Body composition of 161-km ultramarathoners.

This study compares body composition characteristics with performance among participants in a 161-km trail ultramarathon. Height, mass, and percent body fat from bioimpedance spectroscopy were measured on 72 starters (17 women, 55 men). Correlation analyses were used to compare body characteristics with finish time, and unpaired t-tests were used to compare characteristics of finishers with non-finishers. Mean (+/-SD) BMI (kg x m(-2)) was 24.8+/-2.7 (range 19.1-32.2) for the men and 21.2+/-2.1 (range 18.1-26.7) for the women. Among the three fastest runners, BMI values ranged from 22.1 to 23.4 for men and 21.5 to 22.9 for women. Mean (+/-SD) percent body fat values for men and women were 17+/-5 (range 5-35) and 21+/-6 (range 10-29) , and ranged from 6 to 14 and 14 to 27 among the fastest three men and women. There was a significant positive correlation (r(2)=0.23; p=0.0025) between percent body fat and finish time for men but not for women, and percent body fat values were lower for finishers than non-finishers for men (p=0.03) and women (p=0.04). We conclude that despite wide variations in BMI and percent body fat among ultramarathon participants, the faster men have lower percent body fat values than the slower men, and finishers have lower percent body fat values than non-finishers.

Cardiovascular effects of cadence and workload.

Increases in cadence may augment SV during submaximal cycling (> 65 % VO2max) via effects of increased muscle pump activity on preload. At lower workloads (45 - 65 % VO2max), SV tends to plateau, suggesting that effects of increases in cadence on pump activity have little influence on SV. We hypothesized that cadence-induced increases in CO at submaximal workloads, where SV tends to plateau, are due to elevations in HR and/or O2 extraction. SV, CO, HR, VO2, and delta a - vO2 were assessed at 80 and 100 rpm during workloads of 50 % (LO) or 65 % (HI) of VO2max in 11 male cyclists. No changes in SV were seen. CO was higher at 100 rpm in 10 of 11 subjects at LO (18.1 +/- 2.7 vs. 17.2 +/- 2.6 L/min). VO2 at both workloads was greater at 100 than 80 rpm as was HR (LO: 129 +/- 11 vs. 121 +/- 10 beats/min; HI: 146 +/- 13 vs. 139 +/- 14 beats/min) (p < 0.05). delta a - vO2 was greater at HI compared to LO at 80 (15.1 +/- 1.6 vs. 13.6 +/- 1.3 ml) and 100 rpm (16.0 +/- 1.7 vs. 15.1 +/- 1.6 ml) (p < 0.05). Results suggest that increases in O2 demand during low submaximal cycling (50 % VO2max) at high cadences are met by HR-induced increases in CO. At higher workloads (65 % VO2max), inability of higher cadences to increase CO and O2 delivery is offset by greater O2 extraction.

Recovery of (13)CO2 during rest and exercise after [1-(13)C]acetate, [2-(13)C]acetate, and NaH(13)CO3 infusions.

For estimating the oxidation rates (Rox) of glucose and other substrates by use of (13)C-labeled tracers, we obtained correction factors to account for label dilution in endogenous bicarbonate pools and TCA cycle exchange reactions. Fractional recoveries of (13)C label in respiratory gases were determined during 225 min of rest and 90 min of leg cycle ergometry at 45 and 65% peak oxygen uptake (VO(2 peak)) after continuous infusions of [1-(13)C]acetate, [2-(13)C]acetate, or NaH(13)CO(3). In parallel trials, [6,6-(2)H]glucose and [1-(13)C]glucose were given. Experiments were conducted after an overnight fast with exercise commencing 12 h after the last meal. During the transition from rest to exercise, CO(2) production increased (P < 0.05) in an intensity-dependent manner. Significant differences were observed in the fractional recoveries of (13)C label as (13)CO(2) at rest (NaH(13)CO(3), 77.5 +/- 2.8%; [1-(13)C]acetate, 49.8 +/- 2.4%; [2-(13)C]acetate, 26.1 +/- 1.4%). During exercise, fractional recoveries of (13)C label from [1-(13)C]acetate, [2-(13)C]acetate, and NaH(13)CO(3) were increased compared with rest. Magnitudes of label recoveries during both exercise intensities were tracer specific (NaH(13)CO(3), 93%; [1-(13)C]acetate, 80%; [2-(13)C]acetate, 65%). Use of an acetate-derived correction factor for estimating glucose oxidation resulted in Rox values in excess (P < 0.05) of glucose rate of disappearance during hard exercise. We conclude that, after an overnight fast: 1) recovery of (13)C label as (13)CO(2) from [(13)C]acetate is decreased compared with bicarbonate; 2) the position of (13)C acetate label affects carbon dilution estimations; 3) recovery of (13)C label increases in the transition from rest to exercise in an isotope-dependent manner; and 4) application of an acetate correction factor in glucose oxidation measurements results in oxidation rates in excess of glucose disappearance during exercise at 65% of VO(2 peak). Therefore, bicarbonate, not acetate, correction factors are advocated for estimating glucose oxidation from carbon tracers in exercising men.

Autoregulation of glucose production in men with a glycerol load during rest and exercise.

Related to hepatic autoregulation we evaluated hypotheses that 1) glucose production would be altered as a result of a glycerol load, 2) decreased glucose recycling rate (Rr) would result from increased glycerol uptake, and 3) the absolute rate of gluconeogenesis (GNG) from glycerol would be positively correlated to glycerol rate of disappearance (R(d)) during a glycerol load. For these purposes, glucose and glycerol kinetics were determined in eight men during rest and during 90 min of leg cycle ergometry at 45 and 65% of peak O2 consumption (.VO2 (peak)). Trials were conducted after an overnight fast, with exercise commencing 12 h after the last meal. Subjects received a continuous infusion of [6,6-(2)H(2)]glucose, [1-(13)C]glucose, and [1,1,2,3,3-(2)H(5)]glycerol without (CON) or with an additional 1,000 mg (rest: 20 mg/min; exercise: 40 mg/min) of [2-(13)C]- or unlabeled glycerol added to the infusate (GLY). Infusion of glycerol dampened glucose Rr, calculated as the difference between [6,6-(2)H(2)]- and [1-(13)C]glucose rates of appearance (R(a)), at rest [0.35 +/- 0.12 (CON) vs. 0.12 +/- 0.10 mg. kg(-1). min(-1) (GLY), P < 0.05] and during exercise at both intensities [45%: 0.63 +/- 0.14 (CON) vs. 0.04 +/- 0.12 (GLY); 65%: 0.73 +/- 0.14 (CON) vs. 0.04 +/- 0.17 mg. kg(-1). min(-1) (GLY), P < 0.05]. Glucose R(a) and oxidation were not affected by glycerol infusion at rest or during exercise. Throughout rest and both exercise intensities, glycerol R(d) was greater in GLY vs. CON conditions (rest: 0.30 +/- 0.04 vs. 0.58 +/- 0.04; 45%: 0.57 +/- 0.07 vs. 1.19 +/- 0.04; 65%: 0.73 +/- 0.06 vs. 1.27 +/- 0.05 mg. kg(-1). min(-1), CON vs. GLY, respectively). Differences in glycerol R(d) (DeltaR(d)) between protocols equaled the unlabeled glycerol infusion rate and correlated with plasma glycerol concentration (r = 0.97). We conclude that infusion of a glycerol load during rest and exercise at 45 and 65% of .VO2(peak) 1) does not affect glucose R(a) or R(d), 2) blocks glucose Rr, 3) increases whole body glycerol R(d) in a dose-dependent manner, and 4) results in gluconeogenic rates from glycerol equivalent to CON glucose recycling rates.

Endurance training increases gluconeogenesis during rest and exercise in men.

The hypothesis that endurance training increases gluconeogenesis (GNG) during rest and exercise was evaluated. We determined glucose turnover with [6,6-(2)H]glucose and lactate incorporation into glucose by use of [3-(13)C]lactate during 1 h of cycle ergometry at two intensities [45 and 65% peak O(2) consumption (VO(2 peak))] before and after training [65% pretraining VO(2 peak)], same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative intensity (RLT). Nine males (178.1 +/- 2.5 cm, 81.8 +/- 3.3 kg, 27.4 +/- 2.0 yr) trained for 9 wk on a cycle ergometer 5 times/wk for 1 h at 75% VO(2 peak). The power output that elicited 66.0 +/- 1.1% of VO(2 peak) pretraining elicited 54.0 +/- 1.7% posttraining. Rest and exercise arterial glucose concentrations were similar before and after training, regardless of exercise intensity. Arterial lactate concentration during exercise was significantly greater than at rest before and after training. Compared with 65% pretraining, arterial lactate concentration decreased at ABT (4.75 +/- 0.4 mM, 65% pretraining; 2.78 +/- 0.3 mM, ABT) and RLT (3.76 +/- 0.46 mM) (P < 0.05). At rest after training, the percentage of glucose rate of appearance (R(a)) from GNG more than doubled (1.98 +/- 0.5% pretraining; 5.45 +/- 1.3% posttraining), as did the rate of GNG (0.11 +/- 0.03 mg x kg(-1) x min(-1) pretraining, 0.24 +/- 0.06 mg x kg(-1) x min(-1) posttraining). During exercise after training, %glucose R(a) from GNG increased significantly at ABT (2.3 +/- 0.8% at 65% pre- vs. 7.6 +/- 2.1% posttraining) and RLT (6.1 +/- 1.5%), whereas GNG increased almost threefold (P < 0.05) at ABT (0.24 +/- 0.08 mg x kg(-1) x min(-1) 65% pre-, and 0.71 +/- 0.18 mg x kg(-1) x min(-1) posttraining) and RLT (0.75 +/- 0.26 mg x kg(-1) x min(-1)). We conclude that endurance training increases gluconeogenesis twofold at rest and threefold during exercise at given absolute and relative exercise intensities.

Active muscle and whole body lactate kinetics after endurance training in men.

We evaluated the hypotheses that endurance training decreases arterial lactate concentration ([lactate](a)) during continuous exercise by decreasing net lactate release () and appearance rates (R(a)) and increasing metabolic clearance rate (MCR). Measurements were made at two intensities before [45 and 65% peak O(2) consumption (VO(2 peak))] and after training [65% pretraining VO(2 peak), same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative intensity (RLT)]. Nine men (27.4 +/- 2.0 yr) trained for 9 wk on a cycle ergometer, 5 times/wk at 75% VO(2 peak). Compared with the 65% VO(2 peak) pretraining condition (4.75 +/- 0.4 mM), [lactate](a) decreased at ABT (41%) and RLT (21%) (P < 0.05). decreased at ABT but not at RLT. Leg lactate uptake and oxidation were unchanged at ABT but increased at RLT. MCR was unchanged at ABT but increased at RLT. We conclude that 1) active skeletal muscle is not solely responsible for elevated [lactate](a); and 2) training increases leg lactate clearance, decreases whole body and leg lactate production at a given moderate-intensity power output, and increases both whole body and leg lactate clearance at a high relative power output.

Muscle net glucose uptake and glucose kinetics after endurance training in men.

We evaluated the hypotheses that alterations in glucose disposal rate (R(d)) due to endurance training are the result of changed net glucose uptake by active muscle and that blood glucose is shunted to working muscle during exercise requiring high relative power output. We studied leg net glucose uptake during 1 h of cycle ergometry at two intensities before training [45 and 65% of peak rate of oxygen consumption (VO(2 peak))] and after training [65% pretraining VO(2 peak), same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative workload (RLT)]. Nine male subjects (178.1 +/- 2.5 cm, 81.8 +/- 3.3 kg, 27.4 +/- 2.0 yr) were tested before and after 9 wk of cycle ergometer training, five times a week at 75% VO(2 peak). The power output that elicited 66.0 +/- 1.1% of VO(2 peak) before training elicited 54.0 +/- 1.7% after training. Whole body glucose R(d) decreased posttraining at ABT (5.45 +/- 0.31 mg. kg(-1). min(-1) at 65% pretraining to 4.36 +/- 0.44 mg. kg(-1). min(-1)) but not at RLT (5.94 +/- 0.47 mg. kg(-1). min(-1)). Net glucose uptake was attenuated posttraining at ABT (1.87 +/- 0.42 mmol/min at 65% pretraining and 0.54 +/- 0.33 mmol/min) but not at RLT (2.25 +/- 0. 81 mmol/min). The decrease in leg net glucose uptake at ABT was of similar magnitude as the drop in glucose R(d) and thus could explain dampened glucose flux after training. Glycogen degradation also decreased posttraining at ABT but not RLT. Leg net glucose uptake accounted for 61% of blood glucose flux before training and 81% after training at the same relative (65% VO(2 peak)) workload and only 38% after training at ABT. We conclude that 1) alterations in active muscle glucose uptake with training determine changes in whole body glucose kinetics; 2) muscle glucose uptake decreases for a given, moderate intensity task after training; and 3) hard exercise (65% VO(2 peak)) promotes a glucose shunt from inactive tissues to active muscle.

Endurance training increases fatty acid turnover, but not fat oxidation, in young men.

We examined the effects of exercise intensity and a 10-wk cycle ergometer training program [5 days/wk, 1 h, 75% peak oxygen consumption (VO2 peak)] on plasma free fatty acid (FFA) flux, total fat oxidation, and whole body lipolysis in healthy male subjects (n = 10; age = 25.6 +/- 1.0 yr). Two pretraining trials (45 and 65% of VO2 peak) and two posttraining trials (same absolute workload, 65% of old VO2 peak; and same relative workload, 65% of new VO2 peak) were performed by using an infusion of [1-13C]palmitate and [1,1,2,3, 3-2H]glycerol. An additional nine subjects (age 25.4 +/- 0.8 yr) were treated similarly but were infused with [1,1,2,3,3-2H]glycerol and not [1-13C]palmitate. Subjects were studied postabsorptive for 90 min of rest and 1 h of cycling exercise. After training, subjects increased VO2 peak by 9.4 +/- 1.4%. Pretraining, plasma FFA kinetics were inversely related to exercise intensity with rates of appearance (Ra) and disappearance (Rd) being significantly higher at 45 than at 65% VO2 peak (Ra: 8.14 +/- 1.28 vs. 6.64 +/- 0.46, Rd: 8. 03 +/- 1.28 vs. 6.42 +/- 0.41 mol. kg-1. min-1) (P

Evaluation of exercise and training on muscle lipid metabolism.

To evaluate the hypothesis that endurance training increases intramuscular triglyceride (IMTG) oxidation, we studied leg net free fatty acid (FFA) and glycerol exchange during 1 h of cycle ergometry at two intensities before training [45 and 65% of peak rate of oxygen consumption (V(O2) peak)] and after training [65% pretraining V(O2) peak, same absolute workload (ABT), and 65% posttraining V(O2) peak, same relative intensity (RLT)]. Nine male subjects (178.1 +/- 2.5 cm, 81.8 +/- 3.3 kg, 27.4 +/- 2.0 yr) were tested before and after 9 wk of cycle ergometer training, five times per week at 75% V(O2) peak. The power output that elicited 66.1 +/- 1.1% of V(O2) peak before training elicited 54.0 +/- 1.7% after training due to a 14.6 +/- 3.1% increase in V(O2) peak. Training significantly (P < 0.05) decreased pulmonary respiratory exchange ratio (RER) values at ABT (0.96 +/- 0.01 at 65% pre- vs. 0.93 +/- 0.01 posttraining) but not RLT (0.95 +/- 0.01). After training, leg respiratory quotient (RQ) was not significantly different at either ABT (0.98 +/- 0.02 pre- vs. 0.98 +/- 0.03 posttraining) or RLT (1.01 +/- 0.02). Net FFA uptake was increased at RLT but not ABT after training. FFA fractional extraction was not significantly different after training or at any exercise intensity. Net glycerol release, and therefore IMTG lipolysis calculated from three times net glycerol release, did not change from rest to exercise or at ABT but decreased at the same RLT after training. Muscle biopsies revealed minor muscle triglyceride changes during exercise. Simultaneous measurements of leg RQ, net FFA uptake, and glycerol release by working legs indicated no change in leg FFA oxidation, FFA uptake, or IMTG lipolysis during leg cycling exercise that elicits 65% pre- and 54% posttraining V(O2) peak. Training increases working muscle FFA uptake at 65% V(O2) peak, but high RER and RQ values at all work intensities indicate that FFA and IMTG are of secondary importance as fuels in moderate and greater-intensity exercise.

Effects of exercise intensity and training on lipid metabolism in young women.

We examined the effects of exercise intensity and training [12 wk, 5 days/wk, 1 h, 75% peak oxygen consumption (VO2 peak)] on lipolysis and plasma free fatty acid (FFA) flux in women (n = 8; 24.3 +/- 1.6 yr). Two pretraining trials (45 and 65% of VO2 peak) and two posttraining trials [same absolute workload (65% of old VO2 peak; ABT) and same relative workload (65% of new VO2 peak; RLT)] were performed using infusions of [1,1,2,3,3-2H]glycerol and [1-13C]palmitate. Pretraining rates of FFA appearance (Ra), disappearance (Rd), and oxidation (Rox p) were similar between the 65% (6.8 +/- 0.6, 6.2 +/- 0.7, 3.1 +/- 0.3 micromol. kg-1. min-1, respectively) and the 45% of VO2 peak trials. At ABT and RLT training increased FFA Ra to 8.4 +/- 1.0 and 9.7 +/- 1.1 micromol. kg-1. min-1, Rd to 8.3 +/- 1.0 and 9.5 +/- 1.1 micromol. kg-1. min-1, and Rox p to 4.8 +/- 0.4 and 6.7 +/- 0.7 micromol. kg-1. min-1, respectively (P

Training-induced alterations of carbohydrate metabolism in women: women respond differently from men.

We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 12-wk cycle ergometer training program [5 days/wk, 1-h duration, 75% peak O2 consumption (VO2 peak)] in healthy female subjects (n = 17; age 23.8 +/- 2.0 yr). Two pretraining trials (45 and 65% of VO2 peak) and two posttraining trials [same absolute workload (65% of old VO2 peak) and same relative workload (65% of new VO2 peak)] were performed on nine subjects by using a primed-continuous infusion of [1-13C]- and [6,6-2H]glucose. Eight additional subjects were studied by using [6, 6-2H]glucose. Subjects were studied postabsorption for 90 min of rest and 1 h of cycling exercise. After training, subjects increased VO2 peak by 25.2 +/- 2.4%. Pretraining, the intensity effect on glucose kinetics was evident between 45 and 65% of VO2 peak with rates of appearance (Ra: 4.52 +/- 0.25 vs. 5.53 +/- 0.33 mg . kg-1 . min-1), disappearance (Rd: 4.46 +/- 0.25 vs. 5.54 +/- 0.33 mg . kg-1 . min-1), and oxidation (Rox: 2.45 +/- 0.16 vs. 4.35 +/- 0.26 mg . kg-1 . min-1) of glucose being significantly greater (P

Training-induced alterations of glucose flux in men.

We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 10-wk cycle ergometer training program in 19 healthy male subjects. Two pretraining trials [45 and 65% of peak O2 consumption (VO2peak)] and two posttraining trials (same absolute and relative intensities as 65% pretraining) were performed for 90 min of rest and 1 h of cycling exercise. After training, subjects increased VO2peak by 9.4 +/- 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance (R(a); 5.84 +/- 0.23 vs. 4.73 +/- 0.19 mg x kg(-1) x min(-1)), disappearance (R(d); 5.78 +/- 0.19 vs. 4.73 +/- 0.19 mg x kg(-1) x min(-1) x min(-1)), oxidation (R(ox); 5.36 +/- 0.15 vs. 3.41 +/- 0.23 mg x kg(-1) x min(-1)), and metabolic clearance (7.03 +/- 0.56 vs. 5.20 +/- 0.28 ml x kg(-1) x min(-1)) of glucose being significantly greater (P < or = 0.05) in the 65% than the 45% VO2peak trial. When R(d) was expressed as a percentage of total energy expended per minute (R(dE)), there was no difference between the 45 and 65% intensities. Training did reduce R(a) (4.63 +/- 0.25), R(d) (4.65 +/- 0.24), R(ox) (3.77 +/- 0.43), and R(dE) (15.30 +/- 0.40 to 12.85 +/- 0.81) when subjects were tested at the same absolute workload (P < or = 0.05). However, when they were tested at the same relative workload, R(a), R(d), and R(dE) were not different, although R(ox) was lower posttraining (5.36 +/- 0.15 vs. 4.41 +/- 0.42, P < or = 0.05). These results show 1) glucose use is directly related to exercise intensity; 2) training decreases glucose flux for a given power output; 3) when expressed as relative exercise intensity, training does not affect the magnitude of blood glucose use during exercise; 4) training alters the pathways of glucose disposal.

Smoking increases conversion of lactate to glucose during submaximal exercise.

We examined the hypotheses that 1) smoking acutely before exercise (AS) results in a higher rate of lactate production during exercise compared with chronic smoking with preexercise abstinence (CS) and 2) smokers have a higher rate of lactate conversion to glucose during exercise compared with nonsmokers (NS). To test our hypotheses, seven male smokers and seven nonsmokers were studied by using a primed continuous infusion of [3-13C]lactate during 90 min of rest and 60 min of exercise on a cycle ergometer at 50% peak O2 consumption; smokers were studied twice: once after an overnight smoking abstinence and once after smoking three cigarettes before exercise. The rates of lactate appearance and conversion to glucose were increased markedly with exercise compared with rest in all groups (P < 0.05); the rate of lactate appearance for AS was significantly greater (7.87 +/- 0.77 mg.kg-1.min-1) than for both CS (4.64 +/- 0.33 mg.kg-1.min-1) and NS (5.57 +/- 0.60 mg.kg-1.min-1) (P < 0.05). The rate of lactate conversion to glucose was similar between CS and AS (6.49 +/- 1.82 and 6.30 +/- 1.69 mg.kg-1.min-1, respectively) during exercise; NS had a significantly lower rate (3.31 +/- 0.90 mg.kg-1.min-1) compared with CS and AS (P < 0.05). In summary, acute smoking increases lactate flux during exercise; in addition, smokers have a higher rate of lactate to glucose conversion during exercise compared with nonsmokers, which may indicate an increased glucose dependency.

Metabolite and hormonal response in smokers during rest and sustained exercise.

To evaluate the effects of acute and chronic smoking on blood glucose homeostasis, concentrations of metabolites, and hormonal responses at rest and during submaximal exercise, seven male smokers and seven similar nonsmokers were studied after an overnight fast. Nonsmokers (NS) and chronic smokers, abstaining from smoking (CS), were tested during rest and 60 min of cycle ergometry exercise at 49.7 +/- 0.8% of VO2peak. Smokers were restudied after acutely smoking (AS) two cigarettes prior to rest and one prior to exercise. Blood glucose levels were similar among NS, CS, and AS at all times. Lactate levels were elevated in AS compared with NS during exercise (2.32 +/- 0.22 mM vs 1.81 +/- 0.11; P < 0.05), with no differences in alanine. Free fatty acid levels were initially lower at rest in CS (0.45 +/- 0.04 mM) than in either AS (0.77 +/- 0.11) or NS (0.64 +/- 0.06; p < 0.05), but no other differences were found. During exercise, CS had lower glycerol levels (0.31 +/- 0.02 mM) than either AS (0.38 +/- 0.02) or NS (0.41 +/- 0.02; P < 0.05). Nevertheless, respiratory exchange ratio values were not significantly different during steady-state rest or exercise; and insulin, glucagon, and norepinephrine levels were also similar. Smokers effectively maintained normal blood glucose levels with only minor changes in some metabolite and hormone concentrations during rest and sustained exercise.

Increased dependence on blood glucose in smokers during rest and sustained exercise.

To evaluate the hypothesis that smoking increases the dependence on blood glucose as a fuel, seven male smokers [28.7 +/- 1.7 (SE) yr. 77.7 +/- 4.3 kg] and seven nonsmokers (NS; 29.1 +/- 0.9 yr, 78.7 +/- 5.3 kg) were studied in the postabsorptive condition. NS received a primed continuous infusion of [6,6-2H]glucose and [1-13C]glucose during 90 min of rest and 60 min of exercise at 49.7 +/- 0.8% of peak O2 consumption on one occasion; chronic smokers continued their overnight abstinence from smoking (CS) for one trial but, on another occasion, acutely smoked (AS) two cigarettes immediately before resting measurements and another cigarette before exercise. Plasma glucose levels were similar among all groups at all times during the trials; however, the glucose rates of appearance (Ra) at rest in CS (1.96 +/- 0.14 mg.kg-1 x min-1) and AS (2.02 +/- 0.14) were higher than in NS (1.41 +/- 0.15, P < 0.05). With exercise, the glucose Ra values rose in all groups above resting values but were significantly greater in CS (4.76 +/- 0.50) and AS (4.71 +/- 0.53) than in NS (3.31 +/- 0.16). Glucose oxidation during exercise was elevated in smokers (2.31 +/- 0.37 mg.kg-1 x min-1 in CS and 2.18 +/- 0.34 in AS) compared with NS (1.09 +/- 0.18, P < 0.05). Nicotine levels correlated with the glucose Ra in AS (r = 0.93, P < 0.01). In conclusion, the results indicate that long-term smoking, independent of acute smoking, increases the dependence on blood glucose as a fuel during rest and sustained submaximal exercise.