"Every morning in Africa, a gazelle wakes up. It knows it must outrun the fastest lion or it will be killed. Every morning in Africa, a lion wakes up. It knows it must run faster than the slowest gazelle, or it will starve. It doesn't matter whether you're a lion or gazelle - when the sun comes up, you'd better be running." (African Proverb/popular running inspirational quote)
I promised a long time ago to put forth a post on Central Governor Theory (CGT), a term thrown around more and more these days, sometimes fairly inaccurately. The basic premise behind CGT is easily explained through the rental car analogy. You pick up your rental car and the speedometer goes up to 120 miles per hour, and assuming you are in something with more horsepower than a Ford Focus, the car could probably be coaxed up to close to such a speed over a long distance. However, no matter how hard you depress the accelerator, the car won’t go above 80 mph. That’s because the rental car company installed a regulator to prevent you from speeding too fast. The car isn’t doing anywhere near its maximal speed, but you aren’t as likely to kill yourself (or total their car) either.
The actual theory is more complicated, however, and has actually been around quite a while but came back into vogue with an interesting experiment recently published by Samuele Marcora in the European Journal of Applied Physiology (“The limit to exercise tolerance in humans: mind over muscle?” Marcora SM, Staiano W. Eur J Appl Physiol. 2010 Aug;109(6):1225-6.). Ironically, Marcora did not interpret the results to support CGT proper. Instead he put forth the subtly but importantly different “psychobiological model of exercise tolerance.” However, most folks seem to think the difference was semantic, and have taken his striking results as confirmation of the CGT.
So as M.C. Hammer would instruct us, we must break it down.
The existence of a central governor was first put forth by Archibald Hill in 1924, and refined by Tim Noakes, in a string of papers beginning in 1997 and most notably containing his 2001 paper with Peltonen and Rusko, entitled, “Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia.”
Here’s the summary from that article if you wish to “geek out.”
“An enduring hypothesis in exercise physiology holds that a limiting cardiorespiratory function determines maximal exercise performance as a result of specific metabolic changes in the exercising skeletal muscle, socalled peripheral fatigue. The origins of this classical hypothesis can be traced to work undertaken by Nobel Laureate A. V. Hill and his colleagues in London between 1923 and 1925. According to their classical model, peripheral fatigue occurs only after the onset of heart fatigue or failure.
Thus, correctly interpreted, the Hill hypothesis predicts that it is the heart, not the skeletal muscle, that is at risk of anaerobiosis or ischaemia during maximal exercise. To prevent myocardial damage during maximal exercise, Hill proposed the existence of a ‘governor’ in either the heart or brain to limit heart work when myocardial ischaemia developed. Cardiorespiratory function during maximal exercise at different altitudes or at different oxygen fractions of inspired air provides a definitive test for the presence of a governor and its function. If skeletal muscle anaerobiosis is the protected variable then, under conditions in which arterial oxygen content is reduced, maximal exercise should terminate with peak cardiovascular function to ensure maximum delivery of oxygen to the active muscle.
In contrast, if the function of the heart or some other oxygen-sensitive organ
is to be protected, then peak cardiovascular function will be higher during hyperoxia and reduced during hypoxiacompared with normoxia. This paper reviews the evidence that peak cardiovascular function is reduced during maximal exercise in both acute and chronic hypoxia with no evidence for any primary alterations in myocardial function. Since peak skeletal muscle electromyographic activity is also reduced during hypoxia, these data support a model in which a central, neural governor constrains the cardiac output by regulating the mass of skeletal muscle that can be activated during maximal exercise in both acute and chronic hypoxia.”
Pretty straight forward, right?
So basically what they are saying is that this governor in the brain regulates exercise in regard to some neurologically determined safe exertion by the body, particularly the cardiac tissues. That way exercise is controlled so that its intensity cannot threaten the body by causing damage to the heart. The central governor limits exercise by reducing the neural recruitment of muscle fibers, preventing myocardial ischaemia during maximal exertion. This reduced recruitment is what we feel as fatigue. It seems the data support this, because by using altitude to limit oxygen delivery, they showed that peak cardiac output was diminished during max effort without any alterations in normal cardiac function.
Makes sense. Your brain makes sure you don’t exercise till you have a heart attack.
Um…except people die of heart attacks fairly regularly during exercise.
Fair enough. But one can argue the CG is neurologically programmed to protect the normal heart…not the clogged up, weakened model that the average modern adult is toting around. It’s also probably programmed to protect the heart to a certain point, but when the damn thing gets too old and worn then all bets are off (yikes over here). It’s also clear that individuals exist for whom CGT obviously doesn’t apply – they literally race themselves to death.
However, Occam’s razor would suggest that this is a fairly elaborate explanation for a pretty straightforward dilemma – the body protecting itself from exerting itself to death. First of all, how does each individual body know how to neurally calculate its CG? Is it mostly genetic and partially trained like VO2Max? Seems a bit scary…our involuntary responses just guess where the line of cardiac catastrophe is?
Especially when there’s a much simpler way to go about it: if the body FEELS like it’s going to have a heart attack (or other catastrophic physiological breakdown) during maximal exercise it SLOWS DOWN so that said catastrophe doesn’t occur. Otherwise known as rate of perceived exertion (RPE) = 10.
Here’s how Samuele Marcora set about his experiment to prove this. He took 10 professional rugby players – exceptionally fit individuals. He had them do a 5-second maximum voluntary cycling test (MVCT), followed by cycling to exhaustion which took about 10 minutes. Within 1 second of stopping due to exhaustion, they were required to do another 5-second MVCT that they didn’t know was coming.
So here’s the catch. Before hand, this had been widely publicized and made into a contest, with large cash prizes offered to increase motivation. I like the summary on the findings presented by Sweat Science, a great blog on exercise science for normal people.
“Now, if you subscribe to traditional exercise physiology, you’d say that the subjects stopped the test-to-exhaustion when they were no longer physically able to generate enough power to continue. Possible reasons for their failure would include “limited oxygen delivery, metabolic and ionic changes within the active muscles, supraspinal reflex inhibition from muscle afferents sensitive to these changes, and altered cerebral blood flow and metabolism.” But that’s not what Marcora saw. The subjects had to maintain an output of (on average) 242 watts in the test to exhaustion. But as soon as they stopped, one second later, they were able to output (on average) 731 watts in a five-second burst — nearly triple the required power! Clearly the subjects didn’t stop the test because they couldn’t physically produce the needed power.
These results challenge the long-standing assumption that muscle fatigue causes exhaustion during high-intensity aerobic exercise, and suggest that exercise tolerance in highly motivated subjects is ultimately limited by perception of effort.”
Some people argue that this is flawed because when you exercise to exhaustion over a 10 minute period, you are working mainly outside the alactic and gylcolytic energy (anaerobic) systems that you would use for the 5-second burst, and instead are primarily using the aerobic system. At true exhaustion, however, the aerobic system has outstripped the ATP available and the anaerobic system is employed until the 90-120 seconds of glucose/glycogen/ADP/Pi in the muscles is gone (assuming none had been used before which is would have been so in reality this would be even shorter). One second is not enough for the alactic system to recover.
The exception to this would be when glycogen has been depleted to the point where the anaerobic system cannot be employed (another physiological governor since the body holds glycogen in reserve for brain function). Yes – I speak of the true bonk. Unless the subjects had been forced to fast prior to the test, that isn’t going to happen in 10 minutes.
My point is that when they reported exhaustion – if it were true exhaustion – they would have already depleted the ADP/Pi in the muscles that would allow their alactic system to synthesize the ATP necessary for 5 seconds of all-out sprinting. So his conclusion is sound.
Since it’s been proven time and time again that RPE is subjective based on environmental factors, this makes sense for a species developed on the hunt and being hunted. If you have a neurally pre-determined CG that doesn’t allow for you to drive the rental car fast enough to escape the lion, you don’t crash…but you get eaten. Granted, there could be a complex endocrine/neurologic interaction that allows adrenaline inputs to alter the CG’s function. But we already know that if you are outrunning a lion, it doesn’t feel hard – all that limits you is the absolute physiological limits of your neurological recruitment, joints, O2 delivery, and muscular strength. So instead of feeling the pain you just feel too slow – especially when you get caught which you probably will. Ironically, you probably won’t feel that much pain when you get eaten because your adrenaline release and its associated chemical cascade will block your pain receptors….but I digress.
If you are in a footrace with some random guy, competing for a spot in the standings far off the podium and its hot and humid and you have a cramp in your side…your RPE will skyrocket. And for good reason – you are pushing the beginning of the limits of your body, punishing it, and for no biologically necessary reason.
So that’s the distinction between CGT and Psychobiological Model of Exercise Tolerance (PMET), so far as I can tell. CGT is a neurological-cardio regulator preset to prevent cardiac damage from near-maximal exercise, while PMET basically implies that we stop exercising when it gets hard, we go a little farther a little harder when we’re REALLY motivated, but probably don’t realize our full physiological potential until our life is on the line. CGT is one of many regulatory systems that probably kick in when RPE is skewed downward due to environmental factors. Again, some folks seem to be able to convince themselves that their life is on the line when it doesn’t have to be, and keep going when truly redlined. Sometimes they win…sometimes they die.
Like I said, my guess is – and no, I don’t think that an earth sciences degree stands in for one in ex. phys. – that there are a series of regulators in place to guard the body against injury and death. PMET basically takes all of those into account.
• You feel crappy when you run out of sugar…you slow down or stop and find something to eat so that your brain doesn’t run out of fuel and you die
• Your heart is pounding wildly and you are heaving for breath and begin to feel nauseous…so you slow down to puke and let your heart rate come down before causing cardiac damage
• It’s 99 degrees and 100 percent humidity and you begin to feel dizzy forcing you to stop or slow down before you experience heat stroke (or can get to a doc in time to treat it
I think it’s telling that all of these can be trained and acclimated to differing extents in different individuals…but all of them CAN be trained. That means that there IS a buffer that exists between our realized physiological potential and our maximal potential. The fact of the matter is that there are a lot more of us around now who are biologically inferior – either because our bodies don’t sense the impending doom or because our regulators are too active and kick in too quickly – because there are no lions left around to test us and no desperately needed deer to hunt.
I guess the bottom line is that we can learn to push beyond our perceived physical limits, and we can physically accomplish things that we never logically thought possible. But it comes at a risk because there is, in the end, a limit. Push just far enough, and you win the Tour de France (or your AG at your local 5k). Push too far and we’ll see you on the other side.
It all comes down to risk versus reward, just as it did 10,000 years ago. Eventually, I think for most folks, PMET will ultimately tell them when the pain of trying to shave just a few more seconds off the 5k PR just isn’t worth it anymore.
But that might not be until they’ve brought their PR down 10 minutes or more from where they started, each increment gained by making classic physiological gains in oxygen recruitment and distribution, muscle strength, and neurological recruitment, as well as by teaching their minds that each time they push a little harder, life is not at stake.
At least until it is.
0 comments:
Post a Comment