Oxidative stress responses in older men during endurance training and detraining.

PURPOSE: Aging is associated with increased oxidative stress, whereas systematic exercise training has been shown to improve quality of life and functional performance of the aged. This study aimed to evaluate responses of selected markers of oxidative stress and antioxidant status in inactive older men during endurance training and detraining. METHODS: Nineteen older men (65-78 yr) were randomly assigned into either a control (C, N = 8) or an endurance-training (ET, N = 11, three training sessions per week, 16 wk, walking/jogging at 50-80% of HR(max)) group. Before, immediately posttraining, and after 4 months of detraining, subjects performed a progressive diagnostic treadmill test to exhaustion (GXT). Plasma samples, collected before and immediately post-GXT, were analyzed for malondialdehyde (MDA) and 3-nitrotyrosine (3-NT) levels, total antioxidant capacity (TAC), and glutathione peroxidase activity (GPX). RESULTS: ET caused a 40% increase in running time and a 20% increase in maximal oxygen consumption (VO(2max)) (P < 0.05). ET lowered MDA (9% at rest, P < 0.01; and 16% postexercise, P < 0.05) and 3-NT levels (20% postexercise, P < 0.05), whereas it increased TAC (6% at rest, P < 0.01; and 14% postexercise, P < 0.05) and GPX (12% postexercise, P < 0.05). However, detraining abolished these adaptations. CONCLUSIONS: ET may attenuate basal and exercise-induced lipid peroxidation and increase protection against oxidative stress by increasing TAC and GPX activity. However, training cessation may reverse these training-induced adaptations.

Intense basketball-simulated exercise induces muscle damage in men with elevated anterior compartment pressure.

The purpose of the present investigation was to examine the levels of muscle soreness, muscle damage, and performance output in men with (S, n = 24) or without (A, n = 24) chronic compartment syndrome (CACS)-related symptoms after an intense 10-minute basketball-simulated exercise. Anterior compartment pressure (ICP), muscle soreness perception, creatine kinase (CK) and lactate dehydrogenase (LDH) activities, myoglobin (Mb) concentration, leg strength, and knee joint range of motion (KJRM) were measured at rest, immediately after exercise, and at 24, 48, 72 and 96 hours postexercise (ICP was also measured at 5, 15, and 30 minutes postexercise). ICP, muscle soreness, CK, LDH, and myoglobin increased (p < 0.05) immediately postexercise and during the next 4 days of recovery in both groups. However, S demonstrated a far more pronounced and prolonged (p < 0.05) response than A. Leg strength and KJRM declined (p < 0.05) in both groups, but S demonstrated a greater (p < 0.05) performance deterioration than A. The results of this study suggest that intense basketball-simulated exercise increases ICP, muscle soreness, and indices of muscle damage with a concomitant decrease of performance. Men with CACS-related symptoms and/or history appear more sensitive to muscle damage and soreness than asymptomatic men, probably due to a compromised blood flow to the muscle producing fluid shifts from vascular to interstitial space and further increasing compartment pressure and muscle cell disruption. Results of the present investigation provide evidence to support proper diagnosis, monitoring, care, and preventive measures for symptomatic individuals prior to participation in activities such as basketball.