Hyperthermia, dehydration, and osmotic stress: unconventional sources of exercise-induced reactive oxygen species

Abstract

Evidence of increased reactive oxygen species (ROS) production is observed in the circulation during exercise in humans. This is exacerbated at elevated body temperatures and attenuated when normal exercise-induced body temperature elevations are suppressed. Why ROS production during exercise is temperature dependent is entirely unknown. This review covers the human exercise studies to date that provide evidence that oxidant and antioxidant changes observed in the blood during exercise are dependent on temperature and fluid balance. We then address possible mechanisms linking exercise with these variables that include shear stress, effects of hemoconcentration, and signaling pathways involving muscle osmoregulation. Since pathways of muscle osmoregulation are rarely discussed in this context, we provide a brief review of what is currently known and unknown about muscle osmoregulation and how it may be linked to oxidant production in exercise and hyperthermia. Both the circulation and the exercising muscle fibers become concentrated with osmolytes during exercise in the heat, resulting in a competition for available water across the muscle sarcolemma and other tissues. We conclude that though multiple mechanisms may be responsible for the changes in oxidant/antioxidant balance in the blood during exercise, a strong case can be made that a significant component of ROS produced during some forms of exercise reflect requirements of adapting to osmotic challenges, hyperthermia challenges, and loss of circulating fluid volume.

Cryotherapy: biochemical alterations involved in reduction of damage induced by exhaustive exercise

“…There are multiple mechanisms involved in oxidant/antioxidant status during exercise (27). Excessive levels of ROS may alter the muscle, mainly through inflammatory processes (28).…”

Maximizing Cellular Adaptation to Endurance Exercise in Skeletal Muscle

“…Increased tissue temperature activates multiple mediators of the peroxisome proliferator-activated receptor g coactivator 1a (PGC-1a) as well as downstream and parallel transcription and translation factors in the nucleus and mitochondria that encode for mitochondrial and stress proteins (Tamura and Hatta, 2017). Oxidative stress in the form of superoxide may be generated via membrane-bound autocrine process, along with humoral sources (leukocytes or gastrointestinal tract; King et al, 2016). Local heating increases perfusion acutely via metabolic autoregulation during exercise as well as recovery, and chronically via PGC1a-induced increases in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) (Green et al, 2017). synthesis and maintenance, including transport and folding of new proteins and protection of folded shape.…”

Proposal of nursing care plan in people hospitalized with AIDS

“…Thus, it can lead to protein denaturation, loss of large amounts of water and, consequently, exacerbate the clinical situation. Therefore, the nurse should guide the patient to recognize the warning signs of hyperthermia; avoid an environment free of air chain and ingestion of ice-cold liquids; reinforce the importance of hydration; in addition to monitoring body temperature, level of consciousness, ingestion and excretion of liquids and signs of electrolyte imbalance (15)(16) . In hyperthermia, people living with AIDS lose water and electrolytes, essential in the homeostatic stability and dynamics of the body, developing dehydration, which is considered by ICNP® as the reduction of the balance of ingestion and elimination of liquids and electrolytes (14) .…”