Maximum Muscularity II

About the Author: Eric Cressey

by Eric Cressey and Tim Skwiat

In Part 1, Tim and Eric set forth the dietary framework for Maximum Muscularity. Now, training and supplementation take center stage.

* Add Fuel to the Fire…On non-lifting days, we highly recommended that you perform high-intensity interval training (HIIT) in place of the resistance training. The fact that HIIT is most heavily reliant on muscle glycogen during exercise does not mean that it is an inefficient method of exercise for fat loss. On the contrary, HIIT is a much more efficient means of achieving fat loss than steady-state aerobics. Otherwise, you wouldn’t see so many non-spandex deserving aerobics instructors with greater than 30% body fat! When the post-exercise period is factored in and excess post-exercise oxygen consumption (EPOC) is taken into account, the total amount of fat and calories burned as a result of the HIIT is actually greater than with its lower intensity counterparts (20-22). And, let’s not forget that in given the right work: rest ratio, you’ll almost always perform more total work with HIIT than steady-state aerobics. Tremblay et al. found that subjects who performed a HIIT program showed a ninefold greater decrease in the sum of six subcutaneous skinfolds relative to a group of subjects that performed an endurance training program (23). Additionally, interval training is considered to be superior to steady-state, submaximal cardiovascular activity in improving VO2max (24). We know what you’re thinking: “Why should I worry about VO2max? I lift weights; VO2max is only important for spandex-clad cyclists!” Well, even if being a more functional lifter (or athlete, if that’s your cup o’ tea) isn’t reason enough to value VO2max improvements, you will still be interested to know that a greater VO2max value has been associated with increased thermic effect of food (25). That’s right – jack up the VO2max, and the dozen Krispy Kremes that “accidentally” vanish in your presence are less likely to be stored as body fat.

As if all these benefits weren’t enough, let’s consider the explosive nature of HIIT work. Typically, your ball-busting work periods are in the 10-30 second range, a timeframe that closely approximates the duration of most strength training sets. In other words, you’ll be training the same energy systems (ATP-PC and fast glycolysis) as in strength training (13). And, less scientifically, picture yourself digging deep to propel yourself forward during a sprint. Now, think of the last time your hip and knee extensors kicked in as fired out of “the hole” during a set of squats. You can bet that training your explosiveness will carry over to such performances. Finally, when you notice how insanely sore your hams, glutes, quads, calves, obliques, and lower back are after your first sprinting session, you’ll be convinced of how effective HIIT can be in promoting muscle growth.

Okay, now that you understand why HIIT beats steady-state aerobics like a redheaded stepchild, let’s consider the mode and structure of your HIIT sessions. There are plenty of options available: cycling, elliptical trainers (preferably with arm motion included), rowing, jumping rope, and boxing. However, ask any HIIT-aficionado, and he’ll tell you that sprints are king! That said, the table below summarizes some HIIT guidelines to adhere to regardless of your mode of choice. Note: Because we are using interval training for physique enhancement rather than purely for performance improvement, these selections depart from traditional interval training protocols. At the very least, they represent the shortest end of the spectrum in terms of rest intervals, as total recovery should not be reached before the onset of the next work interval.

Work Period Rest Period Work: Rest Ratio Repetitions Duration
10s 50s 1:5 15 15:00
15s 45s 1:3 15 15:00
20s 40s 1:2 15 15:00
30s 60s 1:2 10 15:00

These guidelines are, however, very general; you’ll need to modify them slightly based on your fitness level. With that in mind, suppose you do three HIIT sessions per week. You might opt to do all three at a 1:5 work: rest ratio the first week, and then switch to a 1:2 ratio for the second week. Or, you could add another interval each week. Finally, you could perform each session for the week at a different intensity. That’s one of the beauties of Maximum Muscularity: flexibility. Just be sure to change your protocol of choice every few weeks.

Following the bout of HIIT, a brief (i.e. 5-15 minutes) session of low-intensity aerobics might work to enhance fat loss. It appears that inadequate blood flow to adipose tissue during high-intensity exercise is the culprit behind reduced fat oxidation (26). As a result, immediately upon cessation of high-intensity exercise, there is a marked increase in the concentration of plasma free fatty acids (2). By exercising at an intensity that relies primarily on the use of plasma fatty acids (i.e. less than 60% of heart rate reserve), you will maximize adipose tissue lipolysis and fat oxidation.

On HIIT days, the same schedule (i.e. time of training) need not be followed, but the same diet plan should be preserved. Again, it?s important to remember that high-intensity aerobic exercise (i.e. HIIT) is very heavily glycogen-dependent and can be much more depleting that resistance training. Significant glycogen depletion can occur with a mere 15-30 minutes of exercise performed at very high intensities (i.e. 90-130% of VO2max), which is similar to the protocol that is followed in HIIT-style training (12). Therefore, you should not be at all leery about maintaining your carbohydrate intake after HIIT sessions.

We recommend one complete day of rest from exercise per week. On this activity-free day, you should focus on consuming mostly meals of protein, fats, and fibrous veggies, as described above. That said, on this day, a breakfast of protein and carbs is warranted in most cases, particularly for those who are focusing on gaining muscle mass. Lastly, if your primary goal is muscle growth, you may choose to limit the frequency of HIIT to 1-2 sessions per week. Additionally, for these same individuals, the frequency of the lower intensity aerobic sessions may be reduced or the sessions themselves shortened.

With HIIT completing the training mix, here’s what your sample split might look like:

Upon Rising HIIT Weight training*
Monday: 20-45 minutes Late Afternoon
Tuesday: 20-45 minutes Late Afternoon
Wednesday: Sprints
Thursday: 20-45 minutes Late Afternoon
Friday: 20-45 minutes Late Afternoon
Saturday: Sprints
Sunday: Relax. Kill, cook and eat furry woodland creatures.

*Note: Weight training sessions may be followed by 5-15 minutes of low-intensity aerobics.

*Topping off the Tank…Some individuals may find that after a period of time following these guidelines that glycogen stores are not adequately topped off. Increasing the carbohydrate content of the protein and carb meals and/or increasing overall caloric intake can circumvent this dilemma. However, these increases are not feasible for some, particularly those in a hypoenergetic state who are using this plan as a vehicle for fat loss. That said, many individuals might find that a day of higher carbohydrate intake is needed once every 6-12 days. Obviously, this is a very broad range due to individual differences, so it may take some trial and error (start with every twelfth day). As a rule of thumb, the leaner you are, the more frequently you should carb up. Rather than engaging in an uncontrolled overfeed (consisting of refined, processed, sugary carbs), simply increase the number of protein and carb meals. These meals should be very similar in composition to those that you utilize on a daily basis (healthy carb sources). We encourage you to implement this day of reglycogenation following a weight training session; ideally, the training session would be performed early in the day (i.e. after one protein and fat meal) and be followed by 3-5 protein and carb meals containing 60-100g of carbohydrate each. Total carbohydrate intake will vary based on frequency of reglycogenation periods (i.e. degree of depletion) and activity level on that particular day. To maximize glycogen restoration, a carbohydrate intake of 3-5g/kg of lean body mass is a good starting point; more or less may be optimal. All in all, you’ll need to pay close attention to your response to varying levels of carbohydrate intake, as well as varying frequencies of high-carb days. You will, however, still see comparable results if you opt to incorporate the increased carb intake on a rest day (breakfast should be the largest meal, and carb should slowly be tapered off as the day progresses). This higher carb day will prove beneficial in that it will be very anti-catabolic and will fill up muscle glycogen stores. More importantly for some, it will help to quell any possible mental cravings. Implementing the reglycogenation strategy in a relatively glycogen-depleted state will actually make possible more glycogen storage than if glycogen is restored on a daily basis (27). More glycogen = more energy. More energy = harder training. Harder training = more muscle and less fat.

*Supplements…Although the Maximum Muscularity plan does not require extensive supplementation, several supplements will increase its efficacy. With that in mind, we recommend:

1) BCAAs: These anti-catabolic amino acids will definitely prove valuable in the morning before the fasted-state activity and during your regular HIIT sessions. Xtreme Formulations’ ICE is an excellent choice in this regard, as it also offers an appreciable dose of glutamine.

2) Nootropic: Marc McDougal outlined various nootropic supplements recently in his article, “This is Your Brain on Drugs”. It goes without saying that many of these agents will enhance focus throughout the day ? especially during training sessions – and will help to create the vision of Maximum Muscularity that will keep you going!

3) Glucose disposal agents, particularly R-ALA: These are excellent complements to the protein and carb meals following training as well as the periodic high-carb days. We highly recommend R-lipoic acid (R-ALA) at a dosage of 100mg per 50g carbohydrates consumed in a meal. The capsules should be taken 20-30 minutes prior to the meal. In general, the brands of regular old-school ALA are racemic mixture products; they include both the R+ (naturally occurring form) and S- (synthetic form) isomers. R-ALA has proven more effective than its synthetic counterpart in promoting appropriate glucose disposal in skeletal muscle (28-30). This natural form is, however, pricier, so if cost is an issue or you just happen to have some old stuff kicking around, rest assured that the racemic (traditional) mixtures of ALA will still prove valuable (28,31,32). In short, with improved glucose disposal and enhanced insulin sensitivity, you’ll be storing more carbs as glycogen and promoting anabolism.

4) Yohimbine: Increasing circulating catecholamines via supplementation or exercise results in elevated thermogenesis. Unfortunately, circulating norepinephrine (NEP) is not selective in the receptors to which it binds. While NEP binding to beta receptors stimulates thermogenesis, bindings to alpha 2 receptors trigger a negative feedback response that inhibits further NEP release. Because alpha 2 receptors are activated at low catecholamine levels (32), this phenomenon is most applicable at rest. Therefore, full-force thermogenesis may never be in effect! One way to overcome the alpha-inhibition of lipolysis is to ingest ephedrine and/or caffeine to increase circulating catecholamines, although this potential solution only reduces alpha-induced inhibition of lipolysis to a moderate degree (33). Yohimbine, as a selective alpha 2 receptor antagonist, is the key to maximizing lipolysis (34). By binding and antagonizing alpha 2 receptors, yohimbine inhibits the NEP negative feedback loop. Therefore, by maximizing circulating catecholamines, you also maximize thermogenesis and lipolysis.

An added benefit of yohimbine is increased peripheral blood flow (35,36). Blood flow to adipose tissue is necessary to transport free fatty acids in the bloodstream (after the breakdown of triglycerides in adipose tissue) to tissues for oxidation in the mitochondria. Activation of the alpha receptors (via NEP) causes vasoconstriction, and, consequently, less blood flow, to peripheral tissues (37,38). In this respect, yohimbine’s ability to inhibit the activation of alpha receptors provides maximal peripheral blood flow.

Note: We are speaking of the yohimbine alkaloid from the yohimbe herb (similar to ephedrine being the active alkaloid in ephedra). Therefore, we recommended that you choose the hydrochloride version (i.e. Yohimbine HCl) over the herbal yohimbe in order to ensure purity and avoid unknown side effects of other alkaloids in the same family. If you choose the to go the herbal route, be sure to verify that you are dealing with a reputable company that lists the standardization for yohimbine on the label. The appropriate dosage for Yohimbine HCl is 0.2mg/kg (35,36), with smaller dosages providing less favorable results. A final word of caution: insulin completely blunts the lipolytic actions of yohimbine. Therefore, you should only ingest it before the low-intensity aerobic sessions and at times well separated from carbohydrate-containing meals.

5) Green Tea: This tasty beverage not only gives you a versatile option from water, but it also offers several other benefits of which you can take advantage. Green tea is now being recognized for a plethora of health benefits including those as an anti-oxidant, cholesterol lowering, antidepressant, capillary-strengthening and lipolysis-enhancing agent. As mentioned above, it may also act as a glycemic modifier in that it slows carbohydrate absorption. However, there?s even more exciting benefits than that. Recent research demonstrated that subjects who supplemented with a green tea extract containing 90 mg epigallocatechin gallate (EGCG) and 50mg caffeine three times daily resulted in a 4% greater energy expenditure and significantly lower respiratory quotient (i.e. greater fat oxidation) compared to subjects that consumed 50mg of caffeine alone or subjects that received a placebo (39). The fact that the subjects receiving the green tea extract experienced these benefits and the caffeine group did not clearly illustrates the inherent benefits of the EGCG, which is thought to be the most pharmacologically active catechin polyphenol in green tea. In light of this data, we recommend drinking 5-10 cups of green tea daily, either decaffeinated or caffeinated depending on the timing of ingestion.

Obviously, these supplements should serve as an addendum to your everyday supplements: multivitamin, antioxidants, protein powder, EFAs, and creatine. Beyond these specific recommendations, feel free to include other supplements as your budget allows.

Conclusion

The physique enhancement strategies set forth in the Maximum Muscularity plan are based on thorough evaluation scientific literature and anecdotal evidence. You’ll be optimizing the hormonal milieu to control catabolism and anabolism, manipulating macronutrient and caloric intake for various activities, and paying close attention to nutrient timing as it relates to substrate utilization and storage. Beyond just offering an avenue to aesthetic improvements, Maximum Muscularity is a long-term perspective that enables you to achieve and maintain optimal health status regardless of the short-term goal. Rejoice, Rugged-Brethren! The old-school days of uncomfortable overfeeding followed by painstaking underfeeding are over! The stratagem to getting Huge and Ripped is now reality more than ever. All you have to provide is the determination and effort.

References

1. Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, & Wolfe RR. Regulation of fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol 1993 Sep;265(3 Pt 1):E380-91.

2. Rasmussen BB, Holmback UC, Volpi E, Morio-Liondore B, Paddon-Jones D, Wolfe RR. Malonyl coenzyme A and the regulation of functional carnitine palmitoyltransferase-1 activity and fat oxidation in human skeletal muscle. J Clin Invest 2002 Dec;110(11):1687-93.

3. Sweetman, SC (ed). Martindale: The Complete Drug Reference. Pharmaceutical Press: London, 2002.

4. Dulloo AG, Geissler CA, Horton T, Collins A, & Miller DS. Normal caffeine consumption: influence on thermogenesis and daily energy expenditure in lean and postobese human volunteers. Am J Clin Nutr. 1989 Jan;49(1):44-50.

5. Horowitz, JF, Mora-Rodriguez R, Byerley LO, Coyle EF. Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. Am J Physiol 1997 Oct;273(4 Pt 1):E768-75.

6. Montain SJ, Hppoer MK, Coggan AR, Coyle EF. Exercise metabolism at different time intervals after a meal. J Appl Physiol. 1991 Feb;70(2):882-8.

7. Nair KS, Halliday D, & Garrow JS. Thermic response to isoenergetic protein, carbohydrate or fat meals in lean and obese subjects. Clin Sci (Lond). 1983 Sep;65(3):307-12.

8. Day JL, et al. (1978). Factors governing insulin and glucagon responses during normal meals. Clin Endocrinol (Oxf). 1978 Nov;9(5):443-54.

9. Schade DS, & Eaton RP. Modulation of fatty acid metabolism by glucagon in man. I. Effects in normal subjects. Diabetes. 1975 May;24(5):502-9.

10. Dorgan J, et al. Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. Am J Clin Nutr 64(6): 850-855. 1996.

11. Howarth, NC, E Saltzman, SB Roberts. Dietary fiber and weight regulation. Nutr Rev. 2001 May;59(5):129-39. Review.

12. Lowery, L. Temporal Nutrition, Part 1. Testosterone Magazine. 21 Mar 2003. https://www.t-mag.com/nation_articles/253temp.jsp.

13. Baechle, TR, & Earle, RW. Essentials of Strength and Conditioning: 2nd Edition. Human Kinetics, 2000.

14. Essen-Gustavsson B, & Tesch PA. Glycogen and triglyceride utilization in relation to muscle metabolic characteristics in men performing heavy-resistance exercise. Eur J Appl Physiol Occup Physiol. 1990;61(1-2):5-10.

15. Keizer HA, et al. Influence of liquid and solid meals on muscle glycogen resynthesis, plasma fuel hormone response, and maximal physical working capacity. Int J Sports Med. 1987 Apr;8(2):99-104.

16. Bourghouts LB, & Keizer HA. Exercise and insulin sensitivity: a review. Int J Sports Med. 2000 Jan;21(1):1-12. Review.

17. Zhang J, & Kashket S. Inhibition of salivary amylase by black and green teas and their effects on the intraoral hydrolysis of starch. Caries Res. 1998;32(3):233-8.

18. Lee YS. The effects of various intensities and durations of exercise with and without glucose in milk ingestion on postexercise oxygen consumption. J Sports Med Phys Fitness. 1999 Dec;39(4):341-7.

19. Parker DC, & Rossman LG. Human growth hormone release in sleep: nonsuppression by acute hyperglycemia. J Clin Endocrinol Metab. 1971 Jan;32(1):65-9.

20. Phelain, JF, Reinke E, Harris MA, & Melby CL. Postexercise energy expenditure and substrate oxidation in young women resulting from exercise bouts of different intensity.

J Am Coll Nutr. 1997 Apr;16(2):140-6.

21. Bahr R, & Sejersted OM. Effect of intensity of exercise on excess postexercise O2 consumption. Metabolism. 1991 Aug;40(8):836-41.

22. Smith J, & McNaughton L. The effects of intensity of exercise on excess postexercise oxygen consumption and energy expenditure in moderately trained men and women. Eur J Appl Physiol Occup Physiol. 1993;67(5):420-5.

23. Tremblay A, Simoneau JA, & Bouchard C. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism. 1994 Jul;43(7):814-8.

24. Gorostiaga, EM, Walter CB, Foster C, & Hickson RC. Uniqueness of interval training at the same maintained exercise intensity. Eur. J. Appl. Physiol. 1991;63:(2)101?107.

25. Hill JO, Heymsfield SB, McMannus C 3rd, & DiGirolamo M. Meal size and thermic response to food in male subjects as a function of maximum aerobic capacity. Metabolism 1984 Aug;33(8):743-9.

26. Samra JS, et al. Effects of epinephrine infusion on adipose tissue: interactions between blood flow and lipid metabolism. Am J Physiol. 1996 Nov;271(5 Pt 1):E834-9.

27. Goforth HW Jr, Arnall DA, Bennett BL, & Law PG. Persistence of supercompensated muscle glycogen in trained subjects after carbohydrate loading. J Appl Physiol. 1997 Jan;82(1):342-7.

28. Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, & Tritschler HJ. Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Am J Physiol 1997 Jul;273(1 Pt 1):E185-91.

29. Saengsirisuwan V, Kinnick TR, Schmit MB, & Henriksen EJ. Interactions of exercise training and lipoic acid on skeletal muscle glucose transport in obese Zucker rats. J Appl Physiol 2001 Jul;91(1):145-53.

30. Moini H, Tirosh O, Park YC, Cho KJ, & Packer L. R-alpha-lipoic acid action on cell redox status, the insulin receptor, and glucose uptake in 3T3-L1 adipocytes. Arch Biochem Biophys 2002 Jan 15;397(2):384-91.

31. Jacob S, Henriksen EJ, Schiemann AL, Simon I, Clancy DE, Tritschler HJ, Jung WI, Augustin HJ, & Dietze GJ. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung. 1995 Aug;45(8):872-4.

32. Jacob S, Henriksen EJ, Tritschler HJ, Augustin HJ, & Dietze GJ. Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid. Exp Clin Endocrinol Diabetes. 1996;104(3):284-8.

33. Arner P, Kriegholm E, et al. Adrenergic regulation of lipolysis in situ at rest and during exercise. J Clin Invest. 1990 Mar;85(3):893-8.

34. Goldberg MR, & Robertson D. Yohimbine: a pharmacological probe for study of the alpha 2-adrenoreceptor. Pharmacol Rev. 1983 Sep;35(3):143-80. Review.

35. Berlan M, Galitzky J, Riviere D, et al (1991). Plasma catecholamine levels and lipid mobilization induced by yohimbine in obese and non-obese women. Int J Obes. 1991 May;15(5):305-15.

36. Galitzky J, Taouis M, Berlan M, Riviere D, et al. Alpha 2-antagonist compounds and lipid mobilization: evidence for a lipid mobilizing effect of oral yohimbine in healthy male volunteers. Eur J Clin Invest. 1988 Dec;18(6):587-94.

37. Millet L, Barbe M, Lafontan M, Berlan M, Galitzky J. Catecholamine effects on lipolysis and blood flow in human abdominal and femoral adipose tissue. J Appl Physiol. 1998 Jul;85(1):181-8.

38. Ruffolo RR, Bondinell W, Hieble JP. Alpha- and beta-adrenoceptors: from the gene to the clinic. 2. Structure-activity relationships and therapeutic applications. J Med Chem. 1995 Sep 15;38(19):3681-716. Review.

39. Dulloo, AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Chantre P, & Vandermander J. Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans. Am J Clin Nutr. 1999 Dec;70(6):1040-5.

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