HIGH-INTENSITY EXERCISE TRAINING INDUCES ULTRASTRUCTURAL CHANGES IN THE MITOCHONDRIA OF MICE SKELETAL MUSCLES

Mitochondria are highly adaptable organelles that adjust their morphology and function to cope with the energetic demands of cells in response to a plethora of stimuli. While there is growing evidence of exercise-induced favorable mitochondrial adaptation dynamics, the underlying mechanisms through which high-intensity interval training (HIIT) can impact mitochondrial morphology, efficiency, and network remodeling have been less explored. In a previous study, we demonstrated that HIIT produced a significant increase in the expression of mitochondrial complex enzymes in the muscles of trained mice, compared with sedentary controls. The present study aimed to investigate whether our training paradigm can elicit mitochondrial adaptations through an ultrastructural approach. Mice underwent a prolonged HIIT (5 days/week, 8 weeks), which consisted of brief sequences of intense exercise (at 90% of maximal intensity) interspersed with recovery periods. Ultrastructural morphometry of the mitochondria from gastrocnemius muscle showed that HIIT did not alter sarcomere organization but produced changes in mitochondrial morphology and biogenesis, which consisted of an increase in mitochondria number and size. Compared to sedentary controls, mitochondria from muscles of trained mice showed an increase in maximum (0.51±0.01 vs. 0.44 ±0.01, p<0.01) and minimum diameter (0.35±0.01 vs. 0.32±0.01, p<0.05), and mitochondrial density (0.45±0.03 vs. 0.31±0.05, p<0.05). This study suggests that HIIT can induce mitochondria remodeling, but further research is needed to clarify its impact on mitochondriogenesis, particularly regarding the balance between fission and fusion. As exercise remains a potent therapeutic approach for improving mitochondrial health, understanding these adaptations may have broad clinical implications across many healthcare disciplines.