The effect of high-intensity interval training on the renin-angiotensin system signaling in skeletal muscle of overweight and obese men and women

Abstract

Overactivation of the renin-angiotensin (Ang) system (RAS) has been recently associated with fat accumulation and loss of skeletal muscle mass, common hallmarks of obesity. Angiotensin-converting enzymes (ACE1 and ACE2) catalyse the conversion of Ang to Ang II, which via both Ang II receptors (AT1R and AT2R) modulate ROS, inflammation and may contribute to muscle loss and maintenance. The role of exercise training on the regulation of skeletal muscle RAS signalling remains unknown. Thus, we aim to ascertain how high-intensity training (HIT) modulates RAS signalling in skeletal muscle of overweight and obese individuals and its influence on the changes in body composition. METHODS: Forty-one women (age: 31 yo, weight: 87.1 kg) and 50 men (age: 28.3 yo, weight: 100.9 kg) with overweight or obesity (BMI>27 kg/m2) participated in a HIT program (3 sessions/week x 6 weeks, each consisting in 7 bouts of 1min cycling at 100% of VO2max, with 1 min recovery between bouts or five bouts at a higher intensity with 90s recovery in between). In each volunteer muscle biopsies from vastus lateralis were obtained before, 72h after the last training session, and after 3 weeks of detraining. ACE1, ACE2, AT1R and AT2R protein expression were analysed by Western Blot. Body composition was assessed by DXA. Statistical analysis: repeated-measures ANOVA. RESULTS: VO2max and maximal power output were improved significantly after training (5-10%), while arterial blood pressure was slightly reduced. The protein expression of AT1R was increased by 13% after HIT (P=0.017, n=71) and remained at this level after 3 weeks of detraining (P=0.019). AT2R protein expression was increased after HIT by 33% (P=0.035, n=32), returning to pre-training levels after 3 weeks of detraining. No significant changes were observed in the protein expression levels of ACE1 and ACE2. Men and women responded similarly to HIT (all training variables x sex interactions P>0.10). No significant differences between sex were observed in the protein expression levels of ACE1, ACE2, AT1R and AT2R. CONCLUSION: Increased expression of AT1R and AT2R could facilitate Ang II signalling in skeletal muscle. Some recent studies indicate that the pharmacological blockade of Ang II Receptors may facilitate muscle regeneration, muscle insulin sensitivity and reduced disuse-related atrophy. In turn, increased Ang II signalling in skeletal muscle has been associated with oxidative stress. Given the intensity of the exercise performed and the exhaustive nature of the training program, we cannot rule out these changes as indicative of potential maladaptation to this model of training.