Abstract

Mitochondrial dysfunction is a crucial contributor to heart diseases. Alterations in energetic metabolism affect crucial homeostatic processes, such asATP production, the generation of reactive oxygen species, and the release of pro-apoptotic factors, associated with metabolic abnormalities. In response to energetic deficiency, the cardiomyocytes activate the Mitochondrial Quality Control (MQC), a critical process in maintaining mitochondrial health. This process is compromised in cardiovascular diseases depending on the pathology’s severity and represents, therefore, a potential therapeutic target. Several potential targeting molecules within this process have been identified in the last years, and therapeutic strategies have been proposed to ameliorate mitochondria monitoring and function. In this context, physical exercise is considered a non-pharmacological strategy to protect mitochondrial health. Physical exercise regulates MQC allowing the repair/elimination of damaged mitochondria and synthesizing new ones, thus recovering the metabolic state. In this review, we will deal with the effect of physical exercise on cardiac mitochondrial function tracing its ability to modulate specific steps in MQC both in physiologic and pathologic conditions.

Highlights

  • Mitochondria are considered the “energy power station” of the cells due to their ability to regulate energy metabolism

  • The maximal mitochondrial respiration in muscle fibers increased significantly only after sprint interval training (SIT) and associates with a specific raised content of PGC-1alpha and p53 (Kim et al, 2017). These findings suggest that physical activity (PA), based on training intensity, activates different intracellular pathways that favor new mitochondria synthesis

  • The analysis of mitochondria isolated from hearts of sedentary and exercise-trained rats suggests that exercise can counteract mitochondrial damage: increases antioxidant enzymes and the expression of anti-apoptotic proteins, reduces ROS production, and release of cytochrome c from mitochondria (Kavazis et al, 2008)

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Summary

INTRODUCTION

Mitochondria are considered the “energy power station” of the cells due to their ability to regulate energy metabolism These organelles regulate critical cellular processes, such as calcium homeostasis, and cell survival (Giorgi et al, 2018; Sprenger and Langer, 2019; Fan et al, 2020). Their health is critical to maintaining wellness in organs and tissues (Youle and van der Bliek, 2012; Eisner et al, 2018), especially in high metabolic active tissues that need much energy to support their activities. Physical exercise is emerging as a non-pharmacologic tool to attenuate mitochondrial dysfunction in pathologic conditions, including cardiovascular diseases

THE MOLECULAR MECHANISMS OF MITOCHONDRIA MONITORING IN THE HEART
Mitochondria Fission and Fusion
Mitochondrial Biogenesis
EXERCISE REGULATES MITOCHONDRIAL PHENOTYPES
Exercise and Mitochondrial Biogenesis
Exercise and Mitochondria Turnover
Exercise and Mitochondrial Morphology
Exercise and Mitochondrial Respiration
Exercise and Oxidative Stress
EXERCISE REDUCES CARDIOVASCULAR RISK
EXERCISE AND CARDIAC DISEASES
Exercise and Aging
Myocardial Infarction and Heart Failure
Diabetic Cardiomyopathy
Anthracyclines Dependent Heart Failure
Findings
CONCLUSION

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