Research on the adaptation of skeletal muscle to hypogravity: past and future directions.
Our current understanding of hypogravity-induced atrophy of skeletal muscles is based primarily on studies comparing pre- and post-flight properties of muscles. Interpretations are necessarily qualified by the assumption that the stress of reentry and readjustment to terrestrial gravity do not alter the parameters being analyzed. The neuromuscular system is highly responsive to changes in functional demands and capable of rapid adaptation, making this assumption questionable. A reexamination of the changes in the connective tissue and synaptic terminals of soleus muscles from rats orbited in biosatellites and sampled postflight indicates that these structural alterations represent adaptative responses of the atrophic muscles to the increased workload of returning to 1 G, rather than hypogravity per se. The atrophy of weightlessness is postulated to result because muscles are both underloaded and used less often. Proper testing of this hypothesis requires quantitation of muscle function by monitoring electromyography, force output and length changes during the flight. Experiments conducted in space laboratories, like those being developed for the Space Shuttle, will avoid the complications of reentry before tissue sampling and allow time course atudies of the rate of development of adaptive changes to zero gravity. Another area of great importance for future studies of muscle atrophy is inflight measurement of plasma levels of hormones and tissue receptor levels. Glucocorticoids, thyroid hormone and insulin exert dramatic regulatory influences on muscle structure. Prevention of neuromuscular atrophy becomes increasingly more important as spaceflights increase in duration. Definition of the atrophic mechanism is essential to developing means of preventing neuromuscular atrophy.
Riley
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Department of Anatomy, Medical College of Wisconsin, Milwaukee, USA.
Ellis
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D000222:Adaptation, Physiological; D000818:Animals; D005938:Glucocorticoids / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D051379:Mice; D009046:Motor Neurons / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation* / Q000378:metabolism / Q000502:physiology / Q000503:physiopathology; D009133:Muscular Atrophy / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology* / Q000517:prevention & control; D009469:Neuromuscular Junction / Q000648:ultrastructure; D051381:Rats; D013026:Space Flight; D013963:Thyroid Hormones / Q000378:metabolism; D014893:Weightlessness / Q000009:adverse effects*
D005938:Glucocorticoids; D007328:Insulin; D013963:Thyroid Hormones