scholarly journals Time-Course Analysis of Soleus Muscle Disuse Atrophy Using Myonuclear Number and Domain Size as Indicators

2010 ◽  
Vol 25 (3) ◽  
pp. 363-367
Author(s):  
Kazumi ADACHI ◽  
Toshiaki YAMAZAKI
Aging Cell ◽  
2021 ◽  
Author(s):  
Dennis K. Fix ◽  
H. Atakan Ekiz ◽  
Jonathan J. Petrocelli ◽  
Alec M. Mckenzie ◽  
Ziad S. Mahmassani ◽  
...  

2013 ◽  
Vol 126 (8) ◽  
pp. 557-566 ◽  
Author(s):  
Tim Snijders ◽  
Benjamin T. Wall ◽  
Marlou L. Dirks ◽  
Joan M. G. Senden ◽  
Fred Hartgens ◽  
...  

Two weeks of muscle disuse led to a loss in muscle mass and strength. The loss in muscle mass was attributed to both type I and type II muscle fibre atrophy, and was not accompanied by a decline in satellite cell content.


2017 ◽  
Vol 312 (5) ◽  
pp. E394-E406 ◽  
Author(s):  
Samuel Lee ◽  
Teresa C. Leone ◽  
Lisa Rogosa ◽  
John Rumsey ◽  
Julio Ayala ◽  
...  

Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and -1β serve as master transcriptional regulators of muscle mitochondrial functional capacity and are capable of enhancing muscle endurance when overexpressed in mice. We sought to determine whether muscle-specific transgenic overexpression of PGC-1β affects the detraining response following endurance training. First, we established and validated a mouse exercise-training-detraining protocol. Second, using multiple physiological and gene expression end points, we found that PGC-1β overexpression in skeletal muscle of sedentary mice fully recapitulated the training response. Lastly, PGC-1β overexpression during the detraining period resulted in partial prevention of the detraining response. Specifically, an increase in the plateau at which O2 uptake (V̇o2) did not change from baseline with increasing treadmill speed [peak V̇o2 (ΔV̇o2max)] was maintained in trained mice with PGC-1β overexpression in muscle 6 wk after cessation of training. However, other detraining responses, including changes in running performance and in situ half relaxation time (a measure of contractility), were not affected by PGC-1β overexpression. We conclude that while activation of muscle PGC-1β is sufficient to drive the complete endurance phenotype in sedentary mice, it only partially prevents the detraining response following exercise training, suggesting that the process of endurance detraining involves mechanisms beyond the reversal of muscle autonomous mechanisms involved in endurance fitness. In addition, the protocol described here should be useful for assessing early-stage proof-of-concept interventions in preclinical models of muscle disuse atrophy.


1987 ◽  
Vol 63 (1) ◽  
pp. 130-137 ◽  
Author(s):  
D. B. Thomason ◽  
R. E. Herrick ◽  
D. Surdyka ◽  
K. M. Baldwin

This study examined the time course of adult rodent soleus muscle myofibril and myosin isoform protein expression after 4, 8, 16, 28, and 56 days of hindlimb unweighting by tail suspension (S). The time course of soleus muscle recovery (R) was also examined after 28 days of hindlimb unweighting with an additional 4, 8, 16, and 28 days of unrestricted cage activity. During suspension, soleus muscle myofibril protein rapidly decreased from 34.3 +/- 3.1 (1.96SE) mg/pair in the control (C) group to 6.9 +/- 1.4 (1.96SE) mg/pair in S (t = 56 days). The calculated first-order degradation rate constant for this loss was kd = 0.17 days-1 [half time (t1/2) = 4.1 days]. The estimated slow myosin (SM) isoform content decreased from 13.4 +/- 2.0 (1.96SE) mg/pair in C to 2.1 +/- 0.2 (1.96SE) mg/pair in S (kd = 0.19 days-1, t1/2 = 3.6 days). The relative proportion of other myosin isoforms was increased at 28 and 56 days of suspension, reflecting an apparent de novo synthesis and the loss of SM. Recovery of contractile protein after 28 days of suspension was slower for both the myofibril protein and the SM isoform (kd = 0.07 days-1, t1/2 = 10 days). These data suggest that loss of weight bearing specifically affected the mechanisms of contractile protein expression reflected in soleus muscle protein degradation processes. In addition, the expression of the myosin isoforms were apparently differentially affected by the loss of weight-bearing activity.


2017 ◽  
Vol 98 ◽  
pp. 153-161 ◽  
Author(s):  
Yuji Kanazawa ◽  
Keisuke Ikegami ◽  
Mitsugu Sujino ◽  
Satoshi Koinuma ◽  
Mamoru Nagano ◽  
...  

2019 ◽  
Vol 33 (3) ◽  
pp. 4586-4597 ◽  
Author(s):  
Chris Mcglory ◽  
Stefan H. M. Gorissen ◽  
Michael Kamal ◽  
Ravninder Bahniwal ◽  
Amy J. Hector ◽  
...  

1993 ◽  
Vol 74 (6) ◽  
pp. 2949-2957 ◽  
Author(s):  
K. S. McDonald ◽  
R. H. Fitts

This study characterizes the time course of change in single soleus muscle fiber size and function elicited by hindlimb unweighting (HU) and analyzes the extent to which varying durations of HU altered maximal velocity of shortening (Vo), myofibrillar adenosinetriphosphatase (ATPase), and relative content of slow and fast myosin in individual soleus fibers. After 1, 2, or 3 wk of HU, soleus muscle bundles were prepared and stored in skinning solution at -20 degrees C. Single fibers were isolated and mounted between a motor arm and a transducer, and fiber force, Vo, and ATPase activity were measured. Fiber myosin content was determined by one-dimensional sodium dodecyl sulfate- (SDS) polyacrylamide gel electrophoresis. After 1, 2, and 3 wk of HU, soleus fibers exhibited a progressive reduction in fiber diameter (16, 22, and 42%, respectively) and peak force (42, 48, and 72%, respectively). Peak specific tension was significantly reduced after 1 wk of HU (18%) and showed no further change in 2–3 wk of HU. During 1 and 3 wk of HU, fiber Vo and ATPase showed a significant increase. By 3 wk, Vo had increased from 1.32 +/- 0.04 to 2.94 +/- 0.17 fiber lengths/s and fiber ATPase from 291 +/- 16 to 1,064 +/- 128 microM.min-1 x mm-3. The percent fibers expressing fast myosin heavy chain increased from 4% to 29% by 3 wk of HU, and Vo and ATPase activity within a fiber were highly correlated.(ABSTRACT TRUNCATED AT 250 WORDS)


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