Human skeletal muscle plasmalemma alters its structure to change its Ca2+-handling following heavy-load resistance exercise

Tanya R. Cully, Robyn M. Murphy, Llion Roberts, Truls Raastad, Robert G. Fassett, Jeff S. Coombes, Izzy Jayasinghe and Bradley S. Launikonis ()
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Tanya R. Cully: School of Biomedical Sciences, The University of Queensland
Robyn M. Murphy: La Trobe Institute for Molecular Science, La Trobe University
Llion Roberts: School of Human Movement and Nutritional Sciences, The University of Queensland
Truls Raastad: Norwegian School of Sport Sciences
Robert G. Fassett: School of Human Movement and Nutritional Sciences, The University of Queensland
Jeff S. Coombes: School of Human Movement and Nutritional Sciences, The University of Queensland
Izzy Jayasinghe: School of Biomedical Sciences, The University of Queensland
Bradley S. Launikonis: School of Biomedical Sciences, The University of Queensland

Nature Communications, 2017, vol. 8, issue 1, 1-10

Abstract: Abstract High-force eccentric exercise results in sustained increases in cytoplasmic Ca2+ levels ([Ca2+]cyto), which can cause damage to the muscle. Here we report that a heavy-load strength training bout greatly alters the structure of the membrane network inside the fibres, the tubular (t-) system, causing the loss of its predominantly transverse organization and an increase in vacuolation of its longitudinal tubules across adjacent sarcomeres. The transverse tubules and vacuoles displayed distinct Ca2+-handling properties. Both t-system components could take up Ca2+ from the cytoplasm but only transverse tubules supported store-operated Ca2+ entry. The retention of significant amounts of Ca2+ within vacuoles provides an effective mechanism to reduce the total content of Ca2+ within the fibre cytoplasm. We propose this ability can reduce or limit resistance exercise-induced, Ca2+-dependent damage to the fibre by the reduction of [Ca2+]cyto to help maintain fibre viability during the period associated with delayed onset muscle soreness.

Date: 2017
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DOI: 10.1038/ncomms14266

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