High-Intensity Aerobic Exercise Prevents Angiotensin II-Induced Muscle Atrophy.

PURPOSE: Angiotensin II (Ang II) is widely recognized as a primary factor in the development of hypertension; however, recent research also implicates it in skeletal muscle damage and atrophy. The precise mechanisms by which Ang II impacts muscle morphology and the molecular pathways related to atrophy remain unclear. Moreover, the potential protective effects of aerobic exercise against Ang II-induced muscle alterations have not been fully elucidated. This study aimed to investigate the effects of Ang II on skeletal muscle structure and atrophy-related molecular markers and to assess whether aerobic exercise can confer protective effects against these changes in an Ang II-induced animal model. METHODS: Six-week-old mice (n =48) were divided into 4 groups: (1) control (CON, n =12), (2) Ang II (n =12), (3) Ang II plus low-intensity exercise (Ang II+LIE, n=12), and (4) Ang II plus high-intensity exercise (Ang II+HIE, n=12). Ang II was administered subcutaneously once daily for 4 weeks (1.4 mg/kg/day in phosphate-buffered saline, pH 7.2). The Ang II+LIE and Ang II+HIE groups received daily Ang II injections along with their respective exercise protocols for 4 weeks. RESULTS: The protein expression of inflammatory factors was significantly reduced in the Ang II+HIE group compared to the Ang II group (P < 0.05). Furthermore, the expression of muscle protein synthesis markers, including insulin-like growth factor 1, AKT, mammalian target of rapamycin, and S6K1, was significantly higher in the exercise groups than in the Ang II group (P<0.05). Notably, the expression of autophagy-related factors was also significantly elevated in the Ang II+HIE group compared to the Ang II group (P < 0.05). CONCLUSION: Ang II-induced muscle atrophy was attenuated by aerobic exercise.