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Skeletal muscle atrophy is presumed to be associated with changes in Ca2+ signalling pathways but whether or not intracellular Ca2+ homeostasis is critically affected in that situation and if so how, remains unclear. Furthermore, this question has so far been essentially addressed in slow-twitch muscle and there is very limited related information concerning fast-twitch muscle. Here we characterized properties of flexor digitorum brevis (FDB) muscles following a 2 week period of hindlimb suspension. This protocol resulted in a 19 % reduction in FDB muscle weight and in a corresponding 18 % reduction in fiber diameter. Fibre type distribution remained however unchanged with 12 % of type I, 84 % of type IIa, and 4 % of type IIb fibres. Voltage-clamp measurements showed that the slow Ca2+ current yielded essentially identical properties in control and atrophied fibers. In voltage-clamped fibres loaded with the Ca2+ dye indo-1, neither the resting [Ca2+] level nor the peak change in [Ca2+] elicited by 5-100 ms-long membrane depolarization from -80 to + 10 mV, significantly differed between control and atrophied fibers. However, the rate of [Ca2+] decay after the end of a pulse was reduced by 30-50% in the atrophied fibres (e.g. rate constant of decay was 13.6 ± 1 and 8.8 ± 0.9 s-1 in 20 control and 24 atrophied fibres, respectively, following a 20 ms-long pulse). This effect appears to be consistent with a reduced contribution of both saturable and non-saturable components of myoplasmic Ca2+ removal. Still, western blot analysis showed that the amount of two major components of Ca2+ removal, parvalbumin and type 1 sarco-endoplasmic reticulum Ca2+-ATPase, was not reduced in the atrophied FDB muscles. |
