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.
Terwijl iedereen toch weet dat je altijd moet stoppen met trainen als het uur op een even getal eindigt.
