The Roles of Ionic Processes in Muscular Fatigue During Intense Exercise View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1992-02

AUTHORS

Michael J. McKenna

ABSTRACT

Muscular fatigue is manifested by a decline in force- or power-generating capacity and may be prominent in both submaximal and maximal contractions. Disturbances in muscle electrolytes play an important role in the development of muscular fatigue. Intense muscular contraction is accompanied by an increased muscle water content, distributed in both intracellular and extra-cellular spaces. This water influx will modify ionic changes in both compartments. Changes in muscle intracellular electrolyte concentrations with intense contraction may be summarised as including decreases in potassium (6 to 20%) and in creatine phosphate (up to 70 to 100%) and increases in lactate (more than 10-fold), sodium (2-fold) and small, variable increases in chloride. The net result of these intracellular ionic concentration changes with exercise will be a reduction in the intracellular strong ion difference, with a consequent marked rise in intracellular hydrogen ion concentration. This intracellular acidosis has been linked with fatigue via impairment of regulatory and contractile protein function, calcium regulation and metabolism. Potassium efflux from the contracting muscle cell dramatically decreases the intracellular to extracellular potassium ratio, leading to depolarisation of sarcolemmal and t-tubular membranes. Surprisingly little research has investigated the effects of intense exercise training on electrolyte regulation and fatigue. Intense sprint training in man attenuates muscular fatigue during short term maximal exercise. This is accompanied by improved potassium homeostasis and possibly, improved regulation of muscular acidosis, both factors which may reduce muscular fatigue. More... »

PAGES

134-145

Identifiers

URI

http://scigraph.springernature.com/pub.10.2165/00007256-199213020-00009

DOI

http://dx.doi.org/10.2165/00007256-199213020-00009

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1012526655

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/1373245


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