A single session of physical activity restores the mitochondrial organization disrupted by obesity in skeletal muscle fibers

• Published in: Life sciences (1973) Vol. 256; p. 117965
• Main Authors: Rivera-Alvarez, Irais, Pérez-Treviño, Perla, Chapoy-Villanueva, Héctor, Vela-Guajardo, Jorge E., Nieblas, Bianca, Garza-González, Salvador, García-Rivas, Gerardo, García, Noemí
• Format: Journal Article
• Language: English
• Published: New York Elsevier Inc 01.09.2020; Elsevier BV
• Subjects: AMPK; Calcium; Fibers; Gastrocnemius muscle; Membrane potential; Metabolic syndrome; metabolism; Mitochondria; Mitochondria quality control; Mitochondrial dynamics; mRNA; Muscles; Obesity; Oxidative stress; Physical activity; protein content; proteinases; Proteins; Skeletal muscle; Swimming; Oxidative stress; AMPK; Mitochondria quality control; Metabolic syndrome; Mitochondrial dynamics
• ISSN: 0024-3205; 1879-0631; 1879-0631
• DOI: 10.1016/j.lfs.2020.117965

Several studies have proved that physical activity (PA) regulates energetic metabolism associated with mitochondrial dynamics through AMPK activation in healthy subjects. Obesity, a condition that induces oxidative stress, mitochondrial dysfunction, and low AMPK activity leads to mitochondrial fragmentation. However, few studies describe the effect of PA on mitochondrial dynamics regulation in obesity. The present study aimed to evaluate the effect of a single session of PA on mitochondrial dynamics regulation as well as its effect on mitochondrial function and organization in skeletal muscles of obese rats (Zucker fa/fa). Male Zucker lean and Zucker fa/fa rats aged 12 to 13 weeks were divided into sedentary and subjected-to-PA (single session swimming) groups. Gastrocnemius muscle was dissected into isolated fibers, mitochondria, mRNA, and total proteins for their evaluation. The results showed that PA increased the Mfn-2 protein level in the lean and obese groups, whereas Drp1 levels decreased in the obese group. OMA1 protease levels increased in the lean group and decreased in the obese group. Additionally, AMPK analysis parameters (expression, protein level, and activity) did not increase in the obese group. These findings correlated with the partial restoration of mitochondrial function in the obese group, increasing the capacity to maintain the membrane potential after adding calcium as a stressor, and increasing the transversal organization level of the mitochondria analyzed in isolated fibers. These results support the notion that obese rats subjected to PA maintain mitochondrial function through mitochondrial fusion activation by an AMPK-independent mechanism.