Posted by: SLS | September 17, 2010

What contributes to muscle fatigue?

Here is a problem I’ve been wrestling with now for a few weeks. I’ve been spending most of my time learning biochemistry, reading older journals (to get a baseline of what is “known”) and finding newer material to get an idea of what is “up and coming” in an applied theory sense. Finding the solution is a lot like being lost in a rabbit hole where any one tunnel can lead to an answer or more tunnels to explore. Usually both, which is a problem since I’m the type of person to follow a tangent mid stride if I think it might lead somewhere important. Despite the setbacks, here’s the summary of my most recent research.

Overarching problem: what causes muscle fatigue and how can it be prevented?

Current accepted theory: Muscle fatigue is the decline in ability for actin and myosin bonds to break during prolonged or intense muscle contraction. Breaking the bond is what requires ATP. Lack of sufficient ATP production and use ultimately degrades the cycle of the actin and myosin power stroke. A “power stroke” is the contraction (shortening) of the sarcomeres in the muscle fibers, and the final release back to the “re-cocked” position. Decline in ATP efficacy is thought to result from increasing acidity localized at the muscle cell. This is termed muscle acidosis.

Causes of acidosis: Increasing acidity (decreasing ph level) is due to an accumulation of protons, or a positive charge, usually in the form of positively charged ions such as hydrogen (H+). The metabolic process of ATP production involves a series of reactions which can yield positive, neutral, or negatively charged end products. In anaerobic metabolism, these reactions are broken into 2 main phases (orange text denotes addition or subtraction of free proton):

  1. Glycolysis (glucose-> pyruvate)(+1 for glycogen, +2 for glucose)
  2. Lactate production (2 pyruvate-> 2 lactate) (-2)

Source(s) of net proton gain:

  • ATP hydrolysis (+1 for glycogen, +2 for glucose)
  • Oxidation of glyceraldehyde 3-phosphate (+2)

Source(s) of proton consumption

  • Phosphate group (Pi) removed from ATP to form ADP captures 1+
  • Pyruvate kinase reaction consumes 2+
  • Conversion of 2 pyruvate to 2 lactate consumes 2+

Final outcome:

  • Glucose nets 0
  • Glycogen nets -1

Summary: At the end of anaerobic respiration, glucose nets a proton load of 0, and glycogen nets a -1. It would seem as though acidosis cannot occur based on this analysis. However, the processes described above do not work exactly proportional to one another. In particular, glycolysis (APT hydrolysis to ADP) produces free protons faster than lactate production can take them away. This means that protons actually do build up in the cell despite the buffering attempts of phosphate protonating and lactate production (4).

My end analysis at this point is the realization that prevention of muscle acidosis hinges upon the efficacy of the acid buffering effects of Pi and lactate production, as well as the use of glycogen instead of glucose for glycolysis. Personally I thought it was interesting to know that glycogen use in cellular metabolism halves proton production!

So, in order to delay or prevent acidosis onset, we want to use glycogen, and we want to promote maximum lactate production efficacy. How to do so is the next question!

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