Energy (and Reactive Oxygen Species Generation) Saving Distribution of Mitochondria for the Activation of ATP Production in Skeletal Muscle

Abstract

Exercise produces oxidants from a variety of intracellular sources, including NADPH oxidases (NOX) and mitochondria. Exercise-derived reactive oxygen species (ROS) are beneficial, and the amount and location of these ROS is important to avoid muscle damage associated with oxidative stress. We discuss here some of the evidence that involves ROS production associated with skeletal muscle contraction and the potential oxidative stress associated with muscle contraction. We also discuss the potential role of H2O2 produced after NOX activation in the regulation of glucose transport in skeletal muscle. Finally, we propose a model based on evidence for the role of different populations of mitochondria in skeletal muscle in the regulation of ATP production upon exercise. The subsarcolemmal population of mitochondria has the enzymatic and metabolic components to establish a high mitochondrial membrane potential when fissioned at rest but lacks the capacity to produce ATP. Calcium entry into the mitochondria will further increase the metabolic input. Upon exercise, subsarcolemmal mitochondria will fuse to intermyofibrillar mitochondria and will transfer the mitochondria membrane potential to them. These mitochondria are rich in ATP synthase and will subsequentially produce the ATP needed for muscle contraction in long-term exercise. These events will optimize energy use and minimize mitochondria ROS production.

Moderate physical exercise and ATP modulate the P2X7 receptor and improve cisplatin-induced gastric emptying delay in rats

“…This dysautonomia induced by cisplatin may be associated with sympathetic hyperactivity and a decrease in vagal tone, which induces repercussions in the GI tract, in particular GI motility (19). In this sense, we suggest that exercise has the potential to augment the availability of ATP (20), which can, in turn, exert indirect effects on the aforementioned aspects modulating GE. When we analyzed the co-intervention with BBG and exercise or ATP administration, each intervention prevented GE delay induced by cisplatin.…”

Morroniside Protects C2C12 Myoblasts from Oxidative Damage Caused by ROS-Mediated Mitochondrial Damage and Induction of Endoplasmic Reticulum Stress

“…In particular, excessive mtROS produced in skeletal muscles with high oxygen consumption for contractile activity causes mitochondrial damage, which can lead to loss of muscle function. Therefore, preservation of mitochondrial homeostasis is essential in terms of sustained energy generation for muscle exercise ( Pang et al ., 2021 ; Espinosa et al ., 2023 ). GSH, a ubiquitous cellular thiol compound involved in ROS scavenging and antioxidant defense against electrophiles, serves as a key regulator of redox status within cells.…”

The Impact of Physical Exercise on Oxidative and Nitrosative Stress: Balancing the Benefits and Risks

“…Physical exercise profoundly impacts metabolism by increasing the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS). During aerobic activities, the enhanced oxygen consumption of muscles leads to electron leakage from the mitochondrial electron transport chain, elevating the ROS levels [10]. While potentially compromising cellular integrity, these elevated ROS and RNS levels also serve crucial signaling roles that activate antioxidant defenses and other protective mechanisms [11].…”