Evaluation of arrhythmia scoring systems and exercise-induced cardioprotection.

INTRODUCTION: Exercise is protective against ventricular arrhythmias induced by ischemia (I), the condition of inadequate blood flow, and reperfusion (R), the reestablishment of blood flow. This protection is observed clinically and scientifically by decreased incidence in ECG abnormalities. Numerous scoring systems exist for the quantification of ventricular arrhythmia severity. On the basis of preventricular contractions, ventricular tachycardia, and ventricular fibrillation frequency, these scoring systems are intended to provide more robust ECG outcome indicators than individual arrhythmia variables. Scoring systems vary primarily on continuous versus discontinuous treatment of the data, which should be considered when matching these arrhythmia metrics to scientific applications. PURPOSE: The aim of this investigation was to evaluate seven ECG scoring systems in the assessment of ventricular arrhythmia severity after IR in male Sprague-Dawley rats. METHODS: Animals remained sedentary or exercised (3 d of treadmill exercise for 60 min) before surgically induced IR. A subset of sedentary animals served as sham, undergoing surgical procedure without IR. ECGs were evaluated under blinded conditions by three trained individuals. Single arrhythmia data and the parametric score were analyzed by one-way ANOVA, whereas the Kruskal-Wallis was used to compare group means for all nonparametric scoring systems between groups. RESULTS: IR produced a significant arrhythmic response in exercised and sedentary rats as determined by all arrhythmia scoring systems. Four arrhythmia metrics resulted in significant differences between exercised and sedentary treatments (P < 0.001), whereas three metrics did not. CONCLUSIONS: Continuous versus discontinuous treatment of the data may account for variation in scoring system outcomes. These data confirm that exercise protects against IR-induced arrhythmias, and care must be taken when selecting an arrhythmia scoring system for ECG evaluation.

Mitochondrial KATP channel inhibition blunts arrhythmia protection in ischemic exercised hearts.

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(ATP)) and sarcolemma (sarc K(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(ATP) (5-hydroxydecanoate) or sarc K(ATP) (HMR1098) before IR. Blinded analysis of digital ECG tracings revealed that mito K(ATP) inhibition blunted the anti-arrhythmic effects of exercise, while sarc K(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 K(ATP)-inhibited hearts from exercised animals. These findings suggest that the mito K(ATP) 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.

Beta-glucan, immune function, and upper respiratory tract infections in athletes.

PURPOSE: This study investigated the effects of oat beta-glucan (BG) supplementation on chronic resting immunity, exercise-induced changes in immune function, and self-reported upper respiratory tract infection (URTI) incidence in human endurance athletes. METHODS: Trained male cyclists were randomized to BG (N = 19) or placebo (P; N = 17) groups and under double-blind procedures received BG (5.6 g x d(-1)) or P beverage supplements for 2 wk before, during, and 1 d after a 3-d period in which subjects cycled for 3 h x d(-1) at approximately 57% maximal watts. URTI symptoms were monitored during BG supplementation and for 2 wk afterward. Blood samples were collected before and after 2 wk of supplementation (both samples, 8:00 a.m.), immediately after the 3-h exercise bout on day 3 (6:00 p.m.), and 14 h after exercise (8:00 a.m.) and were assayed for natural killer cell activity (NKCA), polymorphonuclear respiratory burst activity (PMN-RBA), phytohemagglutinin-stimulated lymphocyte proliferation (PHA-LP), plasma interleukin 6 (IL-6), IL-10, IL-1 receptor agonist (IL-1ra), and IL-8, and blood leukocyte IL-10, IL-8, and IL-1ra mRNA expression. RESULTS: Chronic resting levels and exercise-induced changes in NKCA, PMN-RBA, PHA-LP, plasma cytokines, and blood leukocyte cytokine mRNA did not differ significantly between BG and P groups. URTI incidence during the 2-wk postexercise period did not differ significantly between groups. CONCLUSIONS: An 18-d period of BG versus P ingestion did not alter chronic resting or exercise-induced changes in immune function or URTI incidence in cyclists during the 2-wk period after an intensified exercise.

The effect of resistance exercise on humoral markers of oxidative stress.

UNLABELLED: Previous research attempts to identify an oxidative stress response to acute resistance exercise have yielded mixed results. Inconsistencies in the current literature base probably reflect study-to-study variance in resistance exercise protocols; where high volume and short recovery elicit the most identifiable oxidative stress response. PURPOSE: This study examined the effect of resistance exercise intensity on blood oxidative stress. METHODS: To elicit a blood oxidative stress, 10 subjects undertook two different back squat protocols: 1) a hypertrophy protocol of four sets, 10 repetitions with 90 s of rest at 75% one-repetition max (1RM); and 2) a strength protocol of 11 sets, three repetitions with 5 min of rest at 90% 1RM. The resistance exercise protocols were standardized for total volume and completed in a randomized crossover fashion with 1 wk between trials. Blood drawn before (PRE), immediately following exercise (IP), and 60 min following exercise (60POST) was analyzed for markers of oxidative stress and damage. RESULTS: In response to both hypertrophy and strength exercise protein carbonyls were significantly elevated IP and 60POST while plasma lipid hydroperoxides were not. Following the hypertrophy protocol, trolox equivalent antioxidant capacity was elevated IP while urate lower than baseline. At the 60POST time point plasma ferric reducing ability of plasma was elevated following the hypertrophy protocol. Based on protein carbonyl data, a similar oxidative stress was incurred following both hypertrophy and strength protocols. CONCLUSION: Normalization for time of blood draw following the two protocols indicates that the magnitude of blood oxidative protein damage was identical between the protocols. These findings demonstrate that both resistance exercise protocols elicited a blood oxidative stress in a time-dependent fashion.