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The purpose of this study was to determine whether sweat sodium concentration ([Na(+)](sweat)) during exercise in the heat differs between aerobically trained and untrained individuals. On three occasions, ten endurance-trained (Tr) and ten untrained (UTr) subjects (VO2peak = 4.0 ± 0.8 vs. 3.4 ± 0.7 L min(-1), respectively; P < 0.05) cycled in a hot-ventilated environment (36 ± 1°C; 25 ± 2% humidity, airflow 2.5 m s(-1)) at three workloads (i.e., 40, 60, and 80% VO2peak). Whole-body (SR(WB)) and back sweat rates (SR(BACK)) were measured. At the conclusion of the study, Na(+) in sweat and blood samples was analyzed to calculate Na(+) secretion and reabsorption rates. SR(WB) and SR(BACK) were highly correlated in Tr and UTr (r = 0.74 and 0.79, respectively; P < 0.0001). In both groups, SR(BACK) increased with the increases in exercise intensity (P < 0.05). Likewise, [Na(+)](sweat) increased with the exercise intensity in both groups (P < 0.05) and it tended to be higher in Tr than in UTr at 60 and 80% VO2peak (~22 mmol L(-1) higher; P = 0.06). However, when normalized for SR(BACK), [Na(+)](sweat) was not different between groups. In both groups, Na(+) secretion and reabsorption rates increased with the increases in SR(BACK) (P < 0.05). However, Na(+) reabsorption rate was lower in the Tr than in the UTr (mean slope = 48 vs. 82 ηmol cm(-2) min(-1); P = 0.03). In conclusion, using a cross-sectional study design, our data suggest that aerobic fitness level does not reduce sweat Na(+) secretion or enhance Na(+) reabsorption during prolonged exercise in the heat that induced high sweat rates. [ABSTRACT FROM AUTHOR]

Carbohydrate stores within muscle are considered essential as a fuel for prolonged endurance exercise, and regimes for enhancing such stores have proved successful in aiding performance. This study explored the effects of a hyperglycaemic-hyperinsulinemic clamp performed 18 h previously on subsequent prolonged endurance performance in cycling. Seven male subjects, accustomed to prolonged endurance cycling, performed 90 min of cycling at ~65% VO(2max) followed by a 16-km time trial 18 h after a 2-h hyperglycemic-hyperinsulinemic clamp (HCC). Hyperglycemia (10 mM) with insulin infused at 300 mU/m(2)/min over a 2-h period resulted in a total glucose uptake of 275 g (assessed by the area under the curve) of which glucose storage accounted for about 73% (i.e. 198 g). Patterns of substrate oxidation during 90-min exercise at 65% VO(2max) were not altered by HCC. Blood glucose and plasma insulin concentrations were higher during exercise after HCC compared with control (p < 0.05) while plasma NEFA was similar. Exercise performance was improved by 49 s and power output was 10-11% higher during the time trial (p < 0.05) after HCC. These data suggest that carbohydrate loading 18 h previously by means of a 2-h HCC improves cycling performance by 3.3% without any change in pattern of substrate oxidation. [ABSTRACT FROM AUTHOR]

Nutrition is an important co-factor in exercise-induced training adaptations in muscle. We compared the effect of 6 weeks endurance training (3 days/week, 1-2 h at 75% VO(2peak)) in either the fasted state (F; n = 10) or in the high carbohydrate state (CHO, n = 10), on Ca(2+)-dependent intramyocellular signalling in young male volunteers. Subjects in CHO received a carbohydrate-rich breakfast before each training session, as well as ingested carbohydrates during exercise. Before (pretest) and after (posttest) the training period, subjects performed a 2 h constant-load exercise bout (~70% of pretest VO(2peak)) while ingesting carbohydrates (1 g/kg h(-1)). A muscle biopsy was taken from m. vastus lateralis immediately before and after the test, and after 4 h of recovery. Compared with pretest, in the posttest basal eukaryotic elongation factor 2 (eEF2) phosphorylation was elevated in CHO (P < 0.05), but not in F. In the pretest, exercise increased the degree of eEF2 phosphorylation about twofold (P < 0.05), and values returned to baseline within the 4 h recovery period in each group. However, in the posttest dephosphorylation of eEF2 was negated after recovery in CHO, but not in F. Independent of the dietary condition training enhanced the basal phosphorylation status of Phospholamban at Thr(17), 5'-AMP-activated protein kinase α (AMPKα), and Acetyl CoA carboxylase β (ACCβ), and abolished the exercise-induced increase of AMPKα and ACCβ (P < 0.05). In conclusion, training in the fasted state, compared with identical training with ample carbohydrate intake, facilitates post-exercise dephosphorylation of eEF2. This may contribute to rapid re-activation of muscle protein translation following endurance exercise. [ABSTRACT FROM AUTHOR]

This study investigated the energy system contributions of rowers in three different conditions: rowing on an ergometer without and with the slide and rowing in the water. For this purpose, eight rowers were submitted to 2,000 m race simulations in each of the situations defined above. The fractions of the aerobic (W (AER)), anaerobic alactic (W (PCR)) and anaerobic lactic (W ([La-])) systems were calculated based on the oxygen uptake, the fast component of excess post-exercise oxygen uptake and changes in net blood lactate, respectively. In the water, the metabolic work was significantly higher [(851 (82) kJ] than during both ergometer [674 (60) kJ] and ergometer with slide [663 (65) kJ] (P < or = 0.05). The time in the water [515 (11) s] was higher (P < 0.001) than in the ergometers with [398 (10) s] and without the slide [402 (15) s], resulting in no difference when relative energy expenditure was considered: in the water [99 (9) kJ min(-1)], ergometer without the slide [99.6 (9) kJ min(-1)] and ergometer with the slide [100.2 (9.6) kJ min(-1)]. The respective contributions of the W (AER), W (PCR) and W ([La-]) systems were water = 87 (2), 7 (2) and 6 (2)%, ergometer = 84 (2), 7 (2) and 9 (2)%, and ergometer with the slide = 84 (2), 7 (2) and 9 (1)%. VO2, HR and lactate were not different among conditions. These results seem to indicate that the ergometer braking system simulates conditions of a bigger and faster boat and not a single scull. Probably, a 2,500 m test should be used to properly simulate in the water single-scull race. [ABSTRACT FROM AUTHOR]

The aim was to test the hypothesis that one night of sleep deprivation will impair pre-loaded 30 min endurance performance and alter the cardio-respiratory, thermoregulatory and perceptual responses to exercise. Eleven males completed two randomised trials separated by 7 days: once after normal sleep (496 (18) min: CON) and once following 30 h without sleep (SDEP). After 30 h participants performed a 30 min pre-load at 60% [VO(2 max) followed by a 30 min self-paced treadmill distance test. Speed, RPE, core temperature (T(re)), mean skin temperature (T(sk)), heart rate (HR) and respiratory parameters VO(2 max), VCO(2), VE, RER pre-load only) were measured. Less distance (P = 0.016, d = 0.23) was covered in the distance test after SDEP (6037 (759) 95%CI 5527 to 6547 m) compared with CON (6224 (818) 95%CI 5674 to 6773 m). SDEP did not significantly alter T(re) at rest or thermoregulatory responses during the pre-load including heat storage (0.8 degrees C) and T(sk). With the exception of raised VO(2) at 30 min on the pre-load, cardio-respiratory parameters, RPE and speed were not different between trials during the pre-load or distance test (distance test mean HR, CON 174 (12), SDEP 170 (13) beats min(-1): mean RPE, CON 14.8 (2.7), SDEP 14.9 (2.6)). In conclusion, one night of sleep deprivation decreased endurance performance with limited effect on pacing, cardio-respiratory or thermoregulatory function. Despite running less distance after sleep deprivation compared with control, participants' perception of effort was similar indicating that altered perception of effort may account for decreased endurance performance after a night without sleep. [ABSTRACT FROM AUTHOR]

We investigated the impact of 13 days of "living high-training low" (LHTL) on the antioxidant/prooxidant balance in elite endurance swimmers. Eighteen elite swimmers from the French Swimming Federation were submitted to a 13-day endurance training and divided into two groups: one group trained at 1,200 m and lived in hypoxia (2,500-3,000 m simulated altitude) and the second group trained and lived at 1,200 m. The subjects performed an acute hypoxic test (10 min at 4,800 m) before and 1 day after the training period. Plasma levels of advanced oxidation protein products (AOPP), malondialdehydes (MDA), ferric reducing antioxidant power (FRAP), and lipid-soluble antioxidants were measured before and after the 4,800 m tests. After the training, MDA and AOPP responses to the 4,800 m test were lower than before training for both groups (+10 vs. +2%; P = 0.01 for MDA and +80 vs. +14%; P = 0.01 for AOPP). Thirteen days of LHTL did not modify antioxidant status (FRAP and lipid-soluble antioxidants) despite intakes in vitamins A and E below the recommended daily allowances. The LHTL did not affect the antioxidant status in elite swimmers; however, the normoxic endurance training induced preconditioning mechanisms in response to the 4,800 m test. [ABSTRACT FROM AUTHOR]

Investigations of training effects on exercise energy cost have yielded conflicting results. The purpose of the present study was to compare quadriceps energy cost and oxidative capacity between endurance-trained and sedentary subjects during a heavy dynamic knee extension exercise. We quantified the rates of ATP turnover from oxidative and anaerobic pathways with (31)P-MRS, and we measured simultaneously pulmonary oxygen uptake in order to assess both total ATP production [i.e., energy cost (EC)] and O(2) consumption (O(2) cost) scaled to power output. Seven sedentary (SED) and seven endurance-trained (TRA) subjects performed a dynamic standardized rest-exercise-recovery protocol at an exercise intensity corresponding to 35% of maximal voluntary contraction. We showed that during a dynamic heavy exercise, the O(2) cost and EC were similar in the SED and endurance-trained groups. For a given EC, endurance-trained subjects exhibited a higher relative mitochondrial contribution to ATP production at the muscle level (84 +/- 12% in TRA and 57 +/- 12% in SED; P < 0.01) whereas the anaerobic contribution was reduced (18 +/- 12% in TRA and 44 +/- 11% in SED; P < 0.01). Our results obtained in vivo illustrate that on the one hand the beneficial effects of endurance training are not related to any reduction in EC or O(2) cost and on the other hand that this similar EC was linked to a change regarding the contribution of anaerobic and oxidative processes to energy production, i.e., a greater aerobic energy contribution associated with a concomitant reduction of the anaerobic energy supply. [ABSTRACT FROM AUTHOR]

In older healthy men, aerobic exercise capacity is related to postischemic flow-mediated dilation of the brachial artery (FMD), but corresponding data in a younger population is not available. In addition, whether submaximal aerobic exercise performance also correlates with this kind of vasomotor reactivity is not known. Therefore, in 15 nonsmoking young healthy men [age 27 (5) years; body mass index: 24 (2) kg/m(2); mean (SD)] with different levels of ordinary physical activity, but not performing upper-extremity training, we measured FMD at 1 min after reactive hyperemia, and pulmonary oxygen uptake (VO(2)) at ventilatory anaerobic threshold (VO(2)AT) and at peak effort (peak VO(2)) during an incremental exercise on a treadmill. In our participants, FMD was 9.1 (3.4)%, VO(2)AT was 40.72 (5.92) ml/kg per min, and peak VO(2) was 52.95 (8.13) ml/kg per min. Using bivariate Pearson's correlation, and in separate multivariate regression analyses, VO(2)AT and peak VO(2) showed a significant and reasonably good correlation with FMD (r = 0.84, P < 0.001 and r = 0.77, P = 0.001, respectively), independent of age, body mass index and serum total cholesterol (beta = 0.77, P < 0.001, R(2) of the overall model = 0.79 and beta = 0.70, P < 0.005, R(2) of the overall model = 0.69, respectively). Our data provide evidence suggesting that in young healthy men a higher submaximal and maximal aerobic exercise performance is associated with a greater FMD of peripheral conduit arteries. [ABSTRACT FROM AUTHOR]