Quercetin's influence on exercise-induced changes in plasma cytokines and muscle and leukocyte cytokine mRNA.

Trained male cyclists (n = 40) ingested quercetin (Q; n = 20) (1,000 mg/day) or placebo (P; n = 20) supplements under randomized, double-blinded methods for 3 wk before and during a 3-day period in which subjects cycled for 3 h/day at approximately 57% maximal work rate. Blood samples were collected before and after each exercise session and assayed for plasma IL-6, IL-10, IL-1ra, IL-8, TNF-alpha, and monocyte chemoattractant protein 1, and leukocyte IL-10, IL-8, and IL-1ra mRNA. Muscle biopsies were obtained before and after the first and third exercise sessions and assayed for NF-kappaB and cyclooxygenase-2 (COX-2), IL-6, IL-8, IL-1beta, and TNF-alpha mRNA. Postexercise increases in plasma cytokines did not differ between groups, but the pattern of change over the 3-day exercise period tended to be lower in Q vs. P for IL-8 and TNF-alpha (P = 0.094 for both). mRNA increased significantly postexercise for each cytokine measured in blood leukocyte and muscle samples. Leukocyte IL-8 and IL-10 mRNA were significantly reduced in Q vs. P (interaction effects, P = 0.019 and 0.012, respectively) with no other leukocyte or muscle mRNA group differences. Muscle NF-kappaB did not increase postexercise and did not differ between Q and P. Muscle COX-2 mRNA increased significantly postexercise but did not differ between Q and P. In summary, 1 g/day quercetin supplementation by trained cyclists over a 24-day period diminished postexercise expression of leukocyte IL-8 and IL-10 mRNA, indicating that elevated plasma quercetin levels exerted some effects within the blood compartment. Quercetin did not, however, influence any of the muscle measures, including NF-kappaB content, cytokine mRNA, or COX-2 mRNA expression across a 3-day intensified exercise period.     

Effect of creatine supplementation on cycle ergometer exercise in a hyperthermic environment

In order to examine thermoregulatory response to creatine (CR) supplementation, competitive male cyclists and triathletes (n = 7, VO2max = 50.6 +/- 0.8 ml x kg(-1) x min(-1)) completed three 1-hour hyperthermic (ambient temperature = 38.7 +/- 1.0 degrees C, relative humidity = 33 +/- 4%) exercise sessions at 181 +/- 12 W (50% of Wmax, approximately 66% of VO2max). Subjects completed a baseline (BL) session, then 2 sessions following 5 days of CR (20 g x d(-1)) and placebo (PL, 20 g x d(-1)) administered in a double-blind counterbalanced crossover manner with > or = 28-day washout. Pre-exercise BL, CR, and PL body mass were unchanged, with similar decreases in postexercise mass among the three conditions. Tympanic temperature, heart rate, systolic blood pressure, perceived exertion, and lactate, cortisol, and aldosterone concentrations increased similarly during BL, CR, and PL exercise. A greater (p = 0.013) estimated decrease in plasma volume occurred following BL (-16.5 +/- 2.0%) and PL (-17.6 +/- 1.7%) exercise compared to CR (-13.5 +/- 2.1%). Creatine supplementation reduces plasma volume loss during 1 hour of hyperthermic exercise but does not appear to otherwise change thermoregulatory response to hyperthermic exercise.     

Electron spin resonance spectroscopy, exercise, and oxidative stress: an ascorbic acid intervention study.

Oxygen free radicals are highly reactive species that are produced in increased quantities during strenuous exercise and can damage critical biological targets such as membrane phospholipids. The present study examined the effect of acute ascorbic acid supplementation on exercise-induced free radical production in healthy subjects. Results demonstrate increases in the intensity of the alpha-phenyl-tert-butylnitrone adduct (0.05 +/- 0.02 preexercise vs. 0.19 +/- 0.03 postexercise, P = 0.002, arbitrary units) together with increased lipid hydroperoxides (1.14 +/- 0.06 micromol/l preexercise vs. 1.62 +/- 0.19 micromol/l postexercise, P = 0.005) and malondialdehyde (0.70 +/- 0.04 micromol/l preexercise vs. 0.80 +/- 0.04 micromol/l postexercise, P = 0.0152) in the control phase. After supplementation with ascorbic acid, there was no significant increase in the electron spin resonance signal intensity (0.02 +/- 0. 01 preexercise vs. 0.04 +/- 0.02 postexercise, arbitrary units), lipid hydroperoxides (1.12 +/- 0.21 micromol/l preexercise vs. 1.12 +/- 0.08 micromol/l postexercise), or malondialdehyde (0.63 +/- 0.07 micromol/l preexercise vs. 0.68 +/- 0.05 micromol/l postexercise). The results indicate that acute ascorbic acid supplementation prevented exercise-induced oxidative stress in these subjects.     

Carbohydrate loading failed to improve 100-km cycling performance in a placebo-controlled trial.

We evaluated the effect of carbohydrate (CHO) loading on cycling performance that was designed to be similar to the demands of competitive road racing. Seven well-trained cyclists performed two 100-km time trials (TTs) on separate occasions, 3 days after either a CHO-loading (9 g CHO. kg body mass(-1). day(-1)) or placebo-controlled moderate-CHO diet (6 g CHO. kg body mass(-1). day(-1)). A CHO breakfast (2 g CHO/kg body mass) was consumed 2 h before each TT, and a CHO drink (1 g CHO. kg(.)body mass(-1). h(-1)) was consumed during the TTs to optimize CHO availability. The 100-km TT was interspersed with four 4-km and five 1-km sprints. CHO loading significantly increased muscle glycogen concentrations (572 +/- 107 vs. 485 +/- 128 mmol/kg dry wt for CHO loading and placebo, respectively; P < 0.05). Total muscle glycogen utilization did not differ between trials, nor did time to complete the TTs (147.5 +/- 10.0 and 149.1 +/- 11.0 min; P = 0.4) or the mean power output during the TTs (259 +/- 40 and 253 +/- 40 W, P = 0.4). This placebo-controlled study shows that CHO loading did not improve performance of a 100-km cycling TT during which CHO was consumed. By preventing any fall in blood glucose concentration, CHO ingestion during exercise may offset any detrimental effects on performance of lower preexercise muscle and liver glycogen concentrations. Alternatively, part of the reported benefit of CHO loading on subsequent athletic performance could have resulted from a placebo effect.     

Muscle sympathetic nerve responses to physiological changes in prostaglandin production in humans.

Previous studies suggest that prostaglandins may contribute to exercise-induced increases in muscle sympathetic nerve activity (MSNA). To test this hypothesis, MSNA was measured at rest and during exercise before and after oral administration of ketoprofen, a cyclooxygenase inhibitor, or placebo. Twenty-one subjects completed two bouts of graded dynamic and isometric handgrip to fatigue. Each exercise bout was followed by 2 min of postexercise muscle ischemia. The second exercise bouts were performed after 60 min of rest in which 11 subjects were given ketoprofen (300 mg) and 10 subjects received a placebo. Ketoprofen significantly lowered plasma thromboxane B(2) in the drug group (from 36 +/- 6 to 22 +/- 3 pg/ml, P < 0.04), whereas thromboxane B(2) in the placebo group increased from 40 +/- 5 to 61 +/- 9 pg/ml from trial 1 to trial 2 (P < 0.008). Ketoprofen and placebo did not change sympathetic and cardiovascular responses to dynamic handgrip, isometric handgrip, and postexercise muscle ischemia. There was no relationship between thromboxane B(2) concentrations and MSNA or arterial pressure responses during both exercise modes. The data indicate that physiological increases or decreases in prostaglandins do not alter exercise-induced increases in MSNA and arterial pressure in humans. These findings suggest that contraction-induced metabolites other than prostaglandins mediate MSNA responses to exercise in humans.     

Postexercise protein supplementation improves health and muscle soreness during basic military training in Marine recruits.

Elevated postexercise amino acid availability has been demonstrated to enhance muscle protein synthesis acutely, but the long-term impact of postexercise protein supplementation on variables such as health, muscle soreness, and function are unclear. Healthy male US Marine recruits from six platoons (US Marine Corps Base, Parris Island, SC; n = 387; 18.9 +/- 0.1 yr, 74.7 +/- 1.1 kg, 13.8 +/- 0.4% body fat) were randomly assigned to three treatments within each platoon. Nutrients supplemented immediately postexercise during the 54-day basic training were either placebo (0 g carbohydrate, 0 g protein, 0 g fat), control (8, 0, 3), or protein supplement (8, 10, 3). Subjects and observers making measurements and data analysis were blinded to subject groupings. Compared with placebo and control groups, the protein-supplemented group had an average of 33% fewer total medical visits, 28% fewer visits due to bacterial/viral infections, 37% fewer visits due to muscle/joint problems, and 83% fewer visits due to heat exhaustion. Recruits experiencing heat exhaustion had greater body mass, lean, fat, and water losses. Muscle soreness immediately postexercise was reduced by protein supplementation vs. placebo and control groups on both days 34 and 54. Postexercise protein supplementation may not only enhance muscle protein deposition but it also has significant potential to positively impact health, muscle soreness, and tissue hydration during prolonged intense exercise training, suggesting a potential therapeutic approach for the prevention of health problems in severely stressed exercising populations.     

Postexercise carbohydrate-protein supplementation improves subsequent exercise performance and intracellular signaling for protein synthesis

Postexercise carbohydrate-protein (CHO + PRO) supplementation has been proposed to improve recovery and subsequent endurance performance compared to CHO supplementation. This study compared the effects of a CHO + PRO supplement in the form of chocolate milk (CM), isocaloric CHO, and placebo (PLA) on recovery and subsequent exercise performance. Ten cyclists performed 3 trials, cycling 1.5 hours at 70% VO?max plus 10 minutes of intervals. They ingested supplements immediately postexercise and 2 hours into a 4-hour recovery. Biopsies were performed at recovery minutes 0, 45, and 240 (R0, R45, REnd). Postrecovery, subjects performed a 40-km time trial (TT). The TT time was faster in CM than in CHO and in PLA (79.43 ± 2.11 vs. 85.74 ± 3.44 and 86.92 ± 3.28 minutes, p ≤ 0.05). Muscle glycogen resynthesis was higher in CM and in CHO than in PLA (23.58 and 30.58 vs. 7.05 μmol·g?1 wet weight, p ≤ 0.05). The mammalian target of rapamycin phosphorylation was greater at R45 in CM than in CHO or in PLA (174.4 ± 36.3 vs. 131.3 ± 28.1 and 73.7 ± 7.8% standard, p ≤ 0.05) and at REnd in CM than in PLA (94.5 ± 9.9 vs. 69.1 ± 3.8%, p ≤ 0.05). rpS6 phosphorylation was greater in CM than in PLA at R45 (41.0 ± 8.3 vs. 15.3 ± 2.9%, p ≤ 0.05) and REnd (16.8 ± 2.8 vs. 8.4 ± 1.9%, p ≤ 0.05). FOXO3A phosphorylation was greater at R45 in CM and in CHO than in PLA (84.7 ± 6.7 and 85.4 ± 4.7 vs. 69.2 ± 5.5%, p ≤ 0.05). These results indicate that postexercise CM supplementation can improve subsequent exercise performance and provide a greater intracellular signaling stimulus for PRO synthesis compared to CHO and placebo.     

Low-dose estrogen therapy does not change postexercise hypotension, sympathetic nerve activity reduction, and vasodilation in healthy postmenopausal women

The aim of this study was to determine whether estrogen therapy enhances postexercise muscle sympathetic nerve activity (MSNA) decrease and vasodilation, resulting in a greater postexercise hypotension. Eighteen postmenopausal women received oral estrogen therapy (ET; n=9, 1 mg/day) or placebo (n=9) for 6 mo. They then participated in one 45-min exercise session (cycle ergometer at 50% of oxygen uptake peak) and one 45-min control session (seated rest) in random order. Blood pressure (BP, oscillometry), heart rate (HR), MSNA (microneurography), forearm blood flow (FBF, plethysmography), and forearm vascular resistance (FVR) were measured 60 min later. FVR was calculated. Data were analyzed using a two-way ANOVA. Although postexercise physiological responses were unaltered, HR was significantly lower in the ET group than in the placebo group (59+/-2 vs. 71+/-2 beats/min, P<0.01). In both groups, exercise produced significant decreases in systolic BP (145+/-3 vs. 154+/-3 mmHg, P=0.01), diastolic BP (71+/-3 vs. 75+/-2 mmHg, P=0.04), mean BP (89+/-2 vs. 93+/-2 mmHg, P=0.02), MSNA (29+/-2 vs. 35+/-1 bursts/min, P<0.01), and FVR (33+/-4 vs. 55+/-10 units, P=0.01), whereas it increased FBF (2.7+/-0.4 vs. 1.6+/-0.2 ml x min(-1) x 100 ml(-1), P=0.02) and did not change HR (64+/-2 vs. 65+/-2 beats/min, P=0.3). Although ET did not change postexercise BP, HR, MSNA, FBF, or FVR responses, it reduced absolute HR values at baseline and after exercise.     

Repeat exercise normalizes the gas-exchange impairment induced by a previous exercise bout in asthmatic subjects.

Twenty-one subjects with asthma underwent treadmill exercise to exhaustion at a workload that elicited approximately 90% of each subject's maximal O2 uptake (EX1). After EX1, 12 subjects experienced significant exercise-induced bronchospasm [(EIB+), %decrease in forced expiratory volume in 1.0 s = -24.0 +/- 11.5%; pulmonary resistance at rest vs. postexercise = 3.2 +/- 1.5 vs. 8.1 +/- 4.5 cmH2O.l(-1).s(-1)] and nine did not (EIB-). The alveolar-to-arterial Po2 difference (A-aDo2) was widened from rest (9.1 +/- 6.7 Torr) to 23.1 +/- 10.4 and 18.1 +/- 9.1 Torr at 35 min after EX1 in subjects with and without EIB, respectively (P < 0.05). Arterial Po2 (PaO2) was reduced in both groups during recovery (EIB+, -16.0 +/- -13.0 Torr vs. baseline; EIB-, -11.0 +/- 9.4 Torr vs. baseline, P < or = 0.05). Forty minutes after EX1, a second exercise bout was completed at maximal O2 uptake. During the second exercise bout, pulmonary resistance decreased to baseline levels in the EIB+ group and the A-aDo2 and PaO2 returned to match the values seen during EX1 in both groups. Sputum histamine (34.6 +/- 25.9 vs. 61.2 +/- 42.0 ng/ml, pre- vs. postexercise) and urinary 9alpha,11beta-prostaglandin F2 (74.5 +/- 38.6 vs. 164.6 +/- 84.2 ng/mmol creatinine, pre- vs. postexercise) were increased after exercise only in the EIB+ group (P < 0.05), and postexercise sputum histamine was significantly correlated with the exercise PaO2 and A-aDo2 in the EIB+ subjects. Thus exercise causes gas-exchange impairment during the postexercise period in asthmatic subjects independent of decreases in forced expiratory flow rates after the exercise; however, a subsequent exercise bout normalizes this impairment secondary in part to a fast acting, robust exercise-induced bronchodilatory response.     

No effect of short-term 17beta-estradiol supplementation in healthy men on systemic inflammatory responses to exercise

Sex-based differences in inflammatory responses to exercise may be mediated by estrogen through increased muscle membrane stability and/or inhibited cytokine production. In this study, in vivo effects of estrogen on systemic inflammation-related responses to exercise were assessed in healthy men. In a double-blind, placebo-controlled, crossover design, 11 men cycled for 90 min at 65% Vo2 max after 8 days of 17beta-estradiol supplementation (ES; 2 mg/day) or placebo (PL; glucose polymer). After a 2-wk washout, exercise was repeated after 8 days on the alternate treatment. Blood was collected pre- and postexercise to determine IL-6, soluble intercellular adhesion molecule-1 (sICAM-1), neutrophil counts, and cortisol. Preexercise serum was assayed for sex hormones. ES increased estradiol (133+/-71 to 840+/-633 pmol/l, P=0.005) and reduced testosterone (19.9+/-3.7 to 16.1+/-3.9 nmol/l, P=0.007). Exercise increased cortisol (P=0.02), IL-6 (P<0.001) and neutrophil counts (P<0.001) with no influence on sICAM-1 (P=0.34) and no effect of ES on these changes. Postexercise IL-6 and neutrophil counts were correlated (r=0.58, P=0.005); postexercise IL-6 and cortisol (r=0.18, P=0.43) and postexercise cortisol and neutrophil counts (r=0.06, P=0.78) were not. Postexercise sICAM-1 was not correlated with the above variables (P>or=0.79). In conclusion, 8 days of ES in healthy men did not influence systemic inflammation-related responses to acute exercise. Future studies should investigate 17beta-estradiol effects on IL-6 production and neutrophil infiltration within skeletal muscle during and after exercise.     

The effect of a carbohydrate and protein supplement on resistance exercise performance, hormonal response, and muscle damage

The purpose of this study was to determine whether resistance exercise performance and postexercise muscle damage were altered when consuming a carbohydrate and protein beverage (CHO-PRO; 6.2% and 1.5% concentrations). Thirty-four male subjects (age: 21.5 +/- 1.7 years; height: 177.3 +/- 1.1 cm; weight: 77.2 +/- 2.2 kg) completed 3 sets of 8 repetitions at their 8 repetition maximum to volitional fatigue. The exercise order consisted of the high pull, leg curl, standing overhead press, leg extension, lat pull-down, leg press, and bench press. In a double-blind, posttest-only control group design, subjects consumed 355 ml of either CHO-PRO or placebo (electrolyte and artificial sweetener beverage) 30 minutes prior to exercise, 177 ml immediately prior to exercise, 177 ml halfway through the exercise bout, and 355 ml immediately following the exercise bout. There were no significant differences between groups relative to exercise performance. Cortisol was significantly elevated in the placebo group compared to the CHO-PRO group at 24 hours postexercise. Insulin was significantly elevated immediately pre-exercise, after the fourth lift, immediately postexercise, 1 hour, and 6 hours postexercise in CHO-PRO compared to the placebo group. Myoglobin levels in the placebo group approached significance halfway through the exercise bout and at 1 hour postexercise (p = 0.06 and 0.07, respectively) and were significantly elevated at 6 hours postexercise compared to the CHO-PRO group. Creatine kinase levels were significantly elevated in the placebo group at 24 hours postexercise compared to the CHO-PRO group. The CHO-PRO supplement did not improve performance during a resistance exercise bout, but appeared to reduce muscle damage, as evidenced by the responses of both myoglobin and creatine kinase. These results suggest the use of a CHO-PRO supplement during resistance training to reduce muscle damage and soreness.     

Alveolar epithelial integrity in athletes with exercise-induced hypoxemia.

The effect of incremental exercise to exhaustion on the change in pulmonary clearance rate (k) of aerosolized (99m)Tc-labeled diethylenetriaminepentaacetic acid ((99m)Tc-DTPA) and the relationship between k and arterial PO(2) (Pa(O(2))) during heavy work were investigated. Ten male cyclists (age = 25 +/- 2 yr, height = 180.9 +/- 4.0 cm, mass = 80.1 +/- 9.5 kg, maximal O(2) uptake = 5. 25 +/- 0.35 l/min, mean +/- SD) completed a pulmonary clearance test shortly (39 +/- 8 min) after a maximal O(2) uptake test. Resting pulmonary clearance was completed >/=24 h before or after the exercise test. Arterial blood was sampled at rest and at 1-min intervals during exercise. Minimum Pa(O(2)) values and maximum alveolar-arterial PO(2) difference ranged from 73 to 92 Torr and from 30 to 55 Torr, respectively. No significant difference between resting k and postexercise k for the total lung (0.55 +/- 0.20 vs. 0. 57 +/- 0.17 %/min, P > 0.05) was observed. Pearson product-moment correlation indicated no significant linear relationship between change in k for the total lung and minimum Pa(O(2)) (r = -0.26, P > 0.05). These results indicate that, averaged over subjects, pulmonary clearance of (99m)Tc-DTPA after incremental maximal exercise to exhaustion in highly trained male cyclists is unchanged, although the sampling time may have eliminated a transient effect. Lack of a linear relationship between k and minimum Pa(O(2)) during exercise suggests that exercise-induced hypoxemia occurs despite maintenance of alveolar epithelial integrity.     

Influence of high-intensity interval training on adaptations in well-trained cyclists

The purpose of the present study was to examine the influence of 3 different high-intensity interval training regimens on the first and second ventilatory thresholds (VT(1) and VT(2)), anaerobic capacity (ANC), and plasma volume (PV) in well-trained endurance cyclists. Before and after 2 and 4 weeks of training, 38 well-trained cyclists (Vo(2)peak = 64.5 +/- 5.2 ml.kg(-1).min(-1)) performed (a) a progressive cycle test to measure Vo(2)peak, peak power output (PPO), VT(1), and VT(2); (b) a time to exhaustion test (T(max)) at their Vo(2)peak power output (P(max)); and (c) a 40-km time-trial (TT(40)). Subjects were assigned to 1 of 4 training groups (group 1: n = 8, 8 x 60% T(max) at P(max), 1:2 work-recovery ratio; group 2: n = 9, 8 x 60% T(max) at P(max), recovery at 65% maximum heart rate; group 3: n = 10, 12 x 30 seconds at 175% PPO, 4.5-minute recovery; control group: n = 11). The TT(40) performance, Vo(2)peak, VT(1), VT(2), and ANC were all significantly increased in groups 1, 2, and 3 (p < 0.05) but not in the control group. However, PV did not change in response to the 4-week training program. Changes in TT(40) performance were modestly related to the changes in Vo(2)peak, VT(1), VT(2), and ANC (r = 0.41, 0.34, 0.42, and 0.40, respectively; all p < 0.05). In conclusion, the improvements in TT(40) performance were related to significant increases in Vo(2)peak, VT(1), VT(2), and ANC but were not accompanied by significant changes in PV. Thus, peripheral adaptations rather than central adaptations are likely responsible for the improved performances witnessed in well-trained endurance athletes following various forms of high-intensity interval training programs.     

Creatine supplementation influences substrate utilization at rest.

The influence of creatine supplementation on substrate utilization during rest was investigated using a double-blind crossover design. Ten active men participated in 12 wk of weight training and were given creatine and placebo (20 g/day for 4 days, then 2 g/day for 17 days) in two trials separated by a 4-wk washout. Body composition, substrate utilization, and strength were assessed after weeks 2, 5, 9, and 12. Maximal isometric contraction [1 repetition maximum (RM)] leg press increased significantly (P < 0.05) after both treatments, but 1-RM bench press was increased (33 +/- 8 kg, P < 0.05) only after creatine. Total body mass increased (1.6 +/- 0.5 kg, P < 0.05) after creatine but not after placebo. Significant (P < 0.05) increases in fat-free mass were found after creatine and placebo supplementation (1.9 +/- 0.8 and 2.2 +/- 0.7 kg, respectively). Fat mass did not change significantly with creatine but decreased after the placebo trial (-2.4 +/- 0.8 kg, P < 0.05). Carbohydrate oxidation was increased by creatine (8.9 +/- 4.0%, P < 0.05), whereas there was a trend for increased respiratory exchange ratio after creatine supplementation (0.03 +/- 0.01, P = 0.07). Changes in substrate oxidation may influence the inhibition of fat mass loss associated with creatine after weight training.     

Carbohydrate supplementation improves time-trial cycle performance during energy deficit at 4,300-m altitude.

Carbohydrate supplementation (CHOS) typically improves prolonged time-trial (TT) performance at sea level (SL). This study determined whether CHOS also improves TT performance at high altitude (ALT; 4,300 M) despite increased hypoxemia and while in negative energy balance (approximately 1,250 kcal/day). Two groups of fasting, fitness-matched men performed a 720-kJ cycle TT at SL and while living at ALT on days 3 (ALT3) and 10 (ALT10). Eight men drank a 10% carbohydrate solution (0.175 g/kg body wt) and eight drank a placebo (PLA; double blind) at the start of and every 15 min of the TT. Blood glucose during each TT was higher (P < 0.05) for CHOS than for PLA. At SL, TT duration (approximately 59 min) and watts (approximately 218 or approximately 61% of peak watts; %SL Wpeak) were similar for both groups. At ALT, the TT was longer for both groups (P < 0.01) but was shorter for CHOS than for PLA on ALT3 (means +/- SE: 80 +/- 7 vs. 105 +/- 9 min; P < 0.01) and ALT10 (77 +/- 7 vs. 90 +/- 5 min; P < 0.01). At ALT, %SL Wpeak was reduced (P < 0.01) with the reduction on ALT3 being larger for PLA (to 33 +/- 3%) than for CHOS (to 43 +/- 2%; P < 0.05). On ALT3, O2 saturation fell similarly from 84 +/- 2% at rest to 73 +/- 1% during the TT for both groups (P < 0.05), and on ALT10 O2 saturation fell more (P < 0.02) for CHOS (91 +/- 1 to 76 +/- 2%) than for PLA (90 +/- 1 to 81 +/- 1%). %SL Wpeak and O2 saturation were inversely related during the TT for both groups at ALT (r > or = -0.76; P < or = 0.03). It was concluded that, despite hypoxemia exacerbated by exercise, CHOS greatly improved TT performance at ALT in which there was a negative energy balance.     

Effect of caffeine supplementation on the extracellular heat shock protein 72 response to exercise.

The stimulus for the release of 72-kDa heat shock protein (HSP72) during exercise in humans is currently unclear. Recent evidence in an animal model is suggestive of an involvement of catecholamines. The present study, therefore, investigated the effect of caffeine supplementation, a known stimulator of sympathetic activity, on the extracellular (e)HSP72 response to prolonged exercise. Ten healthy male endurance-trained cyclists were recruited (age: 21 +/- 1 yr, maximum O(2) uptake 61.1 +/- 1.7 ml x kg(-1) x min(-1), mean +/- SE). Each subject was randomly assigned to ingest either 6 mg/kg body mass of caffeine (Caff) or placebo (Pla) 60 min before one of two 90-min bouts of cycling at 74 +/- 1% maximum O(2) uptake. Trials were performed at least 7 days apart in a counterbalanced design. Venous blood samples were collected by venepuncture at pretreatment, preexercise, postexercise, and 1 h postexercise. Serum caffeine and plasma catecholamines were determined using a spectrophotometric assay and high-performance liquid chromatography, respectively. Plasma HSP72 and cortisol were determined by ELISA. Serum caffeine concentrations were significantly increased throughout Caff, while no increases were detected in Pla. Caffeine supplementation and exercise was associated with a greater eHSP72 response than exercise alone (postexercise Caff 8.6 +/- 1.3 ng/ml; Pla 5.9 +/- 0.9 ng/ml). This greater eHSP72 response was associated with a greater epinephrine response to exercise in Caff. There was a significant increase in norepinephrine and cortisol, with no intertrial differences. The present data suggest that, in humans, catecholamines may be an important mediator of the exercise-induced increase in eHSP72 concentration.     

Effect of carbohydrate or carbohydrate plus medium-chain triglyceride ingestion on cycling time trial performance.

This study examined the effectiveness of ingesting a carbohydrate or carbohydrate + medium-chain triglycerides (MCT) on metabolism and cycling performance. Eight endurance-trained men [peak O(2) uptake = 4.71 +/- 0.09 (SE) l/min] completed 35 kJ/kg as quickly as possible [time trial (TT)] while consuming 250 ml/15 min of either a 6% (wt/vol) carbohydrate solution (C), a 6% carbohydrate + 4.2% MCT solution (C+M), or a sweet placebo (P). Time to complete the set amount of work was reduced in both C and C+M compared with P by 7 and 5%, respectively (C: 166 +/- 7 min; C+M: 169 +/- 7 min; P: 178 +/- 11 min; P < 0.01). Plasma glucose concentration was maintained at or above resting values throughout both C and C+M trials but decreased (P < 0.05) below resting values in P at the completion of the TT. The estimated rate of carbohydrate oxidation was not different during the first 90 min of exercise but thereafter was reduced (P < 0.05) in P and was maintained in both C and C+M. These data demonstrate that carbohydrate ingestion during exercise improves 100-km TT performance compared with a sweet placebo, but the addition of MCT does not provide any further performance enhancement.     

Effect of carbohydrate supplementation on postexercise GLUT-4 protein expression in skeletal muscle.

The effect of carbohydrate supplementation on skeletal muscle glucose transporter GLUT-4 protein expression was studied in fast-twitch red and white gastrocnemius muscle of Sprague-Dawley rats before and after glycogen depletion by swimming. Exercise significantly reduced fast-twitch red muscle glycogen by 50%. During a 16-h exercise recovery period, muscle glycogen returned to control levels (25.0 +/- 1.4 micromol/g) in exercise-fasted rats (24.2 +/- 0. 3 micro). However, when carbohydrate supplementation was provided during and immediately postexercise by intubation, muscle glycogen increased 77% above control (44.4 +/- 2.1 micromol/g). Exercise-fasting resulted in an 80% increase in fast-twitch red muscle GLUT-4 mRNA but only a 43% increase in GLUT-4 protein concentration. Conversely, exercise plus carbohydrate supplementation elevated fast-twitch red muscle GLUT-4 protein concentration by 88% above control, whereas GLUT-4 mRNA was increased by only 40%. Neither a 16-h fast nor carbohydrate supplementation had an effect on fast-twitch red muscle GLUT-4 protein concentration or on GLUT-4 mRNA in sedentary rats, although carbohydrate supplementation increased muscle glycogen concentration by 40% (35.0 +/- 0.9 micromol/g). GLUT-4 protein in fast-twitch white muscle followed a pattern similar to fast-twitch red muscle. These results indicate that carbohydrate supplementation, provided with exercise, will enhance GLUT-4 protein expression by increasing translational efficiency. Conversely, postexercise fasting appears to upregulate GLUT-4 mRNA, possibly to amplify GLUT-4 protein expression on an increase in glucose availability. These regulatory mechanisms may help control muscle glucose uptake in accordance with glucose availability and protect against postexercise hypoglycemia.     

Effect of carbohydrate ingestion on glycogen resynthesis in human liver and skeletal muscle, measured by (13)C MRS

This study investigated the effect of carbohydrate (CHO) ingestion on postexercise glycogen resynthesis, measured simultaneously in liver and muscle (n = 6) by (13)C magnetic resonance spectroscopy, and subsequent exercise capacity (n = 10). Subjects cycled at 70% maximal oxygen uptake for 83 +/- 8 min on six separate occasions. At the end of exercise, subjects ingested 1 g/kg body mass (BM) glucose, sucrose, or placebo (control). Resynthesis of glycogen over a 4-h period after treatment ingestion was measured on the first three occasions, and subsequent exercise capacity was measured on occasions four through six. No glycogen was resynthesized during the control trial. Liver glycogen resynthesis was evident after glucose (13 +/- 8 g) and sucrose (25 +/- 5 g) ingestion, both of which were different from control (P < 0.01). No significant differences in muscle glycogen resynthesis were found among trials. A relationship between the CHO load (g) and change in liver glycogen content (g) was evident after 30, 90, 150, and 210 min of recovery (r = 0.59-0. 79, P < 0.05). Furthermore, a modest relationship existed between change in liver glycogen content (g) and subsequent exercise capacity (r = 0.53, P < 0.05). However, no significant difference in mean exercise time was found (control: 35 +/- 5, glucose: 40 +/- 5, and sucrose: 46 +/- 6 min). Therefore, 1 g/kg BM glucose or sucrose is sufficient to initiate postexercise liver glycogen resynthesis, which contributes to subsequent exercise capacity, but not muscle glycogen resynthesis.     

Matched work high-intensity interval and continuous running induce similar increases in PGC-1α mRNA, AMPK, p38, and p53 phosphorylation in human skeletal muscle

The aim of the present study was to test the hypothesis that acute high-intensity interval (HIT) running induces greater activation of signaling pathways associated with mitochondrial biogenesis compared with moderate-intensity continuous (CONT) running matched for work done. In a repeated-measures design, 10 active men performed two running protocols consisting of HIT [6 × 3-min at 90% maximal oxygen consumption (Vo(2max)) interspersed with 3-min recovery periods at 50% Vo(2max) with a 7-min warm-up and cool-down period at 70% Vo(2max)] or CONT (50-min continuous running at 70% Vo(2max)). Both protocols were matched, therefore, for average intensity, duration, and distance run. Muscle biopsies (vastus lateralis) were obtained preexercise, postexercise, and 3 h postexercise. Muscle glycogen decreased (P < 0.05) similarly in HIT and CONT (116 ± 11 vs. 111 ± 17 mmol/kg dry wt, respectively). Phosphorylation (P-) of p38MAPK(Thr180/Tyr182) (1.9 ± 0.1- vs. 1.5 ± 0.2-fold) and AMPK(Thr172) (1.5 ± 0.3- vs. 1.5 ± 0.1-fold) increased immediately postexercise (P < 0.05) in HIT and CONT, respectively, and returned to basal levels at 3 h postexercise. P-p53(Ser15) (HIT, 2.7 ± 0.8-fold; CONT, 2.1 ± 0.8-fold), PGC-1α mRNA (HIT, 4.2 ± 1.7-fold; CONT, 4.5 ± 0.9-fold) and HSP72 mRNA (HIT, 4.4 ± 2-fold; CONT, 3.5 ± 1-fold) all increased 3 h postexercise (P < 0.05) although neither parameter increased (P > 0.05) immediately postexercise. There was no difference between trials for any of the above signaling or gene expression responses (P > 0.05). We provide novel data by demonstrating that acute HIT and CONT running (when matched for average intensity, duration, and work done) induces similar activation of molecular signaling pathways associated with regulation of mitochondrial biogenesis. Furthermore, this is the first report of contraction-induced p53 phosphorylation in human skeletal muscle, thus highlighting an additional pathway by which exercise may initiate mitochondrial biogenesis.