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J Appl Physiol (May 21, 2004). doi:10.1152/japplphysiol.00964.2003
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Submitted on September 8, 2003
Accepted on May 14, 2004

Prolonged exercise to fatigue in humans impairs skeletal muscle Na+, K+-ATPase activity, sarcoplasmic reticulum Ca2+ release and Ca2+ uptake

James A Leppik1, Robert J Aughey1, Ivan Medved1, Ian Fairweather1, Michael F Carey2, and Michael J McKenna1*

1 Muscle, Ions and Exercise Group; School of Human Movement, Recreation and Performance, Victoria University of Technology, Melbourne, Victoria, Australia
2 School of Life Sciences and Technology; Centre for Aging, Rehabilitation, Exercise and Sport, Victoria University of Technology, Melbourne, Victoria, Australia

* To whom correspondence should be addressed. E-mail: michael.mckenna{at}vu.edu.au.

Prolonged exhaustive submaximal exercise in humans induces marked metabolic changes, but little is known about effects on muscle Na+, K+ATPase activity and sarcoplasmic reticulum (SR) Ca2+ regulation. We therefore investigated whether these processes were impaired during cycling exercise at 74.3±1.2% VO2peak (mean±SEM) continued until fatigue, in eight healthy subjects (VO2peak 3.93±0.69 l.min-1). A vastus lateralis muscle biopsy was taken at rest, at 10 and 45 min of exercise and at fatigue. Muscle was analyzed for in-vitro Na+, K+ATPase activity (maximal K+-stimulated 3-0-methyl fluorescein phosphatase, 3-O-MFPase activity), Na+K+ATPase content (3[H] ouabain binding sites),SR Ca2+ release rate induced by 4 chloro-m-cresol and SR Ca2+ uptake rate. Cycling time to fatigue was 72.18±6.46 min. Muscle 3-O-MFPase activity [nmol.min-1.(g protein)-1] fell from rest by 6.6±2.1% at 10 min (P<0.05), 10.7±2.3% at 45 min (P<0.01), and by 12.6±1.6% at fatigue (P<0.01), whereas 3[H]ouabain binding site content was unchanged. SR Ca2+ release [mmol.min-1.(g protein)-1] declined from rest by 10.0±3.8% at 45 min (P<0.05) and by 17.9±4.1% at fatigue (P<0.01), whilst SR Ca2+uptake rate fell from rest by 23.8±12.2% at fatigue (P<0.05). However, the decline in muscle 3-O-MFPase activity, Ca2+ uptake and Ca2+ release were variable and not significantly correlated with time to fatigue. Thus, prolonged exhaustive exercise impaired each of the maximal in-vitro Na+,K+ATPase activity, SR Ca2+ release and Ca2+uptake rates. This suggests that acutely downregulated muscle Na+, K+ and Ca2+ transport processes may be important factors in muscle fatigue during prolonged exercise in humans.




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