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L-Ornithine plays an important role in ammonia metabolism via the urea cycle. This study aimed to examine the effect of L-ornithine hydrochloride ingestion on ammonia metabolism and performance after intermittent maximal anaerobic cycle ergometer exercise. Ten healthy young adults (age, 23.8 ± 3.9 year; height, 172.3 ± 5.5 cm; body mass, 67.7 ± 6.1 kg) with regular training experience ingested L-ornithine hydrochloride (0.1 g/kg, body mass) or placebo after 30 s of maximal cycling exercise. Five sets of the same maximal cycling exercise were conducted 60 min after ingestion, and maximal cycling exercise was conducted after a 15 min rest. The intensity of cycling exercise was based on each subject's body mass (0.74 N kg(-1)). Work volume (watt), peak rpm (rpm) before and after intermittent maximal ergometer exercise and the following serum parameters were measured before ingestion, immediately after exercise and 15 min after exercise: ornithine, ammonia, urea, lactic acid and glutamate. Peak rpm was significantly greater with L-ornithine hydrochloride ingestion than with placebo ingestion. Serum ornithine level was significantly greater with L-ornithine hydrochloride ingestion than with placebo ingestion immediately and 15 min after intermittent maximal cycle ergometer exercise. In conclusion, although maximal anaerobic performance may be improved by L-ornithine hydrochloride ingestion before intermittent maximal anaerobic cycle ergometer exercise, the above may not depend on increase of ammonia metabolism with L-ornithine hydrochloride. [ABSTRACT FROM AUTHOR]

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]

The purpose of this study was to determine the influence of transiently elevated endogenous hormone concentrations during exercise on strength training adaptations. Nine subjects performed four unilateral strength training session per week on the elbow flexors for 11 weeks. During two of the weekly sessions, leg exercises were performed to acutely increase the systemic anabolic hormone concentration immediately before the exercises for one of the elbow flexors (L + A). On the two other weekly training sessions, the contralateral elbow flexors were trained without prior leg exercises (A). By randomizing one arm of the subjects to serve as a control and the other as experimental, both conditions have the same nutritional and genetic environment. Serum testosterone and growth hormone was significantly increased during the L - A training session, while no hormonal changes occurred in the A session. Both A and L + A increased 1RM in biceps curl, peak power in elbow flexors at 30 and 60% of 1RM, and muscle volume of the elbow flexors (p < 0.05). However, only L + A achieved increase in CSA at the part of the arm flexors with largest cross sectional area (p < 0.001), while no changes occurred in A. L + A had superior relative improvement in 1RM biceps curl and favorable muscle adaptations in elbow flexors compared to A (p < 0.05). In conclusion, performing leg exercises prior to arm exercises, and thereby increasing the levels of serum testosterone and growth hormone, induced superior strength training adaptations compared to arm training without acute elevation of hormones. [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]

Cardiovascular deconditioning is known to occur in astronauts exposed to microgravity. Endothelial dysfunction at microcirculatory sites might contribute to cardiovascular deconditioning induced by weightlessness. Recent studies have reported changes in the morphology and gene expression of endothelial cells exposed to conditions of simulated microgravity. The present study was aimed at examining the effects of microgravity on the apoptosis of microvascular endothelial cells and the mechanism underlying these effects. We simulated a microgravity environment and found that microgravity induced microvascular endothelial cell apoptosis and that this effect was correlated with the downregulation of the PI3K/Akt pathway, increased expression of NF-κB, and depolymerization of F-actin. These findings may provide important insights into the origin of the adverse physiological changes occurring due to exposure to microgravity conditions. [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]

Both myofibroblast differentiation and extracellular matrix (ECM) deposition are essential components of scar formation in tendons, and hepatocyte growth factor (HGF) is reported to prevent fibrogenic responses in tendons. Matrix metalloproteinases-2(MMP-2) is also involved in the healing process in tendons. Whether HGF protects healed Achilles tendons from injury-induced scar formation and the mechanisms are unknown. Daily for 2 weeks after wounding, except for the non-surgical control group, the Achilles tendons in rats were locally injected with HGF (100 ng 50 μl(-1) per mouse) or phosphate-buffered saline (PBS). Histological examination showed HGF ameliorated disorganized collagen fibers caused by surgical incisions in rats. After transforming growth factor beta-1 (TGF-β1) induced fibrogenic responses in primary Achilles tendon fibroblasts in rats, HGF treatment for 24 h reduced α-smooth muscle actin (α-SMA) (0.60 ± 0.07-fold, P < 0.05) and type III collagen expression (0.39 ± 0.07-fold, P < 0.05). Moreover, HGF elevated MMP-2 expression (1.23 ± 0.11-fold, P < 0.05). The MMP-2 inhibitor, tissue inhibitors of metalloproteinase-1 (TIMP-1), partially blocked the inhibitory effects of HGF on α-SMA expression (from 0.60 ± 0.07-fold to 0.83 ± 0.07-fold, P < 0.05) and type III collagen expression (from 0.39 ± 0.06-fold to 0.86 ± 0.08-fold, P < 0.05). These results indicate HGF attenuates TGF-β1-induced fibrogenic responses in Achilles tendon, which was mediated by MMP-2. These results will aid in developing effective therapeutic approaches for the dysfunctional repair in Achilles tendons. [ABSTRACT FROM AUTHOR]

Optimal levels of membrane fluidity are essential for numerous cell functions including cell growth, solute transport and signal transduction. Since exercise enhances free radical production, our aim was to evaluate in healthy male subjects the effects of an acute bout of maximal and submaximal exercise on the erythrocyte membrane fluidity and its possible relation to the oxidative damage overproduction due to exercise. Subjects (n = 34) performed three cycloergometric tests: a continuous progressive exercise, a strenuous exercise until exhaustion and an acute bout of exercise at an intensity corresponding to 70% of maximal work capacity for 30 min. Venous blood samples were collected before and immediately after these exercises. Erythrocyte membrane fluidity was assessed by fluorescence spectroscopy. Plasma malondialdehyde (MDA) and 4-hydroxyalkenals (4-HDA) concentrations and carbonyl content of plasmatic proteins were used as an index of lipid and protein oxidation, respectively. Exercise produced a dramatic drop in the erythrocyte membrane fluidity as compared to resting time, but this was not accompanied by significant changes in the plasmatic MDA and 4-HDA concentrations. The highest erythrocyte membrane rigidity was detected immediately after strenuous exercise until exhaustion was performed. Protein carbonyl levels were higher after exhaustive exercises than at rest. Continuous progressive and strenuous exercises until exhaustion, but not submaximal workload, resulted in a significant enhanced accumulation of carbonylated proteins in the plasma. These findings are consistent with the idea that exercise exaggerates oxidative damage, which may contribute, at least partially, to explain the rigidity in the membrane of the erythrocytes due to acute exercise. [ABSTRACT FROM AUTHOR]

This investigation reports the effects of caffeinated chewing gum on fatigue and hormone response during repeated sprint performance with competitive cyclists. Nine male cyclists (mean ± SD, age 24 ± 7 years, VO(2max) 62.5 ± 5.4 mL kg(-1) min(-1)) completed four high-intensity experimental sessions, consisting of four sets of 30 s sprints (5 sprints each set). Caffeine (240 mg) or placebo was administered via chewing gum following the second set of each experimental session. Testosterone and cortisol concentrations were assayed in saliva samples collected at rest and after each set of sprints. Mean power output in the first 10 sprints relative to the last 10 sprints declined by 5.8 ± 4.0% in the placebo and 0.4 ± 7.7% in the caffeine trials, respectively. The reduced fatigue in the caffeine trials equated to a 5.4% (90% confidence limit ±3.6%, effect size 0.25; ±0.16) performance enhancement in favour of caffeine. Salivary testosterone increased rapidly from rest (~53%) and prior to treatments in all trials. Following caffeine treatment, testosterone increased by a further 12 ± 14% (ES 0.50; ± 0.56) relative to the placebo condition. In contrast, cortisol concentrations were not elevated until after the third exercise set; following the caffeine treatment cortisol was reduced by 21 ± 31% (ES -0.30; ± 0.34) relative to placebo. The acute ingestion of caffeine via chewing gum attenuated fatigue during repeated, high-intensity sprint exercise in competitive cyclists. Furthermore, the delayed fatigue was associated with substantially elevated testosterone concentrations and decreased cortisol in the caffeine trials. [ABSTRACT FROM AUTHOR]

Acute exercise alters the surface expression of toll-like receptors (TLRs) and HLA.DR on blood monocytes, which could transiently compromise immunity. As serum factors might be responsible, we examined the effects of autologous post-exercise serum exposure on TLR2, TLR4 and HLA.DR expression on resting blood monocytes and their subtypes. Eight trained cyclists completed an ergometer 60 km time trial. PBMCs and serum were obtained before, immediately after and 1 h after exercise. TLR2, TLR4 or HLA.DR expression (gMFI) was determined on blood monocyte subtypes expressing combinations of CD14 and CD16 by flow cytometry, and on resting monocytes exposed to 50% autologous serum (pre, immediately after or 1 h after exercise) for 18 h in culture. Immediately after exercise, total monocyte expression of TLR2 and TLR4 increased by 41 and 27%, respectively, while HLA.DR expression was 39% lower than baseline. TLR2 and TLR4 was 53 and 84% greater 1 h after exercise, respectively, while HLA.DR was 48% lower. Changes in TLR2 and TLR4 expression occurred on the CD14(++bright)/CD16(+dim) monocyte subtype only, while HLA.DR expression changed on the CD14(+dim)/CD16(++bright) subtype. Serum did not affect monocyte TLR2 or TLR4 expression but 1 h post serum increased expression of HLA.DR on total monocytes and the CD14(+dim)/CD16(++bright) subtype, which was in contrast to the change observed at this time after exercise. We conclude that a bout of strenuous aerobic exercise alters the surface expression of TLR2, TLR4 and HLA.DR on blood monocytes and some of their subtypes, but these changes appear to be unrelated to blood serum factors. [ABSTRACT FROM AUTHOR]

The response of calf muscle strength, resting (R (bf)) and post-occlusive (PO(bf)) blood flow were investigated following 4 weeks resistance training with and without blood flow restriction in a matched leg design. Sixteen untrained females performed unilateral plantar-flexion low-load resistance training (LLRT) at either 25% (n = 8) or 50% (n = 8) one-repetition maximum (1 RM). One limb was trained with unrestricted blood flow whilst in the other limb blood flow was restricted with the use of a pressure applied cuff above the knee (110 mmHg). Regardless of the training load, peak PO(bf), measured using venous occlusion plethysmography increased when LLRT was performed with blood flow restriction compared to no change following LLRT with unrestricted blood flow. A significant increase (P < 0.05) in the area under the blood time-flow curve was also observed following LLRT with blood flow restriction when compared LLRT with unrestricted blood flow. No changes were observed in R (bf) between groups following training. Maximal dynamic strength (1 RM), maximal voluntary contraction and isokinetic strength at 0.52 and 1.05 rad s(-1) also increased (P < 0.05) by a greater extent following resistance training with blood flow restriction. Moreover, 1 RM increased to a greater extent following training at 50% 1 RM compared to 25% 1 RM. These results suggest that 4 weeks LLRT with blood flow restriction provides a greater stimulus to increase peak PO(bf) as well as strength parameters than LLRT with unrestricted blood flow. [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]

This study investigated the effect of repeated bouts of short-term, high-intensity cycling exercise on the salivary cortisol, testosterone and immunoglobulin (A) concentrations of 15-16 year old boys. Seventeen apparently healthy schoolchildren (aged 15.5 +/- 0.4 years) participated in this study. All participants completed 6 x 8 s sprints, interspersed with 30 s recovery intervals on a cycle ergometer. Using the passive drool method, salivary samples were taken before, and 5 min after, exercise. The group mean for peak power output was 723.1 +/- 180.3 s. There were significant changes (p < or = 0.05) in both SalT and SalC, 5 min after completing 6 x 8 s cycle sprints. No significant differences (p > 0.05) were recorded for SIg(A). The increases in SalT and SalC reported in this study confirm that repeated bouts of short-term, high-intensity exercise produces significant physiological hormonal responses in adolescent boys, but does not affect mucosal immune function. [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]

The present study was undertaken to evaluate the acute effect of prior resistance training of varying intensities on energy expenditure and substrate utilization during subsequent aerobic exercise. Eleven males and 21 females completed three experimental trials consisting of (1) aerobic exercise only (C), (2) aerobic exercise preceded by a high-intensity resistance training (HI), and (3) aerobic exercise preceded by a low-intensity resistance training (LO). Resistance training produced an equal volume between HI and LO and consisted of six exercises with each performed for three sets of eight repetitions at 90% of 8-RM in HI and three sets of 12 repetitions at 60% of 8-RM in LO. Aerobic exercise was performed on a cycle ergometer at 50% VO(2)peak for 20 min in all trials. Oxygen uptake (VO2), and carbohydrate and fat oxidation were determined throughout each aerobic exercise session. Fat oxidation rate was higher (P < 0.05) in HI than either LO or C in both males and females. VO2 was also higher (P < 0.05) in HI than either LO or C in females. In males, although between-trial differences in VO2 did not reach statistical significance, they were consistent with the trend seen in females. No differences in carbohydrate oxidation rates were observed across the three trials in either gender group. It appears that in training that combines both aerobic and resistance exercises, performing a comparatively higher intensity resistance exercise first would augment fat utilization and energy expenditure during subsequent aerobic exercise. [ABSTRACT FROM AUTHOR]

The reduced arterial oxygen tension at high altitude impairs the ability to work. Acetazolamide improves arterial oxygen saturation (SaO2) by increasing ventilation but is associated with an increased work and cost of breathing. Depending on the settings, sildenafil can also increases SaO2 possibly through a reduction in pulmonary hypertension and interstitial edema, which could improve ventilation–perfusion matching. The objective of this study is to determine the effects of acetazolamide and sildenafil on ventilatory control and breathing efficiency ( VE/ VCO2) during submaximal steady-state hypoxic exercise in healthy individuals. Following 18 h of hypoxic exposure in an altitude tent at an oxygen concentration of 12.5% (simulated altitude of 4,300 m), 15 participants performed 10 min of hypoxic exercise on a stationary bicycle at 40% of their sea level peak oxygen uptake ( VO2) while randomly receiving sildenafil 40 mg (SIL), acetazolamide 125 mg (ACZ) or a placebo (PLA). There was no difference in VO2 during exercise between conditions while SaO2 was greater with acetazolamide compared to both placebo and sildenafil. Acetazolamide increased ventilation (PLA 49.0 ± 3.2, SIL 47.7 ± 3.1, ACZ 52.1 ± 3.0 l/min) and reduced end-tidal CO2 ( PETCO2) (PLA 32.1 ± 0.8, SIL 32.8 ± 0.9, ACZ 29.2 ± 0.7 mmHg) compared to placebo and sildenafil. Breathing was less efficient with acetazolamide (increased VE/ VCO2) in comparison to placebo and sildenafil (PLA 41.5 ± 1.0, SIL 40.4 ± 1.3, ACZ 45.4 ± 1.0) while sildenafil did not change VE/ VCO2 during hypoxic exercise. In conclusion, acetazolamide increased ventilation and reduced breathing efficiency while sildenafil did not affect breathing efficiency despite a trend toward a blunted ventilatory response, possibly due to a reduction in pulmonary hypertension and/or ventilatory drive, during submaximal hypoxic exercise in healthy individuals. [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]

The aims of this study were to evaluate the effects of both noncircular (ROT) and conventional (CON) chainring systems on aerobic and anaerobic cycling performances of professional cyclists, while analyzing the influence of varying the crank angle of maximum crank arm length of ROT. Fifteen professional road cyclists performed both incremental and sub-maximal aerobic tests and the Wingate anaerobic test in the laboratory. There were no statistical differences between CON and ROT in the aerobic tests, even when the best ROT position (ROT+) was selected. However, in the anaerobic test, maximal (4.2-9.1%) and mean (0.7-4.7%) power outputs were higher in ROT (P < 0.05). These differences were greater when the ROT+ was selected (11.2 and 7.0%, respectively). Our findings suggest that ROT is able to improve anaerobic but not aerobic cycling performance in professional cyclists. Nevertheless, it must be adapted to each cyclist to ensure these improvements. [ABSTRACT FROM AUTHOR]

In a placebo-controlled study, the effects of intermittent hypoxic exposures (IHE) or a placebo control for 10 days, were examined on the extent of exercise-induced hypoxemia (EIH), cerebral and muscle oxygenation (near-infrared spectroscopy) and VO(2peak). Eight athletes who had previously displayed EIH (fall in saturation of arterial oxygen (SaO(2)) of >4% from rest) during an incremental maximal exercise test, volunteered for the present research. Prior to (baseline), and 2 days following (post) the IHE or placebo, an incremental maximal exercise test was performed whilst SaO(2), heart rate, cerebral and muscle oxygenation and respiratory gas exchange were measured continuously. After IHE, but not placebo, EIH was less pronounced at VO(2peak) (IHE group, SaO(2) at VO(2peak) baseline 91.23 +/- 1.10%, post 94.10 +/- 2.19%; P < 0.01, mean +/- SD). This reduction was reflected in an increased ventilation (NS), a lower end-tidal CO(2) (P < 0.01), and lowered cerebral TOI during heavy exercise (90% VO(2peak): -6.1 +/- 6.0 Delta%, P = 0.04). Conversely, muscle tHb at maximal exercise, was increased (2.4 +/- 1.8 DeltamicroM, P = 0.01, mean +/- 95 CL) following IHE, whilst de-oxygenated Hb at 90% of VO(2peak) was reduced (-0.9 +/- 0.8 DeltamicroM, P = 0.02). These data indicate that exposure to IHE can attenuate the degree of EIH. Despite a potential compromise in cerebral oxygenation, exposure to IHE may induce some positive physiological adaptations at the muscle tissue level. We speculate that the unchanged VO(2peak) following IHE might reflect a balance between these central (cerebral) and peripheral (muscle) adaptations. [ABSTRACT FROM AUTHOR]

Evidence indicates that repeated-bouts of eccentric exercise (EE) do not exacerbate the extent of muscle damage indices, as compared to a single-bout. We hypothesized that molecular adaptations, under repeated-bouts of EE, would include suppression of muscle repair inhibitory factors such as myostatin and up-regulation of muscle repair positive regulatory factors such as myogenic regulatory factors (MRFs). Fifteen males were recruited for this study. The exercise group (n=9) successfully completed six sets of 15 reps of maximum voluntary eccentric contractions, for six consecutive days, using a dynamometer (Multicont-II). Blood and muscle biopsy samples were obtained from each subject 1 week prior to exercise, 2 days post the first training session, and 24 h after the last training session. Gene expression levels were determined using real-time RT-PCR. Blood samples were analyzed for creatine kinase (CK) and lactate-dehydrogenase (LDH) activity. Repeated-bouts of EE induced a large down-regulation of myostatin mRNA (-73%) which persisted throughout the study. The responses of MRFs were mild. At day 3 only myogenin increased significantly (1.9 fold) while MyoD decreased by 45%. Surprisingly, at day 7, despite the presence of muscle damage indices, all MRFs returned to the pre-exercise levels. The results of the present study showed that repeated-bouts of EE, for six consecutive days, dramatically decreased Myostatin mRNA expression but impaired the expression patterns of MRFs such that, with the exception of myogenin that showed a moderate non-sustained increase, MyoD and MYf5 response was minimal. [ABSTRACT FROM AUTHOR]

The purpose of this study was to evaluate the methodology of Margaria staircase test (MT) for assessment of muscle anaerobic power. Specifically, we hypothesized that due to the scaling effects the outcome of MT calculated using the standard formula that suggests the power output to be proportional to body mass [P = (m . g . h)/T; P = power output, m = body mass, g = 9.81 m/s(2), h = height of stairs climbed, T = running time] overestimates the effect of body size on the calculated muscle power output. Young and physically active subjects (N = 111) were tested and the relationship between P and body size (S; either body mass or height) was assessed by standard allometric model (i.e., P = a . S ( b ); where a and b were the constant multiplier and allometric parameter, respectively). The results supported the hypothesized relationship by revealing b = 0.66 (95%CI = 0.49-0.83; r = 0.59; P < 0.001) and b = 1.13 (95%CI = 0.49-0.83; r = 0.34; P < 0.001) for body mass and body height, respectively. The obtained values of b (i.e., b < 1 for body mass and b < 3 for body height) suggest that the standard formula of MT overestimates the power output of larger subjects and underestimates the power of smaller ones. Since the results were mainly in line with both the experimental findings and theoretical predictions regarding the general effects of scale on human muscle power, we propose a modified formula that provides normalized power: P ( n ) = P/m (0.67) = [(m . g . h)/T]/m (0.67) = (m (0.33) . g . h)/T. The modified formula could provide a body size independent index of muscle power that would both allow for establishing standards and enable comparison of individuals and groups of individuals of different body dimensions. [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]

The chemoreflex system controlling ventilation consists of two subsystems, i.e., the central controller (controlling element), and peripheral plant (controlled element). We developed an integral framework to quantitatively characterize individual ventilatory regulation by experimental determination of an equilibrium diagram using a modified metabolic hyperbola and the CO2 response curve. In 13 healthy males, the steady-state arterial CO2 pressure (PaCO2) and minute ventilation (V? e) were measured. To characterize the central controller, we changed fraction of inspired CO2(0, 3.5, 5 and 6% CO2 in 80% oxygen with nitrogen balance) and measured thePaCO2-V? e relation. To characterize the peripheral plant, we alteredV? e by hyper- or hypoventilation using a visual feedback method, which made it possible to control both tidal volume and breathing frequency, and measured theV? e-PaCO2 relation. The intersection between the two relationship lines gives the operating point. The relationship betweenPaCO2 andV? e for the central controller was reasonably linear in each subject (r2=0.808~0.995). The peripheral plant approximated a modified metabolic hyperbolic curve (r2=0.962~0.996). The operating points of the system estimated from the two relationship lines were in good agreement with those measured under the closed-loop condition. The gain of the central controller was 1.9 (1.0) l min-1 mmHg-1 and that of the peripheral plant was 3.0 (0.5) mmHg l-1 min-1. The total loop gain, the product of the two gains, was 5.3 (2.5). We conclude that human ventilatory regulation by the respiratory chemoreflex system can be quantitatively characterized using an equilibrium diagram. This framework should be useful for understanding the mechanisms responsible for abnormal ventilation under various pathophysiological conditions. [ABSTRACT FROM AUTHOR]