There are many physical, physiological and biochemical changes to skeletal muscle following exposure to microgravity. These changes are similar to, but not identical with, changes seen after ground-based models of weightlessness such as bed rest, hind limb suspension, and limb casting. Considerable data now exists for changes in rodent muscle following variable lengths of spaceflight. Less data exists on human muscle following spaceflight and by the nature of the environment there are problems in interpreting the data. The major problems associated with the human data are: (a) the low subject numbers; (b) little data recorded in-flight; (c) lack of knowledge of diet or compliance with countermeasures; (c) the effects produced by re-entry rather than weightlessness itself; and (d) varying lengths of duration of flight. These problems are probably responsible for the often contradictory results obtained. The major changes observed include muscle and fibre atrophy, decreased force and power, decreased specific force, increased maximal velocity of shortening of fibres, increased susceptibility to damage, increased expression of fast-type myosin isozymes, and increased fatigability. The extent to which these occur is extremely variable in the human studies and is not always related to the duration of exposure. Not all muscles are equally affected by weightlessness, with the antigravity/extensor muscles being more severely affected. In animal muscle the Type 1 fibres undergo the greatest atrophy whereas in the human the Type 2 fibres are more affected. This is thought to relate to the relative size of the different fibre types in rodents as opposed to man. The loss of force observed cannot always be explained by the degree of muscle atrophy and this discrepancy may be partly explained by a decreased neural activation. At a single-fibre level power output can decrease or be unaltered, depending on the relative changes in maximal force and velocity of shortening. In vivo, however, very large changes in maximal power output have been measured after both spaceflight and bed rest. The mechanisms causing the increase in maximal velocity of shortening seen in skinned fibres are not fully understood but has been partly attributed to the shift in fibre type expression and partly to an increase in the thick-to-thin filament spacing due to a preferential loss of actin filaments.

There are several possible mechanisms leading to these changes in the space environment. The most obvious is the lack of loaded physical activity. Other changes include alterations in the endocrine status, nutritional status and microgravity itself. The latter can be studied using tissue-cultured organoid systems and what limited data that exists suggests that significant fibre atrophy can occur as a direct result of space travel. Data on endocrine changes is still deficient and controversial although some bed rest studies have implicated the GH/IGF-1 axis via an involvement of muscle afferent activity.

In order to effectively counteract these muscle changes, we need to more fully understand the molecular events controlling them. Effective countermeasures for the space environment may then be applicable for the older or immobilised person.

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