The effect of pre-exercise ingestion of corinthian currant on endurance performance and blood redox status.

The present study investigated the effect of Corinthian currant pre-exercise supplementation on metabolism, performance and blood redox status during, and after prolonged exercise. Eleven healthy participants (21-45y) performed a 90-min constant-intensity (60-70% VO2max) submaximal-trial, plus a time-trial (TT) to exhaustion (95% VO2max) after consuming an isocaloric (1.5g CHO/kg BM) amount of randomly assigned Corinthian currant or glucose-drink, or water (control). Blood was drawn at baseline, pre-exercise, 30min, 60min, 90min of submaximal-trial, post-TT, and 1h post-TT. Post-ingestion blood glucose (GLU) under Corinthian currant was higher compared with water, and similar compared with glucose-drink throughout the study. Respiratory quotient under Corinthian currant was similar with glucose-drink and higher than water throughout the submaximal trial. Accordingly, higher CHO and lower fat oxidation were observed under Corinthian currant compared with water. The TT performance was similar between Corinthian currant, glucose-drink and water. Redox status were similar under all three conditions. Reduced glutathione (GSH) declined while total antioxidant capacity (TAC) and uric acid increased during exercise. GSH and TAC returned to baseline, while uric acid remained increased the following 1h. Corinthian currant, although did not alter exercise-mediated redox status changes and performance, was equally effective to a glucose-drink in maintaining GLU levels during prolonged cycling.

Evidence of a Redox-Dependent Regulation of Immune Responses to Exercise-Induced Inflammation.

We used thiol-based antioxidant supplementation (n-acetylcysteine, NAC) to determine whether immune mobilisation following skeletal muscle microtrauma induced by exercise is redox-sensitive in healthy humans. According to a two-trial, double-blind, crossover, repeated measures design, 10 young men received either placebo or NAC (20 mg/kg/day) immediately after a muscle-damaging exercise protocol (300 eccentric contractions) and for eight consecutive days. Blood sampling and performance assessments were performed before exercise, after exercise, and daily throughout recovery. NAC reduced the decline of reduced glutathione in erythrocytes and the increase of plasma protein carbonyls, serum TAC and erythrocyte oxidized glutathione, and TBARS and catalase activity during recovery thereby altering postexercise redox status. The rise of muscle damage and inflammatory markers (muscle strength, creatine kinase activity, CRP, proinflammatory cytokines, and adhesion molecules) was less pronounced in NAC during the first phase of recovery. The rise of leukocyte and neutrophil count was decreased by NAC after exercise. Results on immune cell subpopulations obtained by flow cytometry indicated that NAC ingestion reduced the exercise-induced rise of total macrophages, HLA+ macrophages, and 11B+ macrophages and abolished the exercise-induced upregulation of B lymphocytes. Natural killer cells declined only in PLA immediately after exercise. These results indicate that thiol-based antioxidant supplementation blunts immune cell mobilisation in response to exercise-induced inflammation suggesting that leukocyte mobilization may be under redox-dependent regulation.

Age-related responses in circulating markers of redox status in healthy adolescents and adults during the course of a training macrocycle.

Redox status changes during an annual training cycle in young and adult track and field athletes and possible differences between the two age groups were assessed. Forty-six individuals (24 children and 22 adults) were assigned to four groups: trained adolescents, (TAD, N = 13), untrained adolescents (UAD, N = 11), trained adults (TA, N = 12), and untrained adults (UA, N = 10). Aerobic capacity and redox status related variables [total antioxidant capacity (TAC), glutathione (GSH), catalase activity, TBARS, protein carbonyls (PC), uric acid, and bilirubin] were assessed at rest and in response to a time-trial bout before training, at mid- and posttraining. TAC, catalase activity, TBARS, PC, uric acid, and bilirubin increased and GSH declined in all groups in response to acute exercise independent of training status and age. Training improved aerobic capacity, TAC, and GSH at rest and in response to exercise. Age affected basal and exercise-induced responses since adults demonstrated a greater TAC and GSH levels at rest and a greater rise of TBARS, protein carbonyls, and TAC and decline of GSH in response to exercise. Catalase activity, uric acid, and bilirubin responses were comparable among groups. These results suggest that acute exercise, age, and training modulate the antioxidant reserves of the body.

Antioxidation improves in puberty in normal weight and obese boys, in positive association with exercise-stimulated growth hormone secretion.

BACKGROUND: Oxidative stress is associated with obesity while the evidence for the role of GH in pro- and antioxidation is inconclusive. This study investigates the relationships between growth hormone (GH), pro- and antioxidation in relation to obesity and puberty before and after an acute bout of exercise. METHODS: In this case-control study, 76 healthy normal-weight and obese, prepubertal and pubertal boys underwent a blood sampling before and immediately after an aerobic exercise bout until exhaustion at 70% maximal oxygen consumption. Markers of prooxidation (thiobarbituric acid reactive substances (TBARS) and protein carbonyls (PCs)) and antioxidation (glutathione (GSH), oxidized glutathione disulfide (GSSG), GSH/GSSG ratio, glutathione peroxidase (GPX), catalase, and total antioxidant capacity (TAC)) and hormones (GH, insulin-like growth factor (IGF)-1, IGF-BP-3, luteinizing hormone, follicle-stimulating hormone, and testosterone) were measured. RESULTS: Baseline and postexercise TBARS and PCs were greater, while baseline GSH, GSH/GSSG ratio, GPX, and TAC were lower in obese than that in normal-weight participants. In all participants, waist was the best negative and positive predictor for postexercise GPX and TBARS, respectively. Baseline TAC was greater in pubertal than that in pre-pubertal participants. In all participants, baseline GH was the best negative predictor for postexercise PCs. Significant positive linear correlation exists between the exercise-associated GH, and GSSG increases in pubertal normal-weight boys. CONCLUSIONS: Higher prooxidation and lower antioxidation were observed in obese boys, while antioxidation improves with puberty and postexercise, paralleling GH accentuated secretion.

A microcycle of inflammation following a team handball game.

This study investigated the time-course of performance and inflammatory responses during a simulated 6-day in-season microcycle following a team handball (TH) game. Twenty-four handball players participated in a 1-week control trial and in an experimental trial (TH game participation followed by a 6-day training microcycle). Concentrations of lactate, glucose, glycerol, triglycerides, nonesterified fatty acids (NEFAs), and ammonia were measured pregame and postgame. Heart rate (HR) was monitored during the game. Performance (jumping, speed, agility, line-drill testing, and strength), muscle damage (knee range of motion [ROM], knee extensors/flexors delayed onset muscle soreness [DOMS], and creatine kinase activity [CK]), inflammatory (leukocyte count, C-reactive protein, interleukins 1ß and 6 [IL-1ß and IL-6], soluble vascular adhesion molecule 1 [sVCAM-1], p-selectin, uric acid, cortisol, and testosterone), and oxidative stress (malondialdehyde [MDA], protein carbonyls [PC], reduced [GSH] and oxidized glutathione [GSSG], total antioxidant capacity (TAC), catalase, glutathione peroxidase activity [GPX]) markers were determined pregame, postgame, and daily for 6 consecutive days postgame. The game induced a marked rise of HR (∼170 b·min-1), lactate (∼8-fold), glycerol (60%), NEFA (105%), and ammonia (∼62%). Performance deteriorated until 24 hours postgame. Knee ROM decreased (3-5%), whereas DOMS and CK increased (3- to 5-fold and 80-100%, respectively) 24 hours postgame. Leukocyte count, IL-1ß, IL-6, cortisol, MDA, PC, and catalase increased only immediately postgame. C-reactive protein and uric acid increased at 24 hours; sVCAM-1, GSSG, and GPX peaked postgame and remained elevated for 24 hours. The GSH declined until 24 hours postgame. Results suggest that a TH game represents a strong metabolic challenge and induces a short-lived and modest inflammatory response that may affect performance for as long as 24 hours postgame.