The first suggestion that physical exercise results in free radical-mediated damage to tissues appeared in 1978, and the past three decades have resulted in a large growth of knowledge regarding exercise and oxidative stress. Although the sources of oxidant production during exercise continue to be debated, it is now well established that both resting and contracting skeletal muscles produce reactive oxygen species and reactive nitrogen species. Importantly, intense and prolonged exercise can result in oxidative damage to both proteins and lipids in the contracting myocytes. Furthermore, oxidants can modulate a number of cell signaling pathways and regulate the expression of multiple genes in eukaryotic cells. This oxidant-mediated change in gene expression involves changes at transcriptional, mRNA stability, and signal transduction levels. Furthermore, numerous products associated with oxidant-modulated genes have been identified and include antioxidant enzymes, stress proteins, DNA repair proteins, and mitochondrial electron transport proteins. Interestingly, low and physiological levels of reactive oxygen species are required for normal force production in skeletal muscle, but high levels of reactive oxygen species promote contractile dysfunction resulting in muscle weakness and fatigue. Ongoing research continues to probe the mechanisms by which oxidants influence skeletal muscle contractile properties and to explore interventions capable of protecting muscle from oxidant-mediated dysfunction.

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Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production

Reactive oxygen species

Resistance exercise has been shown to elicit a significant acute hormonal response. It appears that this acute response is more critical to tissue growth and remodelling than chronic changes in resting hormonal concentrations, as many studies have not shown a significant change during resistance training despite increases in muscle strength and hypertrophy. Anabolic hormones such as testosterone and the superfamily of growth hormones (GH) have been shown to be elevated during 15-30 minutes of post-resistance exercise providing an adequate stimulus is present. Protocols high in volume, moderate to high in intensity, using short rest intervals and stressing a large muscle mass, tend to produce the greatest acute hormonal elevations (e.g. testosterone, GH and the catabolic hormone cortisol) compared with low-volume, high-intensity protocols using long rest intervals. Other anabolic hormones such as insulin and insulin-like growth factor-1 (IGF-1) are critical to skeletal muscle growth. Insulin is regulated by blood glucose and amino acid levels. However, circulating IGF-1 elevations have been reported following resistance exercise presumably in response to GH-stimulated hepatic secretion. Recent evidence indicates that muscle isoforms of IGF-1 may play a substantial role in tissue remodelling via up-regulation by mechanical signalling (i.e. increased gene expression resulting from stretch and tension to the muscle cytoskeleton leading to greater protein synthesis rates). Acute elevations in catecholamines are critical to optimal force production and energy liberation during resistance exercise. More recent research has shown the importance of acute hormonal elevations and mechanical stimuli for subsequent up- and down-regulation of cytoplasmic steroid receptors needed to mediate the hormonal effects. Other factors such as nutrition, overtraining, detraining and circadian patterns of hormone secretion are critical to examining the hormonal responses and adaptations to resistance training.

Hormonal Responses and Adaptations to Resistance Exercise and Training

In vitro and some animal models have shown that quercetin, a polyphenol derived from plants, has a wide range of biological actions including anti-carcinogenic, anti-inflammatory and antiviral activities; as well as attenuating lipid peroxidation, platelet aggregation and capillary permeability. This review focuses on the physicochemical properties, dietary sources, absorption, bioavailability and metabolism of quercetin, especially main effects of quercetin on inflammation and immune function. According to the results obtained both in vitro and in vivo, good perspectives have been opened for quercetin. Nevertheless, further studies are needed to better characterize the mechanisms of action underlying the beneficial effects of quercetin on inflammation and immunity.

Quercetin, Inflammation and Immunity

Nrf2-Keap1 signaling in oxidative and reductive stress.

Muscle Soreness And Damage During Wildland Firefighter Critical Training: 1424 Board #18 May 28 9:30 AM - 11:00 AM

exercise-induced cardioprotection against apoptosis channels, and ATP Ischemia reperfusion injury, K

TITLE Quercetin's Influence On Exercise-Induced Changes In Plasma Cytokines And Muscle and Leukocyte Cytokine mRNA RUNNING HEAD: Quercetin, Exercise, and Cytokines

Environmental temperature can impact exercise-induced blood oxidative stress; however, the effects of heat acclimation on this response have not been fully elucidated. The purpose of the study was to investigate the effects of hot (33°C) and room temperature (20°C) environments on post-exercise blood oxidative stress responses following 15 temperature acclimation sessions. Untrained participants (n = 38, 26 ± 7 years, VO2peak = 38.0 ± 7.2 years) completed 15 temperature acclimation sessions of a cycling bout at an intensity perceived as “hard” in either a hot (33°C) or room temperature (20°C) environment. Pre and post acclimation exercise tolerance trials were conducted, which involved cycling at 50% Wpeak for one hour. Blood sampling occurred before exercise, immediately after, two hours, and four hours after the exercise tolerance trials. Blood samples were analyzed for oxidative stress markers including lipid hydroperoxides, 8-isoprostanes, protein carbonyls, 3-nitrotyrosine, ferric-reducing ability of plasma, and Trolox-equivalent antioxidant capacity. Exercise-dependent increases were observed in lipid hydroperoxides, Trolox-equivalent antioxidant capacity, and ferric-reducing ability of plasma (p < 0.001). Considering exercise-induced elevations in markers of blood oxidative stress, there were no differences observed between environmental temperatures before or after the acclimation training period.

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John C. Quindry

Papers

Muscle Soreness And Damage During Wildland Firefighter Critical Training: 1424 Board #18 May 28 9:30 AM - 11:00 AM

exercise-induced cardioprotection against apoptosis channels, and ATP Ischemia reperfusion injury, K

TITLE Quercetin's Influence On Exercise-Induced Changes In Plasma Cytokines And Muscle and Leukocyte Cytokine mRNA RUNNING HEAD: Quercetin, Exercise, and Cytokines

Training in a Hot Environment Fails to Elicit Changes in the Blood Oxidative Stress Response

reloadingand attenuates oxidative damage following Intermittent hyperthermia enhances skeletal muscle