Prolonged exercise to fatigue in humans impairs skeletal muscle Na+-K+-ATPase activity, without sarcoplasmic reticulum Ca2+ release; and Ca2+ uptake

• Published in: Journal of applied physiology (1985) 2004-10, Vol.97 (4), p.1414
• Main Authors: Leppik, James A, Aughey, Robert J, Medved, Ivan, Fairweather, Ian
• Format: Article
• Language: English
• Subjects: Calcium; Exercise; Human subjects; Muscular system; Potassium
• ISSN: 8750-7587; 1522-1601

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 x min-1 x 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 x min-1 x 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. [PUBLICATION ABSTRACT]