Resistance exercise training attenuates skeletal muscle atrophy in experimental pulmonary arterial hypertension.

To evaluate the effects of a resistance training (RT) program applied during the development of MCT-induced pulmonary arterial hypertension (PAH) on skeletal muscle atrophy in rats. Twenty-one male Wistar rats were randomly distributed into three experimental groups (n = 7 per group): Sedentary Control (SC), Sedentary Hypertensive (SH), and Trained Hypertensive (TH). PAH was induced by a single intraperitoneal injection of monocrotaline (MCT; 60 mg/kg). Animals in the TH group underwent RT (vertical ladder; 15 climbs with 1-minute interval; 60% of the maximum load supported), 1 session/day, 5 days/week, for approximately 3 weeks. On the 24th day after injection, all animals were euthanized. Subsequently, the biceps brachii were removed, processed and destined for histological or biochemical analyses. RT increased the exercise tolerance (i.e., maximum load supported) in rats with PAH. In addition, RT prevented adverse remodeling in skeletal muscle by preserving the cross-sectional area of myocytes and attenuated total collagen deposition. Furthermore, RT reduced the gene expression of proteolytic agents (i.e., MuRF1, atrogin-1, and myostatin) and attenuated redox imbalance (i.e., CAT, NO, and CP). However, neither PAH nor RT influenced muscle hypertrophy pathways (i.e., Akt, phospo-Akt, eIF4E e phospo- eIF4E) in this model. The RT applied during the development of MCT-induced PAH protects against skeletal muscle atrophy, by mitigating adverse structural remodeling and atrophy through proteolysis modulation and attenuation of redox imbalance.