HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 586/17/4039    most recent jphysiol.2008.155424v2 jphysiol.2008.155424v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Cairns, S. P. Articles by Lindinger, M. I. PubMed PubMed Citation Articles by Cairns, S. P. Articles by Lindinger, M. I. Related Collections Perspectives Skeletal Muscle and Exercise

¹ Institute of Sport and Recreation Research New Zealand, Faculty of Health and Environmental Sciences, AUT University, Auckland 1020, New Zealand
² Department of Human Health and Nutritional Science, University of Guelph, Guelph, ON, Canada N1G 2W1

During intense exercise or electrical stimulation of skeletal muscle the concentrations of several ions change simultaneously in interstitial, transverse tubular and intracellular compartments. Consequently the functional effects of multiple ionic changes need to be considered together. A diminished transsarcolemmal K⁺ gradient per se can reduce maximal force in non-fatigued muscle suggesting that K⁺ causes fatigue. However, this effect requires extremely large, although physiological, K⁺ shifts. In contrast, moderate elevations of extracellular [K⁺] ([K⁺]_o) potentiate submaximal contractions, enhance local blood flow and influence afferent feedback to assist exercise performance. Changed transsarcolemmal Na⁺, Ca²⁺, Cl^– and H⁺ gradients are insufficient by themselves to cause much fatigue but each ion can interact with K⁺ effects. Lowered Na⁺, Ca²⁺ and Cl^– gradients further impair force by modulating the peak tetanic force–[K⁺]_o and peak tetanic force–resting membrane potential relationships. In contrast, raised [Ca²⁺]_o, acidosis and reduced Cl^– conductance during late fatigue provide resistance against K⁺-induced force depression. The detrimental effects of K⁺ are exacerbated by metabolic changes such as lowered [ATP]_i, depleted carbohydrate, and possibly reactive oxygen species. We hypothesize that during high-intensity exercise a rundown of the transsarcolemmal K⁺ gradient is the dominant cellular process around which interactions with other ions and metabolites occur, thereby contributing to fatigue.

(Received 17 April 2008; accepted after revision 20 June 2008; first published online 23 June 2008)
Corresponding author S. Cairns: School of Sport and Recreation, AUT University, Private Bag 92006, Auckland 1020, New Zealand. Email: simeon.cairns{at}aut.ac.nz