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Impaired muscle Ca²⁺ and K⁺ regulation contribute to poor exercise performance post-lung transplantation

¹Muscle, Ions and Exercise Group, School of Human Movement, Recreation and Performance, and ²School of Biomedical Science, Centre for Rehabilitation, Exercise and Sports Science, Victoria University of Technology, Melbourne 8001; ³Department of Allergy, Immunology, and Respiratory Medicine, Alfred Hospital, Melbourne 3004; and ⁴Department of Medicine, Monash University, Melbourne, Victoria 3800, Australia; and ⁵Department of Medicine B, The Heart Centre, Rigshospitalet, 2100 Copenhagen, Denmark

Submitted 20 December 2002 ; accepted in final form 10 June 2003

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 and arterialized venous plasma [K⁺] (where brackets denote concentration) were measured during incremental exercise. Vastus lateralis muscle was biopsied at rest and analyzed for sarcoplasmic reticulum Ca²⁺ release, Ca²⁺ uptake, and Ca²⁺-ATPase activity rates; fiber composition; Na⁺-K⁺-ATPase (K⁺-stimulated 3-O-methylfluorescein phosphatase) activity and content ([³H]ouabain binding sites); as well as for [H⁺] and H⁺-buffering capacity. Peak oxygen consumption 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-methylfluorescein phosphatase activity was 31% higher in LTx (P < 0.05), but [³H]ouabain binding content did not differ significantly. However, during exercise, the rise in plasma [K⁺]-to-work 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.

calcium release; calcium adenosine 5'-triphosphatase; Na⁺-K⁺ pump; muscle fiber type; respiratory disease

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