Soleus biopsies were obtained from four male astronauts 45 days before and within 2 h after a 17 day spaceflight. For all astronauts, single chemically skinned post‐flight fibres expressing only type I myosin heavy chain (MHC) developed less average peak Ca2+ activated force (Po) during fixed‐end contractions (0.78 ± 0.02 vs. 0.99 ± 0.03 mN) and shortened at a greater mean velocity during unloaded contractions (Vo) (0.83 ± 0.02 vs. 0.64 ± 0.02 fibre lengths s−1) than pre‐flight type I fibres. The flight‐induced decline in absolute Po was attributed to reductions in fibre diameter and/or Po per fibre cross‐sectional area. Fibres from the astronaut who experienced the greatest relative loss of peak force also displayed a reduction in Ca2+ sensitivity. The elevated Vo of the post‐flight slow type I fibres could not be explained by alterations in myosin heavy or light chain composition. One alternative possibility is that the elevated Vo resulted from an increased myofilament lattice spacing. This hypothesis was supported by electron micrographic analysis demonstrating a reduction in thin filament density post‐flight. Post‐flight fibres shortened at 30 % higher velocities than pre‐flight fibres at external loads associated with peak power output. This increase in shortening velocity either reduced (2 astronauts) or prevented (2 astronauts) a post‐flight loss in fibre absolute peak power (μN (fibre length) s−1). The changes in soleus fibre diameter and function following spaceflight were similar to those observed after 17 days of bed rest. Although in‐flight exercise countermeasures probably reduced the effects of microgravity, the results support the idea that ground‐based bed rest can serve as a model of human spaceflight. In conclusion, 17 days of spaceflight decreased force and increased shortening velocity of single Ca2+‐activated muscle cells expressing type I MHC. The increase in shortening velocity greatly reduced the impact that impaired force production had on absolute peak power.

The primary goal of this study was to determine the effects of prolonged space flight (∼180 days) on the structure and function of slow and fast fibres in human skeletal muscle. Biopsies were obtained from the gastrocnemius and soleus muscles of nine International Space Station crew members ∼45 days pre-and on landing day (R+0) post-flight. The main findings were that prolonged weightlessness produced substantial loss of fibre mass, force and power with the hierarchy of the effects being soleus type I > soleus type II > gastrocnemius type I > gastrocnemius type II. Structurally, the quantitatively most important adaptation was fibre atrophy, which averaged 20% in the soleus type I fibres (98 to 79 μm diameter). Atrophy was the main contributor to the loss of peak force (P 0 ), which for the soleus type I fibre declined 35% from 0.86 to 0.56 mN. The percentage decrease in fibre diameter was correlated with the initial pre-flight fibre size (r = 0.87), inversely with the amount of treadmill running (r = 0.68), and was associated with an increase in thin filament density (r = 0.92). The latter correlated with reduced maximal velocity (V 0 ) (r = −0.51), and is likely to have contributed to the 21 and 18% decline in V 0 in the soleus and gastrocnemius type I fibres. Peak power was depressed in all fibre types with the greatest loss (∼55%) in the soleus. An obvious conclusion is that the exercise countermeasures employed were incapable of providing the high intensity needed to adequately protect fibre and muscle mass, and that the crew's ability to perform strenuous exercise might be seriously compromised. Our results highlight the need to study new exercise programmes on the ISS that employ high resistance and contractions over a wide range of motion to mimic the range occurring in Earth's 1 g environment.

The purpose of this study was to examine the effect of prolonged bed rest (BR) on the peak isometric force (Po) and unloaded shortening velocity ( V o) of single Ca2+-activated muscle fibers. Soleus muscle biopsies were obtained from eight adult males before and after 17 days of 6° head-down BR. Chemically permeabilized single fiber segments were mounted between a force transducer and position motor, activated with saturating levels of Ca2+, and subjected to slack length steps. V owas determined by plotting the time for force redevelopment vs. the slack step distance. Gel electrophoresis revealed that 96% of the pre- and 87% of the post-BR fibers studied expressed only the slow type I myosin heavy chain isoform. Fibers with diameter >100 μm made up only 14% of this post-BR type I population compared with 33% of the pre-BR type I population. Consequently, the post-BR type I fibers ( n = 147) were, on average, 5% smaller in diameter than the pre-BR type I fibers ( n = 218) and produced 13% less absolute Po. BR had no overall effect on Po per fiber cross-sectional area (Po/CSA), even though half of the subjects displayed a decline of 9–12% in Po/CSA after BR. Type I fiber V oincreased by an average of 34% with BR. Although the ratio of myosin light chain 3 to myosin light chain 2 also rose with BR, there was no correlation between this ratio and V o for either the pre- or post-BR fibers. In separate fibers obtained from the original biopsies, quantitative electron microscopy revealed a 20–24% decrease in thin filament density, with no change in thick filament density. These results raise the possibility that alterations in the geometric relationships between thin and thick filaments may be at least partially responsible for the elevated V o of the post-BR type I fibers.

Soleus muscle atrophy was induced by hindlimb unloading of male Sprague-Dawley rats (305 +/- 15 g) for 4, 7, and 10-14 days. Controls (291 +/- 14 g) were housed in vivarium cages. Soleus electromyogram (EMG) activity was recorded before and during tail suspension. Unloading caused progressive reduction in the muscle-to-body weight ratio. After 14 days, type I and IIa fibers decreased in area 63 and 47%, respectively. Subsarcolemmal mitochondria and myofibrils were degraded more rapidly than intermyofibrillar mitochondria and the cell membrane. After 10 days, 3% of the fibers exhibited segmental necrosis; affected fibers were all high-oxidative type IIa fibers. This suggested ischemic injury. By 13 days, 30% of the fibers possessed central corelike lesions involving primarily type I fibers. Video monitoring revealed abnormal plantar flexion of the hindfeet by 4 days; this posture shortened the soleus working range. Corelike lesions indicated adaptation to the shortened length. No morphological signs of denervation were detected. EMG activity shifted from tonic to phasic, and aggregate activity was 13% of normal after 7 days. These findings indicate that the atrophy and pathological changes result from unloaded contractions, reduced use, compromised blood flow, and shortened working length.

Prolonged exposure to hand-transmitted vibration can cause debilitating neural and vascular dysfunction in humans. It is unclear whether the pathophysiology involves simultaneous or sequential injury of arteries and nerves. The mechanism of vibration injury was investigated in a rat tail model, containing arteries and nerves structurally similar to those in the human hand. Tails were selectively vibrated for 1 or 9 days with the remainder of the animal at rest. One vibration bout of 4 h/day, 60 HZ, 5 g (49 m/s(2)) acceleration, injured endothelial cells. Injury was signaled by elevated immunostaining for NFATc3 transcription factor. Electron microscopy revealed that vibration for 9 days produced loss and thinning of endothelial cells, with activated platelets coating the exposed subendothelial tissue. Endothelial cells and arterial smooth muscle cells contained double membrane-limited, swollen processes indicative of vasoconstriction-induced damage. Laser doppler surface recording demonstrated that 5 min of vibration significantly diminished tissue blood perfusion. These findings indicate that early injury involves vasoconstriction and denuding of the arterial endothelium.