It has been reported that gravitational unloading by actual spaceflight [1][2][3] or simulation models, such as hind limb suspension of rats [3] or human bed rest [4,5] causes atrophy in antigravity muscles. These responses are more profound in slow-twitch than in fasttwitch fibers of ankle plantarflexor muscles [2,3]. It is clear that changes of the muscular properties following gravitational unloading are caused by the decreased normal activity. However, it is not necessarily known what the key factor is for such muscle-specific effects of gravitational unloading. Therefore the effects of various kinds of activities-such as electrical activity estimated by an electromyogram (EMG) recording, contractile activity induced by electrical stimulation at low or high frequencies, and length-related loading on the muscles-on the properties of hind limb muscles were studied in the present investigation.Leonard et al. [6] reported that the mean decrease of lean body mass in nine astronauts was 1.5 kg after 28-84 d of spaceflight, and 1.1 kg was due to water loss. In some studies, the absolute protein content, not Japanese Journal of Physiology, 52, 235-245, 2002 Key words: hind limb suspension, atrophy and growth failure, protein and water contents, electromyogram, muscle length. Abstract:The mechanisms responsible for the morphological and metabolic adaptation of skeletal muscles to the removal of antigravity activity were investigated in rats. Significant atrophy relative to the levels before suspension was induced in ankle plantarflexsors, may be due to a reduced tension production caused by decreased muscle length and electromyogram activity. Growth failure was significant in ankle dorsiflexors, although these muscles did not atrophy. Forced muscle contraction through electrical stimulation at 1 or 100 Hz during hind limb suspension generally had detrimental effects. The percent contribution of water loss to the suspension-related change in weight was 85, 88, and 93% in soleus, plantaris, and extensor digitorum longus, respectively. The total levels of both -hydroxyacyl CoA dehydrogenase (HAD) and lactate dehydrogenase (LDH) were less in the suspended muscles than in the controls, having high positive correlations with the total protein content. The specific activity of HAD, but not of LDH, of the suspended muscles was lower than in the controls (25-61%). These data suggest that the cause of muscle atrophy and changes in metabolic properties may be a decreased tension development, not necessarily the reduction of electrical or contractile activity. Further, it is clearly suggested that electrical stimulation of a muscle group with different composition of fiber phenotype at a certain pattern or frequency is not suitable for the countermeasure. It is also suggested that the major cause of the decreased muscle weight was loss of water, even though protein content was also lowered after suspension. Moreover, the data suggest that the HAD level was affected more than the total protein content and LDH.
SUMMARY1. Responses of enzymic characteristics of gastrocnemius muscle were studied when frogs (Rana pipiens) were exposed to cold environment (4 0C).2. The content of adenosine triphosphate (ATP) decreased significantly after cold exposure. This decrease was greater in starved than in fed frogs.3. Although the glycogen content did not change, lactate levels were lower in coldexposed than room-temperature (control) frogs. No change was observed in glycogen and lactate between fed and unfed frogs kept at 4 0C for 2 months. Lactate dehydrogenase activity tended to increase during chronic cold exposure, but not significantly.4. The activities of citrate synthase, cytochrome oxidase, and ,6-hydroxyacyl CoA dehydrogenase were higher in gastrocnemius of chronically cold-exposed frogs than in room-temperature controls. This increase was statistically significant only in the muscles of starved frogs; these muscles had the greatest decrease in ATP.5. It was suggested that chronic cold exposure decreases skeletal muscle ATP content but may not affect glycolysis. The data also suggested that the decrease in ATP content stimulates mitochondrial biogenesis which increases enzyme activities.
This paper describes an organ culture system that maintains frog sartorius muscles in good condition for 5 days. In the absence of serum and insulin, muscles maintained at approximately 93% of resting length atrophied with significant decreases in dry weight, protein content, and contractile force, and in the levels of activity of citrate synthase, lactate dehydrogenase, and creatine kinase. Inclusion of 1.0 mU/ml of insulin in the culture medium prevented the decreases in muscle mass, twitch tension, and citrate synthase activity and minimized the decreases in lactate dehydrogenase, creatine kinase, and tetanic tension. Inclusion of 10% serum, in addition to 1 mU/ml insulin, in the medium did not have clear cut additional benefits. Stretching muscles to 110% of resting length (L0) resulted in marked deterioration with decreases in total protein, enzyme levels, and contractile force. Keeping muscles at approximately 93% L0 was as effective as maintenance at L0 in preventing atrophy and loss of contractile force and enzyme activities. This organ culture procedure, which maintains frog sartorius muscle in good condition without serum for at least 5 days, may provide a useful model for studying the regulatory mechanisms responsible for a variety of adaptations in muscle.
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