Substrate utilization during endurance exercise in men and women after endurance training

2001 ◽  
Vol 280 (6) ◽  
pp. E898-E907 ◽  
Author(s):  
S. L. Carter ◽  
C. Rennie ◽  
M. A. Tarnopolsky
Keyword(s):  
Endurance Training ◽  
Endurance Exercise ◽  
Cycle Ergometer ◽  
Whole Body ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Glucose Flux ◽  
Before And After ◽  
Glycerol Utilization ◽  
Males And Females

We investigated the effect of endurance training on whole body substrate, glucose, and glycerol utilization during 90 min of exercise at 60% peak O2 consumption (V˙o 2 peak) in males and females. Substrate oxidation was determined before and after 7 wk of endurance training on a cycle ergometer, with posttesting performed at the same absolute (ABS, W) and relative (REL, %V˙o 2 peak) intensities. [6,6-2H]glucose and [1,1,2,3,3-2H]glycerol tracers were used to calculate the respective substrate tracee flux. Endurance training resulted in an increase inV˙o 2 peak for both males and females of 17 and 22%, respectively ( P < 0.001). Females demonstrated a lower respiratory exchange ratio (RER) both pretraining and posttraining compared with males during exercise ( P< 0.001). Glucose rate of appearance (Ra) and rate of disappearance (Rd) were not different between males and females. Glucose metabolic clearance rate (MCR) was lower at 75 and 90 min of exercise for females compared with males ( P < 0.05). Glucose Ra and Rd were lower during exercise at both ABS and REL posttraining exercise intensities compared with pretraining ( P < 0.001). Females had a higher exercise glycerol Ra and Rd compared with males both pre- and posttraining ( P < 0.001). Glycerol Ra was not different at either the ABS or REL posttraining exercise intensities compared with pretraining. We concluded that females oxidize proportionately more lipid and less carbohydrate during exercise compared with males both pre- and posttraining, which was cotemporal with a higher glycerol Ra in females. Furthermore, endurance training resulted in a decrease in glucose flux at both ABS and REL exercise intensities after endurance exercise training.

Training-induced alterations of glucose flux in men

1997 ◽  
Vol 82 (4) ◽  
pp. 1360-1369 ◽  
Author(s):  
Anne L. Friedlander ◽  
Gretchen A. Casazza ◽  
Michael A. Horning ◽  
Melvin J. Huie ◽  
George A. Brooks
Keyword(s):  
Exercise Intensity ◽  
Cycle Ergometer ◽  
Glucose Disposal ◽  
Metabolic Clearance ◽  
Intensity Effect ◽  
Glucose Flux ◽  
Relative Exercise Intensity ◽  
Before And After ◽  
Male Subjects ◽  
Intensity Training

Friedlander, Anne L., Gretchen A. Casazza, Michael A. Horning, Melvin J. Huie, and George A. Brooks. Training-induced alterations of glucose flux in men. J. Appl. Physiol. 82(4): 1360–1369, 1997.—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 (V˙o 2 peak)] 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 increasedV˙o 2 peak by 9.4 ± 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance (Ra; 5.84 ± 0.23 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), disappearance (Rd; 5.78 ± 0.19 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), oxidation (Rox; 5.36 ± 0.15 vs. 3.41 ± 0.23 mg ⋅ kg−1 ⋅ min−1), and metabolic clearance (7.03 ± 0.56 vs. 5.20 ± 0.28 ml ⋅ kg−1 ⋅ min−1) of glucose being significantly greater ( P ≤ 0.05) in the 65% than the 45%V˙o 2 peak trial. When Rd was expressed as a percentage of total energy expended per minute (Rd E), there was no difference between the 45 and 65% intensities. Training did reduce Ra (4.63 ± 0.25), Rd (4.65 ± 0.24), Rox (3.77 ± 0.43), and Rd E (15.30 ± 0.40 to 12.85 ± 0.81) when subjects were tested at the same absolute workload ( P ≤ 0.05). However, when they were tested at the same relative workload, Ra, Rd, and Rd E were not different, although Rox was lower posttraining (5.36 ± 0.15 vs. 4.41 ± 0.42, P ≤ 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.

scholarly journals Training improves the response in glucose flux to exercise in postmenopausal women

2009 ◽  
Vol 107 (1) ◽  
pp. 90-97 ◽  
Author(s):  
Zinta A. Zarins ◽  
Matthew L. Johnson ◽  
Nastaran Faghihnia ◽  
Michael A. Horning ◽  
Gareth A. Wallis ◽  
...  
Keyword(s):  
Endurance Training ◽  
Postmenopausal Women ◽  
Power Output ◽  
Insulin Response ◽  
Cycle Ergometer ◽  
Peak Oxygen Consumption ◽  
Whole Body ◽  
Younger Women ◽  
Glucose Flux ◽  
Ergometer Exercise

We examined the effects of endurance training on parameters of glucose flux during rest and exercise in postmenopausal women. Ten sedentary, but healthy women (55 ± 1 yr) completed 12 wk of endurance exercise training on a cycle ergometer [5 days/wk, 1 h/day, 65% peak oxygen consumption (V̇o2peak)]. Flux rates were determined by primed continuous infusion of [6,6-2H]glucose (D2-glucose) during 90 min of rest and 60 min of cycle ergometer exercise during one pretraining exercise trial [65% V̇o2peak (PRE)] and two posttraining exercise trials [the power output that elicited 65% pretraining V̇o2peak (ABT) and 65% posttraining V̇o2peak (RLT)]. Training increased V̇o2peak by 16.3 ± 3.9% ( P < 0.05). Epinephrine and glucagon were lower during ABT and lactate was lower during ABT and RLT ( P < 0.05), but the apparent insulin response was unchanged. Whole body glucose rate of appearance decreased posttraining during exercise at a given power output (4.58 ± 0.39 mg·kg−1·min−1 during ABT compared with 5.21 ± 0.48 mg·kg−1·min−1 PRE, P < 0.05), but not at the same relative workload (5.85 ± 0.36 mg·kg−1·min−1). Training resulted in a 35% increase in glucose MCR during exercise at the same relative intensity (7.16 ± 0.42 ml·kg−1·min−1 during RLT compared with 5.28 ± 0.42 ml·kg−1·min−1 PRE, P < 0.05). Changes in parameters of glucose kinetics during exercise were accomplished without changes in dietary composition, body weight, or body composition. We conclude that despite changes in the hormonal milieu that occur at menopause, endurance training results in a similar magnitude in training-induced alterations of glucose flux as seen previously in younger women.

Dietary Composition Influences Short-term Endurance Training–Induced Adaptations of Substrate Partitioning during Exercise

2004 ◽  
Vol 14 (1) ◽  
pp. 38-61 ◽  
Author(s):  
Kevin A. Jacobs ◽  
David R. Paul ◽  
Ray J. Geor ◽  
Kenneth W. Hinchcliff ◽  
W. Michael Sherman
Keyword(s):  
Endurance Training ◽  
Time Trial ◽  
Whole Body ◽  
High Fat ◽  
Short Term ◽  
Time Trial Performance ◽  
Glucose Flux ◽  
Before And After ◽  
Substrate Partitioning ◽  
Trial Performance

The purpose of the current study was to examine the influence of dietary composition on short-term endurance training–induced adaptations of substrate partitioning and time trial exercise performance. Eight untrained males cycled for 90 min at ~54% aerobic capacity while being infused with [6,62H]glucose before and after two 10-d experimental phases separated by a 2-week washout period. Time trial performance was measured after the 90-min exercise trials before and after the 2nd experimental phase. During the first 10-d phase, subjects were randomly assigned to consume either a high carbohydrate or high fat diet while remaining inactive (CHO or FAT). During the second 10-d phase, subjects consumed the opposite diet, and both groups performed identical daily supervised endurance training (CHO+T or FAT+T). CHO and CHO+T did not affect exercise metabolism. FAT reduced glucose flux at the end of exercise, while FAT+T substantially increased whole body lipid oxidation during exercise and reduced glucose flux at the end of exercise. Despite these differences in adaptation of substrate use, training resulted in similar improvements in time trial performance for both groups. We conclude that (a) 10-d high fat diets result in substantial increases in whole body lipid oxidation during exercise when combined with daily aerobic training, and (b) diet does not affect short-term training-induced improvements in high-intensity time trial performance.

Isotopic estimation of CO2 production during exercise before and after endurance training

1993 ◽  
Vol 75 (1) ◽  
pp. 70-75 ◽  
Author(s):  
A. R. Coggan ◽  
D. L. Habash ◽  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
C. L. Kien
Keyword(s):  
Endurance Training ◽  
Tricarboxylic Acid Cycle ◽  
Cycle Ergometer ◽  
Submaximal Exercise ◽  
Carbohydrate Oxidation ◽  
Whole Body ◽  
Co2 Production ◽  
Acid Oxidation ◽  
Ergometer Exercise ◽  
Before And After

Endurance training reduces the rate of CO2 release (i.e., VCO2) during submaximal exercise, which has been interpreted to indicate a reduction in carbohydrate oxidation. However, decreased ventilation, decreased buffering of lactate, and/or increased fixation of CO2 could also account for a lower VCO2 after training. We therefore used a primed continuous infusion of NaH13CO3 to determine the whole body rate of appearance of CO2 (RaCO2) in seven men during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2peak) before and after endurance training. RaCO2 is independent of the above-described factors affecting VCO2 but may overestimate net CO2 production due to pyruvate carboxylation and subsequent isotopic exchange in the tricarboxylic acid cycle. Training consisted of cycling at 75–100% VO2peak for 45–90 min/day, 6 days/wk, for 12 wk and increased VO2peak by 28% (P < 0.001). VCO2 during submaximal exercise was reduced from 86.8 +/- 3.7 to 76.2 +/- 4.2 mmol/min, whereas RaCO2 fell from 88.9 +/- 4.0 to 76.4 +/- 4.4 mmol/min (both P < 0.001). VCO2 and RaCO2 were highly correlated in the untrained (r = 0.98, P < 0.001) and trained (r = 0.99, P < 0.001) states, as were individual changes in VCO2 and RaCO2 with training (r = 0.88, P < 0.01). These results support the hypothesis that endurance training decreases CO2 production during exercise. The magnitude and direction of this change cannot be explained by reported training-induced alterations in amino acid oxidation, indicating that it must be the result of a decrease in carbohydrate oxidation and an increase in fat oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

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

1999 ◽  
Vol 87 (5) ◽  
pp. 1684-1696 ◽  
Author(s):  
Bryan C. Bergman ◽  
Eugene E. Wolfel ◽  
Gail E. Butterfield ◽  
Gary D. Lopaschuk ◽  
Gretchen A. Casazza ◽  
...  
Keyword(s):  
Endurance Training ◽  
Power Output ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Lactate Clearance ◽  
Cycle Ergometer ◽  
Whole Body ◽  
Moderate Intensity ◽  
Metabolic Clearance ◽  
Lactate Uptake

We evaluated the hypotheses that endurance training decreases arterial lactate concentration ([lactate]a) during continuous exercise by decreasing net lactate release (L˙) and appearance rates (Ra) and increasing metabolic clearance rate (MCR). Measurements were made at two intensities before [45 and 65% peak O2consumption (V˙o 2 peak)] and after training [65% pretrainingV˙o 2 peak, same absolute workload (ABT), and 65% posttrainingV˙o 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%V˙o 2 peak. Compared with the 65%V˙o 2 peakpretraining condition (4.75 ± 0.4 mM), [lactate]a decreased at ABT (41%) and RLT (21%) ( P < 0.05). L˙ 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.

Letters to the Editor

1998 ◽  
Vol 84 (4) ◽  
pp. 1480-1482
Author(s):  
Andrew Coggan
Keyword(s):  
Exercise Intensity ◽  
Cycle Ergometer ◽  
Glucose Disposal ◽  
Metabolic Clearance ◽  
Letters To The Editor ◽  
Intensity Effect ◽  
Glucose Flux ◽  
Relative Exercise Intensity ◽  
Before And After ◽  
Male Subjects

The following is the abstract of the article discussed in the subsequent letter: Friedlander, Anne L., Gretchen A. Casazza, Michael A. Horning, Melvin J. Huie, and George A. Brooks. Training-induced alterations of glucose flux in men. J. Appl. Physiol. 82(4): 1360–1369, 1997.—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 (V˙o 2 peak)] and two post- training 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 increasedV˙o 2 peak by 9.4 ± 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance (Ra; 5.84 ± 0.23 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), disappearance (Rd; 5.78 ± 0.19 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), oxidation (Rox; 5.36 ± 0.15 vs. 3.41 ± 0.23 mg ⋅ kg−1 ⋅ min−1), and metabolic clearance (7.03 ± 0.56 vs. 5.20 ± 0.28 ml ⋅ kg−1 ⋅ min−1) of glucose being significantly greater ( P ≤ 0.05) in the 65% than the 45%V˙o 2 peak trial. When Rd was expressed as a percentage of total energy expended per minute (Rd E), there was no difference between the 45 and 65% intensities. Training did reduce Ra(4.63 ± 0.25), Rd(4.65 ± 0.24), Rox(3.77 ± 0.43), and Rd E(15.30 ± 0.40 to 12.85 ± 0.81) when subjects were tested at the same absolute workload ( P ≤ 0.05). However, when they were tested at the same relative workload, Ra, Rd, and Rd E were not different, although Roxwas lower posttraining (5.36 ± 0.15 vs. 4.41 ± 0.42, P ≤ 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.

Ten-day endurance training attenuates the hyperosmotic suppression of cutaneous vasodilation during exercise but not sweating

2005 ◽  
Vol 99 (1) ◽  
pp. 237-243 ◽  
Author(s):  
Takashi Ichinose ◽  
Kazunobu Okazaki ◽  
Shizue Masuki ◽  
Hiroyuki Mitono ◽  
Mian Chen ◽  
...  
Keyword(s):  
Endurance Training ◽  
Exercise Intensity ◽  
Plasma Osmolality ◽  
Young Male ◽  
Cycle Ergometer ◽  
Peak Oxygen Consumption ◽  
Cutaneous Vasodilation ◽  
Thermoregulatory Responses ◽  
Before And After ◽  
The Individual

It is well known that hyperosmolality suppresses thermoregulatory responses and that plasma osmolality (Posmol) increases with exercise intensity. We examined whether the decreased esophageal temperature thresholds for cutaneous vasodilation (THFVC) and sweating (THSR) after 10-day endurance training (ET) are caused by either attenuated increase in Posmol at a given exercise intensity or blunted sensitivity of hyperosmotic suppression. Nine young male volunteers exercised on a cycle ergometer at 60% peak oxygen consumption rate (V̇o2 peak) for 1 h/day for 10 days at 30°C. Before and after ET, thermoregulatory responses were measured during 20-min exercise at pretraining 70% V̇o2 peak in the same environment as during ET under isoosmotic or hyperosmotic conditions. Hyperosmolality by ∼10 mosmol/kgH2O was attained by acute hypertonic saline infusion. After ET, V̇o2 peak and blood volume (BV) both increased by ∼4% ( P < 0.05), followed by a decrease in THFVC ( P < 0.05) but not by that in THSR. Although there was no significant decrease in Posmol at the thresholds after ET, the sensitivity of increase in THFVC at a given increase in Posmol [ΔTHFVC/ΔPosmol,°C·(mosmol/kgH2O)−1], determined by hypertonic infusion, was reduced to 0.021 ± 0.005 from 0.039 ± 0.004 before ET ( P < 0.05). The individual reductions in ΔTHFVC/ΔPosmol after ET were highly correlated with their increases in BV around THFVC ( r = −0.89, P < 0.005). In contrast, there was no alteration in the sensitivity of the hyperosmotic suppression of sweating after ET. Thus the downward shift of THFVC after ET was partially explained by the blunted sensitivity to hyperosmolality, which occurred in proportion to the increase in BV.

Effects of training on lactate production and removal during progressive exercise in humans

1992 ◽  
Vol 72 (5) ◽  
pp. 1649-1656 ◽  
Author(s):  
H. S. MacRae ◽  
S. C. Dennis ◽  
A. N. Bosch ◽  
T. D. Noakes
Keyword(s):  
Endurance Training ◽  
Lactate Production ◽  
Metabolic Clearance ◽  
O2 Uptake ◽  
Lower Blood ◽  
Peak Lactate ◽  
Progressive Exercise ◽  
Before And After ◽  
Power Outputs ◽  
Exercise In Humans

To determine whether the reduced blood lactate concentrations [La] during submaximal exercise in humans after endurance training result from a decreased rate of lactate appearance (Ra) or an increased rate of lactate metabolic clearance (MCR), interrelationships among blood [La], lactate Ra, and lactate MCR were investigated in eight untrained men during progressive exercise before and after a 9-wk endurance training program. Radioisotope dilution measurements of L-[U-14C]lactate revealed that the slower rise in blood [La] with increasing O2 uptake (VO2) after training was due to a reduced lactate Ra at the lower work rates [VO2 less than 2.27 l/min, less than 60% maximum VO2 (VO2max); P less than 0.01]. At power outputs closer to maximum, peak lactate Ra values before (215 +/- 28 mumol.min-1.kg-1) and after training (244 +/- 12 mumol.min-1.kg-1) became similar. In contrast, submaximal (less than 75% VO2max) and peak lactate MCR values were higher after than before training (40 +/- 3 vs. 31 +/- 4 ml.min-1.kg-1, P less than 0.05). Thus the lower blood [La] values during exercise after training in this study were caused by a diminished lactate Ra at low absolute and relative work rates and an elevated MCR at higher absolute and all relative work rates during exercise.

Influence of endurance training on muscle [PCr] kinetics during high-intensity exercise

2007 ◽  
Vol 293 (1) ◽  
pp. R392-R401 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Nicolas J. Berger ◽  
Jonathan Fulford
Keyword(s):  
Endurance Training ◽  
High Intensity ◽  
Slow Component ◽  
Knee Extension ◽  
High Intensity Exercise ◽  
Whole Body ◽  
Time To Exhaustion ◽  
Exercise Tests ◽  
Before And After ◽  
Knee Extension Exercise

We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 ± 5 yr) completed 5 wk of single-legged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 ± 2.3 min vs. postintervention group (POST): 19.4 ± 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 ± 1.6 min vs. POST: 22.0 ± 2.2 min; P < 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 ± 13 s vs. POST: 43 ± 10 s) or the trained leg (PRE: 38 ± 8 s vs. POST: 40 ± 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 ± 7 vs. POST: 7 ± 7% change in [PCr]; P < 0.05) with there being no change in the control leg (PRE: 13 ± 8 vs. POST: 12 ± 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.

Long-term mild jogging increases insulin action despite no influence on body mass index or VO2 max

1989 ◽  
Vol 66 (5) ◽  
pp. 2206-2210 ◽  
Author(s):  
Y. Oshida ◽  
K. Yamanouchi ◽  
S. Hayamizu ◽  
Y. Sato
Keyword(s):  
Body Mass Index ◽  
Body Mass ◽  
Clearance Rate ◽  
Insulin Action ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Before And After ◽  
Plasma Insulin Levels ◽  
Improve Glucose Tolerance

Physical training has been shown to improve glucose tolerance and insulin sensitivity. In the present study, insulin action was determined using the euglycemic clamp technique in six untrained nonobese subjects before, during, and after long-term mild regular jogging. After 1 yr of jogging, steady-state plasma insulin levels (I) decreased significantly, and the metabolic clearance rate of insulin was increased by 87%, although insulin infusion rate during the clamp was constant for each individual. The amount of glucose infused (glucose metabolism, M) tended to increase from 6.16 +/- 0.94 to 8.15 +/- 1.94 mg.kg-1.min-1 after regular jogging for 1 yr, although that was not statistically significant. However, M/I increases significantly from 0.060 +/- 0.012 to 0.184 +/- 0.056 (P less than 0.05) after 1 yr. The concentrations of plasma free fatty acids during the hyperinsulinemic clamp decreased more significantly after 1 yr of jogging (P less than 0.05). The concentrations of plasma glycerol decreased gradually before and after long-term regular jogging, showing only a 50–60% reduction in 120 min. Therefore, long-term mild regular jogging, which did not influence either body mass index or maximal O2 uptake, appears to improve insulin action in both carbohydrate and lipid metabolism and to increase the metabolic clearance rate of insulin.

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