In contrast to these findings, analysis of needle biopsy samples from cosmonauts, conducted by the Institute for Biomedical Problems after 76- and 180-day flights, indicated a large degree of individual variation in the extent of myofiber atrophy, with the decrease in myofiber CSA ranging from about 4% to 20%. This variation was attributed to variations in compliance with exercise countermeasures by individual cosmonauts during the flights. More recent muscle biopsy studies have indicated that despite consistent decreases in myofiber CSA in the m. soleus and m. gastrocnemius after spaceflight, MHC expression does not seem to shift, as was previously described by Zhou et al. This discrepancy may reflect the effects of exercise countermeasure protocols carried out by the astronauts during the later flight and the examination of muscles different from those studied in the earlier flight (gastrocnemius and soleus vs. vastus lateralis). Decrements in the aerobic capacity of crewmembers after spaceflight, coupled with a reduction in muscle oxidative capacity, indicate that the vascular supply to skeletal muscle may also be affected by spaceflight. However, at present no consistent relationship is apparent between the degree of muscle atrophy (measured by MRI or myofiber CSA determination after muscle biopsy) and the reported changes in muscle strength and function, although typically loss in muscle strength exceeds the loss in muscle volume. The reasons for these counter-intuitive results are unclear and will probably remain so until resources become available for long-term, on-orbit study of the skeletal muscle atrophic response to spaceflight. In addition to the effects of spaceflight on the myofibrillar component of skeletal muscle, the role of the neural components of skeletal muscle atrophy must not be understated. A functional disruption of neuronal control at the neuromuscular level, which seems to be paralleled by a reduction in the overall electrical activity of the muscle after spaceflight, raises the possibility that neuron-derived factors that play a role in the growth or maintenance of skeletal muscle may be disrupted. The hypothesis that microgravity causes a fundamental alteration in motor control has also been suggested. Studies conducted at JSC by the Exercise Physiology Laboratory showed that two-legged muscle power declines considerably more than can be explained by the loss in muscle mass alone. Additionally, the loss of explosive leg power was associated with a substantial reduction in the electromyography (EMG) activity of the m. rectus femoris, m. vastus lateralis, and m. vastus medialis.