scholarly journals Effect of Loading Frequency on the Recovery Process of Disuse Muscle Atrophy

2021 ◽  
Vol 36 (3) ◽  
pp. 463-466
Author(s):  
Yui MORITA ◽  
Ryo MIYACHI ◽  
Toshiaki YAMAZAKI
2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Ryosuke Nakanishi ◽  
Yusuke Hirayama ◽  
Minoru Tanaka ◽  
Noriaki Maeshige ◽  
Hidemi Fujino

2018 ◽  
Author(s):  
L John Hoffer

This review explains starvation as both a physiologic process and a disease. It includes a detailed explanation of the modifying effects of metabolic adaptation and systemic inflammation, as interpreted in a clinical context. It navigates the reader through the difficult shoals of vague and conflicting terminology that burden this topic and provides current definitions and nuanced explanations of the important but frequently misunderstood terms related to starvation and its modifiers and consequences. It provides a succinct explanation of the physiology of total fasting and its clinical correlates. Finally, it explains the interactions among starvation, sarcopenia, frailty, involuntary weight loss, systemic inflammation, cachexia, and disuse muscle atrophy. The multiple and interacting causes of generalized muscle atrophy are pointed out. Inadequate appreciation of these interactions can result in failure to diagnose and treat starvation-induced diseases. A clinical approach to involuntary weight loss is outlined.   This review contains 6 figures, 2 tables and 56 references Key words: adaptation, cachexia, frailty, hypoalbuminemia, inflammation, ketosis, kwashiorkor, malnutrition, marasmus, muscle atrophy, protein-energy malnutrition, sarcopenia, starvation, systemic inflammation, weight loss


2013 ◽  
Vol 114 (10) ◽  
pp. 1482-1489 ◽  
Author(s):  
Erin E. Talbert ◽  
Ashley J. Smuder ◽  
Kisuk Min ◽  
Oh Sung Kwon ◽  
Scott K. Powers

Prolonged skeletal muscle inactivity results in a rapid decrease in fiber size, primarily due to accelerated proteolysis. Although several proteases are known to contribute to disuse muscle atrophy, the ubiquitin proteasome system is often considered the most important proteolytic system during many conditions that promote muscle wasting. Emerging evidence suggests that calpain and caspase-3 may also play key roles in inactivity-induced atrophy of respiratory muscles, but it remains unknown if these proteases are essential for disuse atrophy in limb skeletal muscles. Therefore, we tested the hypothesis that activation of both calpain and caspase-3 is required for locomotor muscle atrophy induced by hindlimb immobilization. Seven days of immobilization (i.e., limb casting) promoted significant atrophy in type I muscle fibers of the rat soleus muscle. Independent pharmacological inhibition of calpain or caspase-3 prevented this casting-induced atrophy. Interestingly, inhibition of calpain activity also prevented caspase-3 activation, and, conversely, inhibition of caspase-3 prevented calpain activation. These findings indicate that a regulatory cross talk exists between these proteases and provide the first evidence that the activation of calpain and caspase-3 is required for inactivity-induced limb muscle atrophy.


2010 ◽  
Vol 42 ◽  
pp. 19
Author(s):  
Kisuk Min ◽  
Ashley J. Smuder ◽  
Oh-sung Kwon ◽  
Andreas N. Kavazis ◽  
Hazel H. Szeto ◽  
...  

2010 ◽  
Vol 42 ◽  
pp. 18 ◽  
Author(s):  
W. Bradley Nelson ◽  
Ashley J. Smuder ◽  
Matthew B. Hudson ◽  
Erin E. Talbert ◽  
Scott K. Powers

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