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.

Muscular exercise promotes the production of radicals and other reactive oxygen species in the working muscle. Growing evidence indicates that reactive oxygen species are responsible for exercise-i...

Dietary antioxidants and exercise

Exercise-induced cardioprotection against myocardial ischemia–reperfusion injury

The purpose of the current study was to determine the acute neuroendocrine response to hypertrophy (H), strength (S), and power (P) type resistance exercise (RE) equated for total volume. Ten male subjects completed three RE protocols and a rest day (R) using a randomized cross-over design. The protocols included (1) H: 4 sets of 10 repetitions in the squat at 75% of 1RM (90 s rest periods); (2) S: 11 sets of three repetitions at 90% of 1RM (5 min rest periods); and (3) P: 8 sets of 6 repetitions of jump squats at 0% of 1RM (3 min rest periods). Total testosterone (T), cortisol (C), and sex hormone binding globulin (SHBG) were determined prior to (PRE), immediately post (IP), 60 min post, 24 h post, and 48 h post exercise bout. Peak force, rate of force development, and muscle activity from the vastus medialis (VM) and biceps femoris (BF) were determined during a maximal isometric squat test. A unique pattern of response was observed in T, C, and SHBG for each RE protocol. The percent change in T, C, and SHBG from PRE to IP was significantly (p ≤ 0.05) greater in comparison to the R condition only after the H protocol. The percent of baseline muscle activity of the VM at IP was significantly greater following the H compared to the S protocol. These data indicate that significant acute increases in hormone concentrations are limited to H type protocols independent of the volume of work competed. In addition, it appears the H protocol also elicits a unique pattern of muscle activity as well. RE protocols of varying intensity and rest periods elicit strikingly different acute neuroendocrine responses which indicate a unique physiological stimulus.

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Acute hormonal and neuromuscular responses to hypertrophy, strength and power type resistance exercise

Purpose To investigate the influence of intensity versus total energy expenditure on neutrophilia and blood oxidative stress to acute exercise. Methods Nine males (18-30 yr) completed one maximal (Max) and three submaximal exercise sessions: 1) 45 min at 10% above (LT+) lactate threshold (LT), 2) 45 min at 10% below (LT-) LT, and 3) 10% below LT until caloric expenditure equaled the 10%+ trial (LT-kcal). Blood was sampled before (PRE), immediately (POST), 1 h, and 2 h after exercise to measure neutrophils, myeloperoxidase, superoxide (O(2)-), neutrophil activation (O(2)-/neutrophils), ascorbic acid, uric acid, malondialdehyde, and lipid hydroperoxides. Results Intensity-dependent neutrophilia occurred POST exercise with significant increases (P Conclusion Exercise intensity plays a major role in postexercise blood oxidative stress, whereas total exercise energy expenditure does not. Further, neutrophils recruited into circulation during exercise may impose a threshold dependent oxidative stress in blood plasma after exercise.

The effects of acute exercise on neutrophils and plasma oxidative stress.

A wealth of data indicates that performing regular exercise is an important lifestyle modification to prevent cardiovascular disease. Although not fully understood, the cardioprotection by regular exercise may be exerted synergistically through improvement in many risk factors associated with cardio

John C. Quindry

Papers

Dietary antioxidants and exercise

Exercise-induced cardioprotection against myocardial ischemia–reperfusion injury

Acute hormonal and neuromuscular responses to hypertrophy, strength and power type resistance exercise

The effects of acute exercise on neutrophils and plasma oxidative stress.

Exercise and cardioprotection