A Closer Look at Cortisol & Bodybuilding

Every bodybuilder knows that cortisol is bad. Cortisol is one of those nasty catabolic hormones, and catabolism is bad.

At least that’s the logic. Cortisol is a hormone found in your body, in a class of compound called glucocorticoids. It gets its name from the fact that it’s produced in the cortex (outer layer) of the adrenal glands.

The adrenals themselves are heavily involved in the body’s regulation of stress. The body manages it’s overall condition through what is called the hypothalamic-pituitary-adrenal (HPA) axis. The hypothalamus, located in the brain, creates a link between the nervous system and the body’s hormone signals.

Adrenaline, aka epinephrine, is a widely-known stress hormone produced in the adrenal medulla (the inside of the gland). Both cortisol and adrenaline are considered stress hormones due to their actions in the body. They’re the grunt workers involved in managing the body’s responses to stressful conditions.

Much of the negativity around cortisol has come from one simple word: catabolic. In the body, we can summarize metabolic processes as being either positive (anabolic) or negative (catabolic). A state of anabolism has the body building up new tissues; catabolism has those tissues breaking down.

Bodybuilder culture has built up it’s own mythology and lingo, much of it based on bro-lore and a horrible mangling of scientific concepts. This is no exception. In the bodybuilder culture, anything anabolic is good. You know, steroids are anabolic. They’re good. Insulin is anabolic. It’s good. And so on.

Cortisol is a catabolic hormone. Being catabolic is bad, bro.

In this simplified viewpoint, anabolism equates to building muscle, while catabolism means losing muscle. In broad terms, that’s correct. But being an over-simplification, it’s still missing some key information.

Your body is constantly building up and breaking down tissues. This is why we speak in terms of net anabolic or catabolic conditions. Both processes are occurring at the same time. What is relevant is the prevailing trend.

As far as the bodybuilder and lean muscle mass is concerned, we’re talking about the effects on protein metabolism. Muscle size is determined by the amount of protein contained in the muscle fibers. A muscle in a net anabolic state is adding proteins, and thus growing larger. In a state of net catabolism, the muscle is losing proteins and shrinking. Muscle protein synthesis (MPS) and protein breakdown (MPB) are the processes involved here, each controlled by well-identified chemical signals.

As a rule, the growth-influencing (anabolic) hormones like testosterone, insulin, and IGF-1 will tend to increase MPS, as will resistance exercise and ingestion of amino acids. So lifting weights and eating your protein are going to create anabolic conditions in the body by triggering the anabolic signals (Tipton and Ferrando, 2008).

On the opposite side of the coin, we have the stress hormones, which tend to be catabolic. It’s thought that this is a means of short-term stress management, by providing the body with quick sources of energy and helping to shut down processes that are wasteful of energy. Along with this, physical inactivity and conditions of fasting both influence catabolism as well. Indeed, the corticoids influence MPS at the genetic level, working to directly antagonize the anabolic signals; inactivity and fasting will both tend to trigger the atrophy signals that regulate MPB.

If MPS > MPB, you’re anabolic; when MPS < MPB, you’re in a state of catabolism. The actual numbers don’t matter as long as one is greater than the other. Cortisol and it’s friends are necessary for tissue remodeling (that’s muscle growth, to simplify things) to occur. By increasing MPB, cortisol increases the overall rate of protein turnover. In short, it gets rid of old proteins and helps the body replace them with fresh amino acids.

Without cortisol this couldn’t happen, and you’d know it in a hurry. Connective tissues like tendons and ligaments require cortisol in order to stay healthy, as do numerous other tissues in your body. You need tissue breakdown to occur for your body to function properly.

In practice, the body will undergo cycles of hormonal peaks and troughs throughout the day. This is perfectly normal and part of being alive. Conditions change, and your body responds. Natural circadian rhythms will govern this to a large part as well. Both testosterone and cortisol tend to be high in the morning, decreasing throughout the day.

The question is, when does cortisol become a problem? Does it become a problem at all?

Are You Catabolic?

One belief that’s held as “common knowledge” is that you want to keep a workout less than 60 minutes long. The rationale is that testosterone levels will begin to decline around 45 minutes into a workout session, while cortisol levels will increase and stay high. Any training done over an hour is done under catabolic conditions and stresses the body.

That sounds well and good, but looking only at the acute effects without considering the long-term outcome doesn’t tell us a whole lot.

What we need to know is how cortisol itself affects protein metabolism along with exercise and diet. After looking through the research, I can take a strong guess that nobody spouting the “cortisol bad!” line has really bothered to put much thought into this. A review of the literature was pretty illuminating.

Diet is the first key regulator of protein balance. Even in the presence of catabolic hormones, we’ve seen that the anabolic effects of amino acid (AA) intake can help to counteract protein breakdown, with and without carbohydrate (CHO) intake (Hammarqvist et al, 1994; Rankin et al, 2004; Bird et al, 2006b; Baty et al, 2007).

Intake of AA+CHO has been demonstrated to reduce blood levels of cortisol post-exercise (Bird et al 2006a). Interestingly, while AA+CHO has been shown to blunt cortisol levels, AA alone has not (Bird et al 2006c). Some have dubbed this as an “anti-catabolic” effect, as it seems to blunt MPB more than it raises MPS. Intake of CHO alone will affect cortisol levels, but will not affect MPS levels (Thyfault et al, 2004), indicating that AA availability is the key regulator of protein balance, as opposed to cortisol levels.

It’s been shown that inactivity can increase the body’s sensitivity to cortisol, causing an increase in muscle protein breakdown (Ferrando et al, 1999; Fitts et al, 2007). These studies tested the effects of doses of hydrocortisone (chemically very similar to cortisol), dosed as to mimic the cortisol levels of a trauma victim, on bed-resting subjects. Both found that inactivity and high levels of cortisol were the worst possible combination.

Ferrando et al found that hypercortisolemia didn’t affect MPB any more than regular fasting before the period of inactivity. It was only after 14 days of bed-rest that increases in MPB were noted in response to increased cortisol levels. Fitts et al did show that supplementing meals with amino acids and carbohydrates was helpful in preventing atrophy. Likewise, another study (Paddon-Jones et al, 2005) determined that administration of amino acids and carbohydrates added to a normal meal was enough to offset the negative effects on protein balance, under similar conditions.

The results of work by Paddon-Jones et al (2006) showed that during prolonged bed-rest and hypercortisolemia there were no changes in MPB. Instead, atrophy was brought about by a reduction in MPS rates. Wernerman et al (1989) suggest that this is caused by a reduction in the number of ribosomes. Ribosomes are tiny bits inside your cells that are responsible for building proteins; reduce the number of ribosomes, and you reduce MPS rates.

We know that inactivity by itself is enough to reduce MPS and cause atrophy (Ferrando et al, 1996). Inactivity also reduces the body’s overall anabolic response to amino acids (Biolo et al, 2002; 2004). Further, resistance training helps to mitigate the loss of muscle during inactivity specifically by increasing muscle protein synthesis (Ferrando et al, 1997), and calorie restriction during bed-rest also tends to increase the negative protein balance caused by inactivity (Biolo et al, 2007).

It may be a bit hasty to assume that it’s the catabolic hormones at fault; it’s certain that they contribute, but the question is, to what extent? Dramatic muscle loss is only being observed under conditions like extreme inactivity and/or poor nutrition, if not outright injury or illness; these are conditions that reduce or eliminate any increases in MPS. It should go without saying that this won’t reflect what you, the average healthy person, will experience. Even in those extreme cases, just eating properly and exercising is enough to counteract the negative effects on protein balance in all but the cases of physical illness.

The artificially high levels of catabolic hormones seem to make the matter worse, but don’t seem to be causing it when subjects are active and eating properly. This conclusion is also reached in the literature (Bessey et al, 1989; Brown et al, 1994); the authors conclude that stress hormones are a necessary, but not sufficient, factor in creating a negative protein balance.

In other words, the catabolic stress hormones may exacerbate protein loss when present, but aren’t sufficient to cause it on their own. All of this makes it very questionable to implicate cortisol directly, as bodybuilders are wont to do. It doesn’t seem to be helping things, but with proper nutrition in place it doesn’t seem to be doing that much damage, either.

With all this in mind, it doesn’t seem terribly likely that a normal, short-term pulse of cortisol towards the end of a workout is going to make that much difference in your results, assuming you’re getting sufficient amino acids and carbohydrates in your diet.

Wolfe (2001) makes the argument that the MPB rate alone is meaningless without context; it appears that MPB is elevated along with MPS after resistance training, so as not to deplete the amino acid pool. Likewise, we can’t simply look at things on the micro-level and assume they apply to the bigger picture. Looking at the immediate post-exercise effects in the absence of nutritional considerations and any net changes over the long-term just doesn’t cut it. Simply pointing to cortisol as “the culprit”, without any sort of context, is over-simplifying matters.

There are some papers out there indicating a more direct relationship between catabolic hormones and acute MPB in response to exercise (Gore et al, 1993; Hammarqvist et al, 2001; Tarpenning et al, 2001). However, these papers have problems generalizing to the bigger picture.

Tarpenning et al used a four-hour pre-workout fast, followed by administration of either a CHO beverage or a placebo. We already know that a AA is the critical factor regulating protein balance, with CHO only serving to blunt the cortisol response. AA/CHO is also superior to CHO alone (Borsheim et al, 2004a; 2004b).

In all cases, it was held as an assumption that cortisol levels were directly correlated to protein balance, even in the presence of potentially mitigating factors.

We know that exercise will increase MPB, even alongside an increase in MPS rates. We also know that this is a normal response to training, and doesn’t account for overall protein balance.

An earlier paper by Hammarqvist reached the conclusion that amino acid infusion counteracted the MPB caused by stress-hormone infusion (Hammarqvist et al, 1994); so the effects on overall protein balance, and the influence of diet on this, would seem to be important here.

Beyond the lack of any concrete links to protein balance, with no control for dietary factors, there’s also the tiny fact that both testosterone and cortisol tend to peak in the morning, then decline throughout the day. Most research doesn’t account for this, and it could be a potentially large wrench in the works.

Yes, cortisol and it’s relatives are indeed going to increase the levels of protein breakdown in muscle. But net muscle growth occurs when synthesis rates are higher than breakdown rates; even if MPB increases, you can still end up growing if MPS increases more. As Wolfe points out, a simple increase in MPB rates is not necessarily an indicator of net protein loss.

The two things that your average lifter is doing regularly, namely working out and eating protein/carb sources, are also quite effective at countering these negative effects. In short, it’s just not that easy to point out one hormone as the problem, when there’s a whole list of factors involved.

Indicators of Stress

My pet hypothesis is that the acute spike of hormones in response to exercise, including cortisol, is nothing but a marker of an intense stress. Something like a workout, for example. You’d also expect similar changes after any sort of disruptive event; and indeed we do. Physical, mental, and emotional stress of all sorts evokes a similar response. The magnitude of the stress seems to correlate with the magnitude of the hormonal changes.

If we want to talk about using hormones as an indicator of the body’s condition, it’s the chronic changes in the resting levels of the hormones that matter. To see a significant effect on the body, you’re talking about a pretty severe increase over normal resting levels. Conditions of severe injury and trauma are enough to do it. Even then, the research has shown that resistance exercise and adequate AA/CHO intake is sufficient to counter muscle loss.

We’ve got to consider that cortisol is just one of several catabolic and stress-mediating factors. I already mentioned adrenaline, but there’s also a range of inflammatory cytokines that work to put the body in the alert condition. Adrenaline and the cytokines come with their own set of problems, and are often elevated under the same conditions as cortisol. Again, it’s not the short-term that we’re concerned with, but long-term changes in the resting levels.

It’s been observed that positive changes in systemic hormonal state, such as increases in testosterone or growth hormone, aren’t a cause of the training effect on their own (Wilkinson et al, 2006; Spiering et al, 2008), but they can and often do correlate with positive training effects at least in the short-term (Ahtiainen et al, 2005; Crewther et al, 2008; Beaven et al, 2008a; 2008b). This is an important distinction to make. If hormones were a causal factor, then you’d need them in order to see any effects. We can observe muscular changes without any substantial hormonal changes, and hormonal responses to exercise don’t seem to affect anything in the short-term.

It’s reasonable to assume that the short-term hormonal responses to strength training are more of an indicator of stress than a direct cause of adaptation. For example, experienced athletes will have a much different hormonal response than untrained and novice lifters (Ahtiainen et al, 2003a; Ahtiainen et al, 2004), indicating that the body adapts over time.

Testosterone and cortisol are also correlated highly with both the volume and intensity of exercise, with a greater magnitude of either corresponding to greater hormone levels; sensitivity to testosterone (by increases in the amount of androgen receptors) is also increased in proportion to the difficulty of the exercise (Raastad et al, 2000; Ahtiainen et al, 2003b; Smilios et al, 2003; Ratamess et al, 2005). We also see an increase in glucocorticoid receptors under the same conditions (Willoughby, 2004), which is probably an attempt by the body to maintain balance.

Increases in receptor levels indicate a long-term change in the sensitivity of the tissue, and reinforce the idea that it’s not so much the brief spikes that have an effect. If resting levels of the hormones are higher, then increased receptor density will certainly increase their effects; but short-term pulses won’t do much.

I’ll concede that it’s possible that the testosterone spurt might facilitate increased MPS, but we also have to keep in mind that MPS will stay elevated up to 72 hours after a workout. Testosterone levels, unfortunately, do not. If there’s a correlation, it’s subtle; increases in androgen receptor levels probably won’t account for this, although I’ll admit that it’s at least plausible, if not likely.

Considering all the material out there on direct triggers of muscle growth that are independent of systemic hormones (and I’m not even going to try and reference all that, it’s readily available on Pubmed with a quick search for “MAPK”, “mTOR”, or “Akt”), it seems unlikely that acute fluctuations are having any significant effect.

One attempt at an argument is to point at steroid users and say “see, they have increased levels of anabolic hormones and look what it does for them!”. We can’t do that. Steroid use elevates the levels of androgens above the baseline for a long period of time. An average male will make the equivalent of around 70 milligrams of testosterone per week; an average steroid cycle will run doses of 500mg or equivalent amount of testosterone, which some users running double or triple that. Cycles will last anywhere from a few weeks up to several months (or “indefinitely” in the case of many high-level competitors).

By contrast, the post-exercise spike won’t exceed the normal range of human production. In terms of blood levels, the response you get from lifting weights is a drop in the bucket compared to the dose of a steroid cycle. And that blood level stays high for much, much longer. It’s a flawed argument for that reason; there’s just no comparison between chronic elevation and acute spikes.

Over the long-term, changes in the resting levels of testosterone and cortisol, specifically the ratio of testosterone to cortisol (T/C ratio), can serve as an indicator of a deeper, on-going stress to the body (Kilgore and Pendlay, 2001; Haff et al, 2008). Likewise, we can observe a rebound in hormonal status once the work load is reduced (Izquierdo et al, 2007).

As I noted before, we can see that there’s also a correlation between gains and the acute hormonal response, even though the hormone spike isn’t a requirement to see an increase in net protein balance.

Adrenal Fatigue is Snake Oil

One area of concern is trailing the fine line between “working out hard” and pushing yourself past the point of total exhaustion. Too many people get caught up in the idea that they must constantly push themselves, and that they must do this on top of 800 calories a day.

We see that the stress responses to exercise is related to the difficulty of the work done; you’ll increase not only cortisol levels, but adrenaline and markers of inflammation.

We know that exercise isn’t the only thing contributing to your overall physical condition. Stress at work, stress at home, stress from sitting in traffic, lack of sleep, and numerous other matters can all contribute to a physical stress response.

We also know that getting sufficient amounts of amino acids and carbohydrates is a requirement for blunting both cortisol levels and negative protein balance in the body; in contrast, not getting enough causes muscle loss by increasing protein breakdown. This made worse when cortisol levels are increased.

High volumes of exercise combined with not eating enough is a recipe for Bad Things (TM). And that’s not even accounting for other factors in your life. So tell me why exactly you’d want to train with high volumes of intense work, while not eating enough, and expect not to collapse from pure exhaustion? Don’t have a good answer for that one?

It’s been a strong hunch of mine that the quack syndrome “adrenal fatigue” is actually this phenomenon. It’s paraded around under another name that can make people money by convincing you that you’re sick. And that only they have the answers, for just $29.99 if you act now.

Chronically high levels of cortisol tend to mess up insulin sensitivity and can help to kill appetite; same idea with adrenaline. Your body can only stay in the alert condition for so long before it runs out of gas. Feeling like crap is a defense mechanism in the body. It’s caused by inflammatory cytokines (IL-6 and IL-1beta, if you give a damn) that interact with the brain (Smith, 2000; 2004). You feel like crap because you’re supposed to, you know, stop the behavior that’s making you feel like crap.

It’s fairly obvious that this isn’t a pathological condition. There’s no disease state or dysfunction of your adrenal glands. What there is, though, is people that refuse to cut back on the exercise and eat enough food. Of course, that won’t stop the Guru Business Model from capitalizing on it.

Conclusion

Cortisol isn’t bad. It’s essential for our bodies to work properly. In the muscle, it helps increase the rate of protein turnover, which can in turn help with tissue remodeling (growth). Increases in protein breakdown will occur along with increases in protein synthesis, and this is normal. What really makes a difference is the net balance between protein synthesis and breakdown. The rate of protein breakdown on it’s own is meaningless without knowing the overall trend.

Being in a catabolic state is more a function of inactivity and poor diet than it is of hormones. Cortisol on it’s own isn’t likely to cause you problems, but with a poor diet or poor training it can make matters worse. If you’re doing what you’re supposed to be doing, it won’t be an issue.

Hormone spikes that happen in response to exercise are more likely to be an indicator of stress than the cause of adaptation. The blood levels of testosterone and cortisol seem to be directly related to the difficulty of the workout. The spikes are too brief and too low in dose to have any substantial effect on adaptation, although the possibility that they can contribute can’t be ruled out yet. The spikes do seem to correlate with positive gains from training.

When dealing with net adaptation, it’s the chronic changes in resting levels of the hormones that are relevant, and these long-term changes in hormonal status can be used as an effective monitor for overall stress. If you’re getting sick and burned-out from training too much, chances are you’re doing too much work, not eating enough, or both. Chances are that backing off and eating a little more will fix what ails ya.

And adrenal fatigue is a quack syndrome. If you give them money, you help the terrorists win.

References:

  1. Ahtiainen JP, Pakarinen A, Alen M, Kraemer WJ, Häkkinen K. Muscle hypertrophy, hormonal adaptations and strength development during strength training in strength-trained and untrained men. Eur J Appl Physiol. 2003 Aug;89(6):555-63. Epub 2003 May 7.
  2. Ahtiainen JP, Pakarinen A, Kraemer WJ, Häkkinen K. Acute hormonal and neuromuscular responses and recovery to forced vs maximum repetitions multiple resistance exercises. Int J Sports Med. 2003 Aug;24(6):410-8.
  3. Ahtiainen JP, Pakarinen A, Kraemer WJ, Häkkinen K. Acute hormonal responses to heavy resistance exercise in strength athletes versus nonathletes. Can J Appl Physiol. 2004 Oct;29(5):527-43.
  4. Ahtiainen JP, Pakarinen A, Alen M, Kraemer WJ, Häkkinen K. Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men. J Strength Cond Res. 2005 Aug;19(3):572-82.
  5. Baty JJ, Hwang H, Ding Z, Bernard JR, Wang B, Kwon B, Ivy JL. The effect of a carbohydrate and protein supplement on resistance exercise performance, hormonal response, and muscle damage. J Strength Cond Res. 2007 May;21(2):321-9.
  6. Beaven CM, Cook CJ, Gill ND. Significant strength gains observed in rugby players after specific resistance exercise protocols based on individual salivary testosterone responses. J Strength Cond Res. 2008 Mar;22(2):419-25.
  7. Beaven CM, Gill ND, Cook CJ. Salivary testosterone and cortisol responses in professional rugby players after four resistance exercise protocols. J Strength Cond Res. 2008 Mar;22(2):426-32.
  8. Bessey PQ, Jiang ZM, Johnson DJ, Smith RJ, Wilmore DW. Posttraumatic skeletal muscle proteolysis: the role of the hormonal environment. World J Surg. 1989 Jul-Aug;13(4):465-70; discussion 471.
  9. Biolo G, Ciocchi B, Lebenstedt M, Heer M, Guarnieri G. Sensitivity of whole body protein synthesis to amino acid administration during short-term bed rest. J Gravit Physiol. 2002 Jul;9(1):P197-8.
  10. Biolo G, Ciocchi B, Lebenstedt M, Barazzoni R, Zanetti M, Platen P, Heer M, Guarnieri G. Short-term bed rest impairs amino acid-induced protein anabolism in humans. J Physiol. 2004 Jul 15;558(Pt 2):381-8. Epub 2004 May 6.
  11. Biolo G, Ciocchi B, Stulle M, Bosutti A, Barazzoni R, Zanetti M, Antonione R, Lebenstedt M, Platen P, Heer M, Guarnieri G. Calorie restriction accelerates the catabolism of lean body mass during 2 wk of bed rest. Am J Clin Nutr. 2007 Aug;86(2):366-72.
  12. Bird SP, Tarpenning KM, Marino FE. Effects of liquid carbohydrate/essential amino acid ingestion on acute hormonal response during a single bout of resistance exercise in untrained men. Nutrition. 2006 Apr;22(4):367-75. Epub 2006 Feb 10.
  13. Bird SP, Tarpenning KM, Marino FE. Liquid carbohydrate/essential amino acid ingestion during a short-term bout of resistance exercise suppresses myofibrillar protein degradation. Metabolism. 2006 May;55(5):570-7.
  14. Bird SP, Tarpenning KM, Marino FE. Independent and combined effects of liquid carbohydrate/essential amino acid ingestion on hormonal and muscular adaptations following resistance training in untrained men. Eur J Appl Physiol. 2006 May;97(2):225-38. Epub 2006 Mar 24.
  15. Borsheim E, Aarsland A, Wolfe RR. Effect of an amino acid, protein, and carbohydrate mixture on net muscle protein balance after resistance exercise. Int J Sport Nutr Exerc Metab. 2004 Jun;14(3):255-71.
  16. Borsheim E, Cree MG, Tipton KD, Elliott TA, Aarsland A, Wolfe RR. Effect of carbohydrate intake on net muscle protein synthesis during recovery from resistance exercise. J Appl Physiol. 2004 Feb;96(2):674-8. Epub 2003 Oct 31.
  17. Brown JA, Gore DC, Jahoor F. Catabolic hormones alone fail to reproduce the stress-induced efflux of amino acids. Arch Surg. 1994 Aug;129(8):819-24.
  18. Crewther B, Keogh J, Cronin J, Cook C. Possible stimuli for strength and power adaptation: acute hormonal responses. Sports Med. 2006;36(3):215-38.
  19. Ferrando AA, Lane HW, Stuart CA, Davis-Street J, Wolfe RR. Prolonged bed rest decreases skeletal muscle and whole body protein synthesis. Am J Physiol. 1996 Apr;270(4 Pt 1):E627-33.
  20. Ferrando AA, Tipton KD, Bamman MM, Wolfe RR. Resistance exercise maintains skeletal muscle protein synthesis during bed rest. J Appl Physiol. 1997 Mar;82(3):807-10.
  21. Ferrando AA, Stuart CA, Sheffield-Moore M, Wolfe RR. Inactivity amplifies the catabolic response of skeletal muscle to cortisol. J Clin Endocrinol Metab. 1999 Oct;84(10):3515-21.
  22. Fitts RH, Romatowski JG, Peters JR, Paddon-Jones D, Wolfe RR, Ferrando AA. The deleterious effects of bed rest on human skeletal muscle fibers are exacerbated by hypercortisolemia and ameliorated by dietary supplementation. Am J Physiol Cell Physiol. 2007 Jul;293(1):C313-20. Epub 2007 Apr 4.
  23. Gore DC, Jahoor F, Wolfe RR, Herndon DN. Acute response of human muscle protein to catabolic hormones. Ann Surg. 1993 Nov;218(5):679-84.
  24. Haff GG, Jackson JR, Kawamori N, Carlock JM, Hartman MJ, Kilgore JL, Morris RT, Ramsey MW, Sands WA, Stone MH. Force-time curve characteristics and hormonal alterations during an eleven-week training period in elite women weightlifters. J Strength Cond Res. 2008 Mar;22(2):433-46.
  25. Hammarqvist F, von der Decken A, Vinnars E, Wernerman J. Stress hormone and amino acid infusion in healthy volunteers: short-term effects on protein synthesis and amino acid metabolism in skeletal muscle. Metabolism. 1994 Sep;43(9):1158-63.
  26. Hammarqvist F, Ejesson B, Wernerman J. Stress hormones initiate prolonged changes in the muscle amino acid pattern. Clin Physiol. 2001 Jan;21(1):44-50.
  27. Izquierdo M, Ibañez J, González-Badillo JJ, Ratamess NA, Kraemer WJ, Häkkinen K, Bonnabau H, Granados C, French DN, Gorostiaga EM. Detraining and tapering effects on hormonal responses and strength performance. J Strength Cond Res. 2007 Aug;21(3):768-75.
  28. Paddon-Jones D, Sheffield-Moore M, Urban RJ, Aarsland A, Wolfe RR, Ferrando AA. The catabolic effects of prolonged inactivity and acute hypercortisolemia are offset by dietary supplementation. J Clin Endocrinol Metab. 2005 Mar;90(3):1453-9. Epub 2004 Dec 14.
  29. Paddon-Jones D, Sheffield-Moore M, Cree MG, Hewlings SJ, Aarsland A, Wolfe RR, Ferrando AA. Atrophy and impaired muscle protein synthesis during prolonged inactivity and stress. J Clin Endocrinol Metab. 2006 Dec;91(12):4836-41. Epub 2006 Sep 19.
  30. Raastad T, Bjøro T, Hallén J. Hormonal responses to high- and moderate-intensity strength exercise. Eur J Appl Physiol. 2000 May;82(1-2):121-8.
  31. Rankin JW, Goldman LP, Puglisi MJ, Nickols-Richardson SM, Earthman CP, Gwazdauskas FC. Effect of post-exercise supplement consumption on adaptations to resistance training. J Am Coll Nutr. 2004 Aug;23(4):322-30.
  32. Ratamess NA, Kraemer WJ, Volek JS, Maresh CM, Vanheest JL, Sharman MJ, Rubin MR, French DN, Vescovi JD, Silvestre R, Hatfield DL, Fleck SJ, Deschenes MR. Androgen receptor content following heavy resistance exercise in men. J Steroid Biochem Mol Biol. 2005 Jan;93(1):35-42. Epub 2005 Jan 25.
  33. Smilios I, Pilianidis T, Karamouzis M, Tokmakidis SP. Hormonal responses after various resistance exercise protocols. Med Sci Sports Exerc. 2003 Apr;35(4):644-54.
  34. Smith LL .Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress? Med Sci Sports Exerc. 2000 Feb;32(2):317-31.
  35. Smith LL. Tissue trauma: the underlying cause of overtraining syndrome? J Strength Cond Res. 2004 Feb;18(1):185-93.
  36. Spiering BA, Kraemer WJ, Anderson JM, Armstrong LE, Nindl BC, Volek JS, Judelson DA, Joseph M, Vingren JL, Hatfield DL, Fragala MS, Ho JY, Maresh CM. Effects of elevated circulating hormones on resistance exercise-induced Akt signaling. Med Sci Sports Exerc. 2008 Jun;40(6):1039-48.
  37. Thyfault JP, Carper MJ, Richmond SR, Hulver MW, Potteiger JA. Effects of liquid carbohydrate ingestion on markers of anabolism following high-intensity resistance exercise. J Strength Cond Res. 2004 Feb;18(1):174-9.
  38. Tipton KD, Ferrando AA. Improving muscle mass: response of muscle metabolism to exercise, nutrition and anabolic agents. Essays Biochem. 2008;44:85-98.
  39. Wilkinson SB, Tarnopolsky MA, Grant EJ, Correia CE, Phillips SM. Hypertrophy with unilateral resistance exercise occurs without increases in endogenous anabolic hormone concentration. Eur J Appl Physiol. 2006 Dec;98(6):546-55. Epub 2006 Sep 14.
  40. Willoughby DS. Effects of heavy resistance training on myostatin mRNA and protein expression. Med Sci Sports Exerc. 2004 Apr;36(4):574-82.
  41. Wolfe RR. Control of muscle protein breakdown: effects of activity and nutritional states. Int J Sport Nutr Exerc Metab. 2001 Dec;11 Suppl:S164-9.

I write more by email than I do by blog.

Get on the mailing list and it's like having me write a nice letter to you.

Go check your email for a confirmation message.

Something went wrong.

1 thought on “A Closer Look at Cortisol & Bodybuilding”

  1. I can't believe no one has commented yet, this is an amazing and interesting read. I've never seen such a comprehensive view that ties everything together so well. For sever years I have been reading all I can like Pilon, McDonald, Birkham etc and have never seen anthing quite like this. This gets an A+ grade.

Comments are closed.