Posted by: SLS | October 20, 2010

The bee in the honey

It has been far too long since my last post on anything relevant, and as is wont to happen in the information age, the information continues to flow like scattered tributaries coursing towards a central current. My most recent muscle biochemistry read was a kind of ground-shaking article by T.D. Noakes (5) describing different accepted models of muscular fatigue… and how they are wrong.

The slightly disturbing notion that you have spent a great deal of time learning and imbibing information only to find out that your growing paradigm crumbles in light of some new, damnably objective, perspective can and does shake the toughest and most leathery researcher. It sends a great creeping dread down one’s spine that has an incapacitating power. However, it is very possible and quite necessary to shake out the cobwebs of long-standing self-affirmations, grown too accustomed to a welcoming environment, and plunge into the cold, crisp, and slightly biting waters of rational objective skepticism. This I have found from T.D. Noakes’ review article. I’ll summarize briefly below.

The exercise science and muscle biochemistry world recognizes the following concepts as accepted models for muscular fatigue:

  1. The cardiovascular/anaerobic model- performance determined by capacity of heart to pump blood and O2 to muscles
  2. The energy supply/energy depletion model
  3. The muscle recruitment (central fatigue)/muscle power model
  4. The biomechanical model
  5. The psychological/motivational model

Noakes held that some of these models may be partially correct, but ultimately incapable of fully explaining the array of laboratory observations, namely that fatigue occurs long before muscular glycolysis occurs (anaerobisis), before ATP depletion (tetanus) in the muscles, before cardiac ischaemia, and that central fatigue must be resultant from neuronal feedback as to the state of the contracting muscle and associated organ systems.

Noakes countered with one central philosophy regarding muscular fatigue. He stated that all fatigue is essentially neurological controls set to force stop exercise before physiological damage occurs, whether that damage be from cardiac ischaemia, tetanus, heat stroke, cerebral hypoxia, fall in blood pressure, or glucopaenic brain damage from liver glycogen depletion (and obviously poor use of fatty acid metabolism). In other words, our bodies contain governors, much like cars, that cut off activity once some physiological constraint threshold is met.

The other mover and shaker in my world of muscular literature was Pederson et al. 2004 (6), which, by its very title comes out swinging. “Intracellular acidosis enhances the excitability of working muscle,” emphasis mine.  Apparently the acidosis helps increase excitability of the T system, making it easier for the alpha neuron to stimulate the muscle fibers, even as the neuronal signal gets weaker. What does this mean? At rest, the more alkaline pH level stabilizes resting membrane potential and allows high permeability of Cl-, and low permeability of Na+, but Na+ is needed to create an action potential. At higher pH, it takes a larger Na+ current to achieve the action potential, but if the muscle fibers are already acidic (lower pH), a smaller Na+ current is needed to generate an action potential, so acidosis is preserving functionality of the T system in working muscle.  One might say that the signal degrades anyways, even with acidosis, but the fatigue buffering effects aren’t in place to prevent fatigue, only slow its course.

These two articles were a headache, but I think they resonate well when put together. Fatigue is governed by the CNS, simply put, but only as a response to the information feedback from the working muscle and organ systems enacted during exercise.

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