Caffeine Therapy

Desensitize Your Insulin Levels to Stimulate Muscle Growth
150 shared this

The first step in breaking any addiction is admission: My name’s Kiefer and I’m an addict. But even if researchers identify caffeine consumption as a model of drug abuse,(34) I’m not quitting. I love it. Without it, right now, I’d be in bed asleep for the past four hours—but thanks to a strong cup of joe and sugar-free energy drinks, I’ll burn several more hours writing and researching before the caffeine wears off.

For most of my life, I was not a fan of caffeine. It wasn’t because of my religion or some other ideology, but because I thought I didn’t need it. I didn’t know about the true potential that I discovered a few years ago when I began experimenting with carb back-loading. I figured out that with coffee I could bend the timing of circadian insulin sensitivity to my whim. With caffeine, I no longer need to wait until the evening to eat carbs.

For optimum carbohydrate utilization without storing fat, we need to eat carbs at night; this single rule 
is the cornerstone of all my dietary protocols. Post training is even better. I realize that few people have the luxury of picking their training time with infinite latitude. Let’s be honest: How many people live a life where they can train at the same time 
every day, a time of their choosing? Not many, including me. Clients and deadlines don’t give a damn when I want to train. I try to start my training session after 3 p.m.; life, however, often dictates otherwise.

This is where caffeine comes in handy. If I need to train earlier in the day than is optimal, I drink caffeine before my session, and if the training session runs more than an hour, I add some to my post-workout shake as well. I don’t take caffeine for the hunger-curbing cholinomimetic,(1,2) because of the cognitive-enhancing abilities,(3,4) the fat-burning properties,(5-14) nor do I take it because researchers in the International Journal of Sports Nutrition and Exercise Metabolism claim it increases testosterone levels during training(15) or because recent research shows that caffeine increases nitrous oxide (NO) production.(16) I don’t even care that caffeine raises your pain threshold, allowing me to push a little harder.(17-21) I take caffeine because it decreases my sensitivity to insulin.(22-30)

Insulin sensitivity is important
 to health for most people. Doctors normally try to help patients increase their sensitivity to insulin and here I am decreasing mine. This is where diet and medical advice get it wrong. Assumptions about one population cannot be applied to all populations out-of-hand.

You train heavy. That makes you different from 90% of the U.S. population. Someone who’s sedentary and overweight would be advised to stay clear of the morning caffeine. For couch potatoes and desk jockeys, that early morning latte loaded with sugar and caffeine is potentially accelerating their impending diabetes. “I’ll have a scone with that...low-fat, please... I’m watching my figure.”

Getting up to train at 6 a.m. also makes me atypical in the world. As does the fact that I train completely fasted and loaded with caffeine. By having the caffeine, at the end of my workout, I am in a state mimicking the evening reduction in insulin sensitivity, a state that is absolutely critical to the near magical results of my dieting protocols.


The caffeine, by making my fat cells insensitive to insulin, forces
 the carbs into the one tissue that I actually want to grow: my muscles. Skeletal muscle tissue can soak up sugar like a sponge because resistance training forces GLUT4 proteins to the surface of the cells (see my article in the March 2012 issue of FLEX on carb back-loading). The GLUT4 migration to the surface of muscles cells—stimulated by the heavy resistance training—allows sugar to rush into muscle cells regardless of insulin sensitivity. With caffeine and resistance training, you can control which tissue soaks up sugar and which can’t at any time of day. Control is a beautiful thing.

Caffeine use alone does not substitute for the body’s natural daily rhythms. Caffeine is adjunct therapy. If you cannot train after 3 p.m., then this is your best option for simulating an optimal fat burning, muscle-building environment. Caffeine therapy to induce the same physiological state as daytime circadian rhythms is powerful, but you still have other issues to deal with, since the hormonal status in
the morning—i.e., increased cortisol levels—is not as favorable as in the evening for ingesting carbs.

Example for Morning Training:


■ No carbs before training (if you train as soon as you get up, this is pretty easy).


Pre-Workout:


■ 2 cups coffee (about 400mg of caffeine depending on the cup size)


■ 10g isolate and hydrolysate blend (1⁄2 scoop of Blend H)
5g creatine


Post-Workout:


■ 40g isolate and hydrolysate blend (2 scoops of Blend H)


■ 5g leucine


■ 25g fast-acting carb (rilose, dextrose, maltodextrin) or 2 or 3 ripe (mottled brown) bananas


■ 200mg caffeine from a powder or one cup coffee

Afterward, from post-workout until 6 p.m. or so (dinner), stay ultra-low carb. At dinner start eating the carbs. And stay away from “clean,” low-glycemic carbs. As I’ll explain in a future article, high-glycemic carbs trigger powerful anabolic effects at night without interfering with nighttime repair, growth, and fat burning.

In the discussion here, I have primarily focused on simulating the metabolic state that makes back-loading carbs such a powerful dietary protocol, but anyone on a carb-based diet can take advantage of caffeine therapy for faster post-training recovery. When ingested as part of a post-workout recovering drink that includes carbohydrates, levels of caffeine around 3.5mg per pound body weight induce a rapid rate of glycogen recovery,(35,36) stemming,
 in all likelihood, from the same effect (GLUT activation in conjunction with making fat cells insulin insensitive). For a 200-pound male, this would be 700 to 800mg of caffeine, which, for some, may sound like a lot of caffeine. People generally tolerate intakes up to a gram at a time (1,000 mg) well.(37-42)

Note: I mention coffee throughout the article as a source of caffeine 
and there are others such as tea, chocolate, and guarana. Choose guarana, coffee, or energy drinks that specify caffeine for your main sources. Caffeine is a type of methylxanthine found mostly in guarana and coffee beans and is the most potent (31,32) (ephedra is not caffeine and is not chemically related). Theophylline is found in teas and theobromine is the type found in chocolate. They all display the same general characteristics, and the stronger the type, the shorter duration of effects.(33) You might be thinking that you should go for the weaker types (from tea and chocolate) and go for the longer effects. It’s a good thought, but you’re better off taking regular doses of the more potent form, and with a Starbucks on every corner, you have no excuses. You can be an addict too.

 

References: 1. S.Y. Tse, J Pharm Sci. 1991 Jul;80(7):665-9; 2. S.Y. Tse, J Pharm Sci. 1992 May;81(5):449-52; 3. V. Maridakis et al. Int J Neurosci. 2009;119(7):975-94; 4. C. Kourtidou-Papadeli et al., Brain Res Cogn Brain Res. 2002 May;13(3):407-15; 5. R.T. Jung et al.,Clin Sci (Lond). 1981 May;60(5):527- 35; 6. P.J. Arciero et al.,Am J Physiol. 1995 Jun;268(6 Pt 1):E1192-8; 7. J.L. Ivy et al., Med Sci Sports. 1979 Spring;11(1):6-11; 8. K.J. Acheson et al.,Am J Clin Nutr. 2004 Jan;79(1):40-6; 9. V. Mougios et al.,J Appl Physiol. 2003 Feb;94(2):476-84; 10. R.K. Hetzler et al., J Appl Physiol. 1990 Jan;68(1):44-7; 11. R.B. Goldrick and G.M. McLoughlin, J Clin Invest. 1970 Jun;49(6):1213-23; 12. C.A. Raguso et al., Metabolism. 1996 Sep;45(9):1153-60; 13. E.J. Peters et al., Am J Physiol. 1991 Oct;261(4 Pt 1):E500-4; 14. K.J. Acheson et al., Am J Clin Nutr. 1980 May;33(5):989-97; 15. C.M. Beaven et al., Int J Sport Nutr Exerc Metab. 2008 Apr;18(2):131- 41; 16. T. Umemura et al., Am J Cardiol. 2006 Dec 1;98(11):1538-41; 17. J.K. Davis and J.M. Green, Sports Med. 2009;39(10):813-32; 18. M.A. Tarnopolsky, Appl Physiol Nutr Metab. 2008 Dec;33(6):1284-9. Review; 19. J.M. Green et al., Int J Sports Physiol Perform. 2007 Sep;2(3):250-9; 20. M. Tarnopolsky and C. Cupido, J Appl Physiol. 2000 Nov;89(5):1719-24; 21. K. Woolf et al., Int J Sport Nutr Exerc Metab. 2008 Aug;18(4):412-29; 22. H.J. Petrie et al., Am J Clin Nutr. 2004 Jul;80(1):22-8; 23. G.B. Keijzers et al., Diabetes Care. 2002 Feb;25(2):364-9; 24. F. Greer et al., Diabetes. 2001 Oct;50(10):2349-54; 25. T.E. Graham et al., Can J Physiol Pharmacol. 2001 Jul;79(7):559-65; 26. F.S. Thong and T.E. Graham, J Appl Physiol. 2002 Jun;92(6):2347-52; 27. F.S. Thong et al., Diabetes. 2002 Mar;51(3):583-90; 28. L.E. Robinson et al., J Nutr. 2004 Oct;134(10):2528-33; 29. K.L. Johnston et al., Am J Clin Nutr. 2003 Oct;78(4):728-33; 30. M. Sachs and H. Forster, Z Ernahrungswiss. 1984 Sep;23(3):181-205; 31. G.K. Mumford et al.,Psychopharmacology (Berl). 1994 Jun;115(1-2):1-8 ; 32. G. Yu et al., Br J Clin Pharmacol. 1991 Sep; 32(3):341-5; 33. M.J. Arnaud, Prog Drug Res. 1987;31:273-313. Review; 34. S.G. Holtzman, Trends Pharmacol Sci. 1990 Sep;11(9):355- 6. Review; 35. D.J. Pedersen et al., J Appl Physiol. 2008 Jul;105(1):7-13. ; 36. D.S. Battram et al., J Appl Physiol. 2004 Mar;96(3):943-50. ; 37. C.F. Brice and A.P. Smith, Psychopharmacology (Berl). 2002 Nov;164(2):188-92; 38. J.F. Greden, Am J Psychiatry. 1974 Oct;131(10):1089-92; 39. K.N. Stern et al., Psychopharma- cology (Berl). 1989;98(1):81-8; 40. W.W. Eaton and J. McLeod, Am J Public Health. 1984 Jan;74(1):66-8 ; 41. M.A. Lee et al., Psychiatry Res. 1985 Jul;15(3):211-7; 42. M. Rihs et al., Eur Arch Psychiatry Clin Neurosci. 1996;246(2):83-92.

Comments

comments powered by Disqus