Peripheral Fatigue in Exercise

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Peripheral Fatigue in Exercise

by Gavin Curry

Peripheral fatigue is a problem the affects the performance of many athletes. There are many causes for fatigue, although there is debate at to which factors are the primary causes and which have little effect. Factors such as ATP depletion, H? accumulation, Intracellular Pi accumulation, glycogen store depletion and potassium re-distribution are all thought to play an important factor in the fatiguing of muscles.

The aetiology of fatigue is controversial, although the contribution each of these above factors towards fatigue seems to depend on the nature of the exercise (Green, 1997).

Allen (2004) suggested that the accumulation of lactate and extracellular potassium, together with a lowering of the pH, affects membrane excitability. Repeated activation of skeletal muscle causes a variety of changes in its properties, with muscles becoming weaker with intense use (fatigue).

The belief that lactic acid production causes an intracellular acidosis that inhibits the myofibrillar proteins must be questioned. It has been previously thought that lactic acid build-up was the major cause for fatigue. However, there are now several reports of the protective effects of lactate exposure or induced acidosis on potassium-depressed muscle contractions in isolated rodent muscles. Peripheral fatigue in exerciseIn addition, sodium-lactate exposure can attenuate severe fatigue in rat muscle, and suggestions that sodium lactate ingestion can increase time to exhaustion during sprinting in humans (Cairns, 2006). These newer findings have led to the idea that lactate / H+ is ergogenic during exercise and it should not be taken as fact that impairs exercise performance. Experiments on isolated muscle suggest that acidosis has little detrimental effect or may even improve muscle performance during high-intensity exercise (Van Montfoort et al., 2004).

It was found that during repeated stimulation of single fibres of mouse muscle, there was little or no pH change. The reason for the fall in performance was thought to be due to calcium release, and that the precipitation of calcium and phosphate in the sarcoplasmic reticulum contributes to the failure of calcium release (Allen, 2004). Allen (2002) found through experiments on skinned fibre on mice that when intracellular phosphate is increased the amount of Ca2+ released from the sarcoplasmic reticulum (SR) declines. Intracellular calcium release declines during fatigue and this has been shown to contribute to the reduction in force (Dugan and Frontera, 2000).

In summary, although the focus of this abstract has been primarily on the role of lactate, phosphates and calcium, there are many contributing factors, working in unison at any one time to cause fatigue. Lactic acid accumulation does not seem to have as much of a negative influence on fatigue as originally thought, possibly even a positive effect. A major cause of fatigue seems to be due to increased intracellular phosphate levels during exercise which cause a decline in intercellular calcium release, contributing to a reduction of force.

References

Allen DG, Kabbara AA, Westerblad H (2002) Muscle fatigue: The role of intracellular calcium stores Canadian Journal of Applied Physiology 27 (1), pp. 83-96

Allen, DG (2004) Skeletal muscle function: Role of ionic changes in fatigue, damage and disease Clinical and Experimental Pharmacology and Physiology. Volume 31, Issue 8, Pages 485-493

Cairns, SP (2006) Lactic acid and exercise performance: Culprit or friend? Sports Medicine Volume 36, Issue 4, 2006, Pages 279-291

Dugan S.A., Frontera W.R. (2000) Muscle fatigue and muscle injury. Physical Medicine and Rehabilitation Clinics of North America 11 (2) 385-403

Green HJ (1997) Mechanisms of muscle fatigue in intense exercise. Journal of Sports Science, Volume 15: 247-256

Van Montfoort MCE, Van Dieren L, Hopkins WG et al. (2004) Effects of ingestion of bicarbonate, citrate, lactate, and chloride on sprint running. Med Sci Sports Exercise Volume 36: 1239-43

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