Abstract
Cells have the ability to adapt to stressful environments as a part of their evolution. Physical exercise induces an increase of a demand for energy that must be met by mitochondria as the main (ATP) provider. However, this process leads to the increase of free radicals and the so-called reactive oxygen species (ROS), which are necessary for the maintenance of cell signaling and homeostasis. In addition, mitochondrial biogenesis is influenced by exercise in continuous crosstalk between the mitochondria and the nuclear genome. Excessive workloads may induce severe mitochondrial stress, resulting in oxidative damage. In this regard, the objective of this work was to provide a general overview of the molecular mechanisms involved in mitochondrial adaptation during exercise and to understand if some nutrients such as antioxidants may be implicated in blunt adaptation and/or an impact on the performance of exercise by different means.
Highlights
The high-oxygen atmospheric concentrations of a million years ago induced metabolic changes, resulting in the majority of living organisms utilizing more oxygen (O2), promoting the development of aerobic systems
In isolated muscle-cell C2C12 myoblasts, acute exogenous exposure to H2O2 and diethylenetriamine/NO adduct (NO donor) increased TFAM. These results suggest that reactive oxygen species (ROS) and NO are able to regulate the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway to stimulate mitochondrial biogenesis and the expression of antioxidant protection genes [68]
The oxidative stress induced by an imbalance between ROS/reactive nitrogen species (RNS) production and antioxidant systems has been well described in many pathological conditions, such as cancer, diabetes, cardiovascular diseases, immunological, neurodegenerative disorders, and aging
Summary
The high-oxygen atmospheric concentrations of a million years ago induced metabolic changes, resulting in the majority of living organisms utilizing more oxygen (O2), promoting the development of aerobic systems. NO can react with O2− to form peroxynitrite (ONOO−), which is the main cause of the nitration of cellular proteins and the depletion of thiol groups due to its rapid formation. All of these previously mentioned reactive molecules might contribute to oxidative stress (OS), defined as “an imbalance between oxidants and antioxidants in favor of the oxidants, leading to a disruption of redox signaling and control, and/or molecular damage” [3]. Physical work increases energy demands, the O2 uptake, and the formation of ROS [5] In this manner, mitochondria are susceptible to being attacked in high intense or long sports, which might represent a risk for the detriment in muscle force, contraction, and performance. Nutritional insights in terms of the growing evidence with regard to the use of antioxidants and mitochondrial protection are discussed
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