mg EPA and 120 mg DHA per capsule. A good rule of thumb (especially based on the results of the clinical trials) is to consume 3-6 g combined EPA and DHA per day; at this capsule size, you'd need 10-20 capsules per day. For this reason, liquid fish oil is a great alternative.

A small percentage of people will suffer from fish burps with the EPA/DHA supplementation; if you're one of those individuals, I recommend you take all your fish oil with your last meal of the day. That way, if you have salmon belches, they'll be in your sleep! Another alternative is to just eat fatty fish every day, but that can get old very quickly! Finally, be patient! Read the finer details of all of the studies that I've outlined and you'll realize that the majority of them were at least 6-8 weeks in duration (usually longer). Your body needs time to make good use of these healthy raw materials, so count on a few months before you see noticeable results if you have one of the aforementioned conditions. For the rest of you, you probably won't notice much, but I guarantee that you'll be healthier in the long run. References (continued) 34. Belluzzi A, Brignola C, Campieri M, Pera A, Boschi S, Miglioli M. Effect of an enteric-coated fish-oil preparation on relapses in Crohn's disease. N Engl J Med. 1996 Jun 13; 334(24): 1557-60. 35. Barbosa DS, Cecchini R, El Kadri MZ, Rodriguez MA, Burini RC, Dichi I. Decreased oxidative stress in patients with ulcerative colitis supplemented with fish oil omega-3 fatty acids. Nutrition. 2003 Oct;19(10):837-42. 36. Stenson WF, Cort D, Rodgers J, Burakoff R, DeSchryver-Kecskemeti K, Gramlich TL, Beeken W. Dietary supplementation with fish oil in ulcerative colitis. Ann Intern Med. 1992 Apr 15;116(8):609-14. 37. Nagakura T, Matsuda S, Shichijyo K, Sugimoto H, Hata K. Dietary supplementation with fish oil rich in omega-3 polyunsaturated fatty acids in children with bronchial asthma. Eur Respir J. 2000 Nov;16(5):861-5. 38. Mickleborough TD, Murray RL, Ionescu AA, Lindley MR. Fish oil supplementation reduces severity of exercise-induced bronchoconstriction in elite athletes. Am J Respir Crit Care Med. 2003 Nov 15;168(10):1181-9. Epub 2003 Aug 06. 39. De Vizia B, Raia V, Spano C, Pavlidis C, Coruzzo A, Alessio M. Effect of an 8-month treatment with omega-3 fatty acids (eicosapentaenoic and docosahexaenoic) in patients with cystic fibrosis. JPEN J Parenter Enteral Nutr. 2003 Jan-Feb;27(1):52-7. 40. Shahar E, Folsom AR, Melnick SL, Tockman MS, Comstock GW, Gennaro V, Higgins MW, Sorlie PD, Ko WJ, Szklo M. Dietary n-3 polyunsaturated fatty acids and smoking-related chronic obstructive pulmonary disease. Atherosclerosis Risk in Communities Study Investigators. N Engl J Med. 1994 Jul 28;331(4):228-33. 41. Romieu I, Trenga C. Diet and obstructive lung diseases. Epidemiol Rev. 2001;23(2):268-87. 42. Tomer A, Kasey S, Connor WE, Clark S, Harker LA, Eckman JR. Reduction of pain episodes and prothrombotic activity in sickle cell disease by dietary n-3 fatty acids. Thromb Haemost. 2001 Jun;85(6):966-74. 43. Glew RH, Casados JK, Huang YS, Chuang LT, VanderJagt DJ. The fatty acid composition of the serum phospholipids of children with sickle cell disease in Nigeria. Prostaglandins Leukot Essent Fatty Acids. 2002 Oct;67(4):217-22. 44. Deutch B. [Painful menstruation and low intake of n-3 fatty acids]. Ugeskr Laeger. 1996 Jul 15;158(29):4195-8. [Article in Danish] 45. Cellini M, Caramazza N, Mangiafico P, Possati GL, Caramazza R. Fatty acid use in glaucomatous optic neuropathy treatment. Acta Ophthalmol Scand Suppl. 1998; (227): 41-2. 46. Cunnane SC, Ho SY, Dore-Duffy P, Ells KR, Horrobin DF. Essential fatty acid and lipid profiles in plasma and erythrocytes in patients with multiple sclerosis. Am J Clin Nutr. 1989 Oct;50(4):801-6. 47. Gallai V, Sarchielli P, Trequattrini A, Franceschini M, Floridi A, Firenze C, Alberti A, Di Benedetto D, Stragliotto E. Cytokine secretion and eicosanoid production in the peripheral blood mononuclear cells of MS patients undergoing dietary supplementation with n-3 polyunsaturated fatty acids. J Neuroimmunol. 1995 Feb;56(2):143-53. 48. Smuts CM, Huang M, Mundy D, Plasse T, Major S, Carlson SE. A randomized trial of docosahexaenoic acid supplementation during the third trimester of pregnancy. Obstet Gynecol. 2003 Mar;101(3):469-79. 49. Stene LC, Joner G; Norwegian Childhood Diabetes Study Group. Use of cod liver oil during the first year of life is associated with lower risk of childhood-onset type 1 diabetes: a large, population-based, case-control study. Am J Clin Nutr. 2003 Dec;78(6):1128-34. 50. Malcolm CA, McCulloch DL, Montgomery C, Shepherd A, Weaver LT. Maternal docosahexaenoic acid supplementation during pregnancy and visual evoked potential development in term infants: a double blind, prospective, randomised trial. Arch Dis Child Fetal Neonatal Ed. 2003 Sep;88(5):F383-90. 51. Uauy R, Hoffman DR, Mena P, Llanos A, Birch EE. Term infant studies of DHA and ARA supplementation on neurodevelopment: results of randomized controlled trials. J Pediatr. 2003 Oct;143(4 Suppl):S17-25. 52. Uauy R, Hoffman DR, Peirano P, Birch DG, Birch EE. Essential fatty acids in visual and brain development. Lipids. 2001 Sep;36(9):885-95. 53. Dunstan JA, Mori TA, Barden A, Beilin LJ, Taylor AL, Holt PG, Prescott SL. Fish oil supplementation in pregnancy modifies neonatal allergen-specific immune responses and clinical outcomes in infants at high risk of atopy: A randomized, controlled trial. J Allergy Clin Immunol. 2003 Dec;112(6):1178-84. 54. Williams MA, Zingheim RW, King IB, Zebelman AM. Omega-3 fatty acids in maternal erythrocytes and risk of preeclampsia. Epidemiology. 1995 May; 6(3): 232-7. 55. Mayser P, Mrowietz U, Arenberger P, Bartak P, Buchvald J, Christophers E, Jablonska S, Salmhofer W, Schill WB, Kramer HJ, Schlotzer E, Mayer K, Seeger W, Grimminger F. Omega-3 fatty acid-based lipid infusion in patients with chronic plaque psoriasis: results of a double-blind, randomized, placebo-controlled, multicenter trial. J Am Acad Dermatol. 1998 Apr;38(4):539-47. 56. Grimminger F, Mayser P, Papavassilis C, Thomas M, Schlotzer E, Heuer KU, Fuhrer D, Hinsch KD, Walmrath D, Schill WB, et al. A double-blind, randomized, placebo-controlled trial of n-3 fatty acid based lipid infusion in acute, extended guttate psoriasis. Rapid improvement of clinical manifestations and changes in neutrophil leukotriene profile. Clin Investig. 1993 Aug;71(8):634-43. 57. Rhodes LE, White SI. Dietary fish oil as a photoprotective agent in hydroa vacciniforme. Br J Dermatol. 1998 Jan;138(1):173-8. 58. Jain S, Gaiha M, Bhattacharjee J, Anuradha S. Effects of low-dose omega-3 fatty acid substitution in type-2 diabetes mellitus with special reference to oxidative stress--a prospective preliminary study. J Assoc Physicians India. 2002 Aug;50:1028-33. 59. Fernandez-Real JM, Broch M, Vendrell J, Ricart W. Insulin resistance, inflammation, and serum fatty acid composition. Diabetes Care. 2003 May;26(5):1362-8. 60. Salmeron J, Hu FB, Manson JE, Stampfer MJ, Colditz GA, Rimm EB, Willett WC. Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr. 2001 Jun;73(6):1019-26. 61. Chicco, A., D'Alessandro, M. E., Karabatas, L., Gutman, R., and Lombardo, Y. B. Effect of moderate levels of dietary fish oil on insulin secretion and sensitivity, and pancreas insulin content in normal rats. Ann Nutr Metab 40(2), 61-70. 1996. 62. Mori, T. A., Bao, D. Q., Burke, V., Puddey, I. B., Watts, G. F., and Beilin, L. J. Dietary fish as a major component of a weight-loss diet: effect on serum lipids, glucose, and insulin metabolism in overweight hypertensive subjects. Am J Clin Nutr 70(5), 817-25. 1999. 63. Rivellese AA, Maffettone A, Iovine C, Di Marino L, Annuzzi G, Mancini M, Riccardi G. Long-term effects of fish oil on insulin resistance and plasma lipoproteins in NIDDM patients with hypertriglyceridemia. Diabetes Care. 1996 Nov;19(11):1207-13. 64. Woodman RJ, Mori TA, Burke V, Puddey IB, Watts GF, Beilin LJ. Effects of purified eicosapentaenoic and docosahexaenoic acids on glycemic control, blood pressure, and serum lipids in type 2 diabetic patients with treated hypertension. Am J Clin Nutr. 2002 Nov;76(5):1007-15. 65. Berardi, J. The Real World (of Physique Research), Part 3. Testosterone Magazine. 8 Aug 2003. http://www.t-mag.com/nation_articles/273real.jsp. 66. Cha, M. C. and Jones, P. J. Dietary fat type and energy restriction interactively influence plasma leptin concentration in rats. J Lipid Res 39(8), 1655-60. 1998. 67. Peyron-Caso E, Taverna M, Guerre-Millo M, Veronese A, Pacher N, Slama G, Rizkalla SW. Dietary (n-3) polyunsaturated fatty acids up-regulate plasma leptin in insulin-resistant rats. J Nutr. 2002 Aug;132(8):2235-40. 68. Su W, Jones PJ. Dietary fatty acid composition influences energy accretion in rats. J Nutr. 1993 Dec;123(12):2109-14. 69. Maes M, Christophe A, Delanghe J, Altamura C, Neels H, Meltzer HY. Lowered omega3 polyunsaturated fatty acids in serum phospholipids and cholesteryl esters of depressed patients. Psychiatry Res. 1999 Mar 22;85(3):275-91. 70. Hibbeln JR, Salem N Jr. Dietary polyunsaturated fatty acids and depression: when cholesterol does not satisfy. Am J Clin Nutr. 1995 Jul;62(1):1-9. 71. Peet M. Eicosapentaenoic acid in the treatment of schizophrenia and depression: rationale and preliminary double-blind clinical trial results. Prostaglandins Leukot Essent Fatty Acids. 2003 Dec;69(6):477-85. 72. Su KP, Huang SY, Chiu CC, Shen WW. Omega-3 fatty acids in major depressive disorder. A preliminary double-blind, placebo-controlled trial. Eur Neuropsychopharmacol. 2003 Aug;13(4):267-71. 73. Zanarini MC, Frankenburg FR. omega-3 Fatty acid treatment of women with borderline personality disorder: a double-blind, placebo-controlled pilot study. Am J Psychiatry. 2003 Jan;160(1):167-9. 74. Richardson AJ, Puri BK. The potential role of fatty acids in attention-deficit/hyperactivity disorder.Prostaglandins Leukot Essent Fatty Acids. 2000 Jul-Aug;63(1-2):79-87. Review 75. Kidd PM. Attention deficit/hyperactivity disorder (ADHD) in children: rationale for its integrative management. Altern Med Rev. 2000 Oct;5(5):402-28. Review 76. Delarue J, Matzinger O, Binnert C, Schneiter P, Chiolero R, Tappy L. Fish oil prevents the adrenal activation elicited by mental stress in healthy men. Diabetes Metab. 2003 Jun;29(3):289-95. 77. Maes M, Christophe A, Bosmans E, Lin A, Neels H. In humans, serum polyunsaturated fatty acid levels predict the response of proinflammatory cytokines to psychologic stress. Biol Psychiatry. 2000 May 15;47(10):910-20. 78. Harel Z, Gascon G, Riggs S, Vaz R, Brown W, Exil G. Supplementation with omega-3 polyunsaturated fatty acids in the management of recurrent migraines in adolescents. J Adolesc Health. 2002 Aug;31(2):154-61. 79. Rabinovitz S, Mostofsky DI, Yehuda S. Anticonvulsant efficiency, behavioral performance and cortisol levels: a comparison of carbamazepine (CBZ) and a fatty acid compound (SR-3). Psychoneuroendocrinology. 2004 Feb;29(2):113-24. 80. Tamizi far B, Tamizi B. Treatment of chronic fatigue syndrome by dietary supplementation with omega-3 fatty acids--a good idea? Med Hypotheses. 2002 Mar;58(3):249-50. 81.Ernst E. Complementary and alternative medicine in rheumatology. Baillieres Best Pract Res Clin Rheumatol. 2000 Dec;14(4):731-49. 82. Hayashi H, Tanaka Y, Hibino H, Umeda Y, Kawamitsu H, Fujimoto H, Amakawa T. Beneficial effect of salmon roe phosphatidylcholine in chronic liver disease. Curr Med Res Opin. 1999;15(3):177-84.
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Fishy Advice: Part I

By Eric Cressey

If you're even remotely up-to-date on your nutrition-for-health reading, you're well aware of the benefits of fish oil. Moreover, if you're anything like me, you've also gone to great lengths--often to no avail--to convince people that they should be taking it even if it does sound "icky." In an effort to save you and I a lot of future time and energy, I've compiled the following for you to share with your relatives, mailman, proctologist, lunchlady, and anyone else with whom you associate that isn't currently "on da fish." Based on undeniable scientific evidence and anecdotal evidence, I strongly encourage you to incorporate into your diet two specific omega-3 fatty acids: eicosapentaenoic acid (EPA) and docosahexanoic acid (DHA), commonly referred to as fish oils. EPA and DHA deficiencies have been linked to problems that include, but are certainly not limited to heart disease, hypertension, arthritis, cancer, immune disorders, chronic intestinal disorders, growth retardation, liver disorders, skin lesions, reproductive failure, visual problems, kidney disorders, and neurological disorders (1). Dietary alpha-linolenic acid can be converted to EPA and DHA in the body for utilization as important raw materials in healthy cell membranes. Significant amounts of alpha-linolenic acid can be found in the following oils: flaxseed, soybean, hempseed, pumpkinseed, canola, wheat germ and walnut. Products such as margarine and shortening that are derived from these oils also contain modest amounts of alpha-linolenic acid. Some nuts and seeds-- butternuts, walnuts, pumpkinseeds, and flaxseeds-- and vegetables (soybeans) are good sources as well (1). However, the conversion of alpha-linolenic acid to EPA and DHA is quite inefficient; estimates place the conversion rates at less than 5-10% for EPA and 2-5% for DHA (2). Lifestyle factors can also negatively influence these conversions. There is also evidence to suggest that females are more efficient at converting linolenic acid than men; this is likely due to increased demands for EPA and DHA during pregnancy and lactation (3). Even if you eat plenty of the aforementioned foods regularly, you still might come up short on EPA and DHA because the fatty acid quality is often degraded due to the typical overprocessing that occurs in commercial production (4). As such, it is best to get your EPA and DHA directly whenever possible. EPA and DHA are commonly referred to as fish oils because coldwater fish are by far the best sources. Although the terms EPA/DHA and fish oils are substituted for one another in writing and conversation, EPA and DHA are actually just two kinds of fatty acids contained in fish oils (5). These fish include, but are not limited to: salmon, mackerel, bluefish, tuna, mullet, herring, anchovy, and sardines. Infants receive plenty of EPA and DHA from their mothers' milk (1). Certainly, eating fish every day isn't appetizing for most people, and drinking human milk after the age of one is neither feasible nor socially acceptable! Plus, the typical vegetarian diet is extremely low in alpha-linolenic acid, so even if conversion was efficient, these individuals would still be coming up short (clinical studies have proven that vegetarians have insufficient levels of EPA and DHA) (2). Luckily, fish oil supplements in both liquid and softgel form are widely available to ensure that EPA and DHA requirements can be met easily. EPA and DHA exert their most powerful effects in an anti-inflammatory role. Arachidonic acid, which is created out of the omega-6 fatty acids in our diets, serves as the building block for certain eicosanoids that control the synthesis of cytokines that are pro-inflammatory and immunoregulatory; when these cytokines are overproduced, chronic inflammatory diseases (and even septic shock) can result. Omega-3 fatty acids, on the other hand, inhibit the production of arachidonic acid--thus preventing the production of certain mediators of inflammation--and serve as the raw materials for a healthier class of eicosanoids with anti-inflammatory properties (6). Given how out-of-whack the typical diet is in terms of the omega-6: omega-3 ratio, it should come as no surprise that the world is as unhealthy as it is! Here is some pretty impressive data on a variety of fronts: Cardiovascular Health/Atherosclerosis/Hyperlipidemia/Hypertension:

  • An eleven year study of 20,557 male U.S. physicians showed that those who consumed fatty fish at least once per week were 52% less likely to suffer a sudden cardiac death than those who only ate it once per month or less (5).
  • The typical Greenland Eskimo diet is devoid of fruits and vegetables and very high in fats from animal sources: not your traditional "heart healthy diet." However, the Eskimos had far lower instances of coronary heart disease (CHD) than a Denmark population of nearly identical ethnical composition (same ancestors). The Eskimo and Danish diets both consisted of a high percentage of calories from fat (39% and 42%, respectively), so why didn't the Eskimos suffer from such CHD like the Danes and everyone else? The secret lay with the types of fat that the Eskimos were eating. The typical Danish diet consisted of 22% of total calories from saturated fat and less than 1% from omega-3 polyunsaturated fatty acids (PUFAs). Meanwhile, only 9% of total calories in the Eskimo diet came from saturated fat. Perhaps more importantly, 4.2% of the Eskimos' total calories came from omega-3 PUFAs (5). Similar trends are readily apparent in coastal villages of Korea and Japan and throughout Scandinavian countries. Not surprisingly, they all rely extensively on coldwater fish in their everyday lives. Need further proof? A recent comparison of two Japanese villages: one fishing, one farming, found that the farming village had eight times more atherosclerotic plaques than their fishing counterparts (7).
  • In a study of 59 patients with diagnosed heart disease, Durrington et al (2001) monitored the effects of 2 g daily of Omacor, a pharmaceutical grade fish oil concentrate. The researchers found that "there was a sustained significant decrease in serum triglycerides by 20-30% and in very low density lipoprotein (VLDL) cholesterol by 30-40% in patients receiving active Omacor at three, six, and 12 months compared either to baseline or placebo (8)."
  • Not only do fish oils lower serum triglycerides and, in high dosages and combination with dietary modifications, low density lipoprotein (LDL) cholesterol, but they also decrease arterial platelet collection, which can lead to dangerous clots (5).
  • Harper and Jacobsen (2001) reported that randomized clinical trials with fish oils "have demonstrated reductions in risk that compare favorably with those seen in landmark secondary prevention trials with lipid-lowering drugs (5)."
  • Following coronary artery bypass surgery with venous grafts, patients that receive 4 g per day of omega-3 fatty acids have a significantly lower risk of graft occlusion (obstruction/closure) (9).


  • There are like 80 bizillion studies out there proving that fish oil reduces blood pressure (although you'll obviously derive greater benefits if you eat right and exercise, too). That said, 4 g omega-3 fatty acids per day is the minimum you'll need to see an improvement (9). You can expect not only reduced blood pressure, but also decreased vascular wall thickness (10). I've included a few more references (11-13) for those of you that either don't believe me or have a lot of time on your hands for extra reading.

Cardiac Arrhythmias:

  • There is significant backing for the assertion that fish oils' antiarrhymthic capacity is the most important. Without sufficient EFAs, the body is forced to make cell membranes out of saturated fatty acids, which yield membranes that are far less elastic. When cardiac cells are made from EFAs (and are thus appropriately elastic), the heart has an easier time returning to a resting state. However, the rigid cell membranes made from saturated fatty acids can cause arrhythmias and alter the cardiac muscle cell contraction (5).

Inflammatory Diseases of Joints and Connective Tissues:

  • In patients with degenerative and inflammatory joint diseases, supplementation with omega-3 fatty acids decreases both the "degradative and inflammatory aspects of chondrocyte metabolism, whilst having no effect on the normal tissue homeostasis (14)."
  • Chondrocytes are the building blocks of articular cartilage and work with the extracellular matrix of collagen and proteoglycans to dissipate forces. If the cartilage is constantly eroding due to chondrocyte degradation, the structure tends to soften as its water content increases. Interventions with omega-3 fatty acids are effective in reducing these negative trends and their related symptoms in most patients with osteoarthritis (15,16).
  • In more than two dozen studies, researchers have found that fish oil supplementation reduces fatigue and stiffness in rheumatoid arthritis (RA) afflicted individuals. In fact, some studies found the effects to be dramatic enough to allow for substantial decreases in nonsteroidal anti-inflammatory drug (NSAID) dosages (16-18). Generally speaking, in trials of 3 g combined EPA and DHA (the minimum recommended dose for RA patients), the benefits of fish oil supplementation were not noticeable until the 12-week mark, so be patient! On a microscopic level, the omega-3 supplementation tended to limit the release of leukotrien B(4) and interleukin 1 from neutrophils and monocytes. In plain English, this means that two inflammation-causing factors were present in lesser quantities (17).
  • RA patients that supplemented with Vitamin E and fish oil showed an even greater decrease in NSAID requirements, indicating a synergistic effect between the two (18).
  • Raynaud's Phenomenon is a vascular disorder that falls under the inflammatory diseases of joints and connective tissues. In this condition, tiny blood vessels that feed the skin periodically contract (called a "vasospasm"), limiting blood flow to the skin. As oxygen deprivation sets in, the skin--especially in the hands and feet--turns white and eventually blue. There is speculation that this phenomenon is due to the body's overreaction to cold, as the body excessively vasoconstricts these arteries to conserve heat. However, while cold atmospheres are most likely to cause a vasospasm, emotional stress can be a causative factor as well. Because omega-3 fatty acids "induce a favorable response to vascular ischemia," they have been investigated as a potential treatment for Raynaud's. DiGiacomo et al (1989) found that fish oil supplementation improved cold exposure tolerance and significantly delayed the onset of vasospasm in Raynaud's patients. Furthermore, this cold tolerance improvement was associated with a significantly increased digital systolic blood pressure in a cold atmosphere (20).
  • Systemic lupus erythematosus (SLE) -- better known simply as lupus - is a chronic, autoimmune rheumatic disease with a wide variety of symptoms. Typically, this disease affects women of childbearing age (21). Symptoms include arthritis, skin rash, vascular inflammation, and profound effects on the central nervous, renal and cardiopulmonary systems (22). Mohan and Das (1997) found that concentrations of EPA and DHA were low in the plasma phospholipids of SLE patients; this supported pre-existing data that EPA and DHA supplementation could lead to clinical remission without side effects (22).
  • In cases of pediatric SLE, dyslipoproteinemia -- essentially high triglycerides, low HDL, and high LDL - is often present. Provision of fish oil supplements has proven effective in significantly improving blood lipid profiles (decreased serum triglycerides concentrations) in these patients beyond dietary intervention alone (24).


  • Two short-term studies have found that a lower omega-6 to omega-3 fatty acid ratio (achieved via omega-3 supplementation) attenuates bone loss in patients with osteoporosis. These effects are likely due to decreases in the production of Prostaglandin E2 (PGE2), an eicosanoid widely implicated in bone resorption (25). Overall eicosanoid balance is largely dependent on fatty acid intake; so it's important to consider both the quantity of omega-3s and omega-6s present.

Kidney Disease/Renal Failure:

  • Researchers at the Mayo Nephrology Collaborative Clinic found that fish oils slowed the progression of immunoglobin A nephropathy in patients at a high risk for kidney disease (26).
  • Omega-3s have shown promise in reducing urinary calcium levels in kidney stone patients and preventing blood clots in hemodialysis patients (26).
  • Hemodialysis patients given fish oil required 16% less erythropoietin while experiencing a 3.6% increase in serum albumin levels in comparison to a placebo group (27).
  • The side effects (such as skin lesions and hyperlipidemia) of cyclosporine, a medication often prescribed for kidney transplant patients, are noticeably less significant when patients supplement with fish oil (28)

Prostate Cancer:

  • A longitudinal study of 6,272 Swedish men showed that those who regularly consumed fish were approximately 50% less likely to be diagnosed with prostate cancer and roughly 70% less likely to die from it than those who avoided fish. Three servings per week appeared to be the minimum amount needed to attain such benefits (29).
  • Augustsson et al (2003) validated the Swedish study with a larger sample size of 47,882, and noted that the strongest association also existed between fish consumption and metastatic cancer (meaning that it's extensive and spreads to other parts of the body via the blood vessels or lymphatic system). Those men that ate fish more than three times per week were 24% less likely to be diagnosed with metastatic cancer (30).

Colon Cancer:

  • Collett et al noted that incidences of colon cancer in rats were reduced significantly with DHA supplementation in the form of fish oil (31).

Breast Cancer:

  • In a five-year prospective study of 35,298 Singapore Chinese women ages 45-74, high levels of dietary omega-3 fatty acids (mostly from shellfish) were associated with a significantly reduced (26% lower) risk of breast cancer (32).

Skin Cancer:

  • In animals, omega-3 fatty acids have been proven effective as protection against photocarcinogenesis, likely due to the fatty acids' ability to combat oxidative stress. Rhodes et al studied the effect of 4 g/day EPA supplementation "on a range of indicators of ultraviolet radiation (UVR)-induced DNA damage in humans, and assessed effect on basal and post-UVR oxidative status" in 42 healthy subjects. The control group received oleic acid, a monounsaturated fatty acid, for the three-month study. Sunburn sensitivity was reduced in the EPA group only; likewise, other early markers of skin cancer diminished significantly with EPA supplementation. These results imply that there was protection against acute UVR-induced damage by dietary EPA; the researchers hypothesized that "longer-term supplementation might reduce skin cancer in humans (33)."

That concludes part one; hopefully, you've picked up some valuable information. Next month, I'll besiege you with another 8,471 references supporting my argument on a variety of different fronts. Stay tuned! References 1. Whitney, E.N. & Rolfes, S.R. Understanding Nutrition: (8th ed.). Belmont, CA: Wadsworth Publishing Company, 1999. 2. Davis BC, Kris-Etherton PM. Achieving optimal essential fatty acid status in vegetarians: current knowledge and practical implications. Am J Clin Nutr. 2003 Sep;78(3 Suppl):640S-646S. 3. Burdge GC, Wootton SA. Conversion of alpha-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. Br J Nutr. 2002 Oct;88(4):411-20. 4. Colgan, M. Optimum Sports Nutrition. New York: Advanced Research Press, 1993. 5. Harper CR, Jacobson TA. The fats of life: the role of omega-3 fatty acids in the prevention of coronary heart disease. Arch Intern Med. 2001 Oct 8;161(18):2185-92. 6. Calder PC. n-3 polyunsaturated fatty acids and cytokine production in health and disease. Ann Nutr Metab. 1997;41(4):203-34. 7. Yamada T, Strong JP, Ishii T, Ueno T, Koyama M, Wagayama H, Shimizu A, Sakai T, Malcom GT, Guzman MA. Atherosclerosis and omega-3 fatty acids in the populations of a fishing village and a farming village in Japan. Atherosclerosis. 2000 Dec;153(2):469-81. 8. Durrington PN, Bhatnagar D, Mackness MI, Morgan J, Julier K, Khan MA, France M. An omega-3 polyunsaturated fatty acid concentrate administered for one year decreased triglycerides in simvastatin treated patients with coronary heart disease and persisting hypertriglyceridaemia. Heart. 2001 May;85(5):544-8. 9. Nordoy A, Marchioli R, Arnesen H, Videbaek J. n-3 polyunsaturated fatty acids and cardiovascular diseases. Lipids. 2001;36 Suppl:S127-9. 10. Engler MM, Engler MB, Pierson DM, Molteni LB, Molteni A Effects of docosahexaenoic acid on vascular pathology and reactivity in hypertension. Exp Biol Med (Maywood). 2003 Mar;228(3):299-307. 11. Passfall J, Philipp T, Woermann F, Quass P, Thiede M, Haller H. Different effects of eicosapentaenoic acid and olive oil on blood pressure, intracellular free platelet calcium, and plasma lipids in patients with essential hypertension. Clin Investig. 1993 Aug;71(8):628-33. 12. Bhatnagar D, Durrington PN.Omega-3 fatty acids: their role in the prevention and treatment of atherosclerosis related risk factors and complications. Int J Clin Pract. 2003 May;57(4):305-14 13. Holm T, Andreassen AK, Aukrust P, Andersen K, Geiran OR, Kjekshus J, Simonsen S, Gullestad L. Omega-3 fatty acids improve blood pressure control and preserve renal function in hypertensive heart transplant recipients. Eur Heart J. 2001 Mar;22(5):428-36. 14. Curtis CL, Rees SG, Cramp J, Flannery CR, Hughes CE, Little CB, Williams R, Wilson C, Dent CM, Harwood JL, Caterson B. Effects of n-3 fatty acids on cartilage metabolism. Proc Nutr Soc. 2002 Aug;61(3):381-9. 15. Curtis CL, Rees SG, Little CB, Flannery CR, Hughes CE, Wilson C, Dent CM, Otterness IG, Harwood JL, Caterson B. Pathologic indicators of degradation and inflammation in human osteoarthritic cartilage are abrogated by exposure to n-3 fatty acids. Arthritis Rheum. 2002 Jun;46(6):1544-53. 16. Cho SH, Jung YB, Seong SC, Park HB, Byun KY, Lee DC, Song EK, Son JH. Clinical efficacy and safety of Lyprinol, a patented extract from New Zealand green-lipped mussel (Perna Canaliculus) in patients with osteoarthritis of the hip and knee: a multicenter 2-month clinical trial. Allerg Immunol (Paris). 2003 Jun;35(6):212-6. 17. Kremer JM. n-3 fatty acid supplements in rheumatoid arthritis. Am J Clin Nutr. 2000 Jan;71(1 Suppl):349S-51S 18. Tidow-Kebritchi S, Mobarhan S. Effects of diets containing fish oil and vitamin E on rheumatoid arthritis. Nutr Rev. 2001 Oct;59(10):335-8. 19. Rennie KL, Hughes J, Lang R, Jebb SA. Nutritional management of rheumatoid arthritis: a review of the evidence. J Hum Nutr Diet. 2003 Apr;16(2):97-109. 20. DiGiacomo RA, Kremer JM, Shah DM. Fish-oil dietary supplementation in patients with Raynaud's phenomenon: a double-blind, controlled, prospective study. Am J Med. 1989 Feb;86(2):158-64. 21. Ioannou Y, Isenberg DA. Current concepts for the management of systemic lupus erythematosus in adults: a therapeutic challenge. Postgrad Med J. 2002 Oct;78(924):599-606. 22. Das UN. Beneficial effect of eicosapentaenoic and docosahexaenoic acids in the management of systemic lupus erythematosus and its relationship to the cytokine network. Prostaglandins Leukot Essent Fatty Acids. 1994 Sep;51(3):207-13. 23. Mohan IK, Das UN. Oxidant stress, anti-oxidants and essential fatty acids in systemic lupus erythematosus. Prostaglandins Leukot Essent Fatty Acids. 1997 Mar;56(3):193-8. 24. Ilowite NT, Copperman N, Leicht T, Kwong T, Jacobson MS. Effects of dietary modification and fish oil supplementation on dyslipoproteinemia in pediatric systemic lupus erythematosus. J Rheumatol. 1995 Jul;22(7):1347-51. 25. Albertazzi P, Coupland K. Polyunsaturated fatty acids. Is there a role in postmenopausal osteoporosis prevention? Maturitas. 2002 May 20;42(1):13-22. 26. Donadio JV. n-3 Fatty acids and their role in nephrologic practice. Curr Opin Nephrol Hypertens. 2001 Sep;10(5):639-42. 27. Vergili-Nelsen JM. Benefits of fish oil supplementation for hemodialysis patients. J Am Diet Assoc. 2003 Sep;103(9):1174-7. 28. Simopoulos AP. Omega-3 fatty acids in health and disease and in growth and development. Am J Clin Nutr. 1991 Sep;54(3):438-63. 29. Terry P, Lichtenstein P, Feychting M, Ahlbom A, Wolk A. Fatty fish consumption and risk of prostate cancer. Lancet. 2001 Jun 2;357(9270):1764-6. 30. Augustsson K, Michaud DS, Rimm EB, Leitzmann MF, Stampfer MJ, Willett WC, Giovannucci E. A prospective study of intake of fish and marine fatty acids and prostate cancer. Cancer Epidemiol Biomarkers Prev. 2003 Jan;12(1):64-7. 31. Collett ED, Davidson LA, Fan YY, Lupton JR, Chapkin RS. n-6 and n-3 polyunsaturated fatty acids differentially modulate oncogenic Ras activation in colonocytes. Am J Physiol Cell Physiol. 2001 May;280(5):C1066-75. 32. Gago-Dominguez M, Yuan JM, Sun CL, Lee HP, Yu MC. Opposing effects of dietary n-3 and n-6 fatty acids on mammary carcinogenesis: The Singapore Chinese Health Study. Br J Cancer. 2003 Nov 3;89(9):1686-92. 33. Rhodes LE, Shahbakhti H, Azurdia RM, Moison RM, Steenwinkel MJ, Homburg MI, Dean MP, McArdle F, Beijersbergen van Henegouwen GM, Epe B, Vink AA. Effect of eicosapentaenoic acid, an omega-3 polyunsaturated fatty acid, on UVR-related cancer risk in humans. An assessment of early genotoxic markers. Carcinogenesis. 2003 May;24(5):919-25.

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Bogus Biomechanics, Asinine Anatomy: Part II

By Eric Cressey

Last month, I covered the five myths that you're bound to come across in any gym during your time in the iron game. This month, five more!

Myth #6: Stance width dictates recruitment of the different muscles of the quadriceps during squats and leg presses. Contrary to what the local self-proclaimed bodybuilding guru might have told you, this is false. Recruitment is more a function of squat depth than width. McCaw and Melrose (1999) demonstrated that although a wider stance will recruit more of the adductors and glutes, it doesn't change the relative contributions of the four muscles of the quadriceps during a squat (1). In other words, the "feet together for the vastus lateralis" and "wide stance for the vastus medialis" concepts simply don't hold water. The vastus medialis is better recruited with terminal knee extension and any movements that send the knee into valgus. Likewise, anecdotally, knee extension exercises from positions of great knee flexion (e.g. deep squats, lunges, and step-ups) preferentially recruit the vastus medialis. This could result from increased activity of the adductor magnus - which also works as a hip extensor – to assist in hip extension from the low position. Research has shown that because the vastus medialis oblique originates on the adductor magnus tendon, increasing adductor magnus activity will enhance vastus medialis recruitment. This is the premise behind many physical therapists recommending straight leg raises with the knee extended and femur adducted to strengthen the vastus medialis; unfortunately, this rehabilitation model isn't functional at all, and therefore doesn't have much value beyond the initial stages of rehabilitation. The next time someone tells you that stance width is what determines quadriceps recruitment, ask him how we classify single leg movements, where there is no such thing as stance width! Myth #7: The "core" consists of just the abs, and can best be trained with crunches. This statement is accepted as gospel in most mainstream muscle magazines, but it's actually way off the mark. The core actually encompasses far more musculature than the rectus abdominus alone; broadly speaking, it extends from the upper torso and neck to the knees, serving as the link between strength and power in the lower and upper body. Clark (2001) put forth perhaps the best functional anatomy breakdown of the core when he divided it into the local (deep) and global (superficial, prominent) musculature (2). The local musculature – including most notably the transverse abdominus and multifidus – functions primarily to stabilize the spine. Much debate has arisen in the strength training and rehabilitation communities in regards to whether or not the local musculature warrants direct training in healthy individuals. Since it's my article, I'm allowed to give my opinion: in healthy individuals, spinal stabilization occurs involuntarily, so direct training is unproductive, and potentially counterproductive, as McGill has pointed out (3). I'd also like to take this opportunity to say that I think it sucks that most canned tuna has soy hidden in it. Oh yeah, this is also a good spot for my prediction of a third Patriots Super Bowl win in four years. Clark further divided the global musculature into the lateral, deep longitudinal, posterior oblique, and anterior oblique "subsystems." All of these subsystems function as a cohesive unit during complex movements (2), but they warrant mention individually to understand how training can be targeted for improving function in one or more. The lateral subsystem involves the interaction of the gluteus maximus, tensor fascia latae, adductors, and quadratus lumborum (think "inner and outer thighs and hips"). This subsystem plays an important role in stabilizing the body in the frontal plane during activities (especially single-leg work) involving the lower body (2). The deep longitudinal subsystem most notably includes the erector spinae, biceps femoris, sacrotuberous ligament, and thoracolumbar fascia; this system is a crucial component of the powerful posterior chain that you've likely heard discussed by numerous strength coaches. Essentially, this subsystem's primary function is to allow forces generated in the lower body to be carried up to the upper body (and vice versa, in less common occurrences) (2). The posterior oblique subsystem also includes the gluteus maximus and thoracolumbar fascia, but this time in collaboration with the contralateral latissimus dorsi (2). You may have heard of the "serape effect," which relates the gluteus maximus and latissimus dorsi during the gait cycle. Basically, both muscles are extensors; when the right arm is extending (thanks to the right lat) during gait, so is the left leg (thanks in part to the left gluteus maximus). By "posterior oblique," we're referring to the back and across nature of this muscular interaction. This subsystem also has implications in transverse plane stability (2). The anterior oblique subsystem consists of the adductors, internal and external obliques, and external rotators of the hips: gluteus maximus, piriformis, obturator internus and externus, gemelli superior and inferior, quadratus femoris, long head of biceps femoris, posterior fibers of the gluteus medius, sartorius, and adductor complex (at certain degrees of hip flexion). Beyond its obvious role in producing rotational motion, this final system is an important part of transverse plane stabilization (2). Myth #8: You can "isolate" muscles in a resistance training context. True muscular isolation is only possible in fine movements like blinking and twitching. In more gross movements and those involving significant external loading, numerous muscles interact as prime movers, synergists, and stabilizers. While some single-joint exercises will allow you to focus more on one muscle than others in concentric, eccentric, and isometric actions, it's simply impossible to truly isolate a muscle. In fact, the concept of isolated muscle action actually has dangerous implications, as elimination of important stabilizers would undoubtedly compromise exercise safety. If you don't believe me when I say that true isolation is impossible, you can continue to try to isolate your medial gastrocnemius while your bandana-sporting, belt wearing, pretty boy training partner screams in your ear about how badass you are. Meanwhile, those of us who know better will just keep to ourselves and do multi-joint exercises that allow for significant external loading, and we'll see who makes better progress. Myth #9: The secret to healthy shoulders is to have a big, strong chest, lats, delts, and "traps." I've heard this one on several occasions, and it never ceases to crack me up. These larger muscles are usually the problems, not the solutions! When you hammer your pecs, lats, anterior delts, and upper traps mercilessly and ignore their antagonists (external rotators, horizontal abductors, scapular retractors, and scapular depressors), unfavorable postures and movement patterns develop. Specifically, the humeri tend to assume an internally rotated resting position and the scapulae become elevated, winged and anteriorly tilted. These changes mechanically decrease the already-narrow subacromial space, increasing the likelihood that the tendons of the rotator cuff will become irritated when the arm is raised. When the rotator cuff is strong, it serves to depress the humeral head in the glenoid fossa so that this impingement doesn't occur. If the SITS muscles (supraspinatus, infraspinatus, subscapularis, and teres minor) are weak relative to these larger muscles, the humeral head translates superiorly excessively; the pain is most prominent in bench pressing and overhead movements. Summarily, the secret to healthy shoulders is to train the antagonists to the "big dogs" in order to foster appropriate strength ratios and maintain ideal resting posture. Myth #10: Calves won't grow without calf raises. In my experience, calf development is perhaps the single-most genetically influenced aspect of weight training. Some guys are born with high calves, and some have thick ankles attached to tree trunks. That's not to say, however, that training and lifestyle factors can't markedly improve the size of one's calves. Yes, I said lifestyle factors! Take a look at any really fat person, and you'll see a great set of calves. The soleus comprises roughly 2/3 of the lower leg musculature, and since it's largely a postural muscle, it tends to hypertrophy in tubby people even if they don't exercise. It may not seem fair to those of you who are putting in the time with hours upon hours of calf raises, but that's life. Speaking of calf raises, they aren't the only way to train calves. The gastrocnemius works not only in plantarflexion, but also in knee flexion. As such, it gets hit hard with glute-ham raises and leg curls. Moreover, plantarflexion is trained heavily in a variety of more compound movements, including Olympic lifts, sprinting, sled dragging, and farmer's walks (with accentuated pushoffs). Sometimes, ignoring the calf raises altogether and focusing on these compound movements is a great way to spark growth "by accident." Or, they can serve as valuable adjuncts to your regimen of seated, standing, leg press, and donkey calf raises. Finally, the tibialis anterior (muscle on the front of the shin) can contribute to lower leg mass; dorsiflexion exercises and downhill running can be effective means of improving in this regard. Conclusion Hopefully, the past two articles have given you some intellectual firepower to call upon the next time you're confronted with these myths. Then again, old myths die hard, so sometimes it's better to just shake the "gurus" off and do your own thing. References 1. McCaw ST, Melrose DR. Stance width and bar load effects on leg muscle activity during the parallel squat. Med Sci Sports Exerc 1999 Mar;31(3):428-36. 2. Clark, M. Performance Enhancement Specialist Online Manual. National Academy of Sports Medicine, 2001.
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Bogus Biomechanics, Asinine Anatomy: Part I

Kinesiology Myths that Need to Die

By Eric Cressey

Call me anal-retentive, but when intelligent, experienced writers make incorrect statements in their publications, it makes me question their credibility. As we all know only too well, myths abound in the area of weight training ("high reps for toning") and nutrition ("protein is evil"). Since the kinesiology and biomechanics realm is my area of expertise, erroneous statements tend to get on my nerves even more. With that in mind, here's my opportunity to vent with respect to ten of those myths.

Myth #1: You can train the "medial deltoids." I always get a kick out of it when some of the most brilliant strength coaches (I can think of at least five) write about training the medial head of the deltoids with lateral raises or some other shoulder-specific exercise. These are some brilliant guys, so I never have the heart to speak up and tell them that "medial deltoids" don't even exist. Incorporating exercises for this imaginary head is not only impossible, but attempting to do so represents a fundamental lack of knowledge of anatomy. The term "medial" is a directional term that means "toward the midline" of, in this case, the body. From the anatomical position - standing, arms at sides, palms supinated (facing forward), the head of the deltoid that is sandwiched between the anterior and posterior deltoid fibers is actually the farthest away from the midline of the body of all of the heads of the deltoid. If anything, it should be called the lateral head! As such, these fibers are referred to as the "middle deltoid," a term that correctly identifies their position between the anterior and posterior deltoid. Myth #2: You can work on your left and right "bicep" and "tricep." These muscles both have more than one head, so you'd be better off saying, "You can work on your left and right biceps and triceps." Now that we've got the terminology down in a broad sense, let's look at the specific anatomy and how one can prioritize certain heads over the others. An important principle of which you should be aware is active insufficiency, a scenario that occurs when a two-joint muscle cannot contribute optimally to concentric action (i.e. shortening) at one joint because it is already shortened at another. In the case at hand, the long head of both the biceps and triceps can be preferentially recruited or excluded (for the most part) by avoiding or encouraging active insufficiency, respectively. The long (lateral) head of the biceps crosses both the elbow and shoulder joint (and the radio-ulnar joint to act as a supinator, but we won't worry about that right now), acting as an elbow and shoulder flexor. To maximally recruit the long head of the biceps, we need to eliminate one of these joint actions. As such, our options are to a) maintain shoulder extension (preferably past neutral) while flexing the elbow joint (e.g. incline curls) and b) flex the shoulder joint while maintaining elbow extension (e.g. front raise). Both scenarios avoid active insufficiency and force the long head of the biceps to bear the brunt of the load. Likewise, if we want to focus our efforts on the short (medial) head of the biceps, we simply flex the elbow with the shoulder flexed (e.g. preacher curls); because the long head of the biceps is already shortened at the shoulder, it can't contribute effectively to elbow flexion. The long head of the triceps also crosses the shoulder and elbow, but it acts in extension at both joints. If you want to overload this head of the triceps, you can a) maintain shoulder flexion while extending the elbow (e.g. overhead or lying extensions) and b) maintain elbow flexion while extending the shoulder (e.g. bent-arm pullover), although the latter option tends to recruit the lats and teres major more extensively. To reduce involvement of the long head of the triceps in favor of overloading the medial and lateral heads, simply extend the elbow with the shoulder extended (e.g. variations of pressdowns and dips). Myth #3: The traps are just the muscles between your shoulders and neck; they can be trained with just shrugs. This is an unfortunate misconception that has led to countless shoulder injuries in anatomy-ignorant lifters. The trapezius is actually a very large muscle that essentially spans from the lumbar spine all the way to the base of the skull. It can be divided into the lower, middle, and upper fibers; each of the three divisions has unique functions, so it's almost easiest to think of them as separate muscles altogether (much like the different heads of the deltoid). The lower fibers are responsible for scapular depression, retraction, and upward rotation. The middle fibers contribute to scapular retraction, elevation, and upward rotation. Finally, the upper fibers contribute to scapular elevation retraction, and upward rotation, and extension, lateral flexion, and contralateral rotation of the neck. Interestingly, as you may have inferred, the different fibers of the trapezius can act as both antagonists (elevation and depression) and synergists (retraction and upward rotation) to each other! Perhaps more importantly, you hopefully can tell that shrugs only directly train scapular elevation and the upper traps, so you need to use a wider variety of exercises to achieve complete trapezius development. If you didn't pick up on that, you're hopeless; go play in traffic. The rest of you should note that the lower and middle trapezius both play crucial roles in maintaining scapular stability and proper posture, two factors with definite implications in terms of overall shoulder health. Myth #4: Close-grip bench presses are good for the "inner" chest. I've read a lot of anatomy books, but I've never come across the inner head of the pectoralis major. There are clavicular (upper) and sternal (lower) fibers, but selective recruitment of these fibers is a function of angle of inclination of the bench and different movement patterns rather than grip width. Bringing your grip closer together will recruit more triceps, though. Myth #5: Your body doesn't know the differences between similar exercises that target similar musculature. I have been surprised to see this coming from a few prominent writers in the bodybuilding and strength and conditioning industries, so I thought this article would be a good place to air my disagreement with such a statement. Essentially (and pardon the stereotype), this is bodybuilding logic. For the most part, in the bodybuilding world, there are only muscles; in the quest to be big, and not strong or proficient at some athletic endeavor, many bodybuilders completely overlook the role of the nervous system in exercise selection. Let's start with the most basic arguments against this logic. As Mel Siff points out, "Subtle differences apparently as insignificant as a change in grip, stance or head position in regular training can cause significant neural changes which control the way in which the athlete executes a given skill (1)." When we change our grip on standing dumbbell curl variations, for instance, we can shift the emphasis within the elbow flexors among the biceps brachii, brachioradialis, and brachioradialis (among other muscles). Like I said, we're starting with the basics, but let's now make our example a bit more complex by comparing a preacher curl and a standing dumbbell curl. As I mentioned before, there are obvious muscular recruitment changes that occur due to the aforementioned active insufficiency of the long head of the biceps with the flexed-humerus position. Likewise, there are implications in terms of force production capabilities. According to Siff,

Many studies indicate that, in all of the diverse isolated single-joint movements, changes in strength apparently depend upon the role and functions of the joint mechanisms and the relative disposition of the body's links relative to one another. Changes in joint angle alter the conditions of muscular work, since muscle length and angle of pull are changed. Muscular strength and leverage change, and consequently, so does the torque (i.e. moment of force) produced by the muscles about a joint (1).

Keep in mind that the above quote only refers to single-joint movement; as I'm sure you can imagine, when multiple joints are involved, recruitment patterns can differ even more dramatically. Because joint angle affects how muscles produce force, there are clear implications in terms of the overall training effect. For instance, at joint orientations, rate of force development (RFD) will be faster than at others; when dealing with athletes, this is an important consideration. Moreover, strength increases over the entire range of motion depend to a large degree on the joint angle in training at which maximum muscular tension is attained (1). If this strongest position is avoided (via partial reps, for example), the magnitude of the strength increases may be compromised.

Now, let's go back to the preacher curl versus standing dumbbell curl example. Not only are recruitment patterns different within the elbow flexor musculature, but contributions (or lack thereof) from the rest of the kinetic chain are also altered. Far more stabilization must take place at multiple joints in the latter exercise because of the standing position and the lack of support for the upper arms. This underscores the importance of basing all training programs on core exercises; they simply involve more musculature and train recruitment patterns that are functional for our daily lives. It also demonstrates the differential training effect of, say, a floor press when compared to a 2-board press. Both have their place in training programs, but the latter involves greater muscle recruitment and loading in a fixed distance traveled by the bar. Now, let's take this a step further. Which is more neurally draining: a 1RM barbell curl or a 1RM deadlift? If you answered "the curl," it's time to start taking your lower body training more seriously. Very simply, the deadlift is more taxing because it requires more work (force times distance) to be done. Increasing both the force and distance components necessitate increased muscular recruitment via increased neural output. One step further: is a full ROM 1RM barbell curl more neurally draining than a ½ curl? Assuming the same weight it utilized, of course (force stays the same, but distance is greater). However, let's assume you can use enough additional weight on the ½ curl to offset the reduction in distance, and the overall work is the same for both exercises. Then, you certainly have a conundrum. In a broad sense, the neural demands are similar; however, differences exist in terms of rate coding and fiber recruitment, depending again on joint orientation. Here's where a lot of folks want to end the discussion (if they're even gotten this far without getting bored or confused). If we've established that subtle variations in exercises won't markedly change the overall impression left on the nervous system, then we can go ahead and bench 52 weeks per year as long as we change our rep ranges and tempo of execution, right? Yes, but since when is lifting weights about "avoiding stagnation," and not about "getting hella beeeg, fast, and strong?" That's right; I'm talking about optimization of training here. Read on… Training has a far more profound impact on the nervous system than just fiber recruitment. Most attention in the literature is focused on the efferent (motor) and not the afferent (sensory, or feedback) component on the nervous system. However, varying exercise selection – just like varying speed of execution, loading, and volume – is crucial to developing afferent pathways as well. Specifically, I'm referring to the joint receptors.

  • Pacinian corpuscles are rapidly adapting receptors that are highly sensitive to vibration frequency, acceleration, and deceleration.
  • Golgi-Mazzoni corpuscles are sensitive to compression of the joint capsule, therefore supplying crucial information to the CNS regarding how close one is to the end of the range of motion.
  • Ruffini endings are sensitive to capsular stretching with respect to speed and direction; this information complements that gathered by the Pascinian corpuscles.
  • Golgi ligament endings are sensitive to tension and stretch on ligaments, whereas free nerve endings (nociceptive and nonnociceptive) may respond to a variety of mechanical and biochemical stimuli (2,3).

The CNS cannot act without information upon which to base its actions, so efficiency of these joint receptors is of paramount importance in determining not only success, but injury prevention (e.g. knowing when to fire a muscle to decelerate a movement). For this reason, re-education of joint receptors should be an important focus in all rehabilitation and prehabilitation programs. The best way to train these receptors is to expose them to a wide variety of speeds, loads, and positions.

The last few paragraphs are just my two cents on the issue, so I suppose calling this one a "myth" is somewhat of a stretch. Conclusion Next month, I'll cover five more myths that need to be banished from weight rooms for the rest of eternity. In the meantime, be leery of everything you hear from the self-proclaimed gurus at your gym. References 1. Siff, M. Supertraining: 6th Edition. Supertraining Group, 2003. 2. Tiberio, D. Unpublished. 2004.
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Baggett of Tricks, Part I: An Interview with “The Truth About Quickness” Author Kelly Baggett

Today, we have an interview with Kelly Baggett, co-author of The Truth About Quickness.  Kelly's one of the brightest guys in the field of strength and conditioning - but I don't need to tell you that, as you'll get the picture very clearly just by reading the interview below.  Check it out!

EC: Thanks for taking the time to talk shop with me, Kelly. Tell me a little bit about yourself; I don't want our readers to think that I just pulled some lunatic off the street for an interview in order to get an article in on time.

KB: I'm 30 years old and work as a performance enhancement specialist with individuals and coaches of all levels, setting up training, nutrition, and supplementation programs to optimize their progress. I've been fortunate to work in many aspects of the fitness, health, and sports training industry since the age of 18. My passion for these fields isn't limited to team sports; rather, it also includes bodybuilding, which, because of the emphasis on body composition management, has enabled me to pick up many things related to nutrition and apply them to the sports training world. I've pretty much always been into one sport or another; at one time or another over the last 20 years, I've been involved in motocross, baseball, football, basketball, bodybuilding, powerlifting, Olympic lifting, martial arts, boxing, and gymnastics. Now that I think about it - pretty much every sport except for golf!

EC: Yeah, I usually get bored after about five holes, too; there needs to be more violence, cheerleaders, and swearing...but I digress. What were the roots of your passions? KB: I've always been partial to the speed and power dominant sports, but in spite of my yearning to be a great athlete, I really struggled as a youngster. Not only was I very small, but I was also really slow: these two qualities don't add up to much! I grew up with a lot of desire for developing the attributes of superior athleticism and plenty of curiosity and dedication to figure out how best to get the job done. These attributes, of course, include qualities like strength, size, speed, power, agility, quick feet, and, of course, "the look." With consistent training, my own athletic attributes really took off and I knew I was onto something. Fortunately, because of the environments in which I've worked, I've been able to apply the knowledge and experience I've gained toward helping others reach their goals. Nonetheless, I realize this is still the very beginning; right now, we're really just getting started with what can be done. When we look at strength and conditioning fifteen years from now, we'll be amazed at just how far we've come; I just want to do my part and contribute to this advancement as much as I can. EC: One of the things that I've always admired about you is your willingness to think outside the box. Where did this unique perspective originate? KB: It's funny that you'd use the phrase "think outside the box," as I hear that quite a bit; a lot of people comment that I seem to dig up answers from all over the place. When it comes to figuring things out, I probably do tend to stray from the more chosen paths. I guess you could say my overall approach of thinking was solidified by some things I've experienced personally. I developed rheumatoid arthritis (RA) at the age of 25 and was basically told that I would be fortunate if I could walk in a few years. The commonly accepted treatment options for RA are drugs with harsh side effects like medications used during chemotherapy treatment and prednisone: drugs that I would have had to take for the rest of my life to help slow the progression of the disease. Based on what I observed and heard from others, the drugs didn't work consistently and the side effects were harsh. So, I decided to take my own path, which led me to explore alternative treatment options and develop an understanding of the disease in order to treat it holistically. To make a long story short (I have definitely had my fair share of struggles), I've never touched any common prescription medications for RA and am stronger now then I was 25. I pretty much carry that mindset into everything I learn and do; I feel that you can learn from anyone or any situation if you just keep an open mind. When you learn something, you have to immerse yourself in it fully. However, to really take advantage of the information and advance, you must back out and look at things from the outside-in, asking yourself, "How can I best use this and is this really the best way to accomplish my objective?" I'm all for science, but I prefer to start backwards; in other words, how can real world observations be explained by science? EC: That's a perspective that I'd like to see a lot of people in the strength and conditioning industry adopt. All too often, strength and conditioning coaches are afraid to try something new and, as a result, wind up making the same mistakes year after year with different athletes. For instance, I'm amazed at how many people still think that boatloads of boring, steady-state aerobic exercise and a low-fat diet are the best ways to lose fat. All these athletes do is become weak, tired, sick, and apathetic with compromised endocrine status. KB: I agree; conditioning for athletes is a very common area of ignorance in today's coaches. Too many coaches and athletes try to make up for poor diet by running their guy into the ground with conditioning. Not enough attention is paid to diet, and I feel not enough coaches are well versed in dietary approaches. Physically, someone like David Boston, although probably too extreme, is a good example of what can be accomplished with excellent combinations of each - training and diet. EC: While we're on the topic, what do you think are the most prominent errors that strength and conditioning coaches make? KB: Before I get to the errors themselves, we ought to reconsider the use of the term "strength and conditioning," coach, which I feel would be better renamed "performance enhancement" coach. The term "strength and conditioning specialist" conveys that as a coach you must either be busting your athletes' asses in the weight room or running them to death on the field. Too many coaches get caught up on the strength aspect when their time would be better spent focusing on means of improving performance. They should be asking themselves how they can best increase the short- and long-term performance of an athlete, and they should be able to tell you exactly why they're training a certain way at a particular time and know exactly how and why what they're doing is going to improve performance. Often, performance can be improved by doing nothing at all: simply allowing recovery to take place. Or, in some cases, focusing on things unrelated to strength and conditioning like basic sports movement patterns can be of tremendous value.

EC: Excellent observation; recovery is unquestionably one of the most misunderstood and underappreciated facets of not only making people bigger, stronger, and faster, but also improving demeanor. Some athletes just need more time off than others, so you have to know when to back off on volume, do some pool work, or just send them home to eat and go to bed. KB: I agree. That statement also underscores the important of recognizing that one athlete's trash is another athlete's treasure; it's important to assess each athlete's needs individually. I can't tell you how many times I've seen football players with near-zero agility, dynamic flexibility, and reactive movement ability spend their entire summer in the weight room doing nothing but pounding the weights in an effort to get stronger with very little return in playing ability. On the other hand, I can't tell you how many basketball players, runners, and cheerleaders I've seen who have struggled for months and years on end trying to develop their skills when their woes could easily be cured by a solid month in the weight room making friends with the iron. So, it's definitely not a one-way street; the coach needs to understand which direction the athlete should go. EC: Any other common errors? KB: Another thing I see a lot that I don't always agree with is coaches and specialists looking a bit too much to the rehab setting for answers when they should be looking to the real world for answers. Now this is totally different for the general population, but when it comes to athletes, I think you have to draw the line and ask a simple question: "What qualities do the best athletes have and how can one gain those qualities?" To sum it up, list the twenty greatest athletes you can think of in the NFL, NBA, soccer, hockey etc. Out of those twenty, how many of them do you think spent significant time being coached in stability training, core activation, functionally correct linear and lateral movement training, etc. in their youth? Now, if your answer is anything like mine, it's going to be "Not very many!" What is it, then, that separates these athletes from the rest? What are the things that we commonly do now - the best methods to develop these attributes? That's what you need to be doing! Now don't get me wrong, there is a time and place for almost everything, but I feel if something isn't working right, then you can go back step-by-step and correct it. You usually can use drills or exercises that are very close to what you would normally do; there's rarely a need to go back all the way and have this athlete performing a workout that would be more fitting for someone coming out of multiple joint replacement surgery. If your car drives pretty good and you want it to go faster, you'd want to put a bigger engine in it before you waste time trying to make it drive absolutely perfect. Moreover, before you go and start modifying an engine with all sorts of fancy gadgets, you better be able to use the engine you do have in the first place.  This is a theme that resounds in our product, The Truth About Quickness.

To illustrate this concept, let me give a couple of examples from some "Rocky" movies. I'm just going to assume everyone reading this has seen "Rocky." Remember how Micky trained Rocky for speed and agility by having him catch chickens? Sometimes you just have to "turn the chicken loose." If you can catch the chicken, you're most likely able to move functionally well enough! However, if you can't catch the chicken, maybe you should initially spend more time focusing on the things that will more DIRECTLY improve your speed and quickness and see where that takes you instead of worrying about all the often excessively complex functional training techniques. EC: It kind of brings to mind how the term "functional movement training" has been bastardized over the past few years. There were some really smart people on the right track with their definitions and explanations initially; now, commercially-driven goons have redefined it to convince housewives that standing on a stability ball while performing some silly-looking unilateral inverted wiggling motion with a two-pound medicine ball is the optimal way to be "functional and fit." Last time I checked, if a movement got you from point A to point B, it was functional. So, I suppose these people aim to look moronic, then what they're doing is somewhat functional? KB: Sometimes you just have to take that more straightforward approach. Here's another "Rocky example." Recall that in "Rocky IV," Rocky trained in a harsh Siberian environment with nothing but logs, farm equipment, hills, axes, snow, and a pair of sneakers?in short, nothing that even remotely resembled sophistication. Then, you have his Russian opponent training in a pristine scientific environment with every little aspect of his training measured and accounted for. Sure, it's a movie, but I there's still a lesson to be learned. It's fine to use all that science has, but don't forget there are times when it's better just to roll up the sleeves because that's what sporting environments are like anyway; you can't get too far from that mentality. I try to combine optimal amounts of both sophistication and crude toughness.

EC: Another important lesson that I'd like to highlight from that example is that "Rocky IV" is the greatest movie of all time; I'm still upset that it isn't required viewing in high school history classes when the Cold War is the topic of discussion. By the way, you've already covered my favorite movie, but if you can somehow relate "Happy Gilmore" to deadlifting and "Braveheart" to insulin-independent glucose uptake, you'll be on my Christmas card list forever. You mentioned the optimal amounts of different contributing factors; I'm a firm believer that one can't just understand training or nutrition/supplementation. Rather, coaches and athletes need to understand both individually and, more importantly, the synergistic effect of the two. The old adage that success is "90% diet," while admirable in verse, really does send a bad message. Coaches and athletes need to treat training and nutrition/supplementation like they're both 100%. In fact, we ought to also include factors like restoration, motivation, and education in this equation. KB: Well said, in short, coaches need to put their prejudices and preconceived notions aside and look to the end goal: taking an athlete from A to Z even if that means stepping away from tradition. Let performance and needs determine the optimal focus. Learn how to initiate individualized training prescriptions. Learn how to analyze strengths and weaknesses. Learn what training methods are best for a given goal. Optimize the training economy and don't get cute just for the sake of being different. EC: Okay, let's delve into strength training programs for athletes. I'd like to start by getting your perspective on testing athletes. First off, how often? I think that some coaches waste way too much time with testing-only weeks because they test too many different things and get hung up on testing improvements rather than performance improvements in the sport in consideration. KB: Yes, you're exactly right about this. Too many schools spend an entire week or more getting everybody tested and a large part of that time is spent messing around. I don't see any real need for a testing-only week unless part of that week is also going to be used as a regeneration week. It shouldn't take longer than 2-3 days to test everything, anyway. What I have always liked is to incorporate testing into part of the workout or program. This is very similar to what Westside guys do. Those guys are really "testing" every week on their max effort days. All you'd have to do is cut down on volume in the days prior to the testing workouts and do everything nearly the same - that way the testing doesn't become a distraction to the main goal: improving performance. Also, as a coach, I feel the athletes are constantly being tested and evaluated. When I work one-on-one with someone, there is rarely any definite need for testing because during every session I'm observing and usually always know what's going on. Likewise, I can learn a lot and reduce the need for testing just by analyzing someone's training log. If I see a guy improves six inches in two weeks on his depth jump or reduce his times in a sprint drill, I don't need him to run a week of testing to tell me that his sprint times have improved and his vertical jump has improved. If a guy increases by 20 lbs in a strength exercise working in a lower rep range, I don't need to take time off and have him test his 1RM to show he's improved. However, I should note that the one time that can be an advantage is when it used to show an athlete how much he's improved and to boost his confidence, or when a player absolutely needs to be evaluated in the test. For example, if you're preparing for an NFL combine, you have to get used to the testing procedures and learn how to peak at the right time. Times like that are when it's necessary to run a complete battery of tests and train for the tests because they'll be the main focus. I feel as a coach you should be able to tell where your athletes stand just by observing them and their performance in training and what they do on the field. Look for improved function rather than just numbers. EC: I couldn't agree more. In Part II, we'll pick up where we left off with strength testing, and move on to discuss the future of sports training and how to tie all this together for performance and physique enhancement. Thanks for dropping some knowledge bombs on us, Kelly. KB: My pleasure. I look forward to Part II.

In the meantime, for more information on Kelly's methods, check out the product he created along with Alex Maroko, The Truth About Quickness. It's a fantastic product that I highly endorse.

Update: Be sure to read Part 2: Baggett of Tricks, Part 2: An Interview with "The Truth About Quickness" Author Kelly Baggett. Sign-up Today for our FREE Newsletter and receive a four-part video series on how to deadlift!
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Ask EC: Installment II

By: Eric Cressey

Q: I was looking around some internet forums in search of information about training programs for high school basketball players, and your name came up as the expert in that field. If you have any time, I was wondering if you could help me out. Basically, here's the breakdown. I have an athlete who's 18 years old, 6'6, and about 290lbs.  He's never touched a weight before in his life and I get to work with him for a little more than 6 months.  As you can tell, he's fat and slow. So, my main concern is getting his diet in order and shedding some pounds.  Then I want him in the gym 4 days a week working on basketball specific drills. I also want to design workout program for him that will increase his speed, quickness, and strength. That's where I need a little help.  I was wondering if you could help me outline a program for him, or give me any advice at all. If you could, that would greatly be appreciated. Thanks for your time...

A: There are quite a few things that you need to take into account.  First, he's overweight and deconditioned.  The single worst thing that you can do with him right now is getting him doing all sorts of basketball-specific conditioning work where he's running all over the place.  The kid will have a stress fracture, or patellar or Achilles tendinosis so quickly that you'll be amazed.  You need to lean him out to reduce the amount of weight he's going to decelerate with every step and landing, but this can't be done in an exclusively weight-bearing exercise sense.  I recommend you a) clean up his diet (easier said than done with an 18 year-old) and b) incorporate some energy systems work that is comparable metabolically to his sport (i.e. interval training) but is easier on the body (e.g. swimming, elliptical, rowing, and - although I don't really like the idea - biking).  No treadmills or distance running.  He's obviously going to need to be on the court some, but you need to really watch what you do with him right now; I'd stick with skill work specifically and only use a few drills in order to improve his footwork.  Save the more challenging on-court conditioning for when he's more fit.

In terms of resistance training, he's a beginner, so you need to treat him as such.  Start him off with higher reps and lighter weights in order to foster proper technique, build confidence, and promote connective tissue strength.  As he gets more and more neurologically proficient, you can increase the weights a bit.  By six months, he definitely ought to be ready for some significant loading; in fact, his performance will go up simply because the resistance training will teach him to recruit more muscle fibers.

Just because you have to start him from scratch does not mean that you should just plop him on machines with fixed lines of motion, though; get him training with free weights. Taller guys are always more susceptible to the classic postural perturbations, so make a point of including plenty of horizontal rows, glute-activation (supine bridges, X-band walks), and single-leg exercises (most tall guys have terrible frontal plane stability). Above all, you need to hammer on his core strength (specifically from a stabilization standpoint) and posterior chain (most tall guys are very quad-dominant).  Watch to make sure that he isn't hyperextending at the lumbar spine with any overhead lifting that you're doing.  If you have access, a trap bar will be your best friend in his programming.

All in all, just remember to fit the program to the athlete, and not the athlete to the program.  You seem to have a preconceived notion in your head that he needs to be in the gym four days per week; what if his body can't handle that?  You can't run your big men like you run your guards, and although 6-6 isn't giant, it still warrants consideration, especially since he's deconditioned.  Also, you seem to be very enthusiastic about this, but can you say the same for him?  If his heart isn't into it, it won't matter how perfect your programming is; that's one of the fundamental challenges of coaching.

Good luck!

Q: I read your article on Cluster Training in Men's Fitness. In the program you wrote, the clusters were only performed in two of the four sessions; why not include them in all four?

A: The logic behind the cluster training only being done on two of the four training days each week is that it's a very neurologically demanding protocol, so performing clusters at each workout is too much for the vast majority of trainees.  Therefore, we're working on hypertrophy (an increase in cell size) from two different perspectives:

1. Max Strength days - geared toward functional adaptations and maximal protein degradation through heavy training.  These methods lead to sarcomere hypertrophy (increases in the size of the actual muscle proteins - e.g. actin and myosin).

2. Repetition Days - geared toward structural adaptations and sarcoplasmic hypertrophy (proliferation of non-contractile elements - such as collagen - in the muscle cell) and promotion of glycogen storage.

So, basically, twice a week you're going to be hitting it heavy (and then doing assistance work), and twice a week you're going to be focused on just getting your reps in.

Q: I know that stretching is somewhat controversial (if, when, how much, what stretches) and I've tried doing a minimal cardio warm-up (10 or so minutes) just to raise my body temperature a bit and then going directly into my training routine. I still felt stiff, though, and just not anywhere near as good as I did when I did a more adequate cardio and stretch warm-up. I just couldn't give it 100% in training. I also like to stretch between sets sometimes because I've read that it can promote muscle growth (supposedly by stretching the connective tissue surrounding the muscle belly - therefore creating more room for the muscle fibers to increase in size - kind of like how you could fit more sand into a bigger sock). Could you please shed some light on this and include some rationale on why stretching 4-6 hours after is preferable? Should one do some cardio preceding this or can you stretch cold?

A: First off, let me say that warm-ups must be completely unique to the individual; some people take 30 minutes, and some can just go right to it.  I'm an example of the latter; two minutes and a few warm-up sets and I'm good to go.  It has a lot to do with neural efficiency, and also (I'd assume) with resting body temperature.

Be careful how you define flexibility; passive and active flexibility are two completely different things.  Just because you can really get good ROM when you passively force a muscle into a stretch does not mean that the muscle will automatically be able to work through an optimal ROM on its own.  Moreover, hyperflexibility can actually be a problem.

The jury is still out on why static stretching impairs force production, but it's been demonstrated in dozens of studies.  Many (myself included) believe that it has to do with:

a) decreasing stiffness of the cytoskeleton (stiffness is important, as there is lateral pull on the cytoskeleton from the sarcomere - the contractile unit of skeletal muscle - when muscles shorten linearly; if there's no stiffness, there is no lateral "tethering" upon which to base forceful contraction)

b) reduced intramuscular tension, presumably among the contractile units (e.g. actin, myosin) themselves

c) nervous system factors related to motor control and reflex sensitivity; basically, the stretching makes it harder for the nervous system to tell the muscle to fire.

The solution to this problem is dynamic flexibility drills, which consist of controlled movement through joints’ active range of motion. This is something on which the resistance training and performance enhancement communities are light years behind, and they’re really missing out as a result. In light of this ignorance, Mike Robertson and I recently finished shooting our “Magnificent Mobility” DVD, which outlines 32 drills we use as components in more efficient and productive warm-ups. You can pick a copy up at the t-nation.com store (my apologies for the shameless plug). Just give the dynamic warm-up a try and let me know how you feel.  Most people love it and never go back to boring steady-state cardio; it blows this ineffective traditionalist approach out of the water, as you can warm-up and improve your functional range of motion and dynamic flexibility at the same time.

Stretching during training does have its proponents, although it's never been proven in the literature.  Anecdotal evidence is valuable, but personally, I think the value of being able to do extra work on an exercise because you haven't reduced force production capabilities is more valuable than the *possibility* of increased size from stretching.  The best way to implement this, in my opinion, is to simply do it after your last set on a particular movement.  Most of the time, loaded passive stretching is recommended, and keep in mind that this is a pretty damaging protocol; most people will be very sore for the next few days.  As such, it's best to use it for 2-3 weeks here and there rather than during the entire training year.

The 4-6 hours recommendation has to do with avoiding stretching when skeletal muscle blood flow (i.e. "the pump") can actually impair full range of motion.  Given that body temperature is still somewhat elevated at this point, there really isn’t any need to warm-up beforehand.

Q: Just to be sure: My left scapula is elevated and you recommend that I do more work for the left lat?  To me it seems wrong to do more work for the elevated side, so please confirm if this really is right.

A: The latissimus dorsi and upper trapezius are antagonists in their scapular depression and elevation roles, respectively.  By strengthening the lat along with the mid and lower traps and rhomboids, you'll be pulling the scapula downward.  Because you don't have issues with internally rotated humeri, we don't have to worry about the "side effect" of lat training (increased internal rotation of the humerus); your problem is purely at the scapula.

Q: I enjoyed your Cardio Confusion article and I had a question about the best way for a powerlifter to train cardio. I need to get my 2-mile run time down for the Army physical fitness test, but I would like to know the best way to train something like this without sacrificing my lifts. Any advice you can give me would be greatly appreciated.

A: As for your particular question, it's a bit of a different situation from the topic addressed on the forum.  In essence, you have two goals: one maximal strength related and one endurance related.  These goals are completely contrary to one another, so you really have to accept that training for endurance will attenuate the improvements (or even maintenance of maximal strength).  The discussion at t-nation was more related to utilizing aerobic activity as an adjunct to the facilitate strength and speed improvements - not a separate training initiative in itself.

That said, you should work to keep your maximal strength up, obviously.  How you approach this training will be to some extent influenced by your body size.  If you're a really large guy, I'd recommend getting in some non-impact stuff (e.g. rowing, elliptical) for parts of the week to avoid orthopedic problems.  Moreover, I encourage you to watch your diet more closely, as dropping body fat will in itself improve VO2max.  If you're a lighter guy already, you shouldn't have too much of a problem getting into the running; just slowly build up your mileage and frequency.

In terms of specific training initiatives, I'd use longer interval bouts (200-400m) with varying rest periods (diminishing rest intervals over an extended period of time), two-mile runs in themselves (not always at max pace), and some long, slow duration jogs (less than 60% max heart rate) to promote recovery and improve capillarization.

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