Adaptations in the Muscle Cell to Training: Role of the Na+-K+-Atpase

2000 ◽  
Vol 25 (3) ◽  
pp. 204-216 ◽  
Author(s):  
Howard J. Green

The plasticity of skeletal muscle is evident following the onset of regular contractile activity where extensive adaptations can be observed at all levels of organization. Among the properties subject to altered regulation is the Na+-K+-ATPase, an integral membrane protein distributed throughout the sarcolemma and t-tubule, which functions to maintain high Na+ and K+ transmembrane gradients. This protein is uniquely positioned to control muscle excitation and contraction processes, metabolic flux rates, and contractility. Pronounced and rapid upregulation in the Na+-K+-ATPase content can be observed within the first days of exercise and well before the other major ATPase proteins involved in Ca2+ and actomyosin cycling. Moreover, the Na+-K+-ATPase is subject to complex messenger regulation, involved both in the accommodation and the adaptive responses to contractile activity. This emphasizes that adaptive responses can be mediated soon after the onset of training and may have profound affects on muscle contractility and other cellular adaptations. Key Words: muscle, strain, exercise, adaptation, accommodation

2012 ◽  
Vol 90 (9) ◽  
pp. 1209-1217 ◽  
Author(s):  
Robyn Millott ◽  
Elzbieta Dudek ◽  
Marek Michalak

The endoplasmic reticulum has an intricate network of pathways built to deal with the secretory and integral membrane protein synthesis demands of the cell, as well as adaptive responses set up for the endoplasmic reticulum to rely on when stressed. These pathways are both essential and complex, and because of these 2 factors, several situations can lead to a dysfunctional endoplasmic reticulum and result in a dysfunctional cell with the potential to contribute to the progression of disease. The endoplasmic reticulum has been implicated in several metabolic, neurodegenerative, inflammatory, autoimmune, and renal diseases and disorders, and in particular, cardiovascular diseases. The role of the endoplasmic reticulum in cardiovascular disease shows how the change in function of a particular microscopic organelle can lead to macroscopic changes in the form of disease.


2013 ◽  
Vol 11 (1) ◽  
pp. 129 ◽  
Author(s):  
Ludivine Rossard ◽  
Frédéric Favreau ◽  
Sebastien Giraud ◽  
Raphael Thuillier ◽  
Sylvain Le Pape ◽  
...  

2004 ◽  
Vol 287 (1) ◽  
pp. H81-H90 ◽  
Author(s):  
Masakuni Kido ◽  
Hajime Otani ◽  
Shiori Kyoi ◽  
Tomohiko Sumida ◽  
Hiroyoshi Fujiwara ◽  
...  

Dystrophin is an integral membrane protein involved in the stabilization of the sarcolemmal membrane in cardiac muscle. We hypothesized that the loss of membrane dystrophin during ischemia and reperfusion is responsible for contractile force-induced myocardial injury and that cardioprotection afforded by ischemic preconditioning (IPC) is related to the preservation of membrane dystrophin. Isolated and perfused rat hearts were subjected to 30 min of global ischemia, followed by reperfusion with or without the contractile blocker 2,3-butanedione monoxime (BDM). IPC was introduced by three cycles of 5-min ischemia and 5-min reperfusion before the global ischemia. Dystrophin was distributed exclusively in the membrane of myocytes in the normally perfused heart but was redistributed to the myofibril fraction after 30 min of ischemia and was lost from both of these compartments during reperfusion in the presence or absence of BDM. The loss of dystrophin preceded uptake of the membrane-impermeable Evans blue dye by myocytes that occurred after the withdrawal of BDM and was associated with creatine kinase release and the development of contracture. Although IPC did not alter the redistribution of membrane dystrophin induced by 30 min of ischemia, it facilitated the restoration of membrane dystrophin during reperfusion. Also, myocyte necrosis was not observed when BDM was withdrawn after complete restoration of membrane dystrophin. These results demonstrate that IPC-mediated restoration of membrane dystrophin during reperfusion correlates with protection against contractile force-induced myocardial injury and suggest that the cardioprotection conferred by IPC can be enhanced by the temporary blockade of contractile activity until restoration of membrane dystrophin during reperfusion.


1972 ◽  
Vol 50 (10) ◽  
pp. 1017-1019 ◽  
Author(s):  
Keith A. Kelly ◽  
Richard C. La Force

This experiment substantiates the hypothesis that the gastric pacesetter potential sets the pace of gastric contractions. By pacing the gastric pacesetter potential with electrical stimuli during periods of spontaneous and pentagastrin-induced contractile activity, we also paced gastric contractions.


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