Abstract
Many physiological changes occur in response to endurance exercise in order to adapt to the increasing energy needs, mitochondria biogenesis, increased reactive oxygen species (ROS) production and acute inflammatory responses. Mitochondria are organelles within each cell that are crucial for ATP production and are also a major producer of ROS and reactive nitrogen species during intense exercise. Recent evidence shows there is a bidirectional interaction between mitochondria and microbiota. The gut microbiota have been shown to regulate key transcriptional co-activators, transcription factors and enzymes involved in mitochondrial biogenesis such as PGC-1α, SIRT1, and AMPK genes. Furthermore, the gut microbiota and its metabolites, such as short chain fatty acids and secondary bile acids, also contribute to host energy production, ROS modulation and inflammation in the gut by attenuating TNFα- mediated immune responses and inflammasomes such as NLRP3. On the other hand, mitochondria, particularly mitochondrial ROS production, have a crucial role in regulating the gut microbiota via modulating intestinal barrier function and mucosal immune responses. Recently, it has also been shown that genetic variants within the mitochondrial genome, could affect mitochondrial function and therefore the intestinal microbiota composition and activity. Diet is also known to dramatically modulate the composition of the gut microbiota. Therefore, studies targeting the gut microbiota can be useful for managing mitochondrial related ROS production, pro-inflammatory signals and metabolic limits in endurance athletes.
Highlights
Endurance exercise can be defined as cardiovascular exercise—such as running, cross-country skiing, cycling, aerobic exercise or swimming—that is performed for an extended period of time (Joyner and Coyle, 2008; Mach and Fuster-Botella, in press)
peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is involved in thermogenesis, glucose metabolism and oxidative capacity in various tissues and can be phosphorylated by 5′ adenosine monophosphate-activated protein kinase (AMPK), an enzyme involved in mitochondrial biogenesis
Many lines of evidence suggest that mitochondria have a central role in energy production, reactive oxygen species (ROS) and reactive oxygen nitrogen species (RONS) production and regulation of inflammasomes during endurance exercise
Summary
Endurance exercise can be defined as cardiovascular exercise—such as running, cross-country skiing, cycling, aerobic exercise or swimming—that is performed for an extended period of time (Joyner and Coyle, 2008; Mach and Fuster-Botella, in press). Mitochondria, Microbiota, and Endurance Exercise electrolyte and temperature rebalance, (vii) increased production of reactive oxygen species (ROS) and reactive oxygen nitrogen species (RONS), vii) activation of the sympatho-adrenomedullary and hypothalamus-pituitary-adrenal (HPA) axes, which results in the release of stress hormones into these circulatory system (reviewed by Clark and Mach, 2016) as well as systemic inflammation and immune responses (Mach and Fuster-Botella, in press). Mitochondria can use enzymatic pathways of the tricarboxylic acid (TCA) cycle to generate ATP (about 20% of ATP; Papa et al, 2012). These organelles are involved in other essential metabolic and cellular processes, including calcium homeostasis, intracellular signaling, heme biosynthesis, and acute cell death (Wai and Langer, 2016). As a side product of normal respiration, mitochondria produce reactive ROS and RONS (Green et al, 2011), which have important roles in cell signaling and homeostasis, but excessive amount of ROS could
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