Effects of training on potassium, calcium and hydrogen ion regulation in skeletal muscle and blood during exercise

Authors

  • M. J. McKENNA,

    1. Department of Physical Education and Recreation, Centre for Rehabilitation, Exercise and Sports Science, Victoria University of Technology, Footscray, Victoria, Australia
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  • A. R. HARMER,

    1. Department of Biomedical Science, The University of Sydney, Sydney, New South Wales, Australia
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  • S. F. FRASER,

    1. Department of Physical Education and Recreation, Centre for Rehabilitation, Exercise and Sports Science, Victoria University of Technology, Footscray, Victoria, Australia
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  • J. L. LI

    1. Department of Physical Education and Recreation, Centre for Rehabilitation, Exercise and Sports Science, Victoria University of Technology, Footscray, Victoria, Australia
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Dr M. J. McKenna Department of Physical Education and Recreation, Victoria University of Technology, PO Box 14428, MCMC, Melbourne, Victoria, 8001, Australia

Abstract

Ionic regulation is critical to muscle excitation, contraction and metabolism, and thus for muscle function during exercise. This review focuses on the effects of training upon K+, Ca2+ and H+ ion regulation in muscle and K+ regulation in blood during exercise. Training enhances K+ regulation in muscle and blood and reduces muscular fatiguability. Endurance, sprint and strength training in humans induce an increased muscle Na+, K+ pump concentration, usually associated with a reduced rise in plasma [K+] during exercise. Although impaired muscle Ca2+ regulation plays a vital role in fatigue, little is known about possible training effects. In rat fast-twitch muscle, overload-induced hypertrophy and endurance training were associated with reduced sarcoplasmic reticulum Ca2+ uptake, consistent with fast-to-slow fibre transition. In human muscle, endurance and strength training had no effect on muscle Ca2+ ATPase concentration. Whilst muscle Ca2+ uptake, release and Ca2+ ATPase activity were depressed by fatigue, no differences were found between strength athletes and untrained individuals. Muscle H+ accumulation may contribute to fatigue during intense exercise and is also modified by sprint training. Sprint training may increase muscle Lac- and work output with exhaustive exercise, but the rise in muscle [H+] is unchanged or attenuated, indicating a reduced rise in muscle [H+] relative to work performed. Muscle buffering capacity can be dissociated from this improved H+ regulatory capacity after training. Thus, training enhances muscle and blood K+ and muscle H+ regulation during exercise, consistent with improved muscular performance and reduced fatiguability; however, little is known about training effects on muscle Ca2+ regulation during contraction.

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