Effect of elevated FFA on carbohydrate and lipid oxidation during prolonged exercise in humans

Increased availability of circulating free fatty acids (FFA) inhibits the rate of glycolysis in heart and resting skeletal muscle (Randle effect). Whether elevated FFA may play a role in decreasing carbohydrate oxidation during prolonged exercise in humans is more controversial. Using respiratory exchange measurements, we measured substrate utilization during 2.5 h of exercise at approximately 44 +/- 1% maximal O2 uptake (VO2 max) in the presence or absence of elevated FFA levels. After 30 min of base-line determinations, 1,000 U heparin was given intravenously and a 3-h constant infusion of Intralipid 10% (150 g/h) and heparin (500 U/h) was started. After an additional 30 min of rest, subjects exercised for 2.5 h (study 1, n = 6). In another five subjects (study 2) 100 g glucose was ingested after 30 min of exercise. The same protocols (studies 1 and 2) were also performed during a 0.9%-saline infusion. During exercise, without glucose ingestion, higher FFA concentrations prevailed during the Intralipid infusion (1,122 +/- 40 vs. 782 +/- 65 mumol/l), but the relative contributions of carbohydrate (49 +/- 4 vs. 50 +/- 4%) or lipid (49 +/- 4 vs. 47 +/- 6%) oxidation to the total energy expenditure were different only during the first 30 min of exercise. Similarly, higher FFA levels (1,032 +/- 62 vs. 568 +/- 46 mumol/l) did not alter the relative contributions of carbohydrate (62 +/- 4 vs. 69 +/- 2%) or lipid (36 +/- 4 vs. 29 +/- 2%) oxidation to the total energy expenditure after glucose feeding.(ABSTRACT TRUNCATED AT 250 WORDS)     

Separate and combined effects of exercise training and weight loss on exercise efficiency and substrate oxidation

Perturbations in body weight have been shown to affect energy expenditure and efficiency during physical activity. The separate effects of weight loss and exercise training on exercise efficiency or the proportion of energy derived from fat oxidation during physical activity, however, are not known. The purpose of this study was to determine the separate and combined effects of exercise training and weight loss on metabolic efficiency, economy (EC), and fat oxidation during steady-state moderate submaximal exercise. Sixty-four sedentary older (67 +/- 0.5 yr) overweight to obese (30.7 +/- 0.4 kg/m(2)) volunteers completed 4 mo of either diet-induced weight loss (WL; n = 11), exercise training (EX; n = 36), or the combination of both interventions (WLEX; n = 17). Energy expenditure, gross efficiency (GE), EC, and proportion of energy expended from fat (EF) were determined during a 1-h submaximal (50% of peak aerobic capacity) cycle ergometry exercise before the intervention and at the same absolute work rate after the intervention. We found that EX increased GE by 4.7 +/- 2.2%. EC was similarly increased by 4.2 +/- 2.1% by EX. The addition of concomitant WL to EX (WLEX) resulted in greater increases in GE (9.0 +/- 3.3%) compared with WL alone but not compared with EX alone. These effects remained after adjusting for changes in lean body mass. The proportion of energy derived from fat during the bout of moderate exercise increased with EX and WLEX but not with WL. From these findings, we conclude that exercise training, either alone or in combination with weight loss, increases both exercise efficiency and the utilization of fat during moderate physical activity in previously sedentary, obese older adults. Weight loss alone, however, significantly improves neither efficiency nor utilization of fat during exercise.     

Effect of training status on fuel selection during submaximal exercise with glucose ingestion.

In this study, an oral glucose load was enriched with a [U-(13)C]glucose tracer to determine differences in substrate utilization between endurance-trained (T) and untrained (UT) subjects during submaximal exercise at the same relative and absolute workload when glucose is ingested. Six highly trained cyclists/triathletes [maximal workload (Wmax), 400 +/- 9 W] and seven UT subjects (Wmax, 296 +/- 8 W) were studied during 120 min of cycling exercise at 50% Wmax ( approximately 55% maximal O(2) consumption). The T subjects performed a second trial at the mean workload of the UT group (148 +/- 4 W). Before exercise, 8.0 ml/kg of a (13)C-enriched glucose solution (80 g/l) was ingested. During exercise, boluses of 2.0 ml/kg of the same solution were administered every 15 min. Measurements were made in the 90- to 120-min period when a steady state was present in breath (13)CO(2) and plasma glucose (13)C enrichment. Energy expenditure was higher in T than in UT subjects (58 vs. 47 kJ/min, respectively; P < 0.001) at the same relative intensity. This was completely accounted for by an increased fat oxidation (0.57 vs. 0.40 g/min; P < 0.01). At the same absolute intensity, fat oxidation contributed more to energy expenditure in the T compared with the UT group (44 vs. 33%, respectively; P < 0.01). The reduction in carbohydrate oxidation in the T group was explained by a diminished oxidation rate of muscle glycogen (indirectly assessed by using tracer methodology at 0.72 +/- 0.1 and 1.03 +/- 0.1 g/min, respectively; P < 0.01) and liver-derived glucose (0.15 +/- 0.03 and 0.22 +/- 0.02 g/min, respectively; P < 0.05). Exogenous glucose oxidation rates were similar during all trials (+/-0.70 g/min).     

Lipid oxidation in fit young adults during postexercise recovery.

To evaluate the hypothesis that lipid oxidation predominates in postexercise recovery, we examined healthy men (n = 6; age = 21.2 +/- 0.6 yr) and women (n = 6; age = 22.8 +/- 2.1 yr) during and after two exercise tasks [89 min at 45% and 60 min at 65% of peak rate of oxygen consumption (V(O2 peak))] as well as a time-matched resting control trial (Con). Exercise bouts were matched for energy expenditure. Respiratory exchange ratios (RER) during exercise at 65% V(O2 peak) for both men and women (0.95 +/- 0.01 and 0.93 +/- 0.02) were significantly higher than 45% V(O2 peak) (0.89 +/- 0.01 and 0.86 +/- 0.02) and Con trials (0.86 +/- 0.01 and 0.86 +/- 0.02, respectively). During recovery, for men RER values were 0.78 +/- 0.01 and 0.76 +/- 0.01 after 45% and 65% exercise, respectively. For women, values were 0.79 +/- 0.01 and 0.78 +/- 0.01. These were significantly lower than during both the preexercise resting period and the corresponding no-exercise Con period (0.82 +/- 0.01 and 0.83 +/- 0.01, mean RER for men and women, respectively). Hence, the contribution of lipid oxidation to energy supply increased significantly during recovery compared with preexercise levels, and it was greater after exercise than during the time-matched, no-exercise Con period. It is concluded that, although carbohydrate is the major fuel source during moderate- to high-intensity exercise, 1) there is substantial postexercise lipid oxidation; and 2) lipid oxidation is the same during postexercise recovery whether the relative power output is 45% or 65% of V(O2 peak) when energy expenditure of exercise is matched.     

Fat metabolism and acute resistance exercise in trained men.

The purpose of this study was to investigate the effect of acute resistance exercise (RE) on lipolysis within adipose tissue and subsequent substrate oxidation to better understand how RE may contribute to improvements in body composition. Lipolysis and blood flow were measured in abdominal subcutaneous adipose tissue via microdialysis before, during, and for 5 h following whole body RE as well as on a nonexercise control day (C) in eight young (24 +/- 0.7 yr), active (>3 RE session/wk for at least 2 yr) male participants. Fat oxidation was measured immediately before and after RE via indirect calorimetry for 45 min. Dialysate glycerol concentration (an index of lipolysis) was higher during (RE: 200.4 +/- 38.6 vs. C: 112.4 +/- 13.1 micromol/l, 78% difference; P = 0.02) and immediately following RE (RE: 184 +/- 41 vs. C: 105 + 14.6 micromol/l, 75% difference; P = 0.03) compared with the same time period on the C day. Energy expenditure was elevated in the 45 min after RE compared with the same time period on the C day (RE: 104.4 +/- 6.0 vs. C: 94.5 +/- 4.0 kcal/h, 10.5% difference; P = 0.03). Respiratory exchange ratio was lower (RE: 0.71 +/- 0.004 vs. C: 0.85 +/- .03, 16.5% difference; P = 0.004) and fat oxidation was higher (RE: 10.2 +/- 0.8 vs. C: 5.0 +/- 1.0 g/h, 105% difference; P = 0.004) following RE compared with the same time period on the C day. Therefore, the mechanism behind RE contributing to improved body composition is in part due to enhanced abdominal subcutaneous adipose tissue lipolysis and improved whole body fat oxidation and energy expenditure in response to RE.     

Effects of high fat provision on muscle PDH activation and malonyl-CoA content in moderate exercise.

This study examined the effects of elevated free fatty acid (FFA) provision on the regulation of pyruvate dehydrogenase (PDH) activity and malonyl-CoA (M-CoA) content in human skeletal muscle during moderate-intensity exercise. Seven men rested for 30 min and cycled for 10 min at 40% and 10 min at 65% of maximal O(2) uptake while being infused with either Intralipid and heparin (Int) or saline (control). Muscle biopsies were taken at 0, 1 (rest-to-exercise transition), 10, and 20 min. Exercise plasma FFA were elevated (0.99 +/- 0.11 vs. 0.33 +/- 0.03 mM), and the respiratory exchange ratio was reduced during Int (0.87 +/- 0.02) vs. control (0.91 +/- 0.01). PDH activation was lower during Int at 1 min (1.33 +/- 0.19 vs. 2.07 +/- 0.14 mmol. min(-1). kg(-1) wet muscle) and throughout exercise. Muscle pyruvate was reduced during Int at rest [0.17 +/- 0.03 vs. 0.25 +/- 0.03 mmol/kg dry muscle (dm)] but increased above control during exercise. NADH was higher during Int vs. control at rest and 1 min of exercise (0.122 +/- 0.016 vs. 0.102 +/- 0.005 and 0.182 +/- 0.016 vs. 0.150 +/- 0.016 mmol/kg dm), but not at 10 and 20 min. M-CoA was lower during Int vs. control at rest and 20 min of exercise (1.12 +/- 0.22 vs. 1.43 +/- 0.17 and 1.33 +/- 0.16 vs. 1.84 +/- 0.17 micromol/kg dm). The reduced PDH activation with elevated FFA during the rest-to-exercise transition was related to higher mitochondrial NADH at rest and 1 min of exercise and lower muscle pyruvate at rest. The decreased M-CoA may have increased fat oxidation during exercise with elevated FFA by reducing carnitine palmitoyltransferase I inhibition and increasing mitochondrial FFA transport.     

Energy substrate utilization during prolonged exercise with and without carbohydrate intake in preadolescent and adolescent girls.

Little information is available on energy metabolism during exercise in girls, particularly the contribution of exogenous carbohydrate (CHO(exo)). The purpose of this study was to determine substrate utilization during exercise with and without CHO(exo) intake in healthy girls. Twelve-yr-old preadolescent (YG; n = 12) and 14-yr-old adolescent (OG; n = 10) girls consumed flavored water (WT) or (13)C-enriched 6% CHO (CT) while cycling for 60 min at approximately 70% maximal aerobic power (Vo(2max)). Substrate utilization was calculated for the final 15 min of exercise. CHO(exo) decreased fat oxidation by approximately 50% in YG but not in OG (P < 0.001) and decreased endogenous CHO oxidation by approximately 15% in OG but not in YG (P = 0.006). Endogenous CHO oxidation was lower in YG than in OG regardless of trial (P < or = 0.01), whereas fat oxidation was higher in YG only during WT (P < 0.001). CHO(exo) oxidation rate was similar between YG and OG (7.1 +/- 0.5 and 6.8 +/- 0.4 mg.kg(-1).min(-1), respectively, P = 0.67), contributing approximately 19% to total energy expenditure. Serum estradiol levels in all girls correlated with fat (r = -0.50 to -0.59, P = 0.03 to 0.005) and endogenous CHO oxidation (r = 0.50 to 0.63, P = 0.03 to 0.005) but not with CHO(exo) oxidation (r = -0.09, P = 0.71). We conclude that CHO(exo) influences endogenous substrate utilization in an age-dependent manner in healthy girls but that total CHO(exo) oxidation during exercise is not different between YG and OG. Our results also point to potential sex-related differences in energy substrate utilization even during childhood.     

Regulation of fuel metabolism by preexercise muscle glycogen content and exercise intensity.

To date, the results of studies that have examined the effects of altering preexercise muscle glycogen content and exercise intensity on endogenous carbohydrate oxidation are equivocal. Differences in the training status of subjects between investigations may, in part, explain these inconsistent findings. Accordingly, we determined the relative effects of exercise intensity and carbohydrate availability on patterns of fuel utilization in the same subjects who performed a random order of four 60-min rides, two at 45% and two at 70% of peak O(2) uptake (Vo(2 peak)), after exercise-diet intervention to manipulate muscle glycogen content. Preexercise muscle glycogen content was 596 +/- 43 and 202 +/- 21 mmol/kg dry mass (P < 0.001) for high-glycogen (HG) and low-glycogen (LG) conditions, respectively. Respiratory exchange ratio was higher for HG than LG during exercise at both 45% (0.85 +/- 0.01 vs. 0.74 +/- 0.01; P < 0.001) and 70% (0.90 +/- 0.01 vs. 0.79 +/- 0.01; P < 0.001) of Vo(2 peak). The contribution of whole body muscle glycogen oxidation to energy expenditure differed between LG and HG for exercise at both 45% (5 +/- 2 vs. 45 +/- 5%; P < 0.001) and 70% (25 +/- 3 vs. 60 +/- 3%; P < 0.001) of Vo(2 peak). Yet, despite marked differences in preexercise muscle glycogen content and its subsequent utilization, rates of plasma glucose disappearance were similar under all conditions. We conclude that, in moderately trained individuals, muscle glycogen availability (low vs. high) does not influence rates of plasma glucose disposal during either low- or moderate-intensity exercise.     

No effect of menstrual cycle phase on glucose kinetics and fuel oxidation during moderate-intensity exercise

Resting and exercise fuel metabolism was assessed in three different phases of the menstrual cycle, characterized by different levels of estrogen relative to progesterone: early follicular (EF, low estrogen and progesterone), midfollicular (MF, elevated estrogen, low progesterone), and midluteal (ML, elevated estrogen and progesterone). It was hypothesized that exercise glucose utilization and whole body carbohydrate oxidation would decrease sequentially from the EF to the MF to the ML phase. Normal-weight healthy females, experiencing a regular menstrual cycle, were recruited. Subjects were moderately active but not highly trained. Testing occurred after 3 days of diet control and after an overnight fast (12-13 h). Resting (2 h) and exercise (50% maximal O(2) uptake, 90 min) measurements of whole body substrate oxidation, tracer-determined glucose flux, and substrate and hormone concentrations were made. No significant difference was observed in whole body fuel oxidation during exercise in the three phases (nonprotein respiratory exchange ratio: EF 0.84 +/- 0.01, MF 0.85 +/- 0.01, ML 0.85 +/- 0.01) or in rates of glucose appearance or disappearance. There were, however, significantly higher glucose (P < 0.05) and insulin (P < 0.001) concentrations during the first 45 min of exercise in the ML phase vs. EF and MF phases. In conclusion, whole body substrate oxidation and glucose utilization did not vary significantly across the menstrual cycle in moderately active women, either at rest or during 90 min of moderate-intensity exercise. During the ML phase, however, this similar pattern of substrate utilization was associated with greater glucose and insulin concentrations. Both estrogen and progesterone are elevated during the ML phase of the menstrual cycle, suggesting that one or both of these sex steroids may play a role in this response.     

Twenty-four-hour metabolic responses to resistance exercise in women

Seven nonobese adult females (40 +/- 8 years) were studied in a room calorimeter on a day that resistance exercise (REX) was performed (4 sets of 10 exercises) and on a nonexercise control day (CON). Twenty-four-hour energy expenditure (EE) on the REX day (mean +/- SD, 2,328 +/- 327 kcal.d(-1)) was greater than CON (2,001 +/- 369 kcal.d(-1), p < 0.001). The net increase in EE during and immediately after (30 minutes) exercise represented 76 +/- 12% of the total increase in 24-hour EE. Twenty four-hour RQ on the REX day (0.86 +/- 0.06) did not differ from CON (0.87 +/- 0.02). Twenty four-hour carbohydrate oxidation was elevated on the REX day, but 24-hour fat and protein oxidation were not different. Thus, in women, the increase in EE due to resistance exercise is largely seen during and immediately after the exercise. The increased energy demand is met by increased carbohydrate oxidation, with no increase in 24-hour fat oxidation.     

Energy cost of moderate-duration resistance and aerobic exercise

The purpose of this study was to compare energy expenditure of resistance and aerobic exercise matched for total time and relative intensity. Ten trained men (24.3 +/- 3.8 years) performed 30 minutes of intermittent free-weight squatting at 70% of 1 repetition maximum and continuous cycling at 70% of Vo(2)max, in a crossover design. Vo(2), kilocalories (kcal), work, respiratory exchange ratio (RER), V(E), heart rate (HR), and rating of perceived exertion (RPE) data were recorded. Cycling resulted in greater total Vo(2) (87 +/- 3 vs. 53 +/- 3 L, mean +/- SEM), kcal expenditure (441 +/- 17 vs. 269 +/- 13), and work (335 +/- 11 vs. 128 +/- 11 kJ) than squatting did. The mean RER was greater during squatting (1.03 +/- 0.01 vs. 0.94 +/- 0.01), and the V(E) values were greater during cycling (82 +/- 3 vs. 70 +/- 3 L.min(-1)). The HR response was nearly identical between exercise modes (160 +/- 5 vs. 160 +/- 4 bpm), whereas the RPE was greater during squatting (16.96 +/- 0.41 vs. 14.88 +/- 0.42). These data suggest that although lower than similarly matched aerobic exercise, resistance exercise resulted in an energy cost that would meet the recommendations for kcal expenditure as suggested by the American College of Sports Medicine, if performed 4-5 days per week. These findings should be considered by coaches and trainers working with individuals mutually interested in muscular development and weight management, because programs of structured resistance exercise may assist with both.     

Muscle triglyceride utilization during exercise: effect of training

The respiratory exchange ratio (RER) is lower during exercise of the same intensity in the trained compared with the untrained state, even though plasma free fatty acids (FFA) and glycerol levels are lower, suggesting reduced availability of plasma FFA. In this context, we evaluated the possibility that lipolysis of muscle triglycerides might be higher in the trained state. Nine adult male subjects performed a prolonged bout of exercise of the same absolute intensity before and after adapting to a strenuous 12-wk program of endurance exercise. The exercise test required 64% of maximum O2 uptake before training. Plasma FFA and glycerol concentrations and RER during the exercise test were lower in the trained than in the untrained state. The proportion of the caloric expenditure derived from fat, calculated from the RER, during the exercise test increased from 35% before training to 57% after training. Muscle glycogen utilization was 41% lower, whereas the decrease in quadriceps muscle triglyceride concentration was roughly twice as great (12.7 +/- 5.5 vs. 26.1 +/- 9.3 mmol/kg dry wt, P less than 0.001) in the trained state. These results suggest that the greater utilization of FFA in the trained state is fueled by increased lipolysis of muscle triglyceride.     

Acute anemia results in an increased glucose dependence during sustained exercise

We evaluated whether acute anemia results in altered blood glucose utilization during sustained exercise at 26.8 m/min on 0% grade, which elicited approximately 60-70% maximal O2 consumption. Acute anemia was induced in female Sprague-Dawley rats by isovolumic plasma exchange transfusion. Hemoglobin and hematocrit were reduced 33% by exchange transfusion to 8.6 +/- 0.4 g/dl and 26.5 +/- 1%, respectively. Glucose kinetics were determined by primed continuous infusion of [6-3H]glucose. Rates of O2 consumption were similar during rest (pooled means 25.1 +/- 1.8 ml.kg-1.min-1) and exercise (pooled means 46.8 +/- 3.0 ml.kg-1.min-1). Resting blood glucose and lactate concentrations were not different in anemic animals (pooled means 5.1 +/- 0.2 and 0.9 +/- 0.02 mM, respectively). Exercise resulted in significantly decreased blood glucose (4.0 +/- 0.2 vs. 4.6 +/- 0.1 mM) and elevated lactate (6.1 +/- 0.4 vs. 2.3 +/- 0.5 mM) concentrations in anemic animals. Glucose turnover rates (Rt) were not different between anemic and control animals at rest and averaged 58.8 +/- 3.6 mumol.kg-1.min-1. Exercise resulted in a 30% greater increase in Rt in anemic (141.7 +/- 3.2 mumol.kg-1.min-1) than in control animals (111.2 +/- 5.2 mumol.kg-1.min-1). Metabolic clearance rates (MCR = Rt/[glucose]) were not different at rest (11.6 +/- 7.4) but were significantly greater in anemic (55.2 +/- 5.7 ml.kg-1.min-1) than in control animals (24.3 +/- 1.4 ml.kg-1.min-1) during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of a 36-hour fast on human endurance and substrate utilization

To determine if prolonged fasting affects substrate utilization and endurance time, seven trained men exercised to exhaustion on a cycle ergometer at 50% maximum oxygen consumption (VO2max) in an overnight-fasted [postabsorptive (PA)] state and after a 36-h fast (F). Fasting produced significant elevations in the resting concentrations of blood free fatty acids (FFA; 1.16 +/- 0.05 vs. 0.56 +/- 0.06 mM, F vs. PA, respectively, a 107% increase), beta-hydroxybutyrate (beta-OH, 2.06 +/- 0.66 vs. 0.15 +/- 0.06 mM, a 1,270% increase), and glycerol (0.12 +/- 0.03 vs. 0.04 +/- 0.01 mM, a 200% increase), with a significant decline in glucose (79.79 +/- 2.12 vs. 98.88 +/- 3.11 mg/dl, a 19% decrease). Exercise in the F trial increased FFA, decreased glucose, and significantly elevated beta-OH and glycerol over the PA trial. There was no difference in blood glucose concentration between trials at exhaustion. However, F produced a significant decrement in exercise endurance time compared with the PA trial (88.9 +/- 18.3 vs. 144.4 +/- 22.6 min, F vs. PA, a 38% decrease). Based on the respiratory exchange ratio, fasting led to a greater utilization of lipids during rest and exercise. It was concluded that 1) a 36-h fast significantly altered substrate utilization at rest and throughout exercise to exhaustion, 2) glucose levels do not appear to be the single determinant of time to exhaustion in submaximal exercise, and 3) despite the apparent sparing of carbohydrate utilization with the 36-h fast, endurance performance was significantly decreased.     

Different metabolic responses to central and peripheral injection of enterostatin

Enterostatin, a pentapeptide cleaved from procolipase, suppresses fat intake after peripheral and central administration. Chronic treatment of rats with enterostatin decreases body weight and body fat. The effect was greater than could be accounted by the reduction in food intake alone. Hence, we have investigated the effect of enterostatin on energy metabolism. Male Sprague-Dawley rats adapted to a high-fat diet were implanted with lateral cerebral ventricular or amygdala cannulas. The metabolic effects were determined by indirect calorimetry. After habituation to the test cages, fasted rats were injected with either saline vehicle or enterostatin given either intraperitoneally (100 nmol) or intracerebroventricularly (1 nmol) or into specific brain regions [amygdala (0.01 nmol) or paraventricular nucleus (PVN) (0.1 nmol)]. Respiratory quotient (RQ) and energy expenditure were monitored over 2 h. Intraperitoneal enterostatin reduced RQ (saline: 0.81 +/- 0.02 vs. enterostatin: 0.76 +/- 0.01) and increased energy expenditure by 44%. Intracerebroventricular enterostatin increased the energy expenditure without any effects on RQ, whereas PVN enterostatin increased metabolic rate, while preventing the increase in RQ observed in the control animals. In contrast, neither RQ nor energy expenditure was altered after enterostatin was injected into the amygdala. Enterostatin activated AMP-activated protein kinase in primary cultures of human myocytes in a dose- and time-dependent manner and increased the rate of fatty acid beta-oxidation. These findings suggest that enterostatin regulates energy expenditure and substrate partitioning through both peripheral and central effects.     

Changes in 24-h substrate oxidation in older and younger men in response to exercise.

The purpose of this study was to compare 24-h substrate oxidation in older (OM; 60-75 yr, n = 7) and younger (YM; 20-30 yr, n = 7) men studied on sedentary day (Con) and on a day with exercise (Ex; net energy expenditure = 300 kcal). Plasma glucose and free fatty acids were also measured at several time points during the 24-h measurement. Weight was not different in OM and YM (means +/- SD; 84.8 +/- 16.9 vs. 81.4 +/- 10.4 kg, respectively), although percent body fat was slightly higher in OM (25.9 +/- 3.5 vs. 21.9 +/- 9.7%; P = 0.17).Values of 24-h energy expenditure did not differ in OM and YM on the Con (means +/- SE; 2,449 +/- 162 vs. 2,484 +/- 104 kcal/day, respectively) or Ex (2,902 +/- 154 vs. 2,978 +/- 122 kcal/day) days. Under both conditions, 24-h respiratory quotient was significantly lower and fat oxidation significantly higher in OM. Glucose concentrations were not different at any time point, but plasma free fatty acid concentrations were higher in OM, particularly following meals. Thus, under these controlled conditions, 24-h fat oxidation was not reduced and was in fact greater in OM. We speculate that differences in the availability of circulating free fatty acids in the postprandial state contributed to the observed differences in 24-h fat oxidation in OM and YM.     

Glucose kinetics and substrate oxidation during exercise in the follicular and luteal phases.

The purpose of this investigation was to determine whether plasma glucose kinetics and substrate oxidation during exercise are dependent on the phase of the menstrual cycle. Once during the follicular (F) and luteal (L) phases, moderately trained subjects [peak O(2) uptake (V(O(2))) = 48.2 +/- 1.1 ml. min(-1). kg(-1); n = 6] cycled for 25 min at approximately 70% of the V(O(2)) at their respective lactate threshold (70%LT), followed immediately by 25 min at 90%LT. Rates of plasma glucose appearance (R(a)) and disappearance (R(d)) were determined with a primed constant infusion of [6,6-(2)H]glucose, and total carbohydrate (CHO) and fat oxidation were determined with indirect calorimetry. At rest and during exercise at 70%LT, there were no differences in glucose R(a) or R(d) between phases. CHO and fat oxidation were not different between phases at 70%LT. At 90%LT, glucose R(a) (28.8 +/- 4.8 vs. 33.7 +/- 4.5 micromol. min(-1). kg(-1); P < 0.05) and R(d) (28.4 +/- 4.8 vs. 34.0 +/- 4.1 micromol. min(-1). kg(-1); P < 0.05) were lower during the L phase. In addition, at 90%LT, CHO oxidation was lower during the L compared with the F phase (82.0 +/- 12.3 vs. 93.8 +/- 9.7 micromol. min(-1) .kg(-1); P < 0.05). Conversely, total fat oxidation was greater during the L phase at 90%LT (7.46 +/- 1.01 vs. 6.05 +/- 0.89 micromol. min(-1). kg(-1); P < 0.05). Plasma lactate concentration was also lower during the L phase at 90%LT concentrations (2.48 +/- 0.41 vs. 3.08 +/- 0.39 mmol/l; P < 0.05). The lower CHO utilization during the L phase was associated with an elevated resting estradiol (P < 0.05). These results indicate that plasma glucose kinetics and CHO oxidation during moderate-intensity exercise are lower during the L compared with the F phase in women. These differences may have been due to differences in circulating estradiol.     

Oxidation rate of exogenous carbohydrate during exercise is higher in boys than in men.

To determine whether the relative utilization of exogenous carbohydrate (CHO(exo)) differs between children and adults, substrate utilization during 60 min of cycling at 70% peak O(2) uptake was studied in 12 pre- and early pubertal boys (9.8 +/- 0.1 yr) and 10 men (22.1 +/- 0.5 yr) on two occasions. Subjects consumed either a placebo or a (13)C-enriched 6% CHO(exo) beverage (total volume per trial: 24 ml/kg). Substrate utilization was calculated for the final 30 min of exercise. During both trials, total fat oxidation was higher (5.4 +/- 0.5 vs. 3.0 +/- 0.4 mg x kg(-1) x min(-1), P < 0.001) and total CHO oxidation lower (27.4 +/- 1.5 vs. 34.8 +/- 1.2 mg x kg(-1) x min(-1), P < 0.001) in boys than in men, respectively. During the CHO(exo) trial, CHO(exo) oxidation was higher (P < 0.001) in boys (8.8 +/- 0.5 mg x kg(-1) x min(-1)) than in men (6.2 +/- 0.5 mg x kg(-1) x min(-1)) and provided a greater (P < 0.001) relative proportion of total energy in boys (21.8 +/- 1.4%) than in men (14.6 +/- 0.9%). These results suggest that, although endogenous CHO utilization during exercise is lower, the relative oxidation of ingested CHO is considerably higher in boys than in men. The greater reliance on CHO(exo) in boys may be important in preserving endogenous fuels and may be related to pubertal status.     

Glucose ingestion and substrate utilization during exercise in boys with IDDM.

This study was intended to compare exogenous [(13)C]glucose (Glu(exo)) oxidation in boys with insulin-dependent diabetes mellitus (IDDM) and healthy boys of similar age, weight, and maximal O(2) uptake. In a control trial with water intake (CT) and in a (13)C-enriched glucose trial (GT), subjects cycled for 60 min (58.8 +/- 0.9% maximal O(2) uptake) while the utilization of total glucose, total fat, and Glu(exo) was assessed. In CT, total glucose was 84.7 +/- 9.2 vs. 91.3 +/- 6.6 g/60 min (not significantly different) and total fat was 13.3 +/- 2.2 vs. 11.1 +/- 1.7 g/60 min (not significantly different) in IDDM vs. healthy boys, respectively. In GT, Glu(exo) was 10.4 +/- 1.7 vs. 14.8 +/- 1.1 g/60 min, corresponding to 9.0 +/- 1.0 vs. 12.4 +/- 0.5% of the total energy supply in IDDM and healthy boys, respectively (P < 0.05). Endogenous glucose was spared in both groups by 12.6 +/- 3.5% (P < 0.05). Blood glucose and plasma insulin concentrations were two- to threefold higher in IDDM vs. healthy boys in both trials. In conclusion, Glu(exo) is impaired in exercising boys with IDDM, even when plasma insulin levels are elevated.     

Effects of fat adaptation and carbohydrate restoration on prolonged endurance exercise.

We determined the effect of fat adaptation on metabolism and performance during 5 h of cycling in seven competitive athletes who consumed a standard carbohydrate (CHO) diet for 1 day and then either a high-CHO diet (11 g. kg(-1)x day(-1) CHO, 1 g x kg(-1) x day(-1) fat; HCHO) or an isoenergetic high-fat diet (2.6 g x kg(-1) x day(-1) CHO, 4.6 g x kg(-1) x day(-1) fat; fat-adapt) for 6 days. On day 8, subjects consumed a high-CHO diet and rested. On day 9, subjects consumed a preexercise meal and then cycled for 4 h at 65% peak O(2) uptake, followed by a 1-h time trial (TT). Compared with baseline, 6 days of fat-adapt reduced respiratory exchange ratio (RER) with cycling at 65% peak O(2) uptake [0.78 +/- 0.01 (SE) vs. 0.85 +/- 0.02; P < 0.05]. However, RER was restored by 1 day of high-CHO diet, preexercise meal, and CHO ingestion (0.88 +/- 0.01; P < 0.05). RER was higher after HCHO than fat-adapt (0.85 +/- 0.01, 0.89 +/- 0.01, and 0.93 +/- 0.01 for days 2, 8, and 9, respectively; P < 0.05). Fat oxidation during the 4-h ride was greater (171 +/- 32 vs. 119 +/- 38 g; P < 0.05) and CHO oxidation lower (597 +/- 41 vs. 719 +/- 46 g; P < 0.05) after fat-adapt. Power output was 11% higher during the TT after fat-adapt than after HCHO (312 +/- 15 vs. 279 +/- 20 W; P = 0.11). In conclusion, compared with a high-CHO diet, fat oxidation during exercise increased after fat-adapt and remained elevated above baseline even after 1 day of a high-CHO diet and increased CHO availability. However, this study failed to detect a significant benefit of fat adaptation to performance of a 1-h TT undertaken after 4 h of cycling.