Skeletal muscle atrophy and strength loss induced by short-term simulated spaceflight are offset or attenuated by resistance exercise (RE). This study compared the effects of plantar flexor and knee extensor RE on muscle size and function in 17 healthy men (aged 26-41years) subjected to 90 days 6 degrees head-down-tilt bed rest with (BRE; n = 8) or without (BR; n = 9) RE. The RE program consisted of coupled maximal concentric and eccentric actions in the supine squat (4 sets of 7 repetitions) and calf press (4 x 14) every third day employing a gravity-independent flywheel ergometer (FW). Prior to, and following bed rest, muscle volume was assessed using magnetic resonance imaging. Similarly, muscle strength and power and surface electromyographic (EMG) activity were determined during maximal actions using FW or isokinetic dynamometry. In BR, knee extensor and plantar flexor muscle volume decreased (P < 0.05) 18% and 29%, respectively. Torque or force and power decreased (P < 0.05) 31 60% (knee extension) and 37-56% (plantar flexion) while knee extensor and plantar flexor EMG activity decreased 31-38% and 28-35%, respectively following BR. Muscle atrophy in BRE was prevented (P > 0.05; knee extensors) or attenuated (-15%; plantar flexors). BRE maintained task-specific force, power and EMG activity. The decrease in non-task-specific torque was less (P < 0.05) than in BR. The present data imply that the triceps surae and quadriceps muscles show different responsiveness to long-term bed rest with or without resistance exercise. The results also suggest that designing in-flight resistance exercise protocols for space travellers is complex and must extend beyond preserving muscle only.
Muscle biopsies were obtained from the vastus lateralis before and after 84 days of bed-rest from six control (BR) and six resistance-exercised (BRE) men to examine slow-and fast-twitch muscle fibre contractile function. BR did not exercise during bed-rest and had a 17 and 40% decrease in whole muscle size and function, respectively. The BRE group performed four sets of seven maximal concentric and eccentric supine squats 2-3 days per week (every third day) that maintained whole muscle strength and size. Slow (MHC I) and fast (MHC IIa) muscle fibres were studied at 15• C for diameter, peak force (P o ), contractile velocity (V o ) and force-power parameters. SDS-PAGE was performed on each single fibre after the functional experiments to determine MHC isoform composition. MHC I and IIa BR fibres were, respectively, 15 and 8% smaller, 46 and 25% weaker (P o ), 21 and 6% slower (V o ), and 54 and 24% less powerful after bed-rest (P < 0.05). BR MHC I and IIa P o and power normalized to cell size were lower (P < 0.05). BRE MHC I fibres showed no change in size or V o after bed-rest; however, P o was 19% lower (P < 0.05), resulting in 20 and 30% declines (P < 0.05) in normalized P o and power, respectively. BRE MHC IIa fibres showed no change in size, P o and power after bed-rest, while V o was elevated 13% (P < 0.05). BRE MHC IIa normalized P o and power were 10 and 15% lower (P < 0.05), respectively. MHC isoform composition shifted away from MHC I fibres, resulting in an increase (P < 0.05) in MHC I/IIa (BR and BRE) and MHC IIa/IIx (BR only) fibres. These data show that the contractile function of the MHC I fibres was more affected by bed-rest and less influenced by the resistance exercise protocol than the MHC IIa fibres. Considering the large differences in power of human MHC I and IIa muscle fibres (5-to 6-fold), the maintenance of whole muscle function with the resistance exercise programme is probably explained by (1) the maintenance of MHC IIa power and (2) the shift from slow to fast (MHC I → MHC I/IIa) in single fibre MHC isoform composition.
The present data suggest that this resistance exercise paradigm counteracts quadriceps and abates the more substantial triceps surae muscle atrophy in bedridden subjects, and therefore should be an important asset to space travellers.
Adaptive changes of major body systems in astronauts during spaceflight can be simulated by strict anti-orthostatic head-down tilt (HDT) bed rest (BR), a ground-based microgravity (microG) model that provides a meaningful opportunity to study atrophy mechanisms and possible countermeasures under controlled experimental conditions. As nitric oxide (NO) signaling is linked to muscle activity, we investigated altered expression of the three major isoforms of nitric oxide synthase (NOS 1-3) at cellular compartments during prolonged HDT BR without (control group) and with resistance exercise interventions (exercise group) using a flywheel ergometer (FWE). Atrophy detected in mixed (fast-slow) m. vastus lateralis (VL) and slow-type m. soleus (SOL) myofiber Types I and II (minus 35-40% of myofiber cross-sectional area) was prevented by FWE training. Concomitant to muscle atrophy, reduced NOS 1 protein and immunostaining was found in VL not in SOL biopsies. In trained VL, NOS 1 protein and immunostaining at myofibers II were significantly increased at the end of BR. Exercise altered NOS 2/caveolin 3 co-immunostaining patterns of subsarcolemmal focal accumulations in VL or SOL myofibers, which suggests reorganization of sarcolemmal microdomains. In trained VL, increased capillary-to-fiber (C/F) ratio and NOS 3 protein content were documented. Activity-linked NO signaling may be widespread in skeletal muscle cellular compartments that may be directly or indirectly impacted by adequate exercise countermeasure protocols to offset the negative effects induced by disuse, immobilization, or extended exposure to microgravity.
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