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

¹Muscle, Ions, and Exercise Group, School of Human Movement, Recreation and Performance, and ²School of Life Sciences and Technology, Centre for Aging, Rehabilitation, Exercise, and Sport, Victoria University of Technology, Melbourne 8001, Australia

Submitted 8 September 2003 ; accepted in final form 14 May 2004

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 Ca²⁺ regulation. We therefore investigated whether these processes were impaired during cycling exercise at 74.3 ± 1.2% maximal O₂ uptake (mean ± SE) continued until fatigue in eight healthy subjects (maximal O₂ uptake of 3.93 ± 0.69 l/min). 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-O-methylfluorescein phosphatase (3-O-MFPase) activity], Na⁺-K⁺-ATPase content ([³H]ouabain binding sites), sarcoplasmic reticulum Ca²⁺ release rate induced by 4 chloro-m-cresol, and 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), by 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. 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), whereas 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, Ca²⁺ release, and Ca²⁺ uptake rates. This suggests that acutely downregulated muscle Na⁺, K⁺, and Ca²⁺ transport processes may be important factors in fatigue during prolonged exercise in humans.

calcium ion ATPase; sodium-potassium pump; potassium

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