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, Bradley S. Launikonis

High-force eccentric exercise results in sustained increases in cytoplasmic Ca(2+) levels ([Ca(2+)]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 Ca(2+)-handling properties. Both t-system components could take up Ca(2+) from the cytoplasm but only transverse tubules supported store-operated Ca(2+) entry. The retention of significant amounts of Ca(2+) within vacuoles provides an effective mechanism to reduce the total content of Ca(2+) within the fibre cytoplasm. We propose this ability can reduce or limit resistance exercise-induced, Ca(2+)-dependent damage to the fibre by the reduction of [Ca(2+)]cyto to help maintain fibre viability during the period associated with delayed onset muscle soreness.