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.
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).
(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.
In 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.
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
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