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1.
Previously, we examined the effects of carbohydrate (CHO) ingestion on glucose kinetics during exercise at 70% of maximum O2 uptake ( O2,max). Here we repeat those studies in heavier cyclists (n=6 per group) cycling for 3 h at a similar absolute O2 uptake but at a lower (55% of O2,max) relative exercise intensity. During exercise, the cyclists were infused with a 2-3H-glucose tracer and ingested U-14C glucoselabelled solutions of either flavoured water (H2O) or 10 g/100 ml glucose polymer, at a rate of 600 ml/h. Two subjects in the H2O trial fatigued after 2.5 h of exercise. Their rates of glucose appearance (R a) declined from 2.9±0.6 to 2.0±0.1 mmol/min (mean ± SEM) and, as their plasma glucose concentration [Glu] declined from 4.7±0.2 to below 3.5±0.2 mM, their rates of glucose oxidation (R ox) and fat oxidation plateaued at 2.7±0.4 and 1.7±0.1 mmol/min respectively. In contrast, all subjects completed the CHO trial. Although CHO ingestion during exercise reduced the final endogenousR a from 3.4±0.6 to 0.9±0.3 mmol/min at the end of exercise, it increased totalR a to 5.5±0.5 mmol/min (P<0.05). A higher totalR a with CHO ingestion raised [Glu] from 4.3±0.3 to 5.3±0.1 mM and acceleratedR ox from 3.5±0.2 to 5.9±0.2 mmol/min after 180 min of exercise (P<0.05). The increased contribution to total energy production from glucose oxidation (34±1 vs. 20±1 %) decreased energy production from fat oxidation from 51±2 to 40±5% (P=0.08) and produced patterns of glucose, muscle glycogen (plus lactate) and fat utilisation similar to those during exercise at 70% of ( O2,max). Thus, CHO ingestion is necessary to sustain even prolonged, low to moderate intensity exercise and when ingested, it suppresses the higher relative rates of fat oxidation usually observed at exercise intensities less than 60% of O2,max.  相似文献   

2.
Carbohydrate (CHO) ingestion during short-term recovery from prolonged running has been shown to increase the capacity for subsequent exercise in a warm environment. The aim of this study was to examine the effects of the amount of glucose given during recovery on substrate storage and utilisation during recovery and subsequent exercise in a warm environment. A group of 11 healthy male volunteers took part in two experiments in a controlled warm environment (35°C, 40% relative humidity), 1 week apart. On each occasion the subjects completed two treadmill runs (T1 and T2) at a speed equivalent to 60% of maximal oxygen uptake, for 90 min, until they were fatigued, or until aural temperature (T aur) reached 39°C. The two runs were separated by a 4 h recovery period (REC), during which subjects consumed 55 g of naturally enriched [U-13C]-glucose in the form of a 7.5% carbohydrate-electrolyte solution (CES, mass of solution 667 g) immediately after T1. The subjects then consumed either: the same quantity of CES, or an equivalent volume of an electrolyte placebo, at 60, 120 and 180 min during REC, providing a total of 220 g (C220) or 55 g (C55) of [U-13C]-glucose, respectively. Expired gases were collected at 15 min intervals during exercise and 60 min intervals during REC, for determination of total CHO and fat oxidation by indirect respiratory calorimetry, and orally ingested [U-13C]-glucose oxidation, estimated from the 13C:12C ratio of expired CO2. Substrate metabolism did not differ between conditions during T1. Despite the fact that total CHO (P<0.05) and ingested glucose oxidation (P<0.01) were greater during REC of the C220 condition, glycogen synthesis was estimated to be approximately fivefold greater (P<0.01) than in the C55 condition. During T2 the rate of total CHO oxidation was higher (P<0.01) and total fat oxidation lower (P<0.01) at all times during the C220 compared to the C55 condition. The greater CHO oxidation during C220 appeared to be met from ingested sources, as the rate of [U-13C]-glucose oxidation was greater (P<0.01) at all times during T2, compared to C55. Whilst more of the ingested substrate remained unoxidised on completion of T2 during C220, exercise duration was similar in the two experimental conditions, and was limited by thermoregulatory incapacity (T aur>39°C) rather than substrate availability per se. Electronic Publication  相似文献   

3.
Advancing age is associated with changes in fat and carbohydrate (CHO) metabolism, which is considered a risk factor for cardiovascular disease and diabetes. The effects of exercise intensity and duration on fat and CHO metabolism in elderly male subjects were investigated in the present study. Seven trained (63.7 ± 4.7 years) and six untrained (63.5 ± 4.5 years) healthy males performed three 30 min trials on a cycle ergometer at 50, 60 and 70% and two other trials at 60 and 70% in which the total energy expenditure was equal to that for 30 min at 50% Respiratory measures were undertaken throughout the exercise and blood samples taken before and immediately after each trial. Statistical analyses revealed a significant effect of exercise intensity on fat oxidation when the exercise durations were equated as well as when the energy expenditure was held constant for the three trials, though no training effect was noted. Total carbohydrate oxidation increased significantly with exercise intensity (P < 0.05) and with training. Significantly higher levels of non-esterified free fatty acid (NEFA) and glycerol were observed for trained compared with untrained though not for B-hydroxybutyrate (3-OH) or insulin. No differences in NEFA, glycerol, 3-OH were evident for increases in exercise intensity. Carbohydrate and fat oxidation are significantly affected by exercise intensity in elderly males, although only CHO oxidation is influenced by training. Furthermore, training-induced increases in the availability of NEFA and glycerol are not associated with an increase in fat oxidation, rather an increase in CHO oxidation.  相似文献   

4.
Summary Changes in levels of plasma lactate, pyruvate, glucose, free fatty acids (FFA), glycerol and 3-hydroxybutyrate during muscular exercise and recovery in cool (ambient temperature T a = 23 C and water vapor pressure P w = 13 mb) and hot environments (T a = 40 C, P w = 30 mb) were measured in six subjects. Arterial blood samples were collected at fixed time intervals during an initial resting phase of 75 min, an exercise period of 20 min and a recovery period of 125 min. Exercise consisted in pedaling a bicycle ergometer in the supine position at a work load that raised the heart pulse rate to nearly 140 beats min–1 in the cool condition. Heart rate and rectal temperature were significantly higher during exercise and recovery in the hot environment. For samples collected at corresponding times in the cool and the hot conditions, the deviations of the observed blood parameters from their mean values during the whole resting phase seldom differed. However, for the exercise phase as a whole, the mean increases of lactate, pyruvate and glycerol were significantly greater and the mean decrease of glucose significantly smaller, in the hot condition, while the mean decreases of FFA and 3-hydroxybutyrate did not differ significantly. Related to their corresponding mean resting values, the mean changes in all six blood parameters measured were significantly larger during recovery in the hot condition than in the cool. These results verify the enhanced anaerobic metabolism in hot environment already described by previous authors, and show an adipokinetic and hyperglycemic effect of acute exposure to heat.  相似文献   

5.
 The hypothesis that high-intensity (HI) intermittent exercise impairs mitochondrial function was investigated with different microtechniques in human muscle samples. Ten male students performed three bouts of cycling at 130% of peak O2 consumption (V ·O2,peak). Muscle biopsies were taken from the vastus lateralis muscle at rest, at fatigue and after 110 min recovery. Mitochondrial function was measured both in isolated mitochondria and in muscle fibre bundles made permeable with saponin (skinned fibres). In isolated mitochondria there was no change in maximal respiration, rate of adenosine 5’-triphosphate (ATP) production (measured with bioluminescence) and respiratory control index after exercise or after recovery. The ATP production per consumed oxygen (P/O ratio) also remained unchanged at fatigue but decreased by 4% (P<0.05) after recovery. In skinned fibres, maximal adenosine 5’-diphosphate (ADP)-stimulated respiration increased by 23% from rest to exhaustion (P<0.05) and remained elevated after recovery, whereas the respiratory rates in the absence of ADP and at 0.1 mM ADP (submaximal respiration) were unchanged. The ratio between respiration at 0.1 and 1 mM ADP (ADP sensitivity index) decreased at fatigue (P<0.05) but after the recovery period was not significantly different from that at rest. It is concluded that mitochondrial oxidative potential is maintained or improved during exhaustive HI exercise. The finding that the sensitivity of mitochondrial respiration to ADP is reversibly decreased after strenuous exercise may indicate that the control of mitochondrial respiration is altered. Received: 17 June 1998 / Received after revision: 11 November 1998 / Accepted: 26 November 1998  相似文献   

6.
To determine the limits to oxidation of exogenous glucose by skeletal muscle, the effects of euglycaemia (plasma glucose 5 mM, ET) and hyperglycaemia (plasma glucose 10 mM, HT) on fuel substrate kinetics were evaluated in 12 trained subjects cycling at 70% of maximal oxygen uptake (VO2, max) for 2 h. During exercise, subjects ingested water labelled with traces of U-14C-glucose so that the rates of plasma glucose oxidation (R ox) could be determined from plasma 14C-glucose and expired 14CO2 radioactivities, and respiratory gas exchange. Simultaneously, 2-3H-glucose was infused at a constant rate to estimate rates of endogenous glucose turnover (R a), while unlabelled glucose (25% dextrose) was infused to maintain plasma glucose concentration at either 5 or 10 mM. During ET, endogenous liver glucose R a (total R a minus the rate of infusion) declined from 22.4±4.9 to 6.5±1.4 mol/min per kg fat-free mass [FFM] (P<0.05) and during HT it was completely suppressed. In contrast, R ox increased to 152±21 and 61±10 mol/min per kg FFM at the end of HT and ET respectively (P<0.05). HT (i. e., plasma glucose 10 mM) and hyperinsulinaemia (24.5±0.9 U/ml) also increased total carbohydrate oxidation from 203±7 (ET) to 310±3 mol/min per kg FFM (P<0.0001) and suppressed fat oxidation from 51±3 (ET) to 18±2 mol/min per kg FFM (P<0.0001). As the rates of oxidation at more physiological euglycaemic concentrations of glucose were limited to 92±9 mol/ min per kg FFM, and were similar to those reported when carbohydrate is ingested, the results of the current study suggest that the concentrations of glucose and insulin normally present during prolonged, intense exercise may limit the rate of muscle glucose uptake and oxidation.  相似文献   

7.
To determine if bypassing both intestinal absorption and hepatic glucose uptake by intravenous glucose infusion might increase the rate of muscle glucose oxidation above 1 g · min–1, ten endurance-trained subjects were studied during 125 min of cycling at 70% of peak oxygen uptake (VO2 peak). During exercise the subjects ingested either a 15 g · 100 ml–1 U-14C labelled glucose solution or H2O labelled with a U-14C glucose tracer for the determination of the rates of plasma glucose oxidation (Rox) and exogenous carbohydrate (CHO) oxidation from plasma14C glucose and14CO2 specific activities, and respiratory gas exchange. Simultaneously, 2-3H glucose was infused at a constant rate to measure glucose turnover, while unlabelled glucose (25% dextrose) was infused into those subjects not ingesting glucose to maintain plasma glucose concentration at 5 mmol · l–1. Despite similar plasma glucose concentrations [ingestion 5.3 (SEM 0.13) mmol · l–1; infusion 5.0 (0.09) mmol · l–1], compared to glucose infusion, CHO ingestion significantly increased plasma insulin concentrations [12.9 (1.0) vs 4.8 (0.5) mU · l–1;P<0.05], raised total Rox values [9.5 (1.2) vs 6.2 (0.7) mmol · 125 min–1 kg fat free mass–1 (FFM);P<0.05] and rates of CHO oxidation [37.2 (2.8)vs 24.1 (3.9) mmol · 125 min–1 kg FFM–1;P<0.05]. An increased reliance on CHO metabolism with CHO ingestion was associated with a decrease in fat oxidation. Whereas the contribution from fat oxidation to energy production increased to 51 (10)% with glucose infusion, it only reached 18 (4)% with glucose ingestion (P<0.05). Despite these differences in plasma insulin concentration and rates of fat oxidation, the rates of glucose oxidation by muscle were similar after 125 min of exercise for both trials [ingestion 93 (8); infusion 85 (5) mol · min–1 kg FFM–1], suggesting that peak rates of muscle glucose oxidation were primarily dependent on blood glucose concentration which, in turn, regulated the hepatic appearance of ingested CHO.  相似文献   

8.
 The applicability of H2 15O-positron emission tomographic (PET) imaging for the assessment of skeletal muscle perfusion during exercise was investigated in five healthy subjects performing intermittent isometric contractions on a calf ergometer. The workload of the left calf muscles was kept constant in all exercises, while that of the right calf muscles was varied. During exercise H2 15O distribution in the calf muscles was measured by PET. Radioactivity measured in the left calf muscles was used as a reference for the radioactivity measured in the right calf muscles. In all studies, muscles were delineated by uptake of radioactivity. Four subjects demonstrated high radioactivity in the gastrocnemius medialis muscle, in one subject high radioactivity was distributed over the triceps surae muscles. The observed muscles demonstrated also local foci of radioactivity indicating regionally enhanced tissue perfusion. The right-left ratio of radioactivity in the active muscles increased as a function of the load. We conclude that inter- and intramuscle perfusion differences can be measured during exercise by H2 15O-PET imaging. Received: 30 January 1998 / Received after revision and accepted: 9 June 1998  相似文献   

9.

Background

Protein-rich weight-loss diets spare fat-free mass at the cost of fat mass. The objective was to examine if there is a change in stimulated fat oxidation related to protein intake during stable body weight.

Methods

Subjects' (BMI 22 ± 2 kg/m2, age 25 ± 8 years) maximal fat oxidation (Fatmax) was assessed during a graded bicycle test, before and after a 3-month dietary-intervention of 2 MJ/day supplements exchanged with 2 MJ/d of habitual energy intake. The parallel design consisted of protein-rich supplements in the protein group and an isocaloric combination of carbohydrate and fat supplements in the control group. Daily protein intake was determined according to 24-h urine nitrogen. Body composition was measured according to a 4-compartment model by a combination of underwater-weighing technique, deuterium-dilution technique and whole-body dual-energy X-ray absorptiometry (DXA).

Results

Subjects were weight stable and did not change their physical activity. The protein group (n = 12) increased protein intake (11 ± 14 g, P < 0.05) and had significantly higher daily protein intake vs. control (n = 4) (80 ± 21 vs.59 ± 11 g, P < 0.05). Fatmax increased significantly in the protein group (0.08 ± 0.08 g/min, P < 0.01). Fat-free mass increased independent of change in body weight (P < 0.01), and fat mass and fat percentage decreased (P < 0.05). Change in Fatmax was a function of change in protein intake (r = 0.623, P < 0.05), and not of changes in body composition or VO2max.

Conclusion

Increased stimulated fat oxidation was related to increased protein intake.  相似文献   

10.
 It is known that acute physical exercise may have diverse pathophysiological consequences in various organs due to free radical formation. We have investigated whether a period of anaerobic running to exhaustion in rats results in oxidative modification of proteins in the lungs. Six rats of an exercised group (E) ran for two periods of 5 min at a speed of 30 m·min–1 followed by a recovery period of 5 min, and then by a third period of running to exhaustion. Reactive carbonyl derivatives (RCD) were measured by the Western blot technique on lungs of E and control (C) rats. In addition, the activity of glutamine synthetase (GS) was also monitored as marker of oxidative damage to proteins. This investigation revealed significant exercise-induced increases in accumulation of RCD in the lungs of the E group compared with the C group. The RCD signals were visibly stronger in proteins with molecular weight of 55 kDa and 32 kDa. The activity of GS was higher by about 30% in E rats than in C rats. The present data suggest that anaerobic exercise induces protein oxidation in the lungs. Received: 1 August 1997 / Accepted: 13 November 1997  相似文献   

11.
The primary aim of the study was to examine substrate metabolism during combined passive and active exercise in individuals with spinal cord injury (SCI). Nine men and women with SCI (mean age 40.6 ± 3.4 years) completed two trials of submaximal exercise 1 week apart. Two maintained a complete injury and seven had an incomplete injury. Level of injury ranged from thoracic (T4–T6 and T10) to cervical (four C5–C6 and three C6–C7 injuries). During two bouts separated by 1 week, subjects completed two 30 min sessions of active lower-body and passive upper-body exercise, during which heart rate (HR) and gas exchange data were continuously assessed. One-way analysis of variance with repeated measures was used to examine differences in all variables over time. Results demonstrated significant increases (P < 0.05) in HR and oxygen uptake (VO2) from rest to exercise. Respiratory exchange ratio (RER) significantly increased (P < 0.05) during exercise from 0.85 ± 0.02 at rest to 0.95 ± 0.01 at the highest cadence, reflecting increasing reliance on carbohydrate from 50.0 to 83.0% of energy metabolism. Data demonstrate a large reliance on carbohydrate utilization during 30 min of exercise in persons with SCI, with reduced contribution of lipid as exercise intensity was increased. Strategies to reduce carbohydrate utilization and increase lipid oxidation in this population should be addressed.  相似文献   

12.
These studies investigated the effects of 2 weeks of either a high-fat (HIGH-FAT: 70% fat, 7% CHO) or a high-carbohydrate (HIGH-CHO: 74% CHO, 12% fat) diet on exercise performance in trained cyclists (n = 5) during consecutive periods of cycle exercise including a Wingate test of muscle power, cycle exercise to exhaustion at 85% of peak power output [90% maximal oxygen uptake ( O2max), high-intensity exercise (HIE)] and 50% of peak power output [60% O2max, moderate intensity exercise (MIE)]. Exercise time to exhaustion during HIE was not significantly different between trials: nor were the rates of muscle glycogen utilization during HIE different between trials, although starting muscle glycogen content was lower [68.1 (SEM 3.9) vs 120.6 (SEM 3.8) mmol · kg –1 wet mass, P < 0.01] after the HIGH-FAT diet. Despite a lower muscle glycogen content at the onset of MIE [32 (SEM 7) vs 73 (SEM 6) mmol · kg –1 wet mass, HIGH-FAT vs HIGH-CHO, P < 0.01], exercise time to exhaustion during subsequent MIE was significantly longer after the HIGH-FAT diet [79.7 (SEM 7.6) vs 42.5 (SEM 6.8) min, HIGH-FAT vs HIGH-CHO, P<0.01]. Enhanced endurance during MIE after the HIGH-FAT diet was associated with a lower respiratory exchange ratio [0.87 (SEM 0.03) vs 0.92 (SEM 0.02), P<0.05], and a decreased rate of carbohydrate oxidation [1.41 (SEM 0.70) vs 2.23 (SEM 0.40) g CHO · min–1, P<0.05]. These results would suggest that 2 weeks of adaptation to a high-fat diet would result in an enhanced resistance to fatigue and a significant sparing of endogenous carbohydrate during low to moderate intensity exercise in a relatively glycogen-depleted state and unimpaired performance during high intensity exercise.  相似文献   

13.
Summary Four subjects were studied during exercise at 50% of maximum oxygen uptake after a normal diet, after a low carbohydrate (CHO) diet following exercise-induced glycogen depletion, and after a high CHO diet. This regime has previously been shown to cause changes in the amount of glycogen stored in the exercising muscles. Metabolic and respiratory parameters were measured during the exercise. The respiratory exchange ratio, blood lactate, blood pyruvate, blood glucose and plasma triglycerides were lower than normal following the low CHO diet and higher than normal following the high CHO diet. Plasma free fatty acids and plasma glycerol were higher than normal after the low CHO diet and lower than normal after the high CHO diet. The contribution of CHO to metabolism was less than normal after the low CHO diet and greater than normal after the high CHO diet. The altered availability of FFA does not appear to be a result of the variations in the blood lactate content. R. J. M. is in receipt of a Science Research Council Postgraduate Studentship award  相似文献   

14.
This report describes the effects of 9 weeks of endurance-training on the relative rates of lactate removal via oxidation and gluconeogenesis in humans. Before and after training, eight subjects performed incremental (60 W plus 40 W every 6 min) exercise tests, while14C-lactate was infused into one forearm vein and arterialized venous blood was sampled from the other forearm. During the trial, the volume of expired14CO2 and circulating14C-lactate and14C-glucose specific radioactivities were measured. Such measurements revealed that training increased the estimated oxidation of equivalent venous blood lactate concentrations [VLa] of greater than 1.6 mmol/l. These increases in lactate oxidation were more than would be predicted from the approximately 40% higher O2 uptake values at any [VLa] after training. At a [VLa] of 6 mmol/l, rates of lactate oxidation were increased by some 100% following training, from 105±12 to 208±33 mol/min/kg (P<0.01). Improvements in lactate oxidation after training reduced the estimated rates of lactate-to-glucose conversion from 40±3 to 9±2 mol/min/kg at a [VLa] of 2.5 mmol/l (P<0.01). Thus, unlike in rats, human endurance-training does not increase gluconeogenesis. In the final stages of progressive exercise after training, more than 80% of lactate was oxidised and accounted for approximately 45% of overall carbohydrate oxidation.  相似文献   

15.
 To analyse the effect of obesity on exercise-derived heat dissipation, lean and obese Zucker rats were exercised on an inclined treadmill until they would no longer run with gentle prodding. We measured their oxygen consumption, water vapour loss, the concentrations of adenosine tri- and diphosphate, creatine phosphate, and lactate in quick-frozen leg muscles, and the temperature of muscle, skin and blood in the aorta. We determined blood flow to leg muscle, fat and skin by measuring the entrapment of fluorescent microspheres. From the measurements we calculated heat flow rates between hind leg muscle, blood, fat and skin and the environment. The obese rats weighed twice as much as the lean (340–400 g and 175–200 g respectively) and ran half as fast (113 ± 7 m versus 257 ± 17 m). The differences between the two groups for basal oxygen consumption (lean: 6.7 ± 0.9 μmol/min, obese: 5.0 ± 1.9 μmol/min) and exercising oxygen consumption (lean: 37.8 ± 5.6 μmol/min, obese: 22.2 ± 3.8 μmol/min) were not significant. Both groups stopped running after the same time at their maximal speed (lean: 4.5 ± 0.3 min, obese: 4.2 ± 0.2 min). During exercise, lean rats had higher increases in core temperature (lean: 0.7°C, obese: 0.4°C) and muscle temperatures (lean: 1.3°C, obese: 0.7°C) than the obese rats. The calculated heat flows indicated a predominant conductive transfer of heat from muscle through the skin in lean rats but a higher proportion of heat transfer to the blood in obese rats. It is concluded that muscle heat accumulation did not cause fatigue in either case. Received: 30 July 1997 / Received after revision: 24 October 1997 / Accepted: 27 October 1997  相似文献   

16.
Summary We studied rates of exogenous carbohydrate (CHO) oxidation during 90 min of cycling exercise in trained cyclists exercising at 70% of maximal oxygen consumption (VO2max) when they ingested glucose, sucrose, or glucose polymer solutions at concentrations of 7.5%, 10% or 15%. Drinks were labelled with [U-14C]glucose or sucrose and were ingested at a rate of 100 ml · 10 min–1. Rates of oxidation of the ingested CHO were calculated from the specific radio-activity of the labelled CHO, expired14CO2 and carbon dioxide output (VCO2). Total CHO oxidation, determined from oxygen consumption andVCO2 was not influenced by CHO type or concentration. Gastric emptying (P=0.01) and the rate of exogenous CHO oxidation (P=0.028) was greatest for the glucose polymer solutions, and least for glucose. Although gastric emptying (P=0.006) decreased with increasing CHO concentration, CHO delivery to the intestine and exogenous CHO oxidation increased linearly with increasing CHO concentration. The percentage of the CHO delivered to the intestine that was oxidized ranged from 30.0% for 7.5% CHO to 38.1% for 15% CHO. Our results indicated that the rate of gastric emptying for CHO was not controlled to provide a constant rate of energy delivery as is commonly believed and that factors subsequent to gastric emptying limit the rate of exogenous CHO oxidation from the ingested solution.  相似文献   

17.
18.
 In this study we investigated the contribution of diffusion limitation to the exercise-induced hypoxaemia in interstitial lung disease (ILD). We applied isotopic analysis to the composition of the stable isotopic oxygen molecules 16O2 and 16O18O in expiratory gas mixtures obtained from six ILD patients and six healthy subjects at rest and during ergometer work (60 W). The changes in the 16O18O/16O2 ratios were interpreted by using the overall fractionation factor of respiration (α O) which would be increased towards 1.03 on increasing diffusion limitation. In addition, the O2 partial pressures of alveolar gas and arterial blood (P AO2, P aO2) were determined. In the patients, α O was significantly reduced from 1.0066 ± 0.0004 (mean ± SD) at rest to 1.0035 ± 0.0004 during exercise and in the healthy subjects from 1.0072 ± 0.0008 to 1.0044 ± 0.0004. Furthermore, the exercise-induced reduction of P aO2 (from 77 to 69 mmHg) was due to a drop of alveolar PO2 found in each patient, whereas in each healthy subject P aO2 was increased on exercise. On the basis of a resistance model we conclude that the patients’ data were inconsistent with increasing diffusion limitation but showed an increasing impairment of O2 transport by ventilation. Received: 18 September 1997 / Received after revision: 20 November 1997 / Accepted: 26 November 1997  相似文献   

19.
The influence of glucose ingestion on substrate utilization during prolonged exercise in children and adolescents is currently unknown. In the present study we determined the effect of intermittent exogenous glucose (GLUexo) ingestion on substrate utilization during prolonged exercise, in adolescent boys ages 13–17 years. Healthy untrained volunteers performed four 30-min exercise bouts on a cycle ergometer, separated by 5-min rest periods (≅60% maximum O2 consumption), on two occasions spaced 1–4 weeks apart. Two trials were performed, a control trial (CT), in which subjects ingested water intermittently during the exercise, and a glucose trial (GT), in which subjects ingested a 13C-enriched GLUexo drink (≅3 g glucose · kg body mass−1), also intermittently during the exercise. Total free fatty acids (FATtotal), glucose (GLUtotal) and carbohydrate (CHOtotal) oxidation was determined from indirect calorimetry, while GLUexo oxidation was calculated from the 13C/12C ratio in expired air after 5–10 min and 25–30 min of exercise in each bout. Heart rate and rating of perceived exertion (RPE) were determined at the same time intervals. The oxidation of CHOtotal was 169.1 (12.9) g · 120 min−1 and 203.1 (15.9) g · 120 min−1 (P < 0.01) and that of FATtotal was 31.0 (4.2) g · 120 min−1 and 17.1 (2.5) g · 120 min−1 (P < 0.01) in CT and GT, respectively. GLUexo oxidation in GT was 57.8 (4.3) g · 120 min−1, or 34.2 (2.2)% of that ingested. Endogenous glucose oxidation was 169.1 (12.9) g · 120 min−1 and 145.3 (11.9) g · 120 min−1 (P < 0.01) in CT and GT, respectively. Insulin and glucose concentrations were higher in GT than in CT by 226% and 37%, respectively (both P < 0.05). Free fatty acids and glycerol concentrations were lower in GT than in CT, by 27% and 79%, respectively (both P < 0.05). Heart rate was similar between trials, but RPE was lower in GT vs CT at both 115 and 135 min. Thus, under these experimental conditions, GLUexo intake spares endogenous carbohydrate and fat by 16% and 45%, respectively, contributes to approximately 25% of the total energy demand of exercise, and lowers the RPE. Accepted: 21 May 2000  相似文献   

20.
On two occasions, six well-trained, male competitive triathletes performed, in random order, two experimental trials consisting of either a timed ride to exhaustion on a cycle ergometer or a run to exhaustion on a motor-driven treadmill at 80% of their respective peak cycling and peak running oxygen (VO2max) uptakes. At the start of exercise, subjects drank 250 ml of a 15 g·100 ml–1 w/v [U-14C]glucose solution and, thereafter, 150 ml of the same solution every 15 min. Despite identical metabolic rates [VO2 3.51 (0.06) vs 3.51 (0.10) 1·min–1; values are mean (SEM) for the cycling and running trials, respectively], exercise times to exhaustion were significantly longer during cycling than running [96 (14) vs 63 (11) min; P < 0.05]. The superior cycling than running endurance was not associated with any differences in either the rate of blood glucose oxidation [3.8 (0.1) vs 3.9 (0.4) mmol· min–1], or the rate of ingested glucose oxidation [2.0 (0.1) vs 1.7 (0.2) mmol· min–1] at the last common time point (40 min) before exhaustion, despite higher blood glucose concentrations at exhaustion during running than cycling [7.0 (0.9) vs 5.8 (0.5) mmol·1–1; P < 0.05]. However, the final rate of total carbohydrate (CHO) oxidation was significantly greater during cycling than running [24.0 (0.8) vs 21.7 (1.4) mmol C6·min–1; P < 0.01]. At exhaustion, the estimated contribution to energy production from muscle glycogen had declined to similar extents in both cycling and running [68 (3) vs 65 (5)%]. These differences between the rates of total CHO oxidation and blood glucose oxidation suggest that the direct and/or indirect (via lactate) oxidation of muscle glycogen was greater in cycling than running.  相似文献   

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