Voluntary exercise training reversed high-fat diet-induced decreases in cardiac cardiolipins and enhanced mitochondrial complex I activity in mice.
RCT
Randomized
Does voluntary exercise training mitigate the effects of high-fat feeding on cardiac morphology and mitochondrial function in mice?
Voluntary exercise training protects against high-fat diet-induced cardiac mitochondrial dysfunction and cardiolipin depletion in a mouse model.
BACKGROUND: Obesity is a risk factor for developing cardiometabolic disease. Exercise training is pivotal in the treatment of obesity and is associated with reduced cardiovascular mortality. This study examined the effect of high-fat feeding on cardiac morphology and mitochondrial function, alongside the mitigating effects of voluntary exercise training. METHODS: Six-week-old male C57Bl/6 J mice commenced a high fat diet (HFD) or chow diet and were randomized to receive locked (sedentary) or unlocked (voluntary exercise training (VET)) running wheels at 10 weeks of age. Mice were monitored until 30 weeks of age and euthanized for collection of tissues. Magnetic resonance imaging was performed to assess body composition, and echocardiography was performed to assess cardiac function. RESULTS: Compared with chow-fed animals, the HFD increased body weight and adiposity and decreased cardiolipins (CL) in the heart, which are required for maintaining adequate mitochondrial respiration. Importantly, VET reversed these effects and induced physiological cardiac hypertrophy. Cardiac mitochondrial respiratory chain analysis revealed decreased complexes II and IV activity following high fat feeding, while VET enhanced complex I activity, emphasizing the cardioprotective effect of exercise training in obesity. CONCLUSION: This study uncovers mechanisms by which obesity and exercise impact cardiac mitochondrial health and suggests the mitochondria is a therapeutic target in obesity-related cardiovascular diseases.
Perera et al. (Wed,) conducted a rct in Obesity. Voluntary exercise training (VET) vs. Locked (sedentary) running wheels was evaluated on Cardiac morphology and mitochondrial function. Voluntary exercise training reversed high-fat diet-induced decreases in cardiac cardiolipins and enhanced mitochondrial complex I activity in mice.