title: High- versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats.
abstract: Poor skeletal muscle performance was shown to strongly predict mortality and long-term prognosis in a variety of diseases, including heart failure (HF). Despite the known benefits of aerobic exercise training (AET) in improving the skeletal muscle phenotype in HF, the optimal exercise intensity to elicit maximal outcomes is still under debate. Therefore, the aim of the present study was to compare the effects of high-intensity AET with those of a moderate-intensity protocol on skeletal muscle of infarcted rats. Wistar rats underwent myocardial infarction (MI) or sham surgery. MI groups were submitted either to an untrained (MI-UNT); moderate-intensity (MI-CMT, 60% Vo(2)(max)); or matched volume, high-intensity AET (MI-HIT, intervals at 85% Vo(2)(max)) protocol. High-intensity AET (HIT) was superior to moderate-intensity AET (CMT) in improving aerobic capacity, assessed by treadmill running tests. Cardiac contractile function, measured by echocardiography, was equally improved by both AET protocols. CMT and HIT prevented the MI-induced decay of skeletal muscle citrate synthase and hexokinase maximal activities, and increased glycogen content, without significant differences between protocols. Similar improvements in skeletal muscle redox balance and deactivation of the ubiquitin-proteasome system were also observed after CMT and HIT. Such intracellular findings were accompanied by prevented skeletal muscle atrophy in both MI-CMT and MI-HIT groups, whereas no major differences were observed between protocols. Taken together, our data suggest that despite superior effects of HIT in improving functional capacity, skeletal muscle adaptations were remarkably similar among protocols, leading to the conclusion that skeletal myopathy in infarcted rats was equally prevented by either moderate-intensity or high-intensity AET.
authors: School of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil.
authors: José B N
authors: JB
authors: Moreira
authors: Luiz R G
authors: LR
authors: Bechara
authors: Luiz H M
authors: LH
authors: Bozi
authors: Paulo R
authors: PR
authors: Jannig
authors: Alex W A
authors: AW
authors: Monteiro
authors: Paulo M
authors: PM
authors: Dourado
authors: Ulrik
authors: U
authors: Wisløff
authors: Patricia C
authors: PC
authors: Brum
mesh_terms: D000818:Animals; D002950:Citrate (si)-Synthase / Q000378:metabolism; D004195:Disease Models, Animal; D005081:Exercise Therapy / Q000379:methods*; D017079:Exercise Tolerance; D006003:Glycogen / Q000378:metabolism; D006593:Hexokinase / Q000378:metabolism; D008297:Male; D009119:Muscle Contraction; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009133:Muscular Atrophy / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014463:Ultrasonography
chemical_list: D006003:Glycogen; D002950:Citrate (si)-Synthase; D006593:Hexokinase; D046988:Proteasome Endopeptidase Complex