Microgravity and skeletal muscle

Spaceflight (SF) has been shown to cause skeletal muscle atrophy; a loss in force and power; and, in the first few weeks, a preferential atrophy of ex tensors over flexors. The atrophy primarily results from a reduced protein synthesis that is likely triggered by the removal of the antigravity load. Contractile proteins are lost out of proportion to other cellular proteins, and the actin thin filament is lost disproportionately to the myosin thick filament. The decline in contractile protein explains the decrease in forc e per cross-sectional area, whereas the thin-filament loss may explain the observed postflight increase in the maximal velocity of shortening in the t ype I and IIa fiber types. Importantly, the microgravity-induced decline in peak power is partially offset by the increased fiber velocity. Muscle vel ocity is further increased by the microgravity-induced expression of fast-t ype myosin isozymes in slow fibers (hybrid I/II fibers) and by the increase d expression of fast type II fiber types. SF increases the susceptibility o f skeletal muscle to damage, with the actual damage elicited during postfli ght reloading. Evidence in rats indicates that SF increases fatigability an d reduces the capacity for fat oxidation in skeletal muscles. Future studie s will be required to establish the cellular and molecular mechanisms of th e SF-induced muscle atrophy and functional loss and to develop effective ex ercise countermeasures.