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Mythbusters Vol 1

Let me be clear about one thing: with the possible exception of anything that comes out of Larry King's mouth, there are no unimportant interview questions. Every question or comment serves a purpose, whether it's to get the interviewee to open up, show emotion, unleash new information, or just get back on track. Everything matters. But I recently learned that sometimes I should just let the guy ramble. If he wants to rant, my job is to shut up and make sure the tape recorder keeps rolling. Most of the guys I interview are great at going off on tangents. And while the resulting transcript is often a jumbled mess of opinion, applied research, and hard-earned experience, occasionally I get something unexpected: an idea for a completely different article based on the unrelated information or opinion. To paraphrase Rod Stewart, every tangent tells a story. This is a collection of those tangents and tidbits from Dave Tate, Chris Bathke, Matt McGorry, Eric Cressey, and Craig Weller. Continue Reading...
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What I Learned in 2008

In what has become a yearly tradition, it's now time for this year's installment of What I Learned. As always, I learned a ton, but here are a few that stuck out in my mind as I sat down to write this article. Continue Reading... - Eric Cressey
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Invincible Immunity

Invincible Immunity

by Eric Cressey

Of all the lousy things that can happen, this has to be one of the worst. Imagine...You've just completed the most successful bulking cycle of your life, adding twenty pounds of mass; you're on top of the world. Now, all you have to do is train properly and eat plentifully in order to solidify your gains. With your knowledge of diet and training, it should be a snap. Then everything hits the fan... Your girlfriend is so proud of you for making such great gains and transforming your physique that she can't keep her hands off of you. The day before, she had shared a soda with a friend who had just come from the gym. That friend had taken a sip from the water fountain at the gym and accidentally touched her lips to the spout. Ten minutes earlier, that skanky "human sweat gland" guy who spends five hours on the elliptical cross trainer each day had just made out with that same water fountain. That morning, he had kissed his wife goodbye before leaving for his job at the DMV. That wife is the teacher of a kindergarten class. Incidentally, that class happened to be riddled with the flu, and some kid had blown chunks all over her nice new blouse the day before. Sure she cleaned it up, but she still wound up with the flu. Thanks to this incredibly unlikely downward spiral, you are now home sick from work, pitying yourself as you watch the same episode of Sportscenter eight times in a row. All the while, you're thinking about how you would much rather be deadlifting like a madman and showing off your gains at the gym! Unfortunately, you cannot go back in time to prevent yourself from coming down with the flu. Although it may be beneficial to look back and figure out if there was anything you could have done to strengthen your immune system (avoiding overtraining, paying attention to post-workout nutrition, taking certain supplements, getting plenty of sleep, etc.), you need to focus on the task at hand: beating the flu! You see, bodybuilders, powerlifters, and other athletes have to take into account how sickness affects performance and physical appearance, whereas normal folks just worry about "getting rid of their sniffles." Before we get to the specifics, though, I should mention that the term "flu" that we so often use is short for influenza. Influenza (also known as Grippe or Grip) is really only one of several common kinds of viral respiratory infections. Also including on this list are the common cold (upper respiratory infection or acute coryza), pharyngitis, laryngitis, tracheobronchitis, and viral pneumonia (1). Regardless of the clear differences in the nuts and bolts of each infection, they are generally all lumped together and called the flu by the general public. While this oversimplification is erroneous, the human immune system must be strong to prevent and in many cases overcome any type of infection. And, if you're anything like me, you detest the idea of getting loaded up on medications, sugary cough syrups, and lozenges just because your nose is running faster than a sprinter with a rocket up his butt. All that being said, let's get to work on finding a universal approach to maintaining your gains and getting back to optimal health as soon as possible. Diet Proper diet seems like a no-brainer, right? One would think so, but I'm constantly amazed at how people vehemently adhere to this primitive urge that tells them to stuff themselves full of crap foods just because they feel like crap! These crap foods are usually "comfort" foods: Mom's cookies, white toast with cinnamon, sugar, and butter, hot chocolate, a whole gallon of ice cream?. These foods may have made you feel better as a kid when they were used to take your mind off the "boo-boo" on your knee, but they'll only make thing worse when you are a sick adult. They might make you feel all warm and toasty on the inside, but they'll quickly make you soft and fluffy on the outside if you overindulge. So what should you eat and what should you avoid? For starters, remember that total calories are of foremost importance. Don't fall into the trap of dropping calories too low out of fear of gaining fat while "on the shelf." Instead, it's important to assume the mindset of maintaining the status quo physique-wise while bringing the immune system up to par. If you gain a little fat, don't sweat it. Remember, it's a lot easier to shed a little fat than it is to regain a few pounds of lost muscle. In reaching your daily caloric goal, as usual, spread your intake out over six smaller meals. Maintenance caloric intake is highly variable, so rather than multiplying your body weight by a certain number to find your target, base your intake on slightly below (100-150 calories) what you would take in on a normal rest day. This decrease should account for the extra time spent on the couch or in bed. Specific macronutrient recommendations are also of little value in this instance due to individual variations in terms of carb tolerance. As such, adhere to your typical macronutrient ratios with the only exception being a slight reduction in carb intake to compensate for the diminutive calorie reduction and reduced training effect. Furthermore, make sure that you keep protein high (1-1.5g/lb lean body mass) in order to remain in positive nitrogen balance and stop muscle protein catabolism in its tracks. From all our cutting cycles, we're all well aware that protein needs increase during times of stress, and sickness is certainly one of those times. In a study of critically ill children in hypermetabolic and catabolic states, researchers found that a higher protein intake was associated with positive nitrogen balance, whereas a low intake (with total calories held constant) led to a continued state of negative nitrogen balance and muscle protein catabolism (2). A big steak probably won't sound too appealing when you're sick, though, so low carb protein powders (such as Xtreme Ultra Peptide), cottage cheese, omelets, and other "easy to get down" protein sources might turn out to be your best friends. Next, only consume low-glycemic carbs. When you're sick, your body isn't primed for sucking up simple sugars like it is when you've just completed a training session. So, the typical bodybuilding "no-no" foods should be even more off-limits than usual. Your best bet is to focus carb intake early in the day when muscle cells are most receptive to storing glycogen. Keep fats (especially healthy fats) up as well - possibly at the expense of carbohydrates. In the aforementioned study of critically ill children, fat was used preferentially for oxidation. Meanwhile, a high carbohydrate intake was associated with lipogenesis (fat formation) and decreased fat oxidation (2). Thirty percent of total calories is a good figure in order to support endogenous testosterone and overall energy levels (as fat is the primary source of energy at rest). Your body will be forming plenty of new immune cells as you fight off sickness, and fatty acids constitute an important component of each new cell membrane. Therefore, in order to give the body the best raw materials available, make sure that you're getting plenty of omega-3 fatty acids. However, don't fall into the trap of overdoing the omega-3s or fat in general; very high fat diets are associated with impaired lymphocyte (one of the five kinds of leukocytes, or white blood cells) function (3). Furthermore, while fish oil has proven effective in enhancing immune function in certain clinical situations (e.g. rheumatoid arthritis, ulcerative colitis) and in animals, studies of healthy humans are yet to yield consistently favorable results to substantiate the claim that omega-3s enhance immunity (4). As such, there does not appear to be any greater benefit (at least not yet) to increasing omega-3 PUFA intake during times of sickness. Simply stick to your normal intake levels, relying on healthy sources such as fish oil and flaxseed oil for your supplemental fat intake. The last dietary concern that warrants mention is water intake. You might think that because you aren't training, you don't need to worry much about pushing the H2O- big mistake. The body loses a significant amount of fluids each day independent of training. We're constantly losing water as we dissipate heat through our skin and in our breathing without even knowing it. Factor in increased mucus production, the sweating that may be associated with a fever, the fact that your body is constantly constructing new cells (especially during sickness), not to mention your higher protein intake, and you can begin to realize the importance of really emphasizing water intake. Shoot for at least one gallon (preferably more) of water daily. All these considerations in mind, I highly recommend you pick up a copy of Precision Nutrition from Dr. John Berardi.  His information is fantastic, highly effective,  and presented in a user-friendly format. Supplementation First and foremost, be sure to get a flu shot each fall. The optimal time to do so is mid-September through November, as it takes at least a week for the shot to really kick into protective-mode. If you need proof that the influenza vaccine is worth the fee (if you even have to pay for it), look no further than a study conducted on a Brazilian airline company's employees. As I'm sure you can imagine, flight attendants and those in related roles are a population segment that is extremely susceptible to the flu due to their interactions with so many customers (often in confined spaces). Prior to flu season, each of 813 employees received either an influenza vaccination or a placebo. Seven months later, the employees who had received the vaccines showed 39.5% fewer episodes of flu-like illness than the placebo. Additionally, the vaccine group was absent from work due to sickness 26% less often than the placebo group (5). From a weight-training standpoint, that 26% corresponds to a lot of missed training sessions. In addition to the flu shot and your regular multivitamin, you should definitely include the following: Vitamin C Vitamin C (ascorbic acid) is the first immune-booster that comes to mind. A vital component of every cell in the human body, ascorbic acid is perhaps most notably found in high concentrations in leukocytes (white blood cells). The leukocytes are constantly being produced in the bone marrow as safeguards against bad stuff like cottage cheese gone sour, reruns of those obnoxious Subway commercials with Jared, curling in the squat rack, and, oh yeah, infections. During infection, in order to prevent oxidative damage, the vitamin C within the leukocytes is used up faster than a post-training shaker bottle full of Relentless (4)! Thus, it should come as no surprise that reduced leukocyte vitamin C levels are associated with less than optimal immune function. (6) In the worst vitamin C deficit scenario, scurvy, the immune response is entirely inadequate (and sometimes nonexistent) in each of the many components of the immune system. In fact, overall vitamin C status is often measured via an assessment of levels in the leukocytes (4). In terms of preventative supplementation, a true consensus has not yet been met regarding the efficacy of vitamin C in reducing the occurrence of common colds. Several respected studies have found that Vitamin C supplementation is of little value in preventing the common cold (7), whereas others have reported decreased incidences of reported common cold infection among individuals who received large doses of a vitamin C supplement (8,9). However, other studies have verified the assertions that supplementation with vitamin C improves several aspects of the human immune response, effecting positive changes in proliferation and/or function of in three of the five types of leukocytes: lymphocytes, neutrophils, and monocytes (10-16). Adequate vitamin C status is often defined as "a circulating pool of 1500mg" (7). Due to the fact that water-soluble vitamins like vitamin C are not stored by the body as well as fat-soluble vitamins, ascorbic acid must be continuously replenished through diet and supplementation. Doses of up to 10g per day have been used in numerous studies without serious toxicity symptoms. The side effects of such high consumption may include diarrhea and, in serious cases, kidney stones or urate crystals (due to increased uric acid release in the urine). Antonio and Stout state that these risks have "been greatly overstated" (7). Based on the available literature, I recommend 2-2.5g of supplemental vitamin C daily during normal training conditions and 4-5g daily during flu-like symptoms and times increased of training stress. Also, be sure to spread your intake throughout the day in 500mg doses. Dosages of 500mg are proven to increase cellular ascorbic acid absorption by up to 40%, whereas dosages greater do not increase this absorption (17). Vitamin E Perhaps as important as vitamin C is Vitamin E, which works synergistically with selenium in tissues to reduce lipid membrane damage by reactive oxygen species (ROS) during infections (4). Vitamin E has proven effective in improving various parameters of the immune function, including enhanced lymphocyte production, improved antibody response to vaccine, reduced pulmonary viral titers (a measure of virus prevalence in respiratory infections), and "preventing an influenza-mediated decrease in food intake and weight loss" (18-20). No decrease in food intake? Maybe that steak won't sound so bad after all! All that being said, even the slightest deficiency in vitamin E can easily compromise one's immune response. And, the current RDA of 30 IU is barely adequate in preventing deficiency in sedentary, normally healthy individuals, let alone in athletes, the elderly, and the sick and diseased. Granted, one may derive a considerable amount of vitamin E from diet alone, but in order to receive sufficient vitamin E to attain an enhanced immune benefit, one must supplement in excess of the RDA (especially on low-fat diets). Vitamin E is recognized as one of the least toxic vitamins, although one may experience some minor symptoms (nausea, diarrhea, muscle weakness) with very high dosages (7,21). As such, 800-1200 IU throughout the year (regardless of whether you're sick or healthy) is an optimal approach. Glutamine Glutamine is well known as the most abundant amino acid in the human body (including both the plasma and tissue pool). In fact, the intramuscular free amino acid pool is more than 60% glutamine, and the glutamine in skeletal muscle accounts for about 90% of the body's total glutamine pool. Although over 40% of the body's glutamine is devoted to fueling the GI tract, this amino acid also plays a role in the functioning of many other parts of the body, including the liver, brain, muscles (duh!), hair follicles, kidneys, and - you guessed it - the immune system (7,22-24). Adequate levels of glutamine are necessary to ensure optimal proliferation and function of lymphocytes, macrophages, and neutrophils (25,26). Traditionally, because the body can synthesize glutamine endogenously (mostly in the muscle tissue), it has been classified as a nonessential amino acid. However, this classification is made under the assumption that the body is not enduring a stressful physiologic trauma such as sickness (23). Many researchers have now begun to classify glutamine as a conditionally essential amino acid during times of sickness, infection, and malnutrition. Because glutamine is a crucial substrate for a variety of metabolic processes, it is only logical that the body requires increased amounts of the amino acid during infection in order to "bolster" the immune system while maintaining normal physiological functioning (24,26). Unfortunately, as you can see in many cancer patients, the body's response to infection, injury, and stress is protein catabolism. Initially, plasma glutamine levels are depleted. Next, in order to sustain its metabolic processes and replenish plasma glutamine levels, the body takes glutamine from skeletal muscle. Normally, this isn't a problem, as skeletal muscle glutamine synthesis matches glutamine release. However, during times of stress, there is a problem: numerous organs, including the liver and bowel, show marked increases in glutamine uptake during infection. These increases, in combination with the needs of the immune system, GI tract, and the regular metabolic processes, cause glutamine release from skeletal muscle to exceed glutamine synthesis. In fact, skeletal muscle glutamine release may double during infection (23,27). In summary, during infection: 1. Glutamine use increases 2. Glutamine supply decreases 3. A concentration gradient across the muscle cell membrane cannot be reached (23) 4. Your beloved quad sweep becomes fuel for your GI tract and, essentially, your body's lunch. Think about it for a second: when you're sick, is your body going to care more about ensuring appropriate internal organ functioning or maintaining sleeve-splitting biceps? Luckily, numerous studies have proven that exogenous glutamine can help to: maintain positive nitrogen balance (and glutamine levels in skeletal muscle), increase plasma glutamine levels, prevent decreases in ribosomal concentrations, improve muscle protein synthesis rates, and enhance immune function (through such mechanisms as encouraged lymphocyte proliferation) (7, 28-32). Also, let's not forget that glutamine?s "immunoenhancing" effects make it an effective year-round, recovery-promoting supplement (albeit in smaller doses) for hard training athletes who are more susceptible to infection, especially during and shortly after periods of intensive training (7,33,34). Glutamine supplementation is also associated with increased plasma GH concentration, which may also assist in immunity (7,35). During illness, shoot for 0.35-0.4g glutamine per kg body weight, and spread your intake out throughout the day in 3-5g doses. Based on the published clinical studies and for absorbability reasons, I recommend glutamine peptides. L-glutamine (free form), however, tastes better, generally costs less, and will also yield favorable results. Personally, I'll stick with peptides, but it's your call; just make sure to get it in you in some form! Zinc Although most people primarily associate zinc with growth and development, this trace mineral also plays a crucial role in proper immune function. A deficiency of zinc relates to diminished immune response, including low T- and B-cell (the two broad categories of lymphocytes) counts in bone marrow due to decreased proliferation, and reduced antibody production (just to name a few). In some mice, only thirty days of inadequate zinc intake caused an 80% reduction in immune capacity. As such, it should come as no surprise that zinc deficiencies are prevalent in numerous immune system-stressing chronic illnesses, including HIV, renal disease, and alcoholism (4,36). While the complications of zinc deficiency are well established, studies on the benefits of zinc supplementation in enhancing immune function have yielded mixed, but mostly favorable results. Numerous studies have found that zinc supplementation initiated upon the onset of a cold or upper respiratory tract infection decreases the sickness' duration and severity (7,37-39). In a study of twenty burn victims, fewer pulmonary infection rates and shorter hospital stays were observed in patients who received a trace mineral supplement that included zinc (40). Meanwhile, zinc supplementation in long distance runners prevented the typical increase in reactive oxidative species normally seen with endurance activity (41). In terms of preventative supplementation, researchers found that of 609 school children that were given either a zinc supplement or a placebo, those who supplemented with zinc had 45% fewer acute lower respiratory infections over the 120-day study (42). If you take nothing else from all these studies, at least walk away from this article cognizant of how important sufficient intake is, especially for athletes (who are more likely to be deficient than the general population). While high-dose supplementation can actually lead to immunosuppression, moderate supplementation throughout the year with slightly increased dosages beginning at the onset of flu- or cold-like symptoms is an effective and safe supplementation approach (7). During sickness, take at least 25mg zinc (but not more than 100mg) per day. An optimal approach would be to get this supplemental intake in the form of a ZMA supplement, as it will enable you to meet your zinc needs while increasing anabolic hormone levels, improving recovery, and promoting deep, restful sleep. Miscellaneous: the other stuff Here are a few other supplements that are often thrown into the immunity discussion, but will probably not be worthwhile additions to your immune effort: Vitamin A (preformed vitamin A is known as beta-carotene): Although vitamin A is of unquestionable importance to proper immune functioning, there is no definitive evidence to suggest that supplemental vitamin A offers additional benefits over normal dietary intake, especially in those with already adequate status. Excessive vitamin A intakes have been associated with suppression of T- and B-cell function, thus causing a greater susceptibility to infection. Toxicity can also become an issue with higher intakes. Vitamin A deficiency is very uncommon in wealthier nations. As such, if you feel that you need to get more beta-carotene than you diet alone provides, make sure to select a multivitamin with at least 5000 micrograms (4,7). Echinacea: Although a few studies have emerged that show slightly (and relatively insignificantly) shorter respiratory tract infection durations in patients treated with echinacea, most have demonstrated that the herbal product has little or no effect on preventing and treating sickness. This uncertainty is complicated by the fact that there are nine species of the plant, different parts (leaves, stem, roots, flowers) of the plant can be used, and different forms are available (e.g. powder, liquid extract, capsule). Essentially, even if echinacea was definitively proven effective, an argument would still exist over which species, form, and delivery produces the best results. At this point, there is not enough evidence to recommend echinacea as a worthy supplement (7,43-45). Arginine: This nonessential amino acid has shown promise in improving immune response and wound healing via improved lymphocyte production in individuals with compromised health status. Other studies, however, have shown that arginine supplementation is of no benefit in attempting to enhance the immune response, especially in healthy individuals (7). Given that some clinical trials use upwards of 20g L-arginine per day (mostly without appreciable immunity-related results), forty capsules per day seems like far too risky an investment even if you enjoy being a human guinea pig. Then again, even if you do decide to give arginine a try, be careful; excessive intakes can actually blunt the immune response (46). Lifestyle/Training An adequate amount of sleep during sickness is of the utmost importance. The old "8-hours at night" recommendation still holds true...as a minimum. You should also be shooting for a nap or two during the day. It seems like a no-brainer to say that you shouldn't be training when you're sick, but I'm constantly amazed at how many people still go the gym in spite of their wheezing, sore throats, and aches. Before you stumble off the couch and over to your local gym, ask yourself if your body could really recover from a heavy training session if it hasn't even recovered from the flu. The answer should be a resounding "NO!" If it isn't, maybe it will help to think about how your decision to go train will impact others; you'll probably make half the people in the gym sick just like the "human sweat gland" did to you. Stay home, if not for your own sake, then for the sake of everyone else who enjoys his or her health and visits to the gym. Get over the flu and then get back to the gym! Conclusion There you have it: a comprehensive approach to getting back to the gym as soon as possible. To recap: 1. No comfort foods 2. Maintenance calories (factoring in reduced activity level) 3. Normal protein intake 4. Slightly reduced carb intake, consisting of low GI carbs only 5. Normal healthy fat intake 6. Regular Multivitamin 7. 4-5g vitamin C in 500mg doses throughout the day 8. 800-1200 IU vitamin E in 400 IU doses throughout the day 9. 0.35-0.4g glutamine peptides/kg body weight in 3-5g doses throughout the day 10. ZMA supplement (or zinc equivalent providing 25-100mg/day) 11. No training until symptoms are gone 12. R&R It might not sound as appetizing or heart-warming as a bowl of chicken soup, but it beats Nyquil... References 1. The Merck Manual of Diagnosis and Therapy. http://www.merck.com/pubs/mmanual/section13/chapter162/162b.htm; 1995 accessed Sept 2002. 2. Coss-Bu JA et al. Energy metabolism, nitrogen balance, and substrate utilization in critically ill children. Am J Clin Nutr 2001 Nov;74(5):664-9. 3. Calder PC et al. Fatty acids and lymphocyte functions. Br J Nutr 2002 Jan;87 Suppl 1:S31-48. 4. Field C. et al. Nutrients and their role in host resistance to infection. J Leukoc Biol 2002 Jan;71(1):16-32. 5. Mixeu MA et al. Impact of influenza vaccination on civilian aircrew illness and absenteeism. Aviat Space Environ Med 2002 Sep;73(9):876-80 6. Schwager, J. et al. Modulation of interleukin production by ascorbic acid. Vet Immunol Immunopathol. 1998 Jun 30;64(1):45-57. 7. Antonio, J., & Stout, J. Sports Supplements. Lippincott Williams & Wilkins, 2001. 8. Hemila, H. Vitamin C and common cold incidence: a review of studies with subjects under heavy physical stress. Int J Sports Med 1996 Jul;17(5):379-83. 9. Hemila, H. Vitamin C and acute respiratory infections. Int J Tuberc Lung Dis 1999 Sep;3(9):756-61. 10. Kennes, B. et al. Effect of vitamin C supplements on cell-mediated immunity in old people. Gerontology 1983;29(5):305-10. 11. Penn, ND. et al. The effect of dietary supplementation with vitamins A, C and E on cell-mediated immune function in elderly long-stay patients: a randomized controlled trial. Age Ageing 1991 May;20(3):169-74. 12. Shilotri PG, & Bhat KS. Effect of mega doses of vitamin C on bactericidal ativity [sic] of leukocytes. Am J Clin Nutr 1977 Jul;30(7):1077-81 13. de la Fuente, M. et al. Immune function in aged women is improved by ingestion of vitamins C and E. Can J Physiol Pharmacol 1998 Apr;76(4):373-80. 14. Patrone, F. et al. Effects of ascorbic acid on neutrophil function. Studies on normal and chronic granulomatous disease neutrophils. Acta Vitaminol Enzymol 1982;4(1-2):163-8. 15. Prinz, W. The effect of ascorbic acid supplementation on some parameters of the human immunological defense system. Int J Vit Nutr Res 1977; 47:248-57. 16. Woollard, KJ. et al. Effects of oral vitamin C on monocyte: endothelial cell adhesion in healthy subjects. Biochem Biophys Res Commun 2002 Jun 28;294(5):1161-8. 17. Voldani, A. et al. New evidence for antioxidant properties of vitamin C. Cancer Detect Prev. 2000;24(6):508-23. 18. Meydani, SN et al. Vitamin E supplementation enhances cell-mediated immunity in healthy elderly subjects. Am J Clin Nutr. 1990 Sep;52(3):557-63. 19. Meydani, SN et al. Vitamin E supplementation and in vivo immune response in healthy elderly subjects. A randomized controlled trial. JAMA. 1997 May 7; 277(17):1380-6. 20. Han, SN et al. Effect of long-term dietary antioxidant supplementation on influenza virus infection. J Gerontol A Biol Sci Med Sci 2000 Oct;55(10):B496-503. 21. Beharka A. et al. Vitamin E status and immune function. Methods Enzymol 1997;282:247-63 22. Yeh, SL et al. Effects of glutamine-supplemented total parenteral nutrition on cytokine production and T cell population in septic rats. JPEN J Parenter Enteral Nutr. 2001 Sep-Oct;25(5):269-74. 23. van Acker, BA et al. Glutamine: the pivot of our nitrogen economy? JPEN J Parenter Enteral Nutr. 1999 Sep-Oct;23(5 Suppl):S45-8. Review. 24. Newsholme, P. Why is L-glutamine metabolism important to cells of the immune system in health, postinjury, surgery or infection? J Nutr. 2001 Sep;131(9 Suppl):2515S-22S; discussion 2523S-4S. Review. 25. Saito, H. et al. Glutamine as an immunoenhancing nutrient. JPEN J Parenter Enteral Nutr. 1999 Sep-Oct;23(5 Suppl):S59-61. Review. 26. Ziegler, TR. Glutamine supplementation in cancer patients receiving bone marrow transplantation and high dose chemotherapy. J Nutr. 2001 Sep;131(9 Suppl):2578S-84S; discussion 2590S. Review. 27. Karinch AM. et al. Glutamine metabolism in sepsis and infection. J Nutr 2001 Sep;131(9 Suppl):2535S-8S; discussion 2550S-1S. 28. Wilmore, DW. The effect of glutamine supplementation in patients following elective surgery and accidental injury. J Nutr. 2001 Sep;131(9 Suppl):2543S-9S; discussion 2550S-1S. Review. 29. Boelens PG. et al. Glutamine alimentation in catabolic state. J Nutr. 2001 Sep;131(9 Suppl):2569S-77S; discussion 2590S. Review. 30. Yoshida, S. et al. Effects of glutamine supplements and radiochemotherapy on systemic immune and gut barrier function in patients with advanced esophageal cancer. Ann Surg. 1998 Apr;227(4):485-91. 31. Valencia, E. et al. Impact of oral L-glutamine on glutathione, glutamine, and glutamate blood levels in volunteers. Nutrition. 2002 May;18(5):367-70. 32. Yoshida, S. et al. Glutamine supplementation in cancer patients. Nutrition. 2001 Sep;17(9):766-8. 33. Castell LM., & Newsholme EA. The effects of oral glutamine supplementation on athletes after prolonged, exhaustive exercise. Nutrition 1997 Jul-Aug;13(7-8): 738-42. 34. Rosene, MF. et al. Glutamine supplementation may maintain nitrogen balance in wrestlers during a weight reduction program. Med Sci Sports Exerc 1999;31(5): S123. 35. Welbourne, TC. Increased plasma bicarbonate and growth hormone after an oral glutamine load. Am J Clin Nutr. 1995 May;61(5):1058-61. 36. Fraker, PJ. et al. The dynamic link between the integrity of the immune system and zinc status. J Nutr 2000 May;130(5S Suppl):1399S-406S. 37. Prasad AS. et al. Duration of symptoms and plasma cytokine levels in patients with the common cold treated with zinc acetate. A randomized, double-blind, placebo-controlled trial. Ann Intern Med 2000 Aug 15;133(4):245-52. 38. Al-Nakib, W. et al. Prophylaxis and treatment of rhinovirus colds with zinc gluconate lozenges. J Antimicrob Chemother. 1987 Dec;20(6):893-901. 39. Mossad, SB. et al. Zinc gluconate lozenges for treating the common cold. A randomized, double-blind, placebo-controlled study. Ann Intern Med. 1996 Jul 15;125(2):81-8. 40. Berger MM. et al. Trace element supplementation modulates pulmonary infection rates after major burns: a double-blind, placebo-controlled trial. Am J Clin Nutr. 1998 Aug;68(2):365-71. 41. Singh A. et al. Exercise-induced changes in immune function: effects of zinc supplementation. J Appl Physiol 1994 Jun;76(6):2298-303. 42. Sazawal S. et al. Zinc supplementation reduces the incidence of acute lower respiratory infections in infants and preschool children: a double-blind, controlled trial. Pediatrics. 1998 Jul;102(1 Pt 1):1-5. 43. Gunning, K. Echinacea in the treatment and prevention of upper respiratory tract infections. West J Med. 1999 Sep;171(3):198-200. 44. Brinkeborn RM. et al. Echinaforce and other Echinacea fresh plant preparations in the treatment of the common cold. A randomized, placebo controlled, double-blind clinical trial. Phytomedicine. 1999 Mar;6(1):1-6. 45. Grimm, W, & Muller, HH. A randomized controlled trial of the effect of fluid extract of Echinacea purpurea on the incidence and severity of colds and respiratory infections. Am J Med. 1999 Feb;106(2):138-43. 46. Wiebke EA. et al. Effects of L-arginine supplementation on human lymphocyte proliferation in response to nonspecific and alloantigenic stimulation. J Surg Res 1997 Jun;70(1):89-94.
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The Right Way to Stretch the Pecs

Stretches to maintain length of both the pectoralis major and pectoralis minor are really important — especially in the weight-training population, where Mondays, Wednesdays, and Fridays are declared national bench press holidays in all 52 weeks of the year. Simply put, everyone presses too much and pulls too little. However, what few people (including Mike and I, circa 2004) realize is that in the process of stretching out the pecs (particularly pectoralis major) in this fashion, you run the risk of irritating the anterior shoulder capsule, particularly if the shoulder blades aren't stabilized. As the picture below shows, the attachment point of the pectoralis major is further down the humerus. Continue Reading...
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Strength Training for Pitchers

Strength Training for Pitchers

by: Eric Cressey

Recently, I received an email inquiry about the value of strength training for pitchers. The individual emailing me had come across the following quote from a pitching "authority:"

"Training will not teach you how to apply more force...only mechanics can do that. And pitching is not about applying more effort into a pitch but is about producing more skilled movements from better timing of all the parts. That will help produce more force.

"No matter how hard you try, you will not get that from your strength training program...no matter who designed it, how much they have promised you it would or your hope that it will be the secret for you."

To say that this surprised me would be an understatement. I'll start with the positive: I agree with him that pitching is all about producing skilled movements secondary to appropriate timing of all the involved "parts." I've very lucky to work hand-in-hand with some skilled pitching coaches who really know their stuff - and trust in me to do my job to complement the coaching they provide.

With that said, however, I disagree that you can't gain (or lose) velocity based exclusively on your strength and conditioning program. On countless occasions, I've seen guys gain velocity without making any changes to their throwing programs or mechanics. I know what many of the devil's advocates in the crowd are thinking: "you're just making that up!" So, if my word isn't enough, how about we just go to the research?

From: Derenne C, Ho KW, Murphy JC. Effects of general, special, and specific resistance training on throwing velocity in baseball: a brief review. J Strength Cond Res. 2001 Feb;15(1):148-56.

[Note from EC: Yes, it's pathetic that this REVIEW has been out almost seven years and people who are supposedly "in the know" still haven't come across ANY of the studies to which it alludes.]

Practical Applications

Throwing velocity can be increased by resistance training. A rationale for general, special, and specific resistance training to increase throwing velocity has been presented. The following findings and recommendations relevant to strength and conditioning specialists and pitching coaches can be useful from the review of literature.

In the "further reading" section at the end of this article, I have listed ten different studies that each demonstrated a positive effect of weight training on throwing velocity. The authors in the review above also have a table that summarizes 26 studies that examined the effect of different strength protocols on throwing velocity, and 22 of the 26 showed increases over controls who just threw. In other words, throwing and strength training is better than throwing alone for improving velocity -

independent of optimization of mechanics from outside coaching.

The saddest part is that the training programs referenced in this review were nothing short of foo-foo garbage. We're talking 3x10-12 light dumbbell drills and mind-numbing, rubber tubing blasphemy. If archaic stuff works, just imagine what happens when pitchers actually train the right way - and have pitching coaches to help them out?

Oh yeah, 10 mph gains in six months happen - and D1 college coaches and pro scouts start salivating over kids who are barely old enough to drive.

With that rant aside, I'd like to embark on another one: what about the indirect gains associated with strength training? Namely, what about the fact that it keeps guys healthy?

We know that:

a) Pitchers (compared to position players) have less scapular upward rotation at 60 and 90 degrees of abduction -and upward rotation is extremely important for safe overhead activity.

b) 86% of major league pitchers have supraspinatus partial thickness tears.

c) All pitchers have some degree of labral fraying - and the labrum provides approximately 50% of the stability in the glenohumeral joint

d) There is considerable research to suggest that congenital shoulder instability is one of the traits that makes some pitchers better than others (allows for more external rotation during the cocking phase to generate velocity).

e) Most pitchers lack internal rotation range-of-motion due to posterior rotator cuff (and possibly capsular) tightness and morphological changes to bone (retroversion). Subscapularis strength is incredibly important to prevent anterior shoulder instability in this scenario.

We also know that resistance training is the basis for modern physical therapy - which I'm pretty sure is aimed at restoring inappropriate movement patterns which can cause these structural/functional defects/abnormalities from reaching threshold and becoming symptomatic. Do you think that a good resistance training program could strengthen lower traps and serratus anterior to help alleviate this upward rotation problem? Could a solid subscapularis strengthening protocol help with preventing anterior instability? Could a strong rotator cuff and scapular stabilizers allow an individual to work around a torn supraspinatus?

And, last time I checked, strength and conditioning was about more than just being the "weights coach." We do a lot of flexibility/mobility and soft tissue work - and it just so happens that such work does wonders on pec minor, levator scapulae, rhomboids, infraspinatus/teres minor, and a host of other muscles in pitchers.

I also like to tell jokes, do magic tricks, and make shadow puppets on the wall. Am I to assume that these don't play a remarkable role in my athletes' success? I beg to differ. Sure, banging out a set of 20 chin-ups because one of my athletes called me out might make me look like a stupid monkey when my elbows refuse to extend for the subsequent ten minutes, but I still think what we do plays a very important role in our athletes success; otherwise, they wouldn't keep coming back. And, for the record, my shadow puppets are great for building camaraderie and bolstering spirits among the Cressey Performance troops - even if I'm just a "weights coach" or whatever.

This only encompasses a few of the seemingly countless examples I can come up with at a moment's notice. Pitchers are an at-risk population; your number one job in working with a pitcher is to keep him healthy. And, I'm going to go out on a limb and say that a guy who is healthy and super-confident over his monster legs and butt is going to throw a lot harder than a guy who is in pain and as skinny as an Olsen twin because his stubborn pitching coach said strength training doesn't work. You've got to train ass to throw gas!

Last fall, I started working with a pro ball player whose velocity was down from 94 to 88 thanks to a long season - but also because he'd had lower back issues that have prevented him from training. In other words, he counts on strength training to keep his velocity up. And, sure enough, it was a big component of getting him healthy prior to this season.

Putting it into Practice

I suspect that some of the reluctance to recognize strength training as important to pitchers is the notion that it will make pitchers too bulky and ruin pitching-specific flexibility. Likewise, there are a lot of meatheads out there who think that baseball guys can train just like other athletes. While there are a lot of similarities, it's really important to make some specific upper body modifications for the overhead throwing athlete. Contraindicated exercises in our baseball programs include:

  • Overhead lifting (not chin-ups, though)
  • Straight-bar benching
  • Upright rows
  • Front/Side raises (especially empty can - why anyone would do a provocative test as a training measure is beyond me)
  • Olympic lifts aside from high pulls
  • Back squats

The next question, obviously, is "what do you do instead?" Here's a small list:

  • Push-up variations: chain, band-resisted, blast strap
  • Multi-purpose bar benching (neutral grip benching bar)
  • DB bench pressing variations
  • Every row and chin-up you can imagine (excluding upright rows)
  • Loads of thick handle/grip training
  • Medicine ball throws
  • Specialty squat bars: giant cambered bar, safety squat bar
  • Front Squats
  • Deadlift variations

The Take-Home Message

There is nothing fundamentally wrong with strength training program for pitchers. In reality, what is wrong is the assumption that all strength training programs are useless because some are poorly designed and not suited to athletes' needs and limitations. Be leery of people who say strength training isn't important. Everyone - from endurance athletes, to grandmothers, to pitchers - needs it!

Further Reading

1. Bagonzi, J.A. The effects of graded weighted baseballs, free weight training, and simulative isometric exercise on the velocity of a thrown baseball. Master's thesis, Indiana University. 1978.

2. Brose, D.E., and D.L. Hanson. Effects of overload training on velocity and accuracy of throwing. Res. Q. 38:528-533. 1967.

3. Jackson, J.B. The effects of weight training on the velocity of a thrown baseball. Master's thesis, Central Michigan University,. 1994.

4. Lachowetz, T., J. Evon, and J. Pastiglione. The effects of an upper-body strength program on intercollegiate baseball throwing velocity. J. Strength Cond. Res. 12:116-119. 1998.

5. Logan, G.A., W.C. McKinney, and W. Rowe. Effect of resistance through a throwing range of motion on the velocity of a baseball. Percept. Motor Skills. 25:55-58. 1966.

6. Newton, R.U., and K.P. McEvoy. Baseball throwing velocity: A comparison of medicine ball training and weight training. J. Strength Cond. Res. 8:198-203. 1994.

7. Potteiger, J.A., H.N. Williford, D.L. Blessing, and J. Smidt. Effect of two training methods on improving baseball performance variables. J. Appl. Sport Sci. Res. 6:2-6. 1992.

8. Sullivan, J.W. The effects of three experimental training factors upon baseball throwing velocity and selected strength measures. Doctoral dissertation, Indiana University,. 1970.

9. Swangard, T.M. The effect of isotonic weight training programs on the development of bat swinging, throwing, and running ability of college baseball players. Master's thesis, University of Oregon,. 1965.

10. Thompson, C.W., and E.T. Martin. Weight training and baseball throwing speed. J. Assoc. Phys. Mental Rehabil. 19:194-196. 1965.


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Understanding Insulin

Understanding Insulin

By: Eric Cressey

All too often, we overlook the important underlying anatomy and physiology upon which solid training and nutrition recommendations are based. In rushing to get to the "meat and potatoes" (the program or ultimate recommendations) of an article, we fail to truly question and understand the basis for why we do what we do. Take, for example, post-workout nutrition. Ever wonder why you can suck up ridiculous amounts of high-carb foods after you train? In the Rugged mission statement, we promised to make you think; the following article should do just that. And, if it doesn't, you can at least gain an appreciation for one facet of an Exercise Science graduate student's course of study. Without further ado, I present "the insulin response to exercise: carbohydrate, fat, and protein metabolism implications." Introduction Insulin is well recognized as a powerful hormone capable of diverse metabolic effects in a variety of scenarios. Perhaps the most noteworthy of these scenarios is exercise, the stress of which presents significant metabolic demands. The response of insulin to these demands has far-reaching implications in terms of carbohydrate, fat, and protein metabolism. Insulin: Broad Roles in Carbohydrate, Fat, and Protein Metabolism Insulin exerts its most pronounced effects on carbohydrate metabolism at the skeletal muscle and hepatic levels. The hormone facilitates uptake of glucose into skeletal muscle and the liver, thus promoting glycogenesis. Simultaneously, it inhibits hepatic glucose release (glycogenolysis) and production (gluconeogenesis) (1). Insulin appears to demonstrate its most immediate and powerful influence in suppressing glycogenolysis, as more insulin is required to inhibit gluconeogenesis than glycogenolysis in non-diabetic subjects (2). Insulin also plays crucial roles in fat metabolism, regulating both lipolysis and lipogenesis. Lipolysis, the hydrolysis of triglycerides, is a requisite step in fat oxidation, as it liberates fatty acids for transport to mitochondria for oxidation (3). Numerous studies have demonstrated that insulin markedly blunts lipolysis at rest (3-5). Likewise, via facilitation of glucose uptake in liver and adipose tissue, insulin stimulates lipogenesis as well. Glycolytic conversion of glucose to acetyl-CoA is the precursor to fatty acid synthesis (1,6). In terms of protein metabolism, insulin's foremost role is inhibition of protein breakdown. Although the hormone does play a role in promoting protein synthesis, this effect is largely dependent on amino acid availability (7-9). Some studies have noted that insulin elevations without concurrent increases in amino acid availability actually decrease protein synthesis as a result of low plasma amino acid concentrations (10,11). Conversely, dietary amino acids exert their most prominent effect on optimizing protein synthesis rather than reducing protein breakdown (7,8,12). Hormonal Regulation of Blood Glucose: Carbohydrate, Fat, and Protein Metabolism Maintenance of plasma glucose concentrations is of paramount importance to optimal functioning of muscles and the central nervous system. Blood glucose regulation involves interactions of carbohydrate, fat, and protein metabolism; these interactions are even more readily apparent during exercise. While insulin is certainly a powerful modulator of plasma glucose levels, one must also consider several other hormones that exert the opposite physiological effects as insulin. Knowledge of these hormones - glucagon, growth hormone, cortisol, and the catecholamines epinephrine and norepinephrine - is an important prerequisite to comprehending the insulin response to exercise. Glucagon responds to the same stimuli as insulin, but has the exact opposite effects on blood glucose concentrations. These effects are, on the whole, catabolic and anti-anabolic. They include stimulation of glycogenolysis, gluconeogenesis, and protein degradation with concurrent inhibition of protein synthesis (13,14). Some studies have noted that glucagon has a stimulatory effect on lipolysis in human adipose tissue in vitro, and pharmacological interventions to induce dramatic hyperglucagonemia have proven sufficient to stimulate lipolysis (15-17). However, there is insufficient evidence to suggest that normal human hyperglucagonemia can directly induce lipolysis in vivo (18,19). While hypoglycemia is the most potent stimuli for glucagon release from the pancreas, high concentrations of insulin during hypoglycemia can suppress the glucagon response (20). Growth hormone serves as a counter-regulatory hormone to insulin in carbohydrate and fat metabolism, but works synergistically with insulin in establishing an anabolic protein metabolism environment (21). Growth hormone's insulin-antagonistic effects include increased lipolysis, decreased tissue glucose uptake, and enhanced hepatic gluconeogenesis (22-24). Meanwhile, growth hormone has an anabolic effect via enhanced protein synthesis and retention (25-31). Cortisol opposes insulin action in several regards. This glucocorticoid is likely most well known for its catabolic properties, which include stimulation of lipolysis in adipose tissue, protein degradation (the hormone also inhibits protein synthesis), and hepatic gluconeogenesis (32-35). Additionally, in terms of insulin resistance, cortisol not only directly inhibits glucose entry to cells, but also delays insulin action via a post-insulin receptor block (33,36). The catecholamines epinephrine and norepinephrine work in opposition to insulin in the regulation of the plasma glucose concentration. Epinephrine provides a strong stimulus to hepatic glucose mobilization via glycogenolysis and gluconeogenesis (37), although there is a lower threshold for glycogenolysis to occur (38). The catecholamines also stimulate lipolysis in adipose tissue (33,39) and interfere with glucose clearance by insulin (40). While the catecholamines have a catabolic effect on both liver and skeletal muscle glycogen, there is considerable evidence that they have anti-catabolic effects on muscle protein (41-43). Thyroxine is a less recognized regulator of plasma glucose concentrations. While the hormone itself has no direct effect on substrate mobilization at rest or during exercise, it does serve a permissive role for the hormones that are directly involved in plasma glucose regulation. Thyroxine acts by either increasing receptor quantity at the target tissues or by increasing receptor affinity for the aforementioned hormones; during exercise, these effects are more pronounced, as there is an increase in free thyroxine concentrations (33). Hypothyroidism (and the related thyroxine deficiency) has been shown to interfere with fuel mobilization (33). Clearly, a discussion of insulin must include attention to several glucoregulatory hormones, each of which has significant implications in carbohydrate, fat, and protein metabolism. Figure 1 summarizes the roles of those hormones with a direct effect on fuel metabolism in the liver, skeletal muscle, and adipose tissue.


Glucoregulatory Hormone Response to Exercise Insulin is the only glucoregulatory hormone that decreases with exercise under normal physiologic conditions (33). Galbo et al. (1975) found that insulin decreased both during prolonged treadmill running at 76%VO2max and with incremental treadmill exercise at 47% and 77% VO2max (no significant difference was noted at 100% VO2max) (44). Numerous other studies have observed similar decreases (45-47); these decreases are more prominent in longer duration exercise at lower intensities than in short duration, high intensity exercise (47). As a hormone working in direct opposition to insulin, glucagon increases in response to exercise. This effect has been demonstrated in both incremental (44) and prolonged (44,45) endurance exercise. In the aforementioned study by Galbo et al. (1975), the investigators found that glucagon increased more in the longer duration scenario (threefold increase over the resting value) than in incremental exercise (an increase of 35% from rest to VO2max) (44). Others have also noted that glucagon's effects are clearly more prominent in longer duration scenarios (48). Describing plasma growth hormone changes during exercise proves to be a complex task, as numerous physical, psychological, chemical, and exercise modality (both aerobic and resistance training) factors. In a broad sense, plasma growth hormone concentrations increase as exercise intensity increases; plasma GH may increase 25-fold over resting concentrations at VO2max (49). In fact, recent research by Wideman et al. (2003) noted a linear relationship between GH secretion and exercise intensity (50). Bunt et al. (1986) found that plasma GH increased by 500-600% in both runners and non-runners (runners had a higher response) during one hour of treadmill running at 60% VO2max, implying a duration effect for GH secretion as well (33,51). The growth hormone response to resistance training is a product of the work-rest intervals, loads, and volume utilized, with one minute rest periods, 10-repetition maximums, and high volumes proving most beneficial in enhancing GH secretion (50,52). Cortisol increases in response to exercise are related to intensity and duration. A study by Davies and Few (1973) demonstrated the presence of an intensity threshold that must be reached for cortisol increases to occur. In separate exercise sessions, subjects were tested for 60 minutes at 40%, 60%, 80%, and 100% VO2max. Plasma cortisol actually decreased at 40% VO2max over the course of the test, whereas cortisol increased whenever the intensity exceeded 60% VO2max (33). Apparently, light exercise facilitates plasma cortisol removal to the point that it exceeds secretion by the adrenal cortex in response to exercise. At greater intensities, secretion predominated over removal, which had increased even more (33). There also appears to be a duration threshold; Bonen (1973) observed that urinary excretion of cortisol did not change with 10 minutes of exercise at 76% VO2max. However, when the duration increased to 30 minutes, this excretion value doubled (53), likely due to a lag time in the hypothalamic-pituitary-adrenal axis between ACTH and cortisol secretion (54). Numerous studies have found that epinephrine and norepinephrine secretions increase as exercise intensity increases (55-58). However, Kraemer et al. (1985) found that graded exercise did not increase plasma epinephrine above baseline at 54% VO2 max, implying an intensity threshold for catecholamine secretion (59). Several investigators have observed increasing plasma catecholamine concentrations as exercise duration increased (60,61). Galbo et al. (1975) demonstrated that intensity is more influential than duration in the catecholamine response to exercise, as plasma epinephrine increased steadily with prolonged treadmill exercise to exhaustion at 76% VO2 max, but graded exercise in the same subjects at 44, 77, and 100% of VO2 max yielded greater increases (55). Glucose Uptake and Transport during Exercise During exercise, muscle glucose uptake may increase 30-50 fold over resting values (62). There is only a limited supply of muscle glycogen, and it can virtually be depleted with just one hour of exercise at 70-75% VO2max (63); therefore, it is of no surprise that muscle glucose uptake increases so dramatically. Given insulin's key role in promoting glucose uptake in skeletal muscle, it seems counterintuitive that the hormone would actually decrease with exercise. However, numerous physiological factors interact to ensure that plasma glucose is maintained while skeletal muscles receive adequate fuel for the continuation of exercise. First, and perhaps most logically, muscular contractions promote blood flow to skeletal muscles. With blood flow comes more glucose and insulin, so in spite of the fact that insulin is actually decreasing, there is still more opportunity for glucose uptake than at rest (33,64). Meanwhile, a gradient for more rapid glucose diffusion into the cell via increased membrane permeability is created because the muscles are utilizing glucose at a faster rate (64,65). Like insulin, exercise also leads to glucose transporter changes at the sarcolemmal level. In both scenarios, membrane transport capability increases due to translocation of insulin-stimulated GLUT4 transporters to the sarcolemma and transverse tubules from intracellular sites (65-69). Kennedy et al. (1999) demonstrated that 45-60 minutes of bicycling at 60-75% VO2max resulted in acute mean increases of 71-74% in sarcolemmal GLUT4 content in both normal and type 2 diabetic subjects (70). Others have verified this increase in plasma membrane GLUT4 content with exercise (71-73). The mechanism by which muscle contraction facilitates GLUT4 translocation to the plasma membrane is yet to be definitively elucidated; however, the most likely answer is high intramuscular calcium concentrations during exercise. More specifically, protein kinase C (PKC) is an intermediary that is dependent on calcium; PKC downregulation has been associated with reduced contraction-induced glucose transport (33,73). Potential autocrine and paracrine effects on contraction-stimulated glucose transport have also been suggested (73). You can find a scheme of the potential factors influencing GLUT4 translocation in skeletal muscle here (Hayashi et al, Am J Physiol 1997). For the sake of this discussion, it is important to note that insulin and muscular contraction facilitate glucose transport via different pathways, as Yeh et al. (1995) noted that it is possible to inhibit insulin action without inhibiting that of muscle contractions (74). Brozinick et al. (1992) validated this assertion with the observation that contraction-induced facilitated glucose transport is normal in insulin resistant muscle (75). GLUT4 and GLUT1 are two key glucose transporters found in skeletal muscle. Unlike GLUT4, which is responsive to insulin action, GLUT1 exerts its effects on glucose transport independent of insulin stimulation (69). Henriksen et al. (1990) observed that GLUT4 protein concentration is closely associated with maximal glucose transport capability; it logically follows that the overall quantity of glucose transporters (both GLUT4 and GLUT1) in the plasma membrane during exercise is proportional to muscle GLUT4 content (76). However, there is evidence to suggest that GLUT4 transporters are more associated with fast-twitch oxidative-glycolytic fibers, while GLUT1 transporters are associated with slow-twitch oxidative fibers. Additionally, there is evidence to suggest that GLUT1 transporter increases are achieved through several weeks of endurance training, whereas GLUT4 transporters are more responsive to individual exercise bouts (77). Therefore, variations in fiber-type may interfere with this assumption (78). Summarily, with more glucose transporters (both insulin-stimulated and non-insulin-stimulated) present due to both chronic and acute exercise adaptations, less insulin is necessary to have the same physiological effect. On a related note, Ivy (1997) asserted that increased concentrations of enzymes responsible for the phosphorylation, storage, and oxidation of glucose are also responsible for the improved insulin action (68). Conclusions: Bringing it all Together At first glance, it seems counterintuitive for insulin to decrease during exercise, a time when muscle glucose uptake increases rapidly. Upon further review, though, one can recognize that numerous hormonal and intracellular factors interact with this decrease to maintain plasma glucose concentrations, facilitate muscle glucose uptake, and effect appropriate changes in carbohydrate, fat, and protein metabolism. As exercise progresses, skeletal muscle glycogen depletion occurs and the muscles must look to plasma glucose as a fuel source. Assuming no provision of exogenous carbohydrate during exercise, plasma glucose must come from hepatic gluconeogenesis or glycogenolysis. These physiological occurrences are stimulated by the presence of the glucagon, epinephrine, and norepinephrine at the onset of exercise, and growth hormone and cortisol as exercise duration increases (33). As counterregulators to insulin, these five hormones can only be present in sufficient quantities to elicit the desirable effects on plasma glucose maintenance if the plasma insulin concentration is low. While the counterregulatory hormones take care of maintaining plasma glucose, there must be additional physiological adaptations to promote muscle glucose uptake in spite of the decrease in plasma insulin concentrations that occur with exercise. These exercise-induced physiological adaptations include increased skeletal muscle blood flow (and, in turn, glucose and insulin delivery), increased membrane permeability to glucose, translocation of GLUT4 proteins to the sarcolemma and transverse tubules, and increased cellular concentrations of key enzymes involved in glucose utilization. While both insulin and exercise favorably influence glucose uptake, they do so by different pathways. Nonetheless, the positive effects of acute and chronic exercise on insulin action and both insulin-dependent and non-insulin-dependent glucose transporters are undeniable. It is important to also note that glucagon, growth hormone, cortisol, and the catecholamines have effects that extend beyond plasma glucose regulation. All five hormones promote lipolysis, and thus serve as powerful regulators of fat metabolism (which is also dependent on insulin-related lipogenesis). This increased lipolysis favors the increased reliance on free fatty acids with longer durations, lower intensities, and situations of muscle glycogen depletion (79-82). Likewise, some of these hormones - glucagon, the catecholamines, and most notably, cortisol - continue to oppose insulin in protein metabolism by promoting proteolysis and inhibiting protein synthesis. Meanwhile, growth hormone works synergistically with insulin (and amino acids) to achieve an anabolic effect of elevated protein synthesis and decreased protein breakdown. References 1. Khan AH, Pessin JE. Insulin regulation of glucose uptake: a complex interplay of intracellular signalling pathways. Diabetologia. 2002 Nov;45(11):1475-83. Epub 2002 Oct 18. 2. Adkins A, Basu R, Persson M, Dicke B, Shah P, Vella A, Schwenk WF, Rizza R. Higher insulin concentrations are required to suppress gluconeogenesis than glycogenolysis in nondiabetic humans. Diabetes. 2003 Sep;52(9):2213-20. 3. 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. 4. Bonadonna RC, Groop LC, Zych K, Shank M, DeFronzo RA. Dose-dependent effect of insulin on plasma free fatty acid turnover and oxidation in humans. Am J Physiol. 1990 Nov;259(5 Pt 1):E736-50. 5. Campbell PJ, Carlson MG, Hill JO, Nurjhan N. Regulation of free fatty acid metabolism by insulin in humans: role of lipolysis and reesterification. Am J Physiol. 1992 Dec;263(6 Pt 1):E1063-9. 6. Kersten S. Mechanisms of nutritional and hormonal regulation of lipogenesis. EMBO Rep. 2001 Apr;2(4):282-6. 7.Castellino P, Luzi L, Simonson DC, Haymond M, DeFronzo RA. Effect of insulin and plasma amino acid concentrations on leucine metabolism in man. Role of substrate availability on estimates of whole body protein synthesis. J Clin Invest. 1987 Dec;80(6):1784-93. 8.Tessari P, Inchiostro S, Biolo G, Trevisan R, Fantin G, Marescotti MC, Iori E, Tiengo A, Crepaldi G. Differential effects of hyperinsulinemia and hyperaminoacidemia on leucine-carbon metabolism in vivo. Evidence for distinct mechanisms in regulation of net amino acid deposition. J Clin Invest. 1987 Apr;79(4):1062-9. 9. Heslin MJ, Newman E, Wolf RF, Pisters PW, Brennan MF. Effect of hyperinsulinemia on whole body and skeletal muscle leucine carbon kinetics in humans. Am J Physiol. 1992 Jun;262(6 Pt 1):E911-8. 10. McNurlan MA, Garlick PJ. Influence of nutrient intake on protein turnover. Diabetes Metab Rev. 1989 Mar;5(2):165-89. 11. Frexes-Steed M, Lacy DB, Collins J, Abumrad NN. Role of leucine and other amino acids in regulating protein metabolism in vivo. Am J Physiol. 1992 Jun;262(6 Pt 1):E925-35. 12. Svanberg E, Moller-Loswick AC, Matthews DE, Korner U, Andersson M, Lundholm K. Effects of amino acids on synthesis and degradation of skeletal muscle proteins in humans. Am J Physiol. 1996 Oct;271(4 Pt 1):E718-24. 13. Gravholt CH, Moller N, Jensen MD, Christiansen JS, Schmitz O. Physiological levels of glucagon do not influence lipolysis in abdominal adipose tissue as assessed by microdialysis. J Clin Endocrinol Metab. 2001 May;86(5):2085-9. 14. Charlton MR, Adey DB, Nair KS. Evidence for a catabolic role of glucagon during an amino acid load. 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The role of growth hormone in the regulation of protein metabolism with particular reference to conditions of fasting. Horm Res. 2003;59 Suppl 1:62-8. 26. Clemmons DR, Snyder DK, Williams R, Underwood LE: Growth hormone administration conserves lean body mass during dietary restriction in obese subjects. J Clin Endocrinol Metab 1987;64:878-883. 27. Gamrin L, Essen P, Hultman E, McNurlan MA, Garlick PJ, Wernerman J. Protein-sparing effect in skeletal muscle of growth hormone treatment in critically ill patients. Ann Surg. 2000 Apr;231(4):577-86. 28. Lundeberg S, Belfrage M, Wernerman J, von der Decken A, Thunell S, Vinnars E: Growth hormone improves muscle protein metabolism and whole body nitrogen economy in man during a hyponitrogenous diet. Metabolism 1991;40:315-322. 29. Carli F, Webster JD, Halliday D: Growth hormone modulates amino acid oxidation in the surgical patient: leucine kinetics during the fasted and fed state using moderate nitrogenous and caloric diet and recombinant human growth hormone. Metabolism 1997;46:23-28. 30. Copeland KC, Nair KS: Acute growth hormone effects on amino acid and lipid metabolism. J Clin Endocrinol Metab 1994;78:1040-1047. 31. Fryburg DA, Barrett EJ: Growth hormone acutely stimulates skeletal muscle but not whole-body protein synthesis in humans. Metabolism 1993;42:1223-1227. 32. Divertie GD, Jensen MD, Miles JM. Stimulation of lipolysis in humans by physiological hypercortisolemia. Diabetes. 1991 Oct;40(10):1228-32. 33. Powers, SK, Howley, ET. Exercise physiology, 4th edition. Boston: McGraw Hill, 2001. 34. Brillon DJ, Zheng B, Campbell RG, Matthews DE. Effect of cortisol on energy expenditure and amino acid metabolism in humans. Am J Physiol. 1995 Mar;268(3 Pt 1):E501-13. 35. Simmons PS, Miles JM, Gerich JE, Haymond MW. Increased proteolysis. An effect of increases in plasma cortisol within the physiologic range. J Clin Invest. 1984 Feb;73(2):412-20. 36. Rizza RA, Mandarino LJ, Gerich JE. Cortisol-induced insulin resistance in man: impaired suppression of glucose production and stimulation of glucose utilization due to a postreceptor detect of insulin action. J Clin Endocrinol Metab. 1982 Jan;54(1):131-8. 37. Sherwin RS, Sacca L. Effect of epinephrine on glucose metabolism in humans: contribution of the liver. Am J Physiol. 1984 Aug;247(2 Pt 1):E157-65. 38. Sacca L, Vigorito C, Cicala M, Corso G, Sherwin RS. Role of gluconeogenesis in epinephrine-stimulated hepatic glucose production in humans. Am J Physiol. 1983 Sep;245(3):E294-302. 39. Cryer PE. Adrenaline: a physiological metabolic regulatory hormone in humans? Int J Obes Relat Metab Disord. 1993 Dec;17 Suppl 3:S43-6; discussion S68. 40. Rizza R, Haymond M, Cryer P, Gerich J. Differential effects of epinephrine on glucose production and disposal in man. Am J Physiol. 1979 Oct;237(4):E356-62. 41. Fryburg DA, Gelfand RA, Jahn LA, Oliveras D, Sherwin RS, Sacca L, Barrett EJ. Effects of epinephrine on human muscle glucose and protein metabolism. Am J Physiol. 1995 Jan;268(1 Pt 1):E55-9. 42. Miles JM, Nissen SL, Gerich JE, Haymond MW. Effects of epinephrine infusion on leucine and alanine kinetics in humans. Am J Physiol. 1984 Aug;247(2 Pt 1):E166-72. 43. Kraenzlin ME, Keller U, Keller A, Thelin A, Arnaud MJ, Stauffacher W. Elevation of plasma epinephrine concentrations inhibits proteolysis and leucine oxidation in man via beta-adrenergic mechanisms. J Clin Invest. 1989 Aug;84(2):388-93 44. Galbo H, Holst JJ, Christensen NJ. Glucagon and plasma catecholamine responses to graded and prolonged exercise in man. J Appl Physiol. 1975 Jan;38(1):70-6. 45. Miller SL, Maresh CM, Armstrong LE, Ebbeling CB, Lennon S, Rodriguez NR. Metabolic response to provision of mixed protein-carbohydrate supplementation during endurance exercise. Int J Sport Nutr Exerc Metab. 2002 Dec;12(4):384-97. 46. Bonen A, Belcastro AN, MacIntyre K, Gardner J. Hormonal responses during intense exercise preceded by glucose ingestion. Can J Appl Sport Sci. 1980 Jun;5(2):85-90. 47. Tatar P, Kozlowski S, Vigas M, Nazar K, Kvetnansky R, Jezova D, Kaciuba-Uscilko H. Endocrine response to physical efforts with equivalent total work loads but different intensities in man. Endocrinol Exp. 1984 Dec;18(4):233-9. 48. Kjaer M. Hepatic glucose production during exercise. Adv Exp Med Biol. 1998;441:117-27. 49. Sutton J, Lazarus L. Growth hormone in exercise: comparison of physiological and pharmacological stimuli. J Appl Physiol. 1976 Oct;41(4):523-7. 50. Wideman L, Weltman JY, Hartman ML, Veldhuis JD, Weltman A. Growth hormone release during acute and chronic aerobic and resistance exercise: recent findings. Sports Med. 2002;32(15):987-1004. 51. Bunt JC, Boileau RA, Bahr JM, Nelson RA. Sex and training differences in human growth hormone levels during prolonged exercise. J Appl Physiol. 1986 Nov;61(5):1796-801. 52. Baechle, TR, Earle, RW. Essentials of Strength and Conditioning, 2nd edition. Champaign, IL: Human Kinetics, 2001. 53. Bonen A. Effects of exercise on excretion rates of urinary free cortisol. J Appl Physiol. 1976 Feb;40(2):155-8. 54. Rasmuson S, Olsson T, Hagg E. A low dose ACTH test to assess the function of the hypothalamic-pituitary-adrenal axis. Clin Endocrinol (Oxf). 1996 Feb;44(2):151-6. 55. Galbo H, Holst JJ, Christensen NJ. Glucagon and plasma catecholamine responses to graded and prolonged exercise in man. J Appl Physiol. 1975 Jan;38(1):70-6. 56. de Diego Acosta AM, Garcia JC, Fernandez-Pastor VJ, Peran S, Ruiz M, Guirado F. Influence of fitness on the integrated neuroendocrine response to aerobic exercise until exhaustion. J Physiol Biochem. 2001 Dec;57(4):313-20. 57. Kraemer WJ, Dziados JE, Gordon SE, Marchitelli LJ, Fry AC, Reynolds KL. The effects of graded exercise on plasma proenkephalin peptide F and catecholamine responses at sea level. Eur J Appl Physiol Occup Physiol. 1990;61(3-4):214-7. 58. McMurray RG, Forsythe WA, Mar MH, Hardy CJ. Exercise intensity-related responses of beta-endorphin and catecholamines. Med Sci Sports Exerc. 1987 Dec;19(6):570-4. 59. Kraemer WJ, Noble B, Culver B, Lewis RV. Changes in plasma proenkephalin peptide F and catecholamine levels during graded exercise in men. Proc Natl Acad Sci U S A. 1985 Sep;82(18):6349-51. 60. Sothmann MS, Blaney J, Woulfe T, Donahue-Fuhrman S, Lefever K, Gustafson AB, Murthy VS. Plasma free and sulfoconjugated catecholamines during sustained exercise. J Appl Physiol. 1990 Feb;68(2):452-6. 61. Rostrup M, Westheim A, Refsum HE, Holme I, Eide I. Arterial and venous plasma catecholamines during submaximal steady-state exercise. Clin Physiol. 1998 Mar;18(2):109-15. 62. Sahlin K. Muscle glucose metabolism during exercise. Ann Med. 1990 Jun;22(3):85-9. 63. Coggan AR, Coyle EF. Carbohydrate ingestion during prolonged exercise: effects on metabolism and performance. Exerc Sport Sci Rev. 1991;19:1-40. 64. Ivy JL. The insulin-like effect of muscle contraction. Exerc Sport Sci Rev. 1987;15:29-51. 65. Wojtaszewski JF, Richter EA. Glucose utilization during exercise: influence of endurance training. Acta Physiol Scand. 1998 Mar;162(3):351-8. 66. Richter EA, Kristiansen S, Wojtaszewski J, Daugaard JR, Asp S, Hespel P, Kiens B. Training effects on muscle glucose transport during exercise. Adv Exp Med Biol. 1998;441:107-16. 67. Goodyear LJ, Kahn BB. Exercise, glucose transport, and insulin sensitivity. Annu Rev Med. 1998;49:235-61. 68. Ivy JL. Role of exercise training in the prevention and treatment of insulin resistance and non-insulin-dependent diabetes mellitus. Sports Med. 1997 Nov;24(5):321-36. 69. Ivy JL, Kuo CH. Regulation of GLUT4 protein and glycogen synthase during muscle glycogen synthesis after exercise. Acta Physiol Scand. 1998 Mar;162(3):295-304. 70. Kennedy JW, Hirshman MF, Gervino EV, Ocel JV, Forse RA, Hoenig SJ, Aronson D, Goodyear LJ, Horton ES. Acute exercise induces GLUT4 translocation in skeletal muscle of normal human subjects and subjects with type 2 diabetes. Diabetes. 1999 May;48(5):1192-7. 71. Douen AG, Ramlal T, Rastogi S, Bilan PJ, Cartee GD, Vranic M, Holloszy JO, Klip A. Exercise induces recruitment of the "insulin-responsive glucose transporter". Evidence for distinct intracellular insulin- and exercise-recruitable transporter pools in skeletal muscle. J Biol Chem. 1990 Aug 15;265(23):13427-30. 72. Fushiki T, Wells JA, Tapscott EB, Dohm GL. Changes in glucose transporters in muscle in response to exercise. Am J Physiol. 1989 May;256(5 Pt 1):E580-7. 73. Hayashi T, Wojtaszewski JF, Goodyear LJ. Exercise regulation of glucose transport in skeletal muscle. Am J Physiol. 1997 Dec;273(6 Pt 1):E1039-51. 74. Yeh JI, Gulve EA, Rameh L, Birnbaum MJ. The effects of wortmannin on rat skeletal muscle. Dissociation of signaling pathways for insulin- and contraction-activated hexose transport. J Biol Chem. 1995 Feb 3;270(5):2107-11. 75. Brozinick JT Jr, Etgen GJ Jr, Yaspelkis BB 3rd, Ivy JL. Contraction-activated glucose uptake is normal in insulin-resistant muscle of the obese Zucker rat. J Appl Physiol. 1992 Jul;73(1):382-7. 76. Henriksen EJ, Bourey RE, Rodnick KJ, Koranyi L, Permutt MA, Holloszy JO. Glucose transporter protein content and glucose transport capacity in rat skeletal muscles. Am J Physiol. 1990 Oct;259(4 Pt 1):E593-8. 77. Phillips, S., et al. Increments in skeletal muscle GLUT-1 and GLUT-4 after endurance training in humans. Am J Physiol. 1996 Mar;270(3 Pt 1):E456-62. 78. Johannsson, E., Effect of cross-reinnervation on the expression of GLUT-4 and GLUT-1 in slow and fast rat muscles. Am J Physiol. 1996 Jun;270(6 Pt 2):R1355-60. 79. Holloszy JO, Kohrt WM, Hansen PA. The regulation of carbohydrate and fat metabolism during and after exercise. Front Biosci. 1998 Sep 15;3:D1011-27. 80. Jensen MD. Fate of fatty acids at rest and during exercise: regulatory mechanisms. Acta Physiol Scand. 2003 Aug;178(4):385-90. 81. Spriet LL, Watt MJ. Regulatory mechanisms in the interaction between carbohydrate and lipid oxidation during exercise. Acta Physiol Scand. 2003 Aug;178(4):443-52. 82.Coggan AR. Plasma glucose metabolism during exercise in humans. Sports Med. 1991 Feb;11(2):102-24.
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An Interview with Jim “Smitty” Smith

An  Interview with Jim "Smitty" Smith

By: Eric Cressey

I've been following the Diesel Crew guys for a few years, but it wasn't until the past year or so that I had the opportunity to start interacting with Jim "Smitty" Smith regularly.  In the short time that I've known him, Smitty has really impressed me; he is without a doubt one of the most knowledgeable and innovative guys in the "biz."  The interview below is just a small sample of the tremendous amount Smitty has to offer; enjoy! EC: Okay, Smitty, I know quite a bit about you, but that's not to say that our readers can be sure that you're not a complete poser.  Tell is about yourself. JS:  I've been involved in strength training since 1995 and a strength coach since 2001.  I have gotten a few certifications over the years, but have most of my knowledge from years of self study, competing in sports and strongman competitions. I co-founded the Diesel Crew, along with Jedd Johnson, in late 2001 and have been developing the Diesel Method since then.  We've been utilizing powerlifting, odd objects, kettlebells, weightlifting, and Grip strength protocols to build athletes to their greatest potential. I believe we have a solid reputation for being innovators and hopefully provide strength coaches and fitness professionals with new ideas to improve their strength programs. EC: You're about as creative a person in this industry as I've met.  You're like MacGyver; you could train a blind man with no arms and legs with just a book of matches, some Blue Heat, and a burrito.  How did you get so creative?  Do you sniff glue or something? JS: What have you heard?  Let's not talk about college. Seriously, when people first see our products, I am sure they say to themselves, "Damn, I would have never thought of that exercise."  I take a lot of pride in that. When Jedd and I first started, we had no money and no equipment.  All we had was a great desire to succeed.  If we had an idea for an exercise, but we didn't have the equipment, we had to make it or improvise. For instance, in the EliteFTS Q&A Exercise Index, you'll see one unique way to train atlas stones right in a commercial gym without atlas stones and even a cool way to train farmer's walks without farmer's walk implements.  These are just two quick examples. But it is much more than being creative with equipment when you are poor. If athletes or coaches are participating in or training with powerlifting components, they typically only use powerlifting techniques.  If people are utilizing odd objects in their training, they also typically only use these techniques and exercises. But, we saw great potential benefit trying to combine techniques from each protocol into one system.  We called it the Diesel Method. One example would be to take typical keg lifting (odd object) and perform beyond the range (powerlifting) bear hug good mornings.  This BTR hip extension has huge carryover for gluteal firing and neutral lumbar stability endurance. EC: You and Jedd are the go-to guys when it comes to grip training.  What are the most common mistakes you're seeing people make with their grip training? JS: Grip training is not only about getting your hands stronger; it is also about preventing imbalances, training specificity (General, General Specific) for your sport and finally learning how to channel the power generated by your body through your hands.  The body works in integration and everything is connected.  Grip is typically the weakest link in this coordinated kinetic chain.  Strength programs focus on developing limit strength, rate of force development, power, speed, agility and so on - but we still must be able to express this strength through our hands to play any sport!  That is why Grip strength is so important. For example, if you're a boxer whose hands, wrists, and elbows are weak or beat up from tons of sparring, you are very quickly going to: -  become injured from impact - cannot provide adequate contraction of musculature -  become injured from too much tendon and soft tissue trauma - poor restoration -  become limited in your ability to generate a powerful punch - poor neural expression To determine how to implement Grip protocols into your training, check the Needs Analysis for the sport and go from there. EC: I know you're got a pretty good corrective training background; have you been able to apply some of this grip work in that capacity to prevent/rehabilitate injuries to the elbows, forearms, and wrists? JS:  Eric, you know we need to create balance in our movements.  If we have balance in movements, improved soft-tissue quality, neural grooving of firing - then we'll have proper functioning.  The same goes for Grip. You used the example in your Sturdy Shoulder seminar of people who sit in flexion, type in flexion, watch TV in flexion, play video games in flexion all day long.  These people MUST do extension, mobility, and soft tissue work. Similarly, a comprehensive grip protocol would include; flexion (fingers, wrists), extension (fingers, wrists), supination, pronation (radial/ulnar), ulnar / radial deviation (wrist), internal / external rotation (humerus), adduction / abduction (fingers) - everything from the fingertips to the shoulders.  Remember, everything is connected. Now, once these movements, imbalances, and injuries have been addressed, we move to Level II, where we start to learn how to express power through the hands.  That is where irradiation or co-contraction comes into play. The lower arm musculature is part of the whole kinetic chain.   You'll immediately see this when you move into finger into extension against a rubber band or sand (bucket), and the musculature that crosses your elbow contracts.  Why is that?  Because we know that if a muscle crosses a joint it affects that joint.  That is why when you clench your fist as hard as you can, your forearm, biceps, triceps, deltoid, and lat contract as well.  That is how the kinetic chain works, and we can utilize this to our benefit in our training. EC: Let's talk about the Jim Smith library.  What are your top five resources? JS: 1. All the standards: -Essentials of Strength and Conditioning, by Baechle and Earle -Supertraining, by Siff -Science and Practice of Strength Training: 2nd Ed., by Zatsiorsky and Kraemer -Designing Resistance Training Programs, by Kraemer and Fleck 2. The Ultimate Off-Season Training Manual, by Cressey 3. Starting Strength, by Rippletoe and Kilgore 4. Afterburn I & II, by Cosgrove 5. James Smith's Manuals 6. The Coach's Strength Training Playbook, by Kenn 7. Chu's Plyometric books The list goes on and on.  Some I reread regularly, some I use as a reference. I would recommend that your subscribers also do the following: 1. Print out articles and categorize them by topic: nutrition, periodization, sport, protocol, etc.  Now, take these articles and get a bunch of 3-ring binders and create a binder for each category. 2. Make a goal for yourself that each day you will: read one article, read one blog post, add one article to your binder(s), email someone on a question you have, start or create an article yourself. 3. With the idea of always trying to improve yourself, attend every seminar, clinic, and/or conference you can.  I've spent thousands this year in the never-ending pursuit of knowledge. EC: You've got a new manual: "Building the Ultimate MMA Athlete."  Fill us in a bit on it. JS:  I've been a huge MMA for years and coming from a wrestling background, I have been formulating ideas for years to put in this manual, specifically training the functional movement patterns for combat athletics.  It started as a small project and ended up being an eight-month project ending with a 300-page manual. I have gotten an overwhelmingly great response to the book because it is not your standard deadlifts, pull-ups, and cleans type of manual.  Of course, those exercises form the foundation of the program and are in there, but I wanted to go above and beyond that standard school of thought.  I used every implement known to man and took the three functional positions; Standing/Clinch, the Guard, and the Mount, and built the programs and exercises around them. My next manual, Chaos Training, is also going to open a lot of eyes and minds on what "functional" training really is. EC: Cool stuff; thanks a ton for taking the time, Smitty.  How can our readers contact you? JS: The best bet is to go through our websites, www.DieselCrew.com . EC: A note to our readers: Smitty's new Combat Core e-book is an absolutely awesome read that I highly recommend to everyone interested in learning about true "core stability" and "functional training."  I reviewed it HERE.
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A New Model for Training Between Starts: Part 2

A New Model for Training Between Starts: Part 2

By: Eric Cressey

In Part 1 of this article series, I discussed everything that was wrong with distance running for pitchers.  In Part 2, I'll outline my thoughts on how to best integrate conditioning for pitchers between throwing sessions.  This article will focus on managing starters, but I suspect you'll find that managing relievers isn't entirely different aside from the fact that you'll need to "roll with the punches" a bit more. I think the best way to introduce this article is to describe a coincidence from the beginning of the year.    On January 5, I received an email from one of my pro pitchers asking me if I could outline some thoughts on my between-start strength and conditioning mentality, as his old college pitching coach had asked for his input from him, as he was a student of the game and had tried some non-traditional ideas. In response to that email, I replied with essentially everything I'll describe in this article - plus everything I outlined in Part 1 with respect to how bad a choice distance running is. The coincidence didn't become apparent until a week or two later when I got my hands on the January installment of the Journal of Strength and Conditioning Research, which featured a study entitled "Noncompatibility of power and endurance training among college baseball players." These researchers divided a collegiate pitching staff into two groups of eight over the course of a season, and each group did everything identically - except the running portion of their training programs.  Three days per week, the "sprint" group did 10-30 sprints of 15-60m with 10-60s rest between bouts.  The endurance group performed moderate-to-high intensity jogging or cycling 3-4 days per week for anywhere from 20-60 minutes. Over the course of the season, the endurance group's peak power output dropped by an average of 39.5 watts while the sprinting group increased by an average of 210.6 watts (1).  So, basically what I'm saying is that I was right all along - and I'm totally going to brag about it.  Part 1 of this series simply justified all of my thoughts; now it's time to put them into a framework. Some Prerequisite Q&A As a response to Part 1, I got an email from a college pitching coach looking for some further details, and here were his questions (bold) and my answers: Q: Is running 1-2 miles once a week considered distance running? A: I'd call anything over 150m "distance running" in a pitching population, believe it or not.  I haven't had a baseball player run over 60 yards in two years - and even when they go 60, they're build-ups, so only about 50% of that distance is at or near top speed. Q: Is running 10 poles in 30s with one minute of rest considered distance? A: Let's say it takes 30s to run a pole, and then you rest a minute (1:2 work: rest ratio).  Then, you go out and pitch, where you exert effort for one second and rest 20s (1:20 work:rest ratio).  This is the equivalent of a 100m sprinter training like a 1500m runner. Q: Don't you need some endurance to pitch a complete 9-inning game? A: If all endurance was created equal, why didn't Lance Armstrong win the New York or Boston Marathon?  Endurance is very skill specific.  Additionally, there is a huge difference between exerting maximal power over 20-25 individual efforts with near complete rest (a sample inning) and exerting submaximal efforts repeatedly with no or minimal rest. Q: What about guys who are overweight?  What should they do? A: Fat guys should be paperweights, bouncers, sumo wrestlers, or eating contest champions.  If they want to be successful players at the D1 level or beyond, they'll sack up and stop eating crap.  Several years ago, I promised myself that I would never, ever try to use extra conditioning to make up for poor diet. Q: What are your thoughts on interval training? A: We know that interval training is superior to steady state cardio for fat loss, but the important consideration is that it must be specific to the sport in question. These responses should set the stage for the following points: 1. The secret is to keep any longer duration stuff low-intensity (under 70% HRR) and everything else at or above 90% of max effort (this includes starts, agilities, and sprints up to 60yds).  For more background on this, check out the McCarthy et al. study I outlined in Part 1. 2. Ideally, the low-intensity work would involve significant joint ranges-of-motion (more to come on this below). 3. Don't forget that pitchers rarely run more than 15 yards in a game situation. 4. Strength training and mobility training far outweigh running on the importance scale. 5.  If you need to develop pitching specific stamina, the best way to achieve that end is to simply pitch and build pitch counts progressively.  If that needs to be supplemented with something to expedite the process a bit, you can add in some medicine ball medleys - which can also be useful for ironing out side-to-side imbalances, if implemented appropriately.  However, a good off-season throwing program and appropriate management of a pitcher early in the season should develop all the pitching specific endurance that is required. The 5-Day Rotation In a case of a five-day rotation, here is how we typically structure things.  Keep in mind that dynamic flexibility and static stretching are performed every day. Day 0: pitch Day 1 (or right after pitching, if possible): challenging lower body lift, push-up variation (light), horizontal pulling (light), cuff work Day 2: movement training only, focused on 10-15yd starts, agility work, and some top speed work (50-60 yds) Day 3: bullpen (usually), single-leg work, challenging upper body lift (less vertical pulling in-season), cuff work Day 4: low-intensity dynamic flexibility circuits only Day 5: next pitching outing Notes: 1. When a guy happens to get five days between starts, we'll typically split the Day 3 lifting session into two sessions and do some movement training on Day 4 as well. 2. I know a lot of guys (myself included) are advocates of throwing more than once between starts.  For simplicity's sake, I haven't included those sessions. 3.  There are definitely exceptions to this rule.  For instance, if a guy is having a hard time recovering, we'll take Day 2 off altogether and just do our sprint work after the bullpen and before lifting on Day 3.  That adds a full day of rest to the rotation in addition to the really light Day 4. The 7-Day Rotation With a 7-day rotation, we've got a lot more wiggle room to get aggressive with things.  This is why in-season can still be a time of tremendous improvements in the college game, especially since you can work in a good 2-3 throwing sessions between starts.  Again, dynamic flexibility and static stretching are performed every day.  To keep this simple, I'm going to assume we've got a Saturday starter. Saturday: pitch Sunday: challenging lower body lift, light cuff work Monday: movement training only, focused on 10-15yd starts, agility work, and some top speed work (50-60 yds); upper body lift Tuesday: low-Intensity resistance training (<30% of 1RM) circuits, extended dynamic flexibility circuits Wednesday: full-body lift Thursday: movement training only, focused on 10-15yd starts, agility work, and some top speed work (50-60 yds); Friday: low-intensity dynamic flexibility circuits only Saturday: pitch again Of course, traveling logistics can throw a wrench in the plans on this front sometimes, but the good news is that collegiate pitchers have six days to roll with the punches to get back on schedule. Closing Thoughts As you can see, I am a big fan of quality over quantity. Our guys only sprint twice in most weeks - and certainly not more than three times.  This certainly isn't the only way to approach training between starts, but I've found it to be the most effective of what our guys have tried. References 1. Rhea MR, Oliverson JR, Marshall G, Peterson MD, Kenn JG, Ayllón FN. Noncompatibility of power and endurance training among college baseball players. J Strength Cond Res 2008 Jan;22(1):230-4. Sign-up Today for our FREE Baseball Newsletter and Receive a Copy of the Exact Stretches used by Cressey Performance Pitchers after they Throw!
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Lats: Not Just Good for Pulldowns

Imagine, for a second, that I was to tell you that there's a muscle that: a) has serious growth potential b) can dramatically increase your squat and deadlift poundages c) can drive your bench press through the roof d) can keep your shoulders, upper back, lower back, and hips healthy e) can help you run faster f) affects the way you breath You'd probably think I was nuts. Surely the strength training community would've caught on by now, right? Well, I wouldn't say that they haven't caught on; I'd just say that they haven't learned how to utilize this muscle — and it does exist — in the right ways. Perhaps the worst part is that this muscle has a big cross sectional area already, so it's staring people right in the face. I'm talking about the latissimus dorsi, lats for short. Let's get to it... Continue Reading...
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40 Random Thoughts

Like everyone else, I've had my role models and mentors who've looked out for me. My mother has taught high school English for over 20 years, so I owe a lot of my writing success to her. My father taught me to tie a tie and to remember to check the oil in my car. My brother, the accountant, is always a phone call away if I need financial advice. Guys like Alwyn Cosgrove, John Berardi, Dave Tate, and Jason Ferruggia have all been extremely gracious in giving me advice as an up-and-comer in this business. In short, I'm just the sum of many constituent parts: individuals to whom I owe a debt I'll never be able to repay. Continue Reading...
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  • Avoid the most common deadlifting mistakes
  • 9 - minute instructional video
  • 3 part follow up series