scholarly journals Low-Intensity Exercise Improves Aerobic Exercise Capacity in Rats After Myocardial Infarction and the Possible Role of Skeletal Muscle Autophagy

2021 ◽  
Vol 34 (2) ◽  
pp. 226-226
Author(s):  
Li-mei Chen ◽  
Wen-wen Peng ◽  
Gui-qing Xu ◽  
Yue Guo ◽  
Ling-jie Wei ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Exercise Capacity ◽  
Sham Group ◽  
Heart Weight ◽  
Low Intensity ◽  
Aerobic Exercise Capacity ◽  
Low Intensity Exercise

Abstract Background To investigate the effects of low-intensity exercise on aerobic exercise capacity and autophagy of skeletal muscle in rats after myocardial infarction (MI) and its possible mechanisms. Methods Thirty male Sprague Dawley rats, weighing 180–200 g, were randomly divided into sham, MI, and MI with exercise training (MI + Ex) groups. MI was induced by ligation of the left anterior descending artery. One week after surgery, low-intensity exercise training was carried out on a treadmill 5 days per week for 4 weeks. Results Infarct size of MI and MI + Ex groups was 30.8 ± 5.5% and 27.6 ± 5.0% of left ventricle, respectively (P > 0.05). Heart weight and heart to body weight ratio in the MI group were significantly higher than those in the sham group (P < 0.01), and were lowered by exercise training (P < 0.01). The maximal exercise distance and duration in the MI group were lower than those in the sham group (P < 0.01), but were significantly increased by exercise training (P < 0.05). Autophagosome of the gastrocnemius was not detectable in the sham group, scattered in the MI group but clustered in the MI + Ex group. Microtubule-associated protein light chain 3 (LC3-I/II) and Beclin-1 protein levels in the gastrocnemius were similar between MI and sham groups, but were significantly higher in the MI + Ex group (P < 0.05). Conclusions Low-intensity exercise improves exercise capacity in rats after MI. The effect is associated with enhanced autophagy of the skeletal muscle.

scholarly journals Conditional knockout of Mn-SOD targeted to type IIB skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity

2009 ◽  
Vol 297 (6) ◽  
pp. C1520-C1532 ◽  
Author(s):  
Michael S. Lustgarten ◽  
Youngmok C. Jang ◽  
Yuhong Liu ◽  
Florian L. Muller ◽  
Wenbo Qi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Aerobic Exercise ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Contractile Function ◽  
Muscle Fibers ◽  
Conditional Knockout ◽  
Mitochondrial Oxidative Stress ◽  
Aerobic Exercise Capacity

In vitro studies of isolated skeletal muscle have shown that oxidative stress is limiting with respect to contractile function. Mitochondria are a potential source of muscle function-limiting oxidants. To test the hypothesis that skeletal muscle-specific mitochondrial oxidative stress is sufficient to limit muscle function, we bred mice expressing Cre recombinase driven by the promoter for the inhibitory subunit of troponin ( TnIFast-iCre) with mice containing a floxed Sod2 ( Sod2 fl/fl) allele. Mn-SOD activity was reduced by 82% in glycolytic (mainly type II) muscle fiber homogenates from young TnIFastCreSod2 fl/fl mice . Furthermore, Mn-SOD content was reduced by 70% only in type IIB muscle fibers. Aconitase activity was decreased by 56%, which suggests an increase in mitochondrial matrix superoxide. Mitochondrial superoxide release was elevated more than twofold by mitochondria isolated from glycolytic skeletal muscle in TnIFastCreSod2 fl/fl mice. In contrast, the rate of mitochondrial H2O2 production was reduced by 33%, and only during respiration with complex II substrate. F2-isoprostanes were increased by 36% in tibialis anterior muscles isolated from TnIFastCreSod2 fl/fl mice. Elevated glycolytic muscle-specific mitochondrial oxidative stress and damage in TnIFastCreSod2 fl/fl mice were associated with a decreased ability of the extensor digitorum longus and gastrocnemius muscles to produce contractile force as a function of time, whereas force production by the soleus muscle was unaffected. TnIFastCreSod2 fl/fl mice ran 55% less distance on a treadmill than wild-type mice. Collectively, these data suggest that elevated mitochondrial oxidative stress and damage in glycolytic muscle fibers are sufficient to reduce contractile muscle function and aerobic exercise capacity.

scholarly journals Relationship between intermuscular adipose tissue infiltration and myostatin before and after aerobic exercise training

2018 ◽  
Vol 315 (3) ◽  
pp. R461-R468 ◽  
Author(s):  
Adam R. Konopka ◽  
Christopher A. Wolff ◽  
Miranda K. Suer ◽  
Matthew P. Harber
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Aerobic Exercise Training ◽  
Skeletal Muscle Function ◽  
Intermuscular Adipose Tissue ◽  
Before And After

Intermuscular adipose tissue (IMAT) is associated with impaired skeletal muscle contractile and metabolic function. Myostatin and downstream signaling proteins such as cyclin-dependent kinase 2 (CDK2) contribute to the regulation of adipose and skeletal muscle mass in cell culture and animals models, but this relationship remains incompletely understood in humans. The purpose of this study was to determine if the infiltration of IMAT was associated with skeletal muscle myostatin and downstream proteins before and after 12 wk of aerobic exercise training (AET) in healthy older women (OW; 69 ± 2 yr), older men (OM; 74 ± 3 yr), and young men (YM; 20 ± 1 yr). We found that the infiltration of IMAT was correlated with myostatin and phosphorylated CDK2 at tyrosine 15 [P-CDK2(Tyr15)]. IMAT infiltration was greater in the older subjects and was associated with lower skeletal muscle function and exercise capacity. After 12 wk of AET, there was no change in body weight. Myostatin and P-CDK2(Tyr15) were both decreased after AET, and the reduction in myostatin was associated with decreased IMAT infiltration. The decrease in myostatin and IMAT occurred concomitantly with increased exercise capacity, skeletal muscle size, and function after AET. These findings demonstrate that the reduction in IMAT infiltration after AET in weight stable individuals was accompanied by improvements in skeletal muscle function and exercise capacity. Moreover, the association between myostatin and IMAT was present in the untrained state and in response to exercise training, strengthening the potential regulatory role of myostatin on IMAT.

scholarly journals p53 Improves Aerobic Exercise Capacity and Augments Skeletal Muscle Mitochondrial DNA Content

2009 ◽  
Vol 105 (7) ◽  
pp. 705-712 ◽  
Author(s):  
Joon-Young Park ◽  
Ping-yuan Wang ◽  
Takumi Matsumoto ◽  
Ho Joong Sung ◽  
Wenzhe Ma ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dna ◽  
Aerobic Exercise ◽  
Exercise Capacity ◽  
Dna Content ◽  
Mitochondrial Dna Content ◽  
Aerobic Exercise Capacity

Comparison of high- and low-intensity exercise training early after acute myocardial infarction

1988 ◽  
Vol 61 (1) ◽  
pp. 26-30 ◽  
Author(s):  
James A. Blumenthal ◽  
W.Jack Rejeski ◽  
Margaret Walsh-Riddle ◽  
Charles F. Emery ◽  
Henry Miller ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Exercise Training ◽  
Low Intensity ◽  
Low Intensity Exercise

scholarly journals Low Intensity Exercise Training Improves Skeletal Muscle Regeneration Potential

2015 ◽  
Vol 6 ◽  
Author(s):  
Tiziana Pietrangelo ◽  
Ester S. Di Filippo ◽  
Rosa Mancinelli ◽  
Christian Doria ◽  
Alessio Rotini ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration ◽  
Regeneration Potential ◽  
Low Intensity ◽  
Low Intensity Exercise
Sign in / Sign up

Export Citation Format

Share Document