Functional and structural adaptations of skeletal muscle to microgravity

Abstract

SUMMARY Our purpose is to summarize the major effects of space travel on skeletal muscle with particular emphasis on factors that alter function. The primary deleterious changes are muscle atrophy and the associated decline in peak force and power. Studies on both rats and humans demonstrate a rapid loss of cell mass with microgravity. In rats, a reduction in muscle mass of up to 37% was observed within 1 week. For both species, the antigravity soleus muscle showed greater atrophy than the fast-twitch gastrocnemius. However, in the rat, the slow type I fibers atrophied more than the fast type II fibers, while in humans, the fast type II fibers were at least as susceptible to space-induced atrophy as the slow fiber type. Space flight also resulted in a significant decline in peak force. For example, the maximal voluntary contraction of the human plantar flexor muscles declined by 20–48% following 6 months in space, while a 21% decline in the peak force of the soleus type I fibers was observed after a 17-day shuttle flight. The reduced force can be attributed both to muscle atrophy and to a selective loss of contractile protein. The former was the primary cause because, when force was expressed per cross-sectional area (kNm−2), the human fast type II and slow type I fibers of the soleus showed no change and a 4% decrease in force, respectively. Microgravity has been shown to increase the shortening velocity of the plantar flexors. This increase can be attributed both to an elevated maximal shortening velocity (V0) of the individual slow and fast fibers and to an increased expression of fibers containing fast myosin. Although the cause of the former is unknown, it might result from the selective loss of the thin filament actin and an associated decline in the internal drag during cross-bridge cycling. Despite the increase in fiber V0, peak power of the slow type I fiber was reduced following space flight. The decreased power was a direct result of the reduced force caused by the fiber atrophy. In addition to fiber atrophy and the loss of force and power, weightlessness reduces the ability of the slow soleus to oxidize fats and increases the utilization of muscle glycogen, at least in rats. This substrate change leads to an increased rate of fatigue. Finally, with return to the 1g environment of earth, rat studies have shown an increased occurrence of eccentric contraction-induced fiber damage. The damage occurs with re-loading and not in-flight, but the etiology has not been established.

Reciprocal Homer1a and Homer2 Isoform Expression Is a Key Mechanism for Muscle Soleus Atrophy in Spaceflown Mice

“…In other reports, however, muscle atrophy was similarly described in both slow- and fast-twitch myofibers [ 42 ]. An attractive explanation for the relative atrophic response elicited in different muscle types is that microgravity might induce a shift in “neuronal recruitment patterns” of motor units [ 42 , 44 ]. Thus, nerve ending remodeling may play an additional and synergistic role during spaceflight, and altered neuron-derived specific signals (electrical and/or chemical transmitters) [ 45 , 46 ] may contribute to the microgravity effects at the level of single skeletal muscle fibers.…”

Mechanisms of exercise as a preventative measure to muscle wasting

“…Histologically, unloading induces a slow-to-fast myofiber type shift, often contributing to a larger hybrid pool (99,100). At the myofiber level, decreases in power and force are apparent (101,102) and unloaded shortening velocity often increases (103). Furthermore, a 40% reduction in the muscle satellite cell pool (104) may have implications for regenerative capacity upon reloading.…”

The Role of Glycogen Synthase Kinase-3 in the Regulation of Ribosome Biogenesis in Rat Soleus Muscle under Disuse Conditions

“…Skeletal muscle disuse/mechanical unloading occurring during real or simulated microgravity, bedrest, limb immobilization, mechanical ventilation causes a significant reduction in muscle mass, force production and overall function [ 1 , 2 , 3 , 4 , 5 ]. Moreover, transient periods of muscle inactivity can accelerate losses of muscle and strength in older individuals with sarcopenia leading to a variety of negative health outcomes, including an increased risk for falls, fractures and the development of metabolic diseases [ 6 ].…”