Since I get Pubmed updates every Sunday, I usually find one or two papers that catch my eye. I figure it’s worth having a look at them, what they mean, and why they’re interesting to me.
First up, here’s a new one from Stu Phillips’s team up at McMaster University.
The purpose of this study was to investigate associations between acute exercise-induced hormone responses and adaptations to high intensity resistance training in a large cohort (n = 56) of young men. Acute post-exercise serum growth hormone (GH), free testosterone (fT), insulin-like growth factor (IGF-1) and cortisol responses were determined following an acute intense leg resistance exercise routine at the midpoint of a 12-week resistance exercise training study. Acute hormonal responses were correlated with gains in lean body mass (LBM), muscle fibre cross-sectional area (CSA) and leg press strength. There were no significant correlations between the exercise-induced elevations (area under the curve-AUC) of GH, fT and IGF-1 and gains in LBM or leg press strength. Significant correlations were found for cortisol, usually assumed to be a hormone indicative of catabolic drive, AUC with change in LBM (r = 0.29, P < 0.05) and type II fibre CSA (r = 0.35, P < 0.01) as well as GH AUC and gain in fibre area (type I: r = 0.36, P = 0.006; type II: r = 0.28, P = 0.04, but not lean mass). No correlations with strength were observed. We report that the acute exercise-induced systemic hormonal responses of cortisol and GH are weakly correlated with resistance training-induced changes in fibre CSA and LBM (cortisol only), but not with changes in strength.
Any paper with Stu’s name on it gets my attention. It’s hard to get much better than the work coming out from his department, so long as you define “better” as applicable to everyday Gym Stuff. Lately he’s been on a kick to debunk the whole obsession with cortisol, GH, and testosterone — particularly the way those hormones respond to acute stimulus. We’ve seen it in all the textbooks; after an hour of training, test drops off and cortisol spikes, which quashes your gains until you go eat some carbs to spike insulin.
Hormones do wonderful things but the typical Gym Knowledge assigns them a causal power that they just don’t have. Hormones are embedded in a much deeper web of causes and effects that makes it impossible to point to them as causes of anything (and if want to understand wahy, I’ve got three hours of Robert Sapolsky lectures to convince you). Defining cortisol as a cause of muscle wasting or a 30-minute testosterone spike as a cause of muscle gains is horribly wrong on a very deep level.
In any event, this paper is one of several coming out of Stu’s lab that challenges that assumption. The result is kinda funny in itself, where cortisol and GH weakly correlate with CSA (cross-sectional area, the effective size of muscle fibers) and LBM (lean body mass), and there only cortisol has any connection with size gains.
Regular readers will know that “central fatigue” and “overtraining” are two hot-spots that have really captured my attention over the past however many years, and the next two papers touch on that subject from different angles. Much like the Hormonal Causation argument, I think that our notions of recovery and overtraining are way behind the curve. We end up clinging to bodybuilding folk-wisdoms, and that ultimately affects what we can do for ourselves in the gym (not to mention time and money spent on bizarre diets and useless supplements meant to “fix” us).
An important aspect of central fatigue is supraspinal fatigue, or fatigue originating from an insufficient output from the motor cortex. One possible underlying mechanism is that this reaction is evoked by changes in brain neurotransmitters such as dopamine (DA) and noradrenaline (NA). In the present study, we looked into the relation between supraspinal fatigue and changes in brain neurotransmitter concentrations before and after prolonged exercise. Ten well-trained male cyclists participated in this study. Subjects exercised in 18°C and performed 60 min at 55% Wmax followed by a time trial which required the subject to complete a work equal to 30 min at 75% Wmax as quickly as possible. Pharmacological interventions were placebo, methylphenidate (DA reuptake inhibitor) and reboxetine (NA reuptake inhibitor). Voluntary activation and corticospinal excitability changes were tested in the knee extensors using TMS and motor nerve electrical stimulation before and after the cycling exercise. Reaction time and attention were measured using the psychomotor vigilance test (PVT). NA administration decreased performance significantly (9%). This was accompanied by a significant reduction in voluntary activation. No differences were observed for DA reuptake inhibition. No changes in corticospinal excitability were observed. The PVT revealed that reaction time was negatively influenced by reboxetine. Higher NA concentrations in the brain enhance central fatigue. The reduction in both the voluntary activation and reaction time shows that this decrease in performance was centrally mediated.
This one comes from Romain Meeusen’s team at Vrije Universiteit in Belgium. Meeusen is another name that catches my eye for all of his work on the neurochemistry behind central fatigue, and this paper is another piece in that work.
Folk-theories of fatigue suggest that muscles just get tired, but we’re discovering more and more that it isn’t so simple. In exhausting exercise, whether from endurance or high intensity, the brain’s output starts to decline and that decline eventually affects performance. It’s almost like your brain itself gets tired.
Which is pretty much what happens. Much of Meeusen’s previous research has focused on the three monoamine neurotransmitters, dopamine, serotonin, and norepinephrine, which dominate the motor-control pathways in our brains. In this study, Meeusen’s team tested the effects of two different drugs, one which elevates dopamine (DA) and another which elevates norepinephrine (NA), on cycling performance. The result is interesting because it shows that excessive NA impairs performance, whereas NA is typically the “arousal” chemical, with its networks responsible for “turning everything on”. For reference, caffeine and ephedrine work by activating NA nerves.
I haven’t seen this full paper so I really can’t comment further, but previous work from Meeusen has suggested a serotonin hypothesis for fatigue. During hard exercise both serotonin and dopamine levels increase, but at the point of exhaustion dopamine crashes, leaving you with a skewed dopamine to serotonin ratio. Our brain registers that as “tired” and the consequence is that 1. neural output drops off and 2. we experience a sensation of “tired”.
The NA connection is not hard to fit in to that, however. Imagine a day when you drank too much coffee. You were wired up to be sure, but there’s also a such thing as overstimulation. Too much arousal can be as bad as too little. Without having read the whole paper I don’t know if that’s what they’re getting at, but it’s plausible.
Why does this matter? Mainly because strength athletes can undergo something similar. Max-effort intensity and strongman-type exercises that fatigue you both do this magic on the brain, and it isn’t always a matter of “tired muscles” that leave you floored. As I’ve said so often in the past, you can make yourself exhausted just by focusing too hard for too long; the brain centers that control emotional output also control motor output. Volume aside, TRAIN TO FAILURE OR GO HOME!! thinking can lead to burn-out just as easily as — if not easier than — “high volume” training.
Use your RPEs, folks.
The second paper ties right into that suggestion. These pathways between brain and body work in two directions. Again the folk-wisdoms suggest that we “damage” our bodies with exercise and these signals filter up to the brain, which then freaks out, but it’s not so simple.
Skeletal muscle catabolism is a co-morbidity of many chronic diseases and is the result of systemic inflammation. Although direct inflammatory cytokine action on muscle promotes atrophy, nonmuscle sites of action for inflammatory mediators are less well described. We demonstrate that central nervous system (CNS)-delimited interleukin 1β (IL-1β) signaling alone can evoke a catabolic program in muscle, rapidly inducing atrophy. This effect is dependent on hypothalamic-pituitary-adrenal (HPA) axis activation, as CNS IL-1β-induced atrophy is abrogated by adrenalectomy. Furthermore, we identified a glucocorticoid-responsive gene expression pattern conserved in models of acute and chronic inflammatory muscle atrophy. In contrast with studies suggesting that the direct action of inflammatory cytokines on muscle is sufficient to induce catabolism, adrenalectomy also blocks the atrophy program in response to systemic inflammation, demonstrating that glucocorticoids are requisite for this process. Additionally, circulating levels of glucocorticoids equivalent to those produced under inflammatory conditions are sufficient to cause profound muscle wasting. Together, these data suggest that a significant component of inflammation-induced muscle catabolism occurs indirectly via a relay in the CNS.
Inflammation. I’ve written of it before as a potential culprit in sickness feelings and the general post-training ickiness that blights us after a brutal workout. Our friend interleukin-1beta up there in the abstract has come up before, implicated as a potential cause of overtraining.
What you’re seeing in this abstract is roughly as follows: something, like an infection or a lot of unaccustomed exercise, triggers the innate immune system in the damaged tissues. The immune system sets off the inflammation process, releasing lots of inflammatory cytokines (including our friend interleukin-1beta). Inflammatory cytokines reach the brain and set off the HPA axis, which is the “stress manager” system of the body, releasing lots of glucocorticoids as part of the coping strategy.
Normally this is a good thing. Inflammation is, after all, a process of coping and recovering from whatever it was that triggered the response. Likewise for the HPA stress-response.
The keen eyes among you will be wondering why this is a problem if, just scant few paragraphs above, I warned against obsessing over hormones. The main reason is the difference between acute and chronic. A workout is just a workout, so to speak. An acute 30-60 minute elevation of hormones is a normal, expected response to a stressor. It happens, things go back to normal. No big deal.
The problem starts when either 1. the stress happens repeatedly, such that the HPA never gets a chance to turn off or 2. when your HPA, for whatever reasons, doesn’t settle down after you get wound up. Chronic elevation of the HPA and cortisol levels will become a problem.
Set off that cascade by doing lots and lots of training, or training while sick, or any number of activities that would qualify as “overdoing it” and you really are going to cause problems over the long-term.
Cortisol in itself is not the real issue. Bodybuilding folk-wisdom worries about the hormone, but as you can see there’s an identifiable cause in the chain: namely the inflammatory cytokines, and the brain’s response to them. The hormone just does its job; what concerns us is the “upstream” causes — the brain, and the immune-system signals that are altering it.
In training, central matters far more than peripheral; training to deliberately get yourself sore, training to exhaustion at every opportunity, that’s all activating this inflammation-HPA pathway. But even that’s not a huge deal unless you’re one of the truly obsessive personalities that won’t rest for anything.
It’s amazing to me how many people will struggle to control cortisol by fiddling with their workouts and taking crazy supplement regimens that don’t do anything, and completely neglect everything else in their lives. It’s the everything else that really matters, and this paper handily demonstrates why: chronic matters far more than acute. If you live your life in a constant state of Switched On, expect to be sick more often, to have worse subjective “recovery”, and to respond very poorly to anything that pushes you out of the norm.
West DW, & Phillips SM (2011). Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. European journal of applied physiology PMID: 22105707
Roelands B, Klass M, Levenez M, Fontenelle V, Duchateau J, & Meeusen R (2011). Neurotransmitter modulation and supraspinal fatigue. British journal of sports medicine, 45 (15) PMID: 22077003
Braun TP, Zhu X, Szumowski M, Scott GD, Grossberg AJ, Levasseur PR, Graham K, Khan S, Damaraju S, Colmers WF, Baracos VE, & Marks DL (2011). Central nervous system inflammation induces muscle atrophy via activation of the hypothalamic-pituitary-adrenal axis. The Journal of experimental medicine, 208 (12), 2449-63 PMID: 22084407
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