Time course of endothelial adaptation after acute and chronic exercise in patients with metabolic syndrome

Clustering of cardiovascular risk factors may lead to endothelial dysfunction. Physical exercise is an important factor in prevention and treatment of endothelial dysfunction. We wanted to determine the time course of adaptation to a single bout of exercise at either high or moderate intensity upon endothelial function both before and after a 16-week fitness program in patients with metabolic syndrome. Twenty-eight patients with metabolic syndrome participated in the study and were randomized and stratified (according to age and sex) into an aerobic interval exercise training group (AIT, n = 11), a continuously moderate-intensity exercise training group (CME, n = 8) or to a control group (n = 9). Flow-mediated dilatation (FMD) was determined at baseline, immediately, 24, 48, and 72 hours after 1 bout of exercise and repeated after 16 weeks of exercise. In the untrained state, FMD improved from 5 to 11% (p = 0.003) immediately after a single bout of aerobic interval training (AIT), an effect lasting 72 hours postexercise. In comparison, continuous moderate exercise (CME) improved FMD immediately after a single bout of exercise from 5 to 8% (p = 0.02), an effect lasting 24 hours postexercise (group difference, p < 0.001). In the trained state, a single bout of AIT resulted in a 2% (p = 0.007) acute increase of FMD lasting 48 hours postexercise. The CME increased FMD by 3% (p < 0.01), an effect lasting 24 hours postexercise (group difference p = 0.0012). Blood glucose level decreased after 1 single bout of AIT in the untrained state (p < 0.05), and the effect lasted at least 72 hours postexercise (p < 0.01). Acute CME decreased blood glucose with normalization of the values 24 hours postexercise (p < 0.01). A single bout of exercise in the trained state reduced fasting blood glucose by 10% (p < 0.05) after both AIT and CME. Exercise training, especially high intensity, thus appears to be highly beneficial in reducing blood glucose and improving endothelial function.     

Exercise intensity: effect on postexercise O2 uptake in trained and untrained women

Despite many reports of long-lasting elevation of metabolism after exercise, little is known regarding the effects of exercise intensity and duration on this phenomenon. This study examined the effect of a constant duration (30 min) of cycle ergometer exercise at varied intensity levels [50 and 70% of maximal O2 consumption (VO2max)] on 3-h recovery of oxygen uptake (VO2). VO2 and respiratory exchange ratios were measured by open-circuit spirometry in five trained female cyclists (age 25 +/- 1.7 yr) and five untrained females (age 27 +/- 0.8 yr). Postexercise VO2 measured at intervals for 3 h after exercise was greater (P less than 0.01) after exercise at 50% VO2max in trained (0.40 +/- 0.01 l/min) and untrained subjects (0.39 +/- 0.01 l/min) than after 70% VO2max in (0.31 +/- 0.02 l/min) and untrained subjects (0.29 +/- 0.02 l/min). The lower respiratory exchange ratio values (P less than 0.01) after 50% VO2max in trained (0.78 +/- 0.01) and untrained subjects (0.80 +/- 0.01) compared with 70% VO2max in trained (0.81 +/- 0.01) and untrained subjects (0.83 +/- 0.01) suggest that an increase in fat metabolism may be implicated in the long-term elevation of metabolism after exercise. This was supported by the greater estimated fatty acid oxidation (P less than 0.05) after 50% VO2max in trained (147 +/- 4 mg/min) and untrained subjects (133 +/- 9 mg/min) compared with 70% VO2max in trained (101 +/- 6 mg/min) and untrained subjects (85 +/- 7 mg/min).     

Rate of decline in blood lactate after cycling exercise in endurance-trained and -untrained subjects

The purpose of this study was to compare the rate of decline in blood lactate (La) levels in nine trained men [maximal O2 consumption (VO2max) 65.5 +/- 3.3 ml.kg-1.min-1] and eight untrained men (VO2max 42.2 +/- 2.8 ml.kg-1.min-1) during passive recovery from a 3-min exercise bout. Trained and untrained subjects cycled at 85 and 80% VO2max, respectively, to produce similar peak blood La concentrations. Twenty samples of arterialized venous blood were drawn from a heated hand vein during 60 min of recovery and analyzed in an automated La analyzer. The data were then fitted to a biexponential function, which closely described the observed data (r = 0.97-0.98). There was no difference in the coefficient expressing the rate of decline in blood La for trained and untrained groups (0.0587 +/- 0.0111 vs. 0.0579 +/- 0.0100, respectively). However, trained subjects demonstrated a faster time-to-peak La (P = 0.01), indicative of a faster efflux of La from muscle to blood. Thus the rate of decline in blood La after exercise does not appear to be affected by training. The faster decline previously reported for trained subjects may be due to the use of a linear rather than a biexponential curve fit.     

Plasma Met-enkephalin and catecholamine responses to intense exercise in humans.

Native and cryptic Met-enkephalin and catecholamines are coreleased in response to stress. However, it is not known whether Met-enkephalin and catecholamines exhibit concurrent temporal relationships in response to exercise. The purpose of this investigation was to examine the corelease of catecholamines and Met-enkephalin in endurance-trained (n = 6) and untrained (n = 6) male subjects during a 6-min bout of exercise: 4 min at 70% of maximal O2 uptake (VO2max) followed by 2 min at 120% VO2max. Peak catecholamine levels were found at 1 min of recovery. In trained subjects, native Met-enkephalin peaked during exercise at 70% VO2max, declined during exercise at 120% VO2max, and returned to basal levels by 1 min of recovery. In the untrained subjects, native Met-enkephalin peaked at 120% VO2max (6 min) and returned to baseline by 5 min of recovery. In both groups, cryptic Met-enkephalin peaked at 70% VO2max and returned to basal levels during exercise at 120% VO2max. These data demonstrate that during exercise there is a temporal dissociation in plasma levels of Met-enkephalin and catecholamines.     

Oxygen uptake kinetics and time to exhaustion in cycling and running: a comparison between trained and untrained subjects

The objective of the present study was to compare pulmonary gas exchange kinetics (VO2 kinetics) and time to exhaustion (Tlim) between trained and untrained individuals during severe exercise performed on a cycle ergometer and treadmill. Eleven untrained males in running (UR) and cycling (UC), nine endurance cyclists (EC), and seven endurance runners (ER) were submitted to the following tests on separate days: (i) incremental test for determination of maximal oxygen uptake (VO2max) and the intensity associated with the achievement of VO2max (IVO2max) on a mechanical braked cycle ergometer (EC and UC) and on a treadmill (ER and UR); (ii) all-out exercise bout performed at IVO2max to determine the time to exhaustion at IVO2max (Tlim) and the time constant of oxygen uptake kinetics (tau). The tau was significantly faster in trained group, both in cycling (EC = 28.2 +/- 4.7s; UC = 63.8 +/- 25.0s) and in running (ER = 28.5 +/- 8.5s; UR = 59.3 +/- 12.0s). Tlim of untrained was significantly lower in cycling (EC = 384.4 +/- 66.6s vs. UC; 311.1 +/- 105.7 s) and higher in running (ER = 309.2 +/- 176.6 s vs. UR = 439.8 +/- 104.2 s). We conclude that the VO2 kinetic response at the onset of severe exercise, carried out at the same relative intensity is sensitive to endurance training, irrespective of the exercise type. The endurance training seems to differently influence Tlim during exercise at IVO2max in running and cycling.     

Exercise effects on chromium excretion of trained and untrained men consuming a constant diet

Chromium excretion of eight trained and five sedentary men was determined on rest days and after exercise to exhaustion at 90% of maximum O2 consumption (VO2max) to determine if degree of physical fitness affects urinary Cr losses. Subjects were fed a constant daily diet containing approximately 9 micrograms Cr/1,000 kcal. VO2max of the trained runners was in the good or above range based on their age and that of the sedentary subjects was average or below. While consuming the control diet, basal urinary Cr excretion of subjects who exercise regularly was significantly lower than that of the sedentary control subjects, 0.09 +/- 0.01 and 0.21 +/- 0.03 microgram/day (mean +/- SE), respectively. When subjects consumed self-chosen diets, basal urinary Cr excretion of the trained subjects was also significantly lower than that of the untrained subjects. Daily urinary Cr excretion of trained subjects was significantly higher on the day of a single exercise bout at 90% VO2max compared with nonexercise days, 0.12 +/- 0.02 and 0.09 +/- 0.01 microgram/day, respectively. Urinary Cr excretion of sedentary subjects was not altered after controlled exercise. These data demonstrate that basal urinary Cr excretion and excretion in response to exercise are related to VO2max and therefore degree of physical fitness.     

Enhanced endothelium-dependent vasodilation in older endurance-trained men.

We hypothesized that abnormal endothelium-dependent vasodilation (EDD) found in older otherwise healthy subjects can be attenuated with long-term endurance training. Ten endurance-trained men, 68.5 +/- 2.3 yr old, and 10 healthy sedentary men, 64.7 +/- 1.4 yr old, were studied. Aerobic exercise capacity (VO(2 max)), fasting plasma cholesterol, insulin, and homocysteine concentrations were measured. Master athletes had higher VO(2 max) (42 +/- 2.3 vs. 27 +/- 1.4 ml. kg(-1). min(-1), P < 0.001), slightly higher total cholesterol (226 +/- 8 vs. 199 +/- 8 mg/dl, P = 0.05), similar insulin, and higher homocysteine (10.7 +/- 1.3 vs. 9.2 +/- 1.4 micromol/ml, p = 0.02) concentrations. Brachial arterial diameter, determined with vascular ultrasound, during the hyperemic response was greater in the master athletes than in controls (P = 0.005). Peak vasodilatory response was 109.1 +/- 2 vs. 103.6 +/- 2% (P < 0.05) in the athletes and controls, respectively. Endothelium-independent vasodilation in response to nitroglycerin was similar between the two groups. The increased arterial diameter during the hyperemic response correlated significantly with the VO(2 max) in the entire population (r = 0.66, P < 0.002). Our results suggest that long-term endurance exercise training in older men is associated with systemic enhanced EDD, which is even detectable in the conduit arteries of untrained muscle.     

Enhanced protein breakdown after eccentric exercise in young and older men

The effects of eccentric exercise on whole body protein metabolism were compared in five young untrained [age 24 +/- 1 yr, maximal O2 uptake (VO2max) = 49 +/- 6 ml.kg-1.min-1] and five older untrained men (age 61 +/- 1 yr, VO2max = 34 +/- 2 ml.kg-1.min-1). They performed 45 min of eccentric exercise on a cycle ergometer at a power output equivalent to 80% VO2max (182 +/- 18 W). Beginning 5 days before exercise and continuing for at least 10 days after exercise, they consumed a eucaloric diet providing 1.5 g.kg-1.day-1 of protein. Leucine metabolism in the fed state was measured before, immediately after, and 10 days after exercise, with intravenous L-[1-13C]leucine as a tracer (0.115 mumol.kg-1.min-1). Leucine flux increased 9% immediately after exercise (P less than 0.011) and remained elevated 10 days later, with no effect of age. Leucine oxidation increased 19% immediately after exercise and remained 15% above baseline 10 days after exercise (P less than 0.0001), with no effect of age. In the young men, urinary excretion of 3-methylhistidine per gram of creatinine did not increase until 10 days postexercise (P less than 0.05), but in the older men, it increased 5 days after exercise and remained high through 10 days postexercise (P less than 0.05), averaging 37% higher than in the young men. These data suggest that eccentric exercise produces a similar increase in whole body protein breakdown in older and young men, but myofibrillar proteolysis may contribute more to whole body protein breakdown in the older group.     

Effect of food intake on exercise fatigue in trained and untrained subjects

The effects of carbohydrate and fat intake on exercise-induced fatigue was investigated in 30 untrained--(VO2max of 40.6 +/- 2.7 ml X kg-1 X min-1) and 24 trained-subjects (VO2max of 52.3 +/- 2.7 ml X kg-1 X min-1) performing a 34 km march with a 25 kg backpack. Marching time was 8 1/2 h and 6 1/3 h in the untrained and trained-subjects respectively. The subjects were divided into 3 dietary groups. One group had free access to sugar cubes, the second group was offered almonds and the third one served as a control. Triglyceride levels decreased by 65 mg X dl-1 in untrained, and by 115 mg X dl-1 in trained subjects, while blood glucose remained at normal levels. In the untrained subjects, ingestion of almonds delayed the subjective sensation of exhaustion, while 50% of the controls and the sugar consuming subjects complained of exhaustion. The data suggest that ingestion of food containing fat delays exercise induced exhaustion or fatigue to a greater extent than does carbohydrate ingestion.     

Lymphocyte proliferation responses after exercise in men: fitness, intensity, and duration effects

This study investigated the effects of intensity and duration of exercise on lymphocyte proliferation as a measure of immunologic function in men of defined fitness. Three fitness groups--low [maximal O2 uptake (VO2max) = 44.9 +/- 1.5 ml O2.kg-1.min-1 and sedentary], moderate (VO2max = 55.2 +/- 1.6 ml O2.kg-1.min-1 and recreationally active), and high (VO2max = 63.3 +/- 1.8 ml O2.kg-1.min-1 and endurance trained)--and a mixed control group (VO2max = 52.4 +/- 2.3 ml O2.kg-1.min-1) participated in the study. Subjects completed four randomly ordered cycle ergometer rides: ride 1, 30 min at 65% VO2max; ride 2, 60 min at 30% VO2max; ride 3, 60 min at 75% VO2max; and ride 4, 120 min at 65% VO2max. Blood samples were obtained at various times before and after the exercise sessions. Lymphocyte responses to the T cell mitogen concanavalin A were determined at each sample time through the incorporation of radiolabeled thymidine [( 3H]TdR). Despite differences in resting levels of [3H]TdR uptake, a consistent depression in mitogenesis was present 2 h after an exercise bout in all fitness groups. The magnitude of the reduction in T cell mitogenesis was not affected by an increase in exercise duration. A trend toward greater reduction was present in the highly fit group when exercise intensity was increased. The reduction in lymphocyte proliferation to the concanavalin A mitogen after exercise was a short-term phenomenon with recovery to resting (preexercise) values 24 h after cessation of the work bout. These data suggest that single sessions of submaximal exercise transiently reduce lymphocyte function in men and that this effect occurs irrespective of subject fitness level.     

Effects of aging and training status on ventilatory response during incremental cycling exercise

The aim of this study was to examine the effect of aging and training status on ventilatory response during incremental cycling exercise. Eight young (24 ± 5 years) and 8 older (64 ± 3 years) competitive cyclists together with 8 young (27 ± 4 years) and 8 older (63 ± 2 years) untrained individuals underwent a continuous incremental cycling test to exhaustion to determine ventilatory threshold (VT), respiratory compensation point (RCP), and maximal oxygen uptake (VO?max). In addition, the isocapnic buffering (IB) phase was calculated together with the hypocapnic hyperventilation. Ventilatory threshold occurred at similar relative exercise intensities in all groups, whereas RCP was recorded at higher intensities in young and older cyclists compared to the untrained subjects. The IB phase, reported as the difference between VT and RCP and expressed either in absolute (ml·min?1·kg?1 VO?) or in relative terms, was greater (p < 0.01) in both young and older trained cyclists than in untrained subjects, who were also characterized by a lower exercise capacity. Isocapnic buffering was particularly small in the older untrained volunteers. Although young untrained and older trained subjects had a similar level of VO?max, older athletes exhibited a larger IB. In addition, a higher absolute but similar relative IB was observed in young vs. older cyclists, despite a higher VO?max in the former. In conclusion, the present study shows that aging is associated with a reduction of the IB phase recorded during an incremental exercise test. Moreover, endurance training induces adaptations that result in an enlargement of the IB phase independent of age. This information can be used for the characterization and monitoring of the physiological adaptations induced by endurance training.     

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.     

Effects of recovery beverages on glycogen restoration and endurance exercise performance

The restorative capacities of a high carbohydrate-protein (CHO-PRO) beverage containing electrolytes and a traditional 6% carbohydrate-electrolyte sports beverage (SB) were assessed after glycogen-depleting exercise. Postexercise ingestion of the CHO-PRO beverage, in comparison with the SB, resulted in a 55% greater time to exhaustion during a subsequent exercise bout at 85% maximum oxygen consumption (VO(2)max). The greater recovery after the intake of the CHO-PRO beverage could be because of a greater rate of muscle glycogen storage. Therefore, a second study was designed to investigate the effects of after exercise CHO-PRO and SB supplements on muscle glycogen restoration. Eight endurance-trained cyclists (VO(2)max = 62.1 +/- 2.2 ml.kg(-1) body wt.min(-1)) performed 2 trials consisting of a 2-hour glycogen-depletion ride at 65-75% VO(2)max. Carbohydrate-protein (355 ml; approximately 0.8 g carbohydrate (CHO).kg(-1) body wt and approximately 0.2 g protein.kg(-1) body wt) or SB (355 ml; approximately 0.3 g CHO.kg(-1) body wt) was provided immediately and 2 hours after exercise. Trials were randomized and separated by 7-15 days. Ingestion of the CHO-PRO beverage resulted in a 17% greater plasma glucose response, a 92% greater insulin response, and a 128% greater storage of muscle glycogen (159 +/- 18 and 69 +/- 32 micromol.g(-1) dry weight for CHO-PRO and SB, respectively) compared with the SB (p < 0.05). These findings indicate that the rate of recovery is coupled with the rate of muscle glycogen replenishment and suggest that recovery supplements should be consumed to optimize muscle glycogen synthesis as well as fluid replacement.     

Total nitrogen oxide following exercise testing reflects endothelial function and discriminates health status

Nitric oxide (NO) bioavailability is important in vascular health, but unsuitable as a clinical measure due to biological oxidation. Total nitrogen oxides (NO(x)) are stable but background nitrate levels make it difficult to detect disease-based variation. We investigated the clinical discriminatory value of NO(x) as it relates to exercise capability (VO(2peak)) and brachial artery reactivity (BAR, an NO-dependent measure of endothelial health), in healthy (H), increased risk (RF), and known cardiovascular disease (CVD) subjects. BAR was measured using forearm occlusion/hyperemia stimulus. Subjects performed a maximal graded exercise test (GXT). Blood at rest, exercise termination, and 10 min into recovery was mixed equally with 0.1 M NaOH at 4 degrees C, filtered, and stored at -70 degrees C. NO(x) was measured by chemiluminescence. Seven of the RF group then exercise-trained for 6 months prior to retesting. The H group (n = 12) was younger, had higher VO(2peak), HDL levels, and baseline NO(x) values than the RF (n = 15) and CVD (n = 10) groups. NO(x) increased from baseline to recovery in the H group only (75.85 +/- 19.04 microM vs 97.76 +/- 31.93 microM; P 相似文献   

Standards and predicted values of anaerobic threshold

Mean values for body size, body composition and endurance indices have been obtained from a homogeneous group of 125 physically active men to find predicted values of AT (age 23.4 +/- 4.3 years; height 175.9 +/- 6.5 cm; weight 72.2 +/- 8.9 kg; body fat 17.9 +/- 4.7% body weight, muscularity index 19.0 +/- 1.5 kg fat-free mass/cm2 X 10(-4) height; forced vital lung capacity 5667 +/- 815 cm3; VO2max 48.5 +/- 6.0 cm3 X kg-1 X min-1; anaerobic threshold 61.0 +/- 7.8% VO2max). Endurance performance and fitness indices were a little higher than average, but about 10% lower than in endurance-trained athletes. The authors suggest that standards of anaerobic threshold (AT) for ergonomics and endurance training should be about 55-65% VO2max, but not lower than 1800 cm3 O2 X min-1. The coefficients of correlation of AT relating to VO2max, PFO2 and submaximal load were significant at the 0.01 level. Using regression analysis, predicted values of AT were developed. A predicted value of AT can be obtained from the regression line of AT on Lsubmax used as a nomogram, during a simple PWC170 exercise test without blood or gas analysis.     

Effects of acute exercise and detraining on insulin action in trained men

Seven endurance-trained subjects [maximal O2 consumption (VO2max) 64 +/- 1 (SE) ml.min-1.kg-1] underwent sequential hyperinsulinemic euglycemic clamps on three occasions: 1) in the "habitual state" 15 h after the last training bout (C), 2) after 60 min of bicycle exercise at 72 +/- 3% of VO2max performed in the habitual state (E), and 3) 5 days after the last ordinary training session (detrained, DT). Sensitivity for insulin-mediated whole-body glucose uptake was not affected by acute exercise [insulin concentrations eliciting 50% of maximal insulin-mediated glucose uptake being 44 +/- 2 (C) vs. 46 +/- 3 (E) microU/ml] but was decreased after detraining (54 +/- 2 microU/ml, P less than 0.05) to levels comparable to those found in untrained subjects [Am. J. Physiol. 254 (Endocrinol. Metab. 17): E248-E259, 1988]. Near-maximal insulin-mediated glucose uptake (responsiveness) was higher than in untrained subjects and not influenced by acute exercise or detraining [13.4 +/- 1.2 (C), 12.2 +/- 0.9 (E), and 12.2 +/- 0.3 (DT) mg.min-1.kg-1]. Calculated by indirect calorimetry, the glucose-to-glycogen conversion was not influenced by E but was reduced during detraining (P less than 0.05) yet remained higher than previously found in untrained subjects (P less than 0.05). However, only on E days did muscle glycogen increase during insulin infusion. Glycogen synthase activity was increased on E and decreased on DT compared with C days.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of inhaled nitric oxide on gas exchange during normoxic and hypoxic exercise in highly trained cyclists.

This study tested the effects of inhaled nitric oxide [NO; 20 parts per million (ppm)] during normoxic and hypoxic (fraction of inspired O(2) = 14%) exercise on gas exchange in athletes with exercise-induced hypoxemia. Trained male cyclists (n = 7) performed two cycle tests to exhaustion to determine maximal O(2) consumption (VO(2 max)) and arterial oxyhemoglobin saturation (Sa(O(2)), Ohmeda Biox ear oximeter) under normoxic (VO(2 max) = 4.88 +/- 0.43 l/min and Sa(O(2)) = 90.2 +/- 0.9, means +/- SD) and hypoxic (VO(2 max) = 4.24 +/- 0.49 l/min and Sa(O(2)) = 75.5 +/- 4.5) conditions. On a third occasion, subjects performed four 5-min cycle tests, each separated by 1 h at their respective VO(2 max), under randomly assigned conditions: normoxia (N), normoxia + NO (N/NO), hypoxia (H), and hypoxia + NO (H/NO). Gas exchange, heart rate, and metabolic parameters were determined during each condition. Arterial blood was drawn at rest and at each minute of the 5-min test. Arterial PO(2) (Pa(O(2))), arterial PCO(2), and Sa(O(2)) were determined, and the alveolar-arterial difference for PO(2) (A-aDO(2)) was calculated. Measurements of Pa(O(2)) and Sa(O(2)) were significantly lower and A-aDO(2) was widened during exercise compared with rest for all conditions (P < 0.05). No significant differences were detected between N and N/NO or between H and H/NO for Pa(O(2)), Sa(O(2)) and A-aDO(2) (P > 0.05). We conclude that inhalation of 20 ppm NO during normoxic and hypoxic exercise has no effect on gas exchange in highly trained cyclists.     

Blood pressure and plasma catecholamine responses to various challenges during exercise-recovery in man

The purpose of this study was to assess the effects of a 2 h cycle exercise (50% VO2max) on heart rate (HR) and blood pressure (BP), and on plasma epinephrine (E) and norepinephrine (NE) concentrations, during the recovery period in seven normotensive subjects. Measurements were made at rest in supine (20 min) and standing (10 min) positions, during isometric exercise (hand-grip, 3 min, 25% maximal voluntary, contraction), in response to a mild psychosocial challenge (Stroop conflicting color word task) and during a 5-min period of light exercise (42 +/- 3% VO2max). Data were compared to measurements taken on another occasion under similar experimental conditions, without a previous exercise bout (control). The results showed HR to be slightly elevated in all conditions following the exercise bout. However, diastolic and systolic BP during the recovery period following exercise were not significantly different from the values observed in the control situation. Plasma NE concentrations in supine position and in response to the various physiological and/or psychosocial challenges were similar in the control situation and during the recovery period following exercise. On the other hand plasma E (nmol.1-1) was about 50% lower at rest (0.11 +/- 0.03 vs 0.23 +/- 0.04) as well as in response to hand-grip (0.21 +/- 0.04 vs 0.41 +/- 0.20) and the Stroop-test (0.21 +/- 0.05 vs 0.41 +/- 0.15) following the exercise bout.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity.

This study investigates whether a 6-wk intermittent hypoxia training (IHT), designed to avoid reductions in training loads and intensities, improves the endurance performance capacity of competitive distance runners. Eighteen athletes were randomly assigned to train in normoxia [Nor group; n = 9; maximal oxygen uptake (VO2 max) = 61.5 +/- 1.1 ml x kg(-1) x min(-1)] or intermittently in hypoxia (Hyp group; n = 9; VO2 max = 64.2 +/- 1.2 ml x kg(-1) x min(-1)). Into their usual normoxic training schedule, athletes included two weekly high-intensity (second ventilatory threshold) and moderate-duration (24-40 min) training sessions, performed either in normoxia [inspired O2 fraction (FiO2) = 20.9%] or in normobaric hypoxia (FiO2) = 14.5%). Before and after training, all athletes realized 1) a normoxic and hypoxic incremental test to determine VO2 max and ventilatory thresholds (first and second ventilatory threshold), and 2) an all-out test at the pretraining minimal velocity eliciting VO2 max to determine their time to exhaustion (T(lim)) and the parameters of O2 uptake (VO2) kinetics. Only the Hyp group significantly improved VO2 max (+5% at both FiO2, P < 0.05), without changes in blood O2-carrying capacity. Moreover, T(lim) lengthened in the Hyp group only (+35%, P < 0.001), without significant modifications of VO2 kinetics. Despite similar training load, the Nor group displayed no such improvements, with unchanged VO2 max (+1%, nonsignificant), T(lim) (+10%, nonsignificant), and VO2 kinetics. In addition, T(lim) improvements in the Hyp group were not correlated with concomitant modifications of other parameters, including VO2 max or VO2 kinetics. The present IHT model, involving specific high-intensity and moderate-duration hypoxic sessions, may potentialize the metabolic stimuli of training in already trained athletes and elicit peripheral muscle adaptations, resulting in increased endurance performance capacity.     

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.