Listening to the Noakes podcast posted recently on this forum (see here: Podcast) and a recent thread on Letsrun sparked my interest in central governor theory. The idea that a central nervous system mechanism protects the body from damage by limiting performance is an appealing one, but I’m struggling to figure out how it fits with the energy systems model, or if it supercedes it.
Could the level of lactate or other metabolites be “monitored” by the central governor, and used to determine the permitted level of muscle fibre activation? If so, by what mechanism? Some of Noakes’ evidence (lactate concentrations at altitude) seems to suggest that lactate doesn’t explain fatigue. Is the basis of fatigue more neural than biochemical?
Even if we accept the idea of a central governor, it seems to me it doesn’t change much in terms of how we train, but rather how we explain why our training methods work. It also implies that physiological tests (VO2max, LT) may be less important than previously thought. It’s been known for a while that velocity at VO2max is a better predictor of performance than VO2max itself, and central governor theory could explain this.
Are L4 intervals on the bike and tempo runs effective because sustained periods of work at an uncomfortable level of effort reset our central governor?
Does central governor theory suggest that treadmill training, where the pace is set by the machine and not self-selected, might be extremely effective?
Interesting review article on central governor theory here.
Schillings and friends actually tried to quantify the difference between central and peripheral fatigue in a paper… I’ll have to see if I can find it for you today.
I heard this theory about a year or two ago. They were saying that bonking was a response like this and that through training we diminish this response. They were pointing out how pro/elite level athletes will bonk at the end of a IM marathon and physically collapse, while average joe blow runner would have been forced to stop a long time before it got that bad.
If you get his book you can read about 4 or 5 other theories too. It’s worth looking into.
jaretj
I second this suggestion. One of the things I like about his book is that although Noakes clearly has a strong opinion on this, he presents a lot of the research on all angles of exercise phys, and he clearly delineates what is known or not known, and what the logical connections are supposed to be (between theory and empirical support). The book could have used some editing (it is repetitious in places), but overall it is a good source of info subject to its publication date and your willingness to wade through all the details.
Interesting review article on central governor theory here.
I find his arguements weak compared to the numerous models that demonstrate fatigue is peripheral under most every circumstance. He’s certainly got a lot of mileage out his theory but I don’t see a paradigm shift coming anytime soon. We may not a have a good idea what exactly causes fatigue, the old lactic acid theory has taken a pounding the last several years, but from my reading of the literature it’s almost certainly peripheral.
I imagine why we’re having such a hard time determining underlying mechanism with fatigue is that it has multiple underlying mechanism that vary in importance depending on the means by which you’re causing the fatigue.
Theoretically we could probably test his theory by using electrical stimulation (thereby by-passing any volitional control) to activate the muscle and see if VO2max increased, or we caused heart damage, etc.
Are L4 intervals on the bike and tempo runs effective because sustained periods of work at an uncomfortable level of effort reset our central governor?
Does central governor theory suggest that treadmill training, where the pace is set by the machine and not self-selected, might be extremely effective?
Samples size N=1…in my lead up to A races, this is why I do some really hard short duration stuff. One of it is to set my “pain threshold” from a mental tolerance perspective.
With respect to the treadmill or CT ergo mode, have you guys noticed that after doing a “pyramid” where you incrementally increase the load reach the “top of the pyramid” (with respect to load) and then bring it down, how the perceived effort on the way down seems so much lower? Granted, it might be because one is fully warmed up and firing, but sometimes I feel it is just a “relative thing” from a neural receptor perspective.
I imagine why we’re having such a hard time determining underlying mechanism with fatigue is that it has multiple underlying mechanism that vary in importance depending on the means by which you’re causing the fatigue.
I tend to agree with this. As far as I know there’s no reason to assume that the mechanisms underlying fatigue are identical for 800m, 10k and marathon distances.
We may not a have a good idea what exactly causes fatigue, the old lactic acid theory has taken a pounding the last several years, but from my reading of the literature it’s almost certainly peripheral.
What about a model that incorporates central and peripheral mechanisms? Current models of chronic pain, another poorly understood phenomenon, suggest that changes to pain-conducting peripheral afferents as well as changes to the “central modulation” of pain stimuli, combine to produce chronic pain. This model accounts for the known impact of affective disturbances (e.g. depression) on pain, just as emotional stimuli produced by a competitive atmosphere can modify fatigue thresholds.
Theoretically we could probably test his theory by using electrical stimulation (thereby by-passing any volitional control) to activate the muscle and see if VO2max increased, or we caused heart damage, etc.
I think Noakes suggested that his theory could explain the effectiveness of amphetamines in improving endurance performance in that they affect the central nervous system in such a way that they cause disinhibition or central governor desensitisation. Amphetamines are a known CNS stimulant at doses used to treat ADHD, and at those doses they also delay fatigue. I’m not sure if at those doses they are known to affect peripheral lactate metabolism, etc. If they don’t, this is definitely evidence in Noakes’ favour.
“With respect to the treadmill or CT ergo mode, have you guys noticed that after doing a “pyramid” where you incrementally increase the load reach the “top of the pyramid” (with respect to load) and then bring it down, how the perceived effort on the way down seems so much lower? Granted, it might be because one is fully warmed up and firing, but sometimes I feel it is just a “relative thing” from a neural receptor perspective.”
I get the same thing whenever I get shot out of the back of a fast group ride, as long as I haven’t blown myself all to hell. I can’t maintain that scary fast speed, but a normally solo tempo pace/pwr almost feels like I’m soft pedalling for 30 minutes or so.
When I used to train exclusively for Olympic tri, right before my weekly track session, I’d do this 20 min warmup run (easy) and then I had a super steep ~15-25% grade hill for no more than 200m that I would sprint up till I nearly collapesed. After that, the 15x400m session felt much easier than when I had to do my track work away from my “home track” and the hill was not there to “clean the pipes”. It think there is something to be said about desensitizing the brain to a super high level of pain before embarking on less intense sets over longer duration…or maybe it is in my head…same reason why I do the 10x15 second all out sprints after my warmup before a tri race start…seems to make the chaos and high intensity of the mass start more bearable!
If so, by what mechanism? Some of Noakes’ evidence (lactate concentrations at altitude) seems to suggest that lactate doesn’t explain fatigue. This is well accepted, and has been for a while Is the basis of fatigue more neural than biochemical?
Technically, can the two really be separated, assuming that by neural, you aren’t talking specifically about recruitment? Even if we accept the idea of a central governor, it seems to me it doesn’t change much in terms of how we train, but rather how we explain why our training methods work. It also implies that physiological tests (VO2max, LT) may be less important than previously thought. True - how many top pro’s do you know that got there as a result of regular lab testing? Are L4 intervals on the bike and tempo runs effective because sustained periods of work at an uncomfortable level of effort reset our central governor? Good point, and probable - constant higher intensity effort is suggested to impact upon tolerance to the higher systolic BP associated with high int exercise - partly a centrally regulated process
i like the governor theory, for two reasons: from my POV as a medical anthropologist, a central governor makes good evolutionary sense. especially considering how many adaptations we have to deal with heat stress, i can imagine a ‘central’ process that effectively shuts us down to limit the amount of damage we’re capable of doing to ourselves. sort of like how swelling is our body’s way of immobilizing a joint.
the second reason i like it is because it’s elegant. the ‘peripheral’ theory has definitely been around for ages and is tried and tested, but as far as occam’s razor goes, i’ll take noakes. i realize this argument is totally unscientific, but that’s why nobody pays me to be a physiologist. . .
Are L4 intervals on the bike and tempo runs effective because sustained periods of work at an uncomfortable level of effort reset our central governor? Good point, and probable - constant higher intensity effort is suggested to impact upon tolerance to the higher systolic BP associated with high int exercise - partly a centrally regulated process
What do you mean by tolerance to higher systolic BP? Plenty of people walk around with chronic hypertension with no awareness or acute ill effects. What’s the proposed mechanism - baroreceptor desensitisation?
Is the basis of fatigue more neural than biochemical?
Technically, can the two really be separated, assuming that by neural, you aren’t talking specifically about recruitment?
Of course synaptic transmission is a biochemical process, but I suppose my question was really whether the focus of fatigue research should shift to focus less on peripheral biochemical markers of cellular metabolism (serum lactate or others) to investigating centrally governed skeletal muscle recruitment patterns/limitations/feedback mechanisms.
i like the governor theory, for two reasons: from my POV as a medical anthropologist, a central governor makes good evolutionary sense. especially considering how many adaptations we have to deal with heat stress, i can imagine a ‘central’ process that effectively shuts us down to limit the amount of damage we’re capable of doing to ourselves. sort of like how swelling is our body’s way of immobilizing a joint.
I don’t think anyone is discounting central fatigue as a player in certain circumstances, heat stress is regularly cited as an example of central fatigue.
Noakes’ arguement though is that if our muscles or heart worked as hard as they could then the heart would become ischemic so therefore something central must either limit how hard our muscles or heart can work, it’s a fine theory but it lacks almost any support and there is a good bit of support that the limitation in muscle performance occurs in the muscles themselves.
Personally I believe it is primarily an issue of energetics in the muscle, the problem is we don’t know what that energy sensor is or how it works, and I’m not a biochemist or biophysicist so I’m certianly not going to figure it out.
Muscle starts to fatigue within seconds of activity as PCr is depleted, starts to recover almost instantly when activity stops as PCr is resynthesized (and recovery can be prevented by stopping the blood supply since PCr resynthesis is oxidative), we know you reach a steady-state of muscle performance once anaerobic sources of energy are depleted, that is, ATP consumption is matched by the muscles’ rate of oxidative regeneratation of ATP, and this performance very slowly and gradually declines as excercise duration increases probably because some muscle fibers are depleting their glycogen and then must rely on the slower process of fat oxidation to regenerate ATP.
There are likely other factors as well, whether it is metabolites or acidosis inhibiting glycolysis or the issues surrounding Calcium handling during very intense exercise.
I imagine why we’re having such a hard time determining underlying mechanism with fatigue is that it has multiple underlying mechanism that vary in importance depending on the means by which you’re causing the fatigue.
I tend to agree with this. As far as I know there’s no reason to assume that the mechanisms underlying fatigue are identical for 800m, 10k and marathon distances.
We may not a have a good idea what exactly causes fatigue, the old lactic acid theory has taken a pounding the last several years, but from my reading of the literature it’s almost certainly peripheral.
What about a model that incorporates central and peripheral mechanisms? Current models of chronic pain, another poorly understood phenomenon, suggest that changes to pain-conducting peripheral afferents as well as changes to the “central modulation” of pain stimuli, combine to produce chronic pain. This model accounts for the known impact of affective disturbances (e.g. depression) on pain, just as emotional stimuli produced by a competitive atmosphere can modify fatigue thresholds.
Theoretically we could probably test his theory by using electrical stimulation (thereby by-passing any volitional control) to activate the muscle and see if VO2max increased, or we caused heart damage, etc.
I think Noakes suggested that his theory could explain the effectiveness of amphetamines in improving endurance performance in that they affect the central nervous system in such a way that they cause disinhibition or central governor desensitisation. Amphetamines are a known CNS stimulant at doses used to treat ADHD, and at those doses they also delay fatigue. I’m not sure if at those doses they are known to affect peripheral lactate metabolism, etc. If they don’t, this is definitely evidence in Noakes’ favour.
Couldn’t we just give rats or dogs or whatver ampthetamines and exercise them at extreme intensities? If the percentage of VO2max they are able to sustain doesn’t increase or their heart doesn’t become ischemic this would speak against the central limiter, or at least the ability of amphetamines to over ride it.