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1 School of Human Movement, Recreation and Performance; Centre for Rehabilitation, Exercise and Sports Science, Victoria University of Technology, Melbourne, Victoria, Australia
2 School of Life Sciences and Technology; Centre for Rehabilitation, Exercise and Sports Science, Victoria University of Technology, Melbourne, Victoria, Australia
3 Department of Respiratory Medicine, Alfred Hospital and Monash University, Melbourne, Victoria, Australia
4 Department of Medicine B, The Heart Centre, Rigshospitalet, Copenhagen, Denmark
* To whom correspondence should be addressed. E-mail: michael.mckenna{at}vu.edu.au.
Lung transplant recipients (LTx) exhibit marked peripheral limitations to exercise. We investigated whether skeletal muscle Ca2+ and K+ regulation might be abnormal in eight LTx and eight healthy controls. Peak oxygen consumption (VO2peak) and arterialised venous plasma [K+] were measured during incremental exercise. Vastus lateralis muscle was biopsied at rest and analysed for sarcoplasmic reticulum Ca2+ release, Ca2+ uptake and Ca2+ATPase activity rates; fiber composition; Na+,K+-ATPase activity (K+-stimulated 3-O-methylfluorescein phosphatase; 3-O-MFPase activity) and Na+,K+-ATPase content (3H-ouabain binding sites), as well as for [H+] and H+-buffering capacity. VO2peak was 47% less in LTx (P<0.05). LTx had lower Ca2+ release (34%), Ca2+ uptake (31%) and Ca2+ATPase activity (25%)than controls (P<0.05), despite their higher Type II fiber proportion (LTx, 75.0±5.8, Controls 43.5±2.1%). Muscle [H+] was elevated in LTx (P<0.01), but buffering capacity was similar to Controls. Muscle 3-O-MFPase activity was 31% higher in LTx (P<0.05), but 3H-ouabain binding site content did not differ significantly. However, during exercise the rise in plasma [K+].work-1 ratio was 2.6-fold greater in LTx (P<0.05), indicating impaired K+ regulation. Thus grossly subnormal muscle calcium regulation, with impaired potassium regulation, may contribute to poor muscular performance in LTx.
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