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Previous reports have shown that loss of basal autophagy activity in cardiac or skeletal muscle leads to abnormal development, and cardiac failure and skeletal muscle atrophy, respectively;, therefore, (inducible) tissue-specific knockout of autophagy genes in these organs would not be a suitable approach for examining the physiological effects of deficient exercise-induced autophagy.
To quantify the effect of hamstrings muscle action on stability of the anterior cruciate ligament deficient knee during isokinetic exercise at various speeds.
While even a marginal magnesium deficiency can impair exercise performance, magnesium supplementation can also boost training performance in athletes, particularly in magnesium-deficient individuals [ 2, 4].
The force generated by nNOSμ-deficient muscles during simulated exercise plateaus at a significantly lower level than controls (Figure 3B).
After 40 s of simulated exercise, nNOSμ-deficient muscles begin to show deficits in force production (Figure 3A).
The impaired performance of nNOSμ-deficient skeletal muscle during exercise is unlikely to be due to an increased predisposition to contraction-induced injury.
We also assessed dysferlin-deficient animals following eccentric exercise induced by exhaustive downhill running.
These abnormalities in glucose metabolism during acute exercise in mice deficient in exercise-induced autophagy led us to investigate whether autophagy might contribute to some of the beneficial metabolic effects of chronic exercise training.
The objective of this study was to investigate the chondrogenic response to voluntary exercise in dystrophin-deficient mice.
Studies in TP53-deficient mice have shown a reduced exercise capacity associated with a lower mitochondrial density in skeletal muscle [ 16- 18].
These physiologic changes drive changes in health behaviors; we are more likely to eat poorly and obtain less vigorous exercise when we are sleep deficient.
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