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Abstract
Physical exercise promotes cardiorespiratory fitness, and is considered the mainstream of non-pharmacological therapies along with lifestyle modification for various chronic diseases, in particular cardiovascular diseases. Physical exercise may positively affect various cardiovascular risk factors including body weight, blood pressure, insulin sensitivity, lipid and glucose metabolism, heart function, endothelial function, and body fat composition. With the ever-rising prevalence of obesity and other types of metabolic diseases, as well as sedentary lifestyle, regular exercise of moderate intensity has been indicated to benefit cardiovascular health and reduce overall disease mortality. Exercise offers a wide cadre of favorable responses in the cardiovascular system such as improved dynamics of the cardiovascular system, reduced prevalence of coronary heart diseases and cardiomyopathies, enhanced cardiac reserve capacity, and autonomic regulation. Ample clinical and experimental evidence has indicated an emerging role for autophagy, a conservative catabolism process to degrade and recycle cellular organelles and nutrients, in exercise training-offered cardiovascular benefits. Regular physical exercise as a unique form of physiological stress is capable of triggering adaptation while autophagy in particular selective autophagy seems to be permissive to such cardiovascular adaptation. Here in this mini-review, we will summarize the role for autophagy in particular mitochondrial selective autophagy namely mitophagy in the benefit versus risk of physical exercise on cardiovascular function.
Highlights
Regular physical exercise is a part of healthy lifestyle, with multiple cross-sectional studies consolidating reduced overall risk of cardiovascular diseases and cardiac events associated with habitual or leisure physical exercises [1,2]
In-depth analysis was carried out by Luan and associates in an effort to recapitulate beneficial effects of various types of exercise on 26 forms of chronic diseases, including cardiovascular diseases. These authors have concluded that long-term aerobic or home-based exercise seems to benefit patients with coronary artery diseases the most, while high-intensity interval training (HIIT) significantly enhances cardiac performance in patients with chronic heart failure [12]
Preserved prepare the organism for the bout of activity [40]. This is possibly achieved through autophagy glucose uptake has been documented in insulin-resistant muscle following exercise [42]
Summary
Regular physical exercise is a part of healthy lifestyle, with multiple cross-sectional studies consolidating reduced overall risk of cardiovascular diseases and cardiac events associated with habitual or leisure physical exercises [1,2]. Regular physical exercise is becoming a non-pharmacological remedy to lower cardiovascular morbidity and mortality courtesy of the exercise-induced cardiovascular benefit [6,7] Such maneuver drastically improves the overall cardiovascular survival despite the poor success for current pharmaceutical. There is a growing concern of physiological adaptation and induction of autophagy, a conserved evolutionary process responsible for the degradation of multiple cellular components [1,14,15,16] Under stress conditions such as starvation and increased physical activity, autophagy is usually turned on to recycle long-lived or damaged cellular organelles and proteins for the resynthesis of new organelles and ATP. Mitophagy might be instrumental to a better understanding of how exercise impacts the overall organismal health In this mini-review, we will highlight the essential role of mitophagy in exercise-induced effects on cardiovascular system
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