Abstract

Overview

Mitochondria play a dual role as both a primary provider of ATP and a pivotal regulator of cell death, crucial for physiological muscle functions. Ca2+ is integral in mitochondrial functioning, particularly during muscle contractions where it aids in activating enzymes critical for energy production.

Findings

• Pathophysiological conditions like skeletal muscle denervation lead to elevated mitochondrial Ca2+ levels, exacerbating ROS generation and other deleterious processes causing muscle atrophy.
• Conversely, acute and long-term endurance exercises, and electrical stimulation have shown to mitigate ROS production and help in muscle preservation.
• A recent study highlights the beneficial role of rapid mitochondrial Ca2+ transients in maintaining mPTP in a closed state, thus reducing mitochondrial ROS production.

Conclusion

This review article aims to further discuss and explore the differential impacts of physiological and pathological mitochondrial Ca2+ alterations on skeletal muscle ROS production.