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Muscle Fatigue Essay

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Contrary to what was long thought, muscle fatigue is not due to the accumulation of lactate in our muscles. Indeed, it is the concentration of H + protons and not the lactate concentration which intervenes in the acid-base modifications responsible for fatigue. Moreover, we know that the most important production of this latter, results from the hydrolysis of ATP and not glycogenolysis. However, muscle fatigue depends on many factors and in our time, is still not very well understood.
Indeed, in vitro, the accumulation of H + protons leads to a significant decrease in the cellular pH (7 → 6) which inhibits the activity of the enzyme regulating glycolysis: phosphofructokinase or PFK. But in vivo the add of inorganic phosphate (Pi), ADP, AMP
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Moreover, always in vitro, this inhibition would entail the stopping of the glycolysis and consequently the stopping of the synthesis of the ATP, thus a decrease in the contractile force, synonymous with functional incapacity. Then, the protons would compete with the calcium ions, preventing them from interacting with the troponin calcium sites. Under these conditions, the removal of the inhibition exerted at rest by the troponin-tropomyosin complex on the formation of the actomyosin bridges could not be realized: the muscular contraction could not therefore take place. However, in vivo, two to three minutes of rest are sufficient for the muscle to regain its functional capacity after stopping by exhaustion following intense exercise causing a large drop in pH.
Second, lactate is often mistakenly accused of causing muscle cramps. In fact, cramps are caused by mineral deficiencies or hydromineral imbalances. Indeed, if it was because of the lactate concentration, every time you do some sports you would be prone to cramps. It is
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