Time of sampling is crucial for measurement of cell-free plasma DNA following acute aseptic inflammation induced by exercise.

OBJECTIVES: To determine the time-course changes of cell-free plasma DNA (cfDNA) following heavy exercise. METHODS: cfDNA concentration, C-reactive protein levels (hs-CRP), uric acid concentration (UA), creatine kinase activity (CK) were measured before and post-exercise (immediately post, 0.5h, 1h, 2h, 3h, 4h, 5h, 6h, 8h, 10h, 24h). RESULTS: cfDNA increased (15-fold) 30-min post-exercise and normalized thereafter. hs-CRP increased (56%, p<0.001) 1h post-exercise, remained elevated throughout recovery (52-142%, p<0.0001), and peaked (200% rise, p<0.0001) at 24h post-exercise. UA and CK increased (p<0.05), immediately post-exercise, remained elevated throughout recovery (p<0.0001), and peaked (p<0.0001) at 24h of post-exercise recovery. CONCLUSIONS: cfDNA sampling timing is crucial and a potential source of error following aseptic inflammation.

Time-course of changes in inflammatory and performance responses following a soccer game.

OBJECTIVE: : To study the effects of a single soccer game on indices of performance, muscle damage, and inflammation during a 6-day recovery period. DESIGN: : Participants were assigned to either an experimental group (E, played in the game; n = 14) or a control group (C, did not participate in the game; n = 10). SETTING: : Data were collected on a soccer field and at the Physical Education and Sports Science laboratory of the Democritus University of Thrace before and after the soccer game. PARTICIPANTS: : Twenty-four elite male soccer players (age, 20.1 +/- 0.8 years; height, 1.78 +/- 0.08 m; weight, 75.2 +/- 6.8 kg). MAIN OUTCOME MEASUREMENTS: : Muscle strength, vertical jumping, speed, DOMS, muscle swelling, leukocyte count, creatine kinase (CK), lactate dehydrogenase (LDH), C-reactive protein (CRP), cortisol, testosterone, cytokines IL-6 and IL-1b, thioburbituric acid-reactive substances (TBARS), protein carbnyls (PC), and uric acid (UA). RESULTS: : Performance deteriorated 1 to 4 days post-game. An acute-phase inflammatory response consisted of a post-game peak of leukocyte count, cytokines, and cortisol, a 24-hour peak of CRP, TBARS, and DOMS, a 48-hour peak of CK, LDH, and PC, and a 72-hour peak of uric acid. CONCLUSION: : A single soccer game induces short-term muscle damage and marked but transient inflammatory responses. Anaerobic performance seems to deteriorate for as long as 72-hour post-game. The acute phase inflammatory response in soccer appears to follow the same pattern as in other forms of exercise. These results clearly indicate the need of sufficient recovery for elite soccer players after a game.

Acute exercise may exacerbate oxidative stress response in hemodialysis patients.

BACKGROUND/AIMS: Hemodialyzed patients (HD) demonstrate elevated oxidative stress (OXS) levels. Exercise effects on OXS response and antioxidant status of HD was investigated in the present study. METHODS: Twelve HD and 12 healthy controls (HC) performed a graded exercise protocol. Blood samples, collected prior to and following exercise, were analyzed for lactate, thiobarbituric acid-reactive substances (TBARS), protein carbonyls (PC), reduced (GSH) and oxidized glutathione (GSSG), total antioxidant capacity (TAC), catalase, and glutathione peroxidase (GPX) activity. RESULTS: HC demonstrated higher time-to-exhaustion (41%), lactate (41%) and VO2 peak (55%) levels. At rest, HD exhibited higher TBARS, PC, and catalase activity values and lower GSH, GSH/GSSG, TAC, and GPX levels. Although exercise elicited a marked change of OXS markers in both groups, these changes were more pronounced (p < 0.05) in HD patients. After adjusting for VO2 peak, differences between groups disappeared. VO2 peak was highly correlated with GSH/GSSG, TBARS, TAC and PC at rest and after exercise. CONCLUSIONS: These results imply that HD demonstrate higher OXS levels and a lower antioxidant status than HC at rest and following exercise. Acute exercise appears to exacerbate OXS response in hemodialyzed patients probably due to diminished antioxidant defense. However, aerobic capacity level seems to be related to OXS responses in this population.

Oxidative stress biomarkers responses to physical overtraining: implications for diagnosis.

Overtraining syndrome is characterized by declining performance and transient inflammation following periods of severe training with major health implications for the athletes. Currently, there is no single diagnostic marker for overtraining. The present investigation examined the responses of oxidative stress biomarkers to a resistance training protocol of progressively increased and decreased volume/intensity. Twelve males (21.3+/-2.3 years) participated in a 12-week resistance training consisting of five 3-week periods (T1, 2 tones/week; T2, 8 tones/week; T3, 14 tones/week; T4, 2 tones/week), followed by a 3-week period of complete rest. Blood/urine samples were collected at baseline and 96 h following the last training session of each period. Performance (strength, power, jumping ability) increased after T2 and declined thereafter, indicating an overtraining response. Overtraining (T3) induced sustained leukocytosis, an increase of urinary isoprostanes (7-fold), TBARS (56%), protein carbonyls (73%), catalase (96%), glutathione peroxidase, and oxidized glutathione (GSSG) (25%) and a decline of reduced glutathione (GSH) (31%), GSH/GSSG (56%), and total antioxidant capacity. Isoprostanes and GSH/GSSG were highly (r=0.764-0.911) correlated with performance drop and training volume increase. In conclusion, overtraining induces a marked response of oxidative stress biomarkers which, in some cases, was proportional to training load, suggesting that they may serve as a tool for overtraining diagnosis.

Dose-related effects of prolonged NaHCO3 ingestion during high-intensity exercise.

PURPOSE: Sodium bicarbonate (NaHCO3) ingestion may prevent exercise-induced perturbations in acid-base balance, thus resulting in performance enhancement. This study aimed to determine whether different levels of NaHCO3 intake influences acid-base balance and performance during high-intensity exercise after 5 d of supplementation. METHODS: Twenty-four men (22 +/- 1.7 yr) were randomly assigned to one of three groups (eight subjects per group): control (C, placebo), moderate NaHCO3 intake (MI, 0.3 g x kg(-1) x d(-1)), and high NaHCO3 intake (HI, 0.5 g x kg(-1) x d(-1)). Arterial pH, HCO3(-), PO2, PCO2, K+, Na, base excess (BE), lactate, and mean power (MP) were measured before and after a Wingate test pre- and postsupplementation. RESULTS: HCO3(-) increased proportionately to the dosage level. No differences were detected in C. Supplementation increased MP (W x kg(-)) in MI (7.36 +/- 0.7 vs 6.73 +/- 1.0) and HI (7.72 +/- 0.9 vs 6.69 +/- 0.6), with HI being more effective than MI. NaHCO3 ingestion resulted postexercise in increased lactate (mmol x L(-1)) (12.3 +/- 1.8 vs 10.3 +/- 1.9 and 12.4 +/- 1.2 vs 10.4 +/- 1.5 in MI and HI, respectively), reduced exercise-induced drop of pH (7.305 +/- 0.04 vs 7.198 +/- 0.02 and 7.343 +/- 0.05 vs 7.2 +/- 0.01 in MI and HI, respectively) and HCO3(-) (mmol x L(-1)) (13.1 +/- 2.4 vs 17.5 +/- 2.8 and 13.2 +/- 2.7 vs 19.8 +/- 3.2 for HCO3 in MI and HI, respectively), and reduced K (3.875 +/- 0.2 vs 3.625 +/- 0.3 mmol x L(-1) in MI and HI, respectively). CONCLUSION: NaHCO3 administration for 5 d may prevent acid-base balance disturbances and improve performance during anaerobic exercise in a dose-dependent manner.

Resistance training and detraining effects on flexibility performance in the elderly are intensity-dependent.

The present investigation attempted to determine whether resistance exercise intensity affects flexibility and strength performance in the elderly following a 6-month resistance training and detraining period. Fifty-eight healthy, inactive older men (65- 78 yrs) were randomly assigned to 1 of 4 groups: a control group (C, n = 10), a low-intensity resistance training group (LI, n = 14, 40% of 1 repetition maximum [1RM]), a moderate-intensity resistance training group (MI, n = 12, 60% of 1RM), or a high-intensity resistance training group (HI, n = 14, 80% of 1RM). Subjects in exercise groups followed a 3 days per week, whole-body (10 exercises, 3 sets per exercise) protocol for 24 weeks. Training was immediately followed by a 24-week detraining period. Strength (bench and leg press 1RM) and range of motion in trunk, elbow, knee, shoulder, and hip joints were measured at baseline and during training and detraining. Resistance training increased upper- (34% in LI, 48% in MI, and 75% in HI) and lower-body strength (38% in LI, 53% in MI, and 63% in HI) in an intensity-dependent manner. Flexibility demonstrated an intensity-dependent enhancement (3-12% in LI, 6-22% in MI, and 8-28% in HI). Detraining caused significant losses in strength (70-98% in LI, 44-50% in MI, and 27-29% in HI) and flexibility (90-110% in LI, 30-71% in MI, and 23-51% in HI) in an intensity-dependent manner. Results indicate that resistance training by itself improves flexibility in the aged. However, intensities greater than 60% of 1RM are more effective in producing flexibility gains, and strength improvement with resistance training is also intensity-dependent. Detraining seems to reverse training strength and flexibility gains in the elderly in an intensity-dependent manner.

Cell-free plasma DNA as a novel marker of aseptic inflammation severity related to exercise overtraining.

BACKGROUND: Circulating free plasma DNA is implicated in conditions associated with tissue injury, including exercise-induced inflammation, and thus is a potential marker for athletic overtraining. METHODS: We measured free plasma DNA along with C-reactive protein (CRP), creatine kinase (CK), and uric acid (UA) in 17 recreationally trained men participating in a 12-week resistance training regimen (8 resistance multi-joint exercises selected to stress the entire musculature: bench press, squat, leg press, snatch, hang clean, dead lifts, barbell arm curls, and rowing), consisting of 4 training periods (t1, t2, t3, and t4). RESULTS: Plasma DNA concentrations increased markedly after t1, t2, and t3 and returned to baseline after t4. There were substantial differences between t2 and t1 and between t3 and t2 plasma DNA concentrations. CRP increased by 300% after t2 and by 400% after t3 (there was no difference between t2 and t3 CRP values) compared with baseline (t0). CK increased only after t3. UA increased after t2 and t3, with a greater increase after t3. CONCLUSIONS: This study demonstrates that, after chronic excessive resistance exercise, plasma DNA concentrations increase in proportion to training load, suggesting that plasma DNA may be a sensitive marker for overtraining-induced inflammation.

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.