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Duchenne muscular dystrophy (DMD), caused by deficiency of functional dystrophin protein, is a fatal, progressive muscle disease that frequently includes metabolic dysregulation. Herein, we explore the physiologic consequences of dystrophin deficiency within the context of obesity and insulin resistance. We hypothesized that dystrophin deficiency increases the frequency of insulin resistance, and insulin resistance potentiates muscle pathology caused by dystrophin deficiency. [ABSTRACT FROM AUTHOR]

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 Troloxequivalent 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. [ABSTRACT FROM AUTHOR]

The mechanisms responsible for anti-arrhythmic protection during ischemia-reperfusion (IR) in exercised hearts are not fully understood. The purpose of this investigation was to examine whether the ATP-sensitive potassium channels in the mitochondria (mito [K.sub.ATP]) and sarcolemma (sarc [K.sub.ATP]) provide anti-arrhythmic protection in exercised hearts during IR. Male Sprague-Dawley rats were randomly assigned to cardioprotective treadmill exercise or sedentary conditions before IR (I = 20 min, R = 30 min) in vivo. Subsets of exercised animals received pharmacological inhibitors for mito [K.sub.ATP] (5-hydroxydecanoate) or sarc [K.sub.ATP] (HMR1098) before IR. Blinded analysis of digital ECG tracings revealed that mito [K.sub.ATP] inhibition blunted the anti-arrhythmic effects of exercise, while sarc [K.sub.ATP] inhibition did not. Endogenous antioxidant enzyme activities for total, CuZn, and Mn superoxide dismutase, catalase, and glutathione peroxidase from ischemic and perfused ventricular tissue were not mitigated by IR, although oxidative stress was elevated in sedentary and mito KATP-inhibited hearts from exercised animals. These findings suggest that the mito KATP channel provides anti-arrhythmic protection as part of exercise-mediated cardioprotection against IR. Furthermore, these data suggest that the observed anti-arrhythmic protection may be associated with preservation of redox balance in exercised hearts. cardioprotection; ischemia-reperfusion; myocardial; oxidative stress; preconditioning doi: 10.1152/ajpheart.01211.2009.

The objective of this study was to evaluate the effects of three different drinks (commercially formulated water, bottled water, and a carbohydrate-electrolyte beverage) on blood and urinary markers of hydration after acute dehydration in collegiate wrestlers. Twenty-one athletes were recruited to perform a randomized, crossover study comparing the effectiveness of commercially formulated water, carbohydrateelectrolyte (60/0 or 60 g.[L.sup.- 1]), or regular bottled water (placebo) in promoting rehydration after a 30/0 reduction in body mass. Urine specific gravity [U.sub.sg]), urine osmolarity ([U.sub.osm]), plasma osmolarity ([P.sub.osm]), and plasma volume were measured pre--and post-dehydration and at 1 hour after rehydration. Statistical analyses used a 3 (conditions) X 3 (times) repeated measures analysis of variance. Significant (p < 0.01) interactions were found for [P.sub.osm] [U.sub.osm] and [U.sub.sg.] [P.sub.osm], returned to baseline levels and [U.sub.osm] remained in a lower balance after 1 hour of rehydration in the trials of the commercially formulated water and regular bottled water. No significant interactions were found for plasma volume shift. The findings of this study demonstrate that the commercially formulated water was no more effective in promoting rehydration than either a carbohydrate-electrolyte solution or plain water in collegiate wrestlers after a 3% reduction in body mass and a rehydration period of 1 hour when consuming 100% of their body weight loss. KEY WORDS fluid balance, electrolyte balance, rehydration, dehydration, plasma osmolarity

The expression of myocardial heat shock protein 72 (HSP72) postexercise is initiated by the activation of heat shock transcription factor 1 (HSF1). However, it remains unknown which physiological stimuli govern myocardial HSF1 activation during exercise. These experiments tested the hypothesis that thermal stress and mechanical load, concomitant with simulated exercise, provide independent stimuli for HSF1 activation and ensuing cardiac HSP72 gene expression. To elucidate the independent roles of increased temperature and cardiac workload in the exercise-mediated upregulation of left-ventricular HSP72, hearts from adult male Sprague-Dawley rats were randomly assigned to one of five simulated exercise conditions. Upon reaching a surgical plane of anesthesia, each experimental heart was isolated and perfused using an in vitro working heart model, while independently varying temperatures (i.e., 37[degrees]C vs. 40[degrees]C) and cardiac workloads (i.e., low preload and afterload vs. high preload and afterload) to mimic exercise responses. Results indicate that hyperthermia, independent of cardiac workload, promoted an increase in nuclear translocation and phosphorylation of HSF1 compared with normothermic left ventricles. Similarly, hyperthermia, independent of workload, resulted in significant increases in cardiac levels of HSP72 mRNA. Collectively, these data suggest that HSF1 activation and HSP72 gene transcriptional competence during simulated exercise are linked to elevated heart temperature and are not a direct function of increased cardiac workload. heat shock protein 72; heat shock transcription factor 1; working heart; exercise; phosphorylation

The [Ca.sup.2+]-activated protease calpain has been shown to play a deleterious role in the heart during ischemia-reperfusion (I/R). We tested the hypothesis that exercise training would minimize I/R-induced calpain activation and provide cardioprotection against I/R-induced injury. Hearts from adult male rats were isolated in a working heart preparation, and myocardial injury was induced with 25 min of global ischemia followed by 45 min of reperfusion. In sedentary control rats, I/R significantly increased calpain activity and impaired cardiac performance (cardiac work during reperfusion = 24% of baseline). Compared with sedentary animals, exercise training prevented the I/R-induced rise in calpain activity and improved cardiac work (recovery = 80% of baseline). Similar to exercise, pharmacological inhibition of calpain activity resulted in comparable cardioprotection against I/R injury (recovery = 86% of baseline). The exercise-induced protection against I/R-induced calpain activation was not due to altered myocardial protein levels of calpain or calpastatin. However, exercise training was associated with increased myocardial antioxidant enzyme activity (Mn-SOD, catalase) and a reduction in oxidative stress. Importantly, exercise training also prevented the I/R-induced degradation of sarco(endo)plasmic reticulum [Ca.sup.2+]-ATPase (SERCA)2a. These findings suggest that increases in endogenous antioxidants may diminish the free radical-mediated damage and/or degradation of [Ca.sup.2+] handling proteins (such as SERCA2a) typically observed after I/R. In conclusion, these results support the concept that calpain activation is an important component of I/R-induced injury and that exercise training provides cardioprotection against I/R injury, at least in part, by attenuating I/R-induced calpain activation. antioxidants; oxidative stress; cardioprotection