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Abstract
Spaceflight causes muscle wasting. The Sarcolab pilot study investigated two astronauts with regards to plantar flexor muscle size, architecture, and function, and to the underlying molecular adaptations in order to further the understanding of muscular responses to spaceflight and exercise countermeasures. Two crew members (A and B) spent 6 months in space. Crew member A trained less vigorously than B. Postflight, A showed substantial decrements in plantar flexor volume, muscle architecture, in strength and in fiber contractility, which was strongly mitigated in B. The difference between these crew members closely reflected FAK-Y397 abundance, a molecular marker of muscle’s loading history. Moreover, crew member A showed downregulation of contractile proteins and enzymes of anaerobic metabolism, as well as of systemic markers of energy and protein metabolism. However, both crew members exhibited decrements in muscular aerobic metabolism and phosphate high energy transfer. We conclude that countermeasures can be effective, particularly when resistive forces are of sufficient magnitude. However, to fully prevent space-related muscular deterioration, intersubject variability must be understood, and intensive exercise countermeasures programs seem mandatory. Finally, proteomic and metabolomic analyses suggest that exercise benefits in space may go beyond mere maintenance of muscle mass, but rather extend to the level of organismic metabolism.
Highlights
Physical deconditioning is known to occur during spaceflight since Skylab and Mir missions
Muscle function During postflight session 1 (PF-1, performed 0−4 days after return to Earth), plantar flexor muscle strength was reduced by 30.6% in crew member A, whereas B depicted no change from baseline (Fig. 2)
Muscle size and architecture Medial gastrocnemius (GM) muscle volume, pennation angle (PA), and fascicle length (Lf) at PF-1 were all substantially reduced in crew member A, but much less in B (Table 1)
Summary
Physical deconditioning is known to occur during spaceflight since Skylab and Mir missions. Muscle atrophy results from imbalance between protein synthesis and degradation. This imbalance can be caused by enhanced muscle protein breakdown (MPB), controlled by catabolic pathways (ubiquitin proteasome and autophagy), and by inhibited muscle protein synthesis (MPS), controlled by the Akt/mTOR/p70S6K pathway.[9] To date, the relative contribution of MPB and MPS is still unclear.[10] The determination of the actual rates of protein synthesis and degradation in humans is challenging. The relative activation of intracellular pathways involved varies across species and disuse conditions. It is unclear whether a metabolic program plays a relevant role in causing disuse atrophy in humans. It has been suggested that mitochondrial dysfunction is a major trigger of MPB and MPS imbalance.[11,12] Solving these open issues is important for spaceflight
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