High-Intensity Resistance Training with Insufficient Recovery Time Between Bouts Induce Atrophy and Alterations in Myosin Heavy Chain Content in Rat Skeletal Muscle

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)The aim of this study was to test whether high-intensity resistance training with insufficient recovery time between bouts, could result in a decrease of muscle fiber cross-sectional area (CSA), alter fiber-type frequencies and myosin heavy chain (MHC) isoform content in rat skeletal muscle. Wistar rats were divided into two groups: trained (Tr) and control (Co). Tr group were subjected to a high-intensity resistance training program (5 days/week) for 12 weeks, involving jump bouts into water, carrying progressive overloads based on percentage body weight. At the end of experiment, animals were sacrificed, superficial white (SW) and deep red (DR) portions of the plantaris muscle were removed and submitted to mATPase histochemical reaction and SDS-PAGE analysis. Throughout the experiment, both groups increased body weight, but Tr was lower than Co. There was a significant reduction in IIA and IID muscle fiber CSA in the DR portion of Tr compared to Co. Muscle fiber-type frequencies showed a reduction in Types I and IIA in the DR portion and IID in the SW portion of Tr compared to Co; there was an increase in Types IIBD frequency in the DR portion. Change in muscle fiber-type frequency was supported by a significant decrease in MHCI and MHCIIa isoforms accompanied by a significant increase in MHCIIb isoform content. MHCIId showed no significant differences between groups. These data show that high-intensity resistance training with insufficient recovery time between bouts promoted muscle atrophy and a transition from slow-to-fast contractile activity in rat plantaris muscle. Anat Rec, 294: 1393-1400, 2011. (C) 2011 Wiley-Liss, Inc.294813931400Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP [130628/2008-5, 08/52641-1

NFAT Isoforms Regulate Muscle Fiber Type Transition without Altering CaN during Aerobic Training

The purpose of this study was to determine whether the aerobic training-induced fiber-type transition in different muscles is associated with alterations in NFAT isoforms gene expression. We hypothesized that the aerobic training-induced fiber-type transition would be mediated by NFATc1-c3 isoforms without altering the CaN expression. Male Wistar rats (80 days old) were divided into a trained group (T; n=8) that underwent an 8-wk swimming endurance training program (5 days/week) and a control group (C; n=8). After the experimental period, the animals were sacrificed, and the soleus (SOL) and plantaris (PL) muscles were collected for morphometrical, histochemical and molecular analyses. Aerobic training induced a type I-to-type IIA fiber transition in the SOL muscle and a type IIB-to-type IIA fiber transition in the PL muscle, which were concomitant with a significant (p<0.05) increase in NFATc1-c3 gene expression in both the SOL and PL muscles. In contrast, the expression levels of calcineurin (CaN) and NFATc4 remained unchanged. Therefore, our results showed that fiber type switching induced by aerobic training is mediated by NFATc1-c3 isoforms without altering the CaN expression.341086186

Aerobic Exercise Training Prevents Heart Failure-Induced Skeletal Muscle Atrophy by Anti-Catabolic, but Not Anabolic Actions

Heart failure (HF) is associated with cachexia and consequent exercise intolerance. Given the beneficial effects of aerobic exercise training (ET) in HF, the aim of this study was to determine if the ET performed during the transition from cardiac dysfunction to HF would alter the expression of anabolic and catabolic factors, thus preventing skeletal muscle wasting.We employed ascending aortic stenosis (AS) inducing HF in Wistar male rats. Controls were sham-operated animals. At 18 weeks after surgery, rats with cardiac dysfunction were randomized to 10 weeks of aerobic ET (AS-ET) or to an untrained group (AS-UN). At 28 weeks, the AS-UN group presented HF signs in conjunction with high TNF-α serum levels; soleus and plantaris muscle atrophy; and an increase in the expression of TNF-α, NFκB (p65), MAFbx, MuRF1, FoxO1, and myostatin catabolic factors. However, in the AS-ET group, the deterioration of cardiac function was prevented, as well as muscle wasting, and the atrophy promoters were decreased. Interestingly, changes in anabolic factor expression (IGF-I, AKT, and mTOR) were not observed. Nevertheless, in the plantaris muscle, ET maintained high PGC1α levels.Thus, the ET capability to attenuate cardiac function during the transition from cardiac dysfunction to HF was accompanied by a prevention of skeletal muscle atrophy that did not occur via an increase in anabolic factors, but through anti-catabolic activity, presumably caused by PGC1α action. These findings indicate the therapeutic potential of aerobic ET to block HF-induced muscle atrophy by counteracting the increased catabolic state