Imental trial, the subjects exercised for 45 min at 70-75% V˙O2max and then at 90% V˙O2max to exhaustion on a treadmill; in the control trial, the subjects remained at rest. Blood samples were drawn before and after exercise (immediately after exercise and at 0.5, 1, 2, 3, 4, 5, 6, 8, 10, and 24 h). Reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, thiobarbituric acid-reactive substances (TBARS), protein carbonyls, catalase activity, and total antioxidant capacity (TAC) were determined. Results: The time to lowest concentration after exercise was 1.7 ± 0.7 h (mean ± SD) for GSH/GSSG, and the time to highest concentration after exercise was 1.2 ± 0.6 h for TBARS, 4.4 ± 0.5 h for protein carbonyls, 0.5 ± 0.4h for catalase, and 2.2 ± 0.9 h for TAC. The greatest change after exercise was −74 ± 9% for GSH/GSSG, 129 ± 29% for TBARS, 135 ± 53% for protein carbonyls, 51 ± 16% for catalase, and 24 ± 10% for TAC. Conclusion: There is no best time point applying to all markers for collecting blood samples after aerobic exercise. The optimum postexercise time points for blood collection in untrained individuals are immediately after exercise for catalase, 1 h for TBARS, 2 h for TAC, GSH, and GSSG, and 4 h after exercise for protein carbonyls....

Exercise-induced muscle damage is associated with an acute-phase inflammatory response characterized by phagocyte infiltration into muscle and free radical production. Although soccer includes intense eccentric muscle actions that cause muscle damage, the oxidative stress responses after a soccer game are currently unknown. The present investigation attempted to determine the responses of circulating levels of oxidative stress and antioxidant status markers during recovery from a soccer game. Twenty soccer players (experimental group) were assigned to 2 different teams that competed against each other (2 × 45 minutes). Ten other players served as controls (rested). Creatine kinase (CK) activity, uric acid, leukocyte count, malondialdehyde (MDA), protein carbnyls (PC), reduced (GSH) and oxidized glutathione (GSSG), antioxidant capacity (TAC), catalase, glutathione peroxidase activity (GPX), delayed-onset of muscle soreness (DOMS), and anaerobic performance (speed, vertical jump performance) were measured before and following (immediately post, 24 hours, 48 hours, 72 hours) the game. Performance deteriorated (2-17%, p < 0.05) throughout recovery. Leukocytosis developed (p < 0.05) immediately following the game and at 24 hours. Both CK and DOMS (3-8-fold, p < 0.05) increased from baseline and remained elevated (p < 0.05) through 48 hours. Thiobarbituric acid reactive substances (TBARS), PC, uric acid, GPX, and TAC increased (13-67%, p < 0.05) throughout recovery, whereas catalase was elevated (38%, p < 0.05) only immediately after the game. GSH/GSSG declined (17-75%, p < 0.05) throughout recovery. Our results suggest that oxidative stress is markedly upregulated by a soccer game, probably as a part of the exercise-induced inflammatory response, and is accompanied by a marked deterioration of anaerobic performance for as long as 72 hours.

Plyometric training (PT) is a widely used method to improve muscle ability to generate explosive power. This study aimed to determine whether preadolescent boys exhibit plyometric trainability or not. Forty-five children were randomly assigned to either a control (CG, N = 21, 10.6 ± 0.5 years; participated only in regular soccer practice) or a plyometric training group (PTG, N = 24, 10.6 ± 0.6 years; participated in regular soccer practice plus a plyometric exercise protocol). Both groups trained for 12 weeks during the in-season period. The PT exercises (forward hopping, lateral hopping, shuffles, skipping, ladder drills, skipping, box jumps, low-intensity depth jumps) were performed twice a week. Preadolescence was verified by measuring Tanner stages, bone age, and serum testosterone. Speed (0-10, 10-20, 20-30 m), leg muscle power (static jumping, countermovement jumping, depth jumping [DJ], standing long jump [SLJ], multiple 5-bound hopping [MB5]), leg strength (10 repetition maximum), anaerobic power (Wingate testing), and soccer-specific performance (agility, kicking distance) were measured at baseline, midtraining, and posttraining. The CG caused only a modest (1.2-1.8%) increase in speed posttraining. The PTG induced a marked (p < 0.05) improvement in all speed tests (1.9-3.1% at midtraining and 3-5% at posttraining) and vertical jump tests (10-18.5% at midtraining and 16-23% at posttraining), SLJ (2.6% at midtraining and 4.2% at posttraining), MB5 (14.6% at midtraining and 23% at posttraining), leg strength (15% at midtraining and 28% at posttraining), agility (5% at midtraining and 23% at posttraining), and kicking distance (13.6% at midtraining and 22.5% at posttraining). Anaerobic power remained unaffected in both groups. These data indicate that (a) prepubertal boys exhibit considerable plyometric trainability, and (b) when soccer practice is supplemented with a PT protocol, it leads to greater performance gains.

The objectives of the present investigation were to study the inflammatory and performance responses after an acute bout of intense plyometric exercise during a prolonged recovery period. Participants were randomly assigned to either an experimental group (P, n = 12) that performed intense plyometric exercises or a control group (C, n = 12) that rested. The delayed onset of muscle soreness (DOMS), knee range of motion (KROM), creatine kinase (CK) and lactate dehydrogenase (LDH) activities, white blood cell count, C reactive protein (CRP), uric acid (UA), cortisol, testosterone, IL-6, IL-1b strength (isometric and isokinetic), and countermovement (CMJ) and static (SJ) jumping performance were measured at rest, immediately postexercise and at 24, 48, 72, 96, and 120 hours of recovery. Lactate was measured at rest and postexercise. Strength remained unchanged throughout recovery, but CMJ and SJ declined (p < 0.05) by 8-20%. P induced a marked rise in DOMS, CK, and LDH (peaked 24-48 hours postexercise) and a KROM decline. An acute-phase inflammatory response consisting of leukocytosis (postexercise and at 24 hours), an IL-6, IL-1b, CRP, and cortisol elevation (during the first 24 hours of recovery) and a delayed increase of UA (peaked at 48 hours) and testosterone (peaked at 72 hours) was observed in P. The results of this investigation indicate that performing an acute bout of intense plyometric exercise may induce a short-term muscle damage and marked but transient inflammatory responses. Jumping performance seems to deteriorate for as long as 72 hours postexercise, whereas strength appears to remain unchanged. The acute-phase inflammatory response after a plyometric exercise protocol appears to follow the same pattern as in other exercise models. These results clearly indicate the need of sufficient recovery between successive plyometric exercise training sessions.

Background: The major thiol-disulfide couple of reduced glutathione (GSH) and oxidized glutathione is a key regulator of major transcriptional pathways regulating aseptic inflammation and recovery of skeletal muscle after aseptic injury. Antioxidant supplementation may hamper exercise-induced cellular adaptations.