Post-160-km race illness rates and decreases in granulocyte respiratory burst and salivary IgA output are not countered by quercetin ingestion.

This study measured the influence of the flavonoid quercetin on immune changes and incidence rates of upper respiratory tract infections in ultramarathoners competing in the 160-km Western States Endurance Run. Sixty-three runners were randomized to quercetin and placebo groups, and under double-blinded methods ingested 1000 mg/day quercetin for 3 wks before, during, and 2 wks after the race. Thirty-nine of the 63 subjects (n = 18 for quercetin, n = 21 for placebo) finished the race and provided blood and saliva samples the morning before the race and 15 - 30 min postrace. Upper respiratory tract infections were assessed during the week before and the 2-wk period after the race using an illness symptom checklist. Race times did not differ significantly between quercetin and placebo groups. Significant pre- to postrace decreases were measured for natural killer cells (43 %), granulocyte respiratory burst activity (55 %), and salivary IgA output (48 %), and increases for neutrophil (288 %) and monocyte (211 %) cell counts, with no significant group differences. Postrace illness rates did not differ between groups. In conclusion, quercetin supplementation for 3 wks before and 2 wks after the Western States Endurance Run had no effect on illness rates, perturbations in leukocyte subset counts, or decreases in granulocyte respiratory burst activity and salivary IgA.

Effect of pharmacological lowering of plasma urate on exercise-induced oxidative stress.

Urate is a metabolic end product of purine metabolism that contributes about 66% of the antioxidant capacity of plasma. The objective of this study was to evaluate the importance of plasma urate as an antioxidant using pharmacological lowering and examining the impact on plasma antioxidant capacity and oxidative stress after intense exercise. Fifteen subjects ran for 45 min at approximately 80% VO2 max under the influence of probenecid (1 g/d) (PRO) or placebo (PLA) in a double-blind, crossover design. Blood samples obtained at baseline, pre-exercise, and immediately post-exercise were analyzed for F2-isoprostanes, lipid hydroperoxides (LHs), ferric-reducing ability of plasma (FRAP), urate, ascorbate (AA), and nitrite. A 2 (group)x2 (time) repeated-measures analysis of variance (ANOVA), one-way ANOVA, Tukey-Kramer multiple comparison tests, and Student's t tests were used for statistical analysis. PRO exhibited lowered urate and FRAP compared with baseline (p

Effect of NSAID on muscle injury and oxidative stress.

Indirect markers of muscle damage and delayed onset muscle soreness were examined and correlated to changes in oxidative stress, plasma antioxidant potential, and use or nonuse of non-steroidal anti-inflammatory drugs in 60 ultra-marathoners following the Western States Endurance Run. Blood was collected prior to and immediately following the race and analyzed for muscle damage by creatine phosphokinase and oxidative stress by F (2)-isoprostanes, protein carbonyls, and lipid hydroperoxides and antioxidant potential by the ferric reducing ability of plasma. Subjects recorded delayed onset muscle soreness during the week following the race. Lipid hydroperoxide concentrations were unchanged, but F (2)-isoprostanes, protein carbonyls, ferric reducing ability of plasma, creatine phosphokinase, and delayed onset muscle soreness increased significantly postrace. Protein carbonyls were significantly higher postrace in nonsteroidal anti-inflammatory drug users versus nonusers (p < 0.05). However, there was no difference between users and non-users for all other markers. Postrace creatine phosphokinase concentrations were not correlated with oxidative stress markers but were correlated with changes in delayed onset muscle soreness. Based upon these findings, caution should be used when consuming nonsteroidal anti-inflammatory drugs during ultra distance events.

Carbohydrate effect: hormone and oxidative changes.

Carbohydrate administration during exercise diminishes stress hormone release, but the relationship of these hormones with oxidative stress has not been examined. Fifteen subjects functioned as their own controls and ingested carbohydrate (6 %) or placebo in a randomized design while cycling for 2.5-h ( approximately 75 % V.O (2peak)). Blood and skeletal muscle samples were collected 30 min pre-exercise, immediately post-exercise, and 12-h post-exercise and analyzed for F (2)-isoprostanes, ferric reducing ability of plasma, glucose, insulin, cortisol, epinephrine, and muscle glycogen, respectively. Statistical design was a 2 (treatment) x 3 (time) repeated measures analysis of variance. Glucose, insulin, and ferric reducing ability of plasma were significantly higher and F (2)-isoprostanes, cortisol, and epinephrine significantly lower in carbohydrate versus placebo. The decrease in muscle glycogen was not different. During cycling exercise, oxidative stress appears to be heavily influenced by carbohydrate ingestion and increased stress hormones.

Immune changes: 2 h of continuous vs. intermittent cycling.

Immune changes following 2 h of intensive cycling with or without rest intervals were measured in trained cyclists (n = 12) who functioned as their own controls during two test sessions that were separated by two weeks. Subjects cycled for 2.0 h at approximately 64 % Watts(max) continuously (C) or with 3-min rest intervals (R) interspersed every 10 min (2.6 h total time), with the order of the sessions randomized. Blood samples were collected 30-min pre-exercise, and immediately and 1-h postexercise, and assayed for blood leukocyte subset counts, plasma IL-6, IL-10, IL-1ra, IL-8, PHA-induced lymphocyte proliferation, and natural killer cell activity (NKCA). Significant time effects were measured for all immune measures, but no significant differences in the pattern of change were found between C and R exercise trials. In conclusion, immune changes induced by 2 h of intense and prolonged exercise paralleled those measured when athletes rested 3 min every 10 min of exercise.

Hyperthermia increases exercise-induced oxidative stress.

The purpose of this investigation was to examine oxidative markers after exercise in a hyperthermic environment (35 degrees C, 70 % RH) (Hot) versus a neutral environment (25 degrees C, 40 % RH) (Con). Hyperthermia may exacerbate oxidative stress by uncoupling the mitochondrial respiratory chain or by inhibiting antioxidant defense mechanisms, but this has not been assessed in vivo. Six male subjects performed low-intensity exercise (50 % VO(2max)) on a treadmill in Hot until a core temperature of 39.5 degrees C was reached, and for an equivalent time in Con. Blood samples were drawn before and immediately after exercise and at 8 min and 15 min following exercise. Samples were analyzed for F2 isoprostanes (FIP), lipid hydroperoxides (LPO), and lactate. A 2 x 4 repeated measures ANOVA was used to test for treatment, time, and interaction effects for FIP, LPO, and lactate. Differences in VO(2) were tested with Student's t-test. Significance was set at p < 0.05. Oxygen consumption was not significantly different between Hot and Con. The pattern of change of FIP and lactate in Hot was significant versus exercise in Con. LPO was significantly elevated over time in both Hot and Con, but the pattern of change was not significantly different. Ending core temperatures and heart rates were significantly elevated in Hot versus Con. These data indicate that hyperthermia increases oxidative stress and selectively affects specific lipid markers, independent of oxygen consumption.

Influence of carbohydrate ingestion on immune changes after 2 h of intensive resistance training.

Thirty strength-trained subjects were randomized to carbohydrate (CHO) or placebo (Pla) groups and lifted weights for 2 h (10 exercises, 4 sets each, 10 repetitions, with 2- to 3-min rest intervals). Subjects received 10 ml x kg(-1) x h(-1) CHO (6%) or Pla beverages during the weight training bout. Blood, saliva, and vastus lateralis muscle biopsy samples were collected before and after exercise. Blood cell counts were determined, and plasma was analyzed for IL-6, IL-10, IL-1 receptor antagonist (IL-1ra), IL-8, and cortisol. Muscle was analyzed for glycogen content and relative gene expression of 13 cytokines (IL-1alpha, IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p35, IL-12p40, IL-15, IFN-gamma, TNF-alpha) by use of real-time quantitative RT-PCR. Significant but modest increases were measured for plasma IL-6, IL-10, IL-1ra, and IL-8, but the pattern of increase did not differ between CHO and Pla groups. The rate of decrease in muscle glycogen content did not differ between CHO and Pla (P = 0.463). Muscle cytokine mRNA was detected preexercise for IL-1beta, IL-6, IL-15, IL-8, and TNF-alpha, and of these, IL-1beta, IL-6, IL-8, and TNF-alpha were significantly increased after the 2-h weight training bout. The increase in mRNA (fold difference from preexercise) did not differ between CHO and Pla groups. In summary, CHO vs. Pla ingestion did not alter modest increases measured for plasma IL-6, IL-10, IL-1ra, and IL-8, and muscle gene expression for IL-1beta, IL-6, IL-8, and TNF-alpha in strength-trained subjects lifting weights intensively for 2 h.

Immune and oxidative changes during and following the Western States Endurance Run.

Changes in immune and oxidative stress parameters were measured in ultramarathon runners competing in the 160-km Western States Endurance Run. Forty-five runners agreed to provide blood and saliva samples the morning before the race event, at the 90-km aid station, and 5 - 10 min post-race. Upper respiratory tract infection (URTI) during the two-week period post-race was assessed retrospectively by telephone interviews. Forty subjects completed 90-km (race time, 13.1 +/- 0.3 h), and 31 completed the 160-km race event (27.0 +/- 0.4 h). The blood neutrophil and monocyte counts rose 249 % and 214 %, respectively, in the 31 finishers. Salivary IgA (sIgA) secretion rate decreased significantly from 508 +/- 40 micro g/min pre-race, to 287 +/- 39 micro g/min at 90-km, and 254 +/- 30 micro g/min post-race (50 % decrease). Significant increases were measured in cytokines at 90-km and post-race, with post-race IL-10 increasing 9.5-fold, IL-1ra 6.1-fold, IL-6 50.2-fold, and IL-8 2.5-fold over pre-race levels. Post-race indicators of oxidative stress, F (2)-isoprostane and lipid hydroperoxides, increased 33 % and 88 %, respectively. Pearson product-moment correlations revealed positive correlations at 90-km between F (2)-isoprostane and IL-6 (r = 0.31, p = 0.048), IL-10 (r = 0.31, p = 0.050), and IL-8 (r = 0.43, p = 0.005), but no other significant relationships between immune and oxidative stress indicators at 90-km and post-race. In the group of runners completing at least 90 km of the race, 26 % reported an URTI episode during the two-week period post-race. A low sIgA secretion rate at 90-km was the best predictor of post-race URTI (173 +/- 34 micro g/min in those who later acquired URTI compared to 325 +/- 40 micro g/min in those without URTI, p = 0.007). In conclusion, a modest correlation was found between cytokines and F (2)-isoprostane at 90-km when the greatest oxidative stress occurred, but no other significant correlations in immune and oxidative stress indicators during and following a 160-km ultramarathon race event were noted. About one in four ultramarathoners reported URTI during the two-week period post-race, and a low sIgA secretion rate mid-race best predicted URTI occurrence.

Carbohydrate ingestion influences skeletal muscle cytokine mRNA and plasma cytokine levels after a 3-h run.

Sixteen experienced marathoners ran on treadmills for 3 h at approximately 70% maximal oxygen consumption (Vo(2 max)) on two occasions while receiving 1 l/h carbohydrate (CHO) or placebo (Pla) beverages. Blood and vastus lateralis muscle biopsy samples were collected before and after exercise. Plasma was analyzed for IL-6, IL-10, IL-1 receptor agonist (IL-1ra), IL-8, cortisol, glucose, and insulin. Muscle was analyzed for glycogen content and relative gene expression of 13 cytokines by using real-time quantitative RT-PCR. Plasma glucose and insulin were higher, and cortisol, IL-6, IL-10, and IL-1ra, but not IL-8, were significantly lower postexercise in CHO vs. Pla. Change in muscle glycogen content did not differ between CHO and Pla (P = 0.246). Muscle cytokine mRNA content was detected preexercise for seven cytokines in this order (highest to lowest): IL-15, TNF-alpha, IL-8, IL-1beta, IL-12p35, IL-6, and IFN-gamma. After subjects ran for 3 h, gene expression above prerun levels was measured for five of these cytokines: IL-1beta, IL-6, and IL-8 (large increases), and IL-10 and TNF-alpha (small increases). The increase in mRNA (fold difference from preexercise) was attenuated in CHO (15.9-fold) compared with Pla (35.2-fold) for IL-6 (P = 0.071) and IL-8 (CHO, 7.8-fold; Pla, 23.3-fold; P = 0.063). CHO compared with Pla beverage ingestion attenuates the increase in plasma IL-6, IL-10, and IL-1ra and gene expression for IL-6 and IL-8 in athletes running 3 h at 70% Vo(2 max) despite no differences in muscle glycogen content.