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)

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.

Endurance training decreases plasma glucose turnover and oxidation during moderate-intensity exercise in men

1990 ◽  
Vol 68 (3) ◽  
pp. 990-996 ◽  
Author(s):  
A. R. Coggan ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
D. M. Bier ◽  
J. O. Holloszy
Keyword(s):  
Endurance Training ◽  
Plasma Glucose ◽  
Cycle Ergometer ◽  
Fat Free Mass ◽  
Strenuous Exercise ◽  
Moderate Intensity ◽  
Glucose Turnover ◽  
Moderate Intensity Exercise ◽  
Ergometer Exercise ◽  
Before And After

To assess the effects of endurance training on plasma glucose kinetics during moderate-intensity exercise in men, seven men were studied before and after 12 wk of strenuous exercise training (3 days/wk running, 3 days/wk cycling). After priming of the glucose and bicarbonate pools, [U-13C] glucose was infused continuously during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2) to determine glucose turnover and oxidation. Training increased cycle ergometer peak VO2 by 23% and decreased the respiratory exchange ratio during the final 30 min of exercise from 0.89 +/- 0.01 to 0.85 +/- 0.01 (SE) (P less than 0.001). Plasma glucose turnover during exercise decreased from 44.6 +/- 3.5 mumol.kg fat-free mass (FFM)-1.min-1 before training to 31.5 +/- 4.3 after training (P less than 0.001), whereas plasma glucose clearance (i.e., rate of disappearance/plasma glucose concentration) fell from 9.5 +/- 0.6 to 6.4 +/- 0.8 ml.kg FFM-1.min-1 (P less than 0.001). Oxidation of plasma-derived glucose, which accounted for approximately 90% of plasma glucose disappearance in both the untrained and trained states, decreased from 41.1 +/- 3.4 mumol.kg FFM-1.min-1 before training to 27.7 +/- 4.8 after training (P less than 0.001). This decrease could account for roughly one-half of the total reduction in the amount of carbohydrate utilized during the final 30 min of exercise in the trained compared with the untrained state.

Effect of prolonged exercise on muscle citrate concentration before and after endurance training in men

1993 ◽  
Vol 264 (2) ◽  
pp. E215-E220 ◽  
Author(s):  
A. R. Coggan ◽  
R. J. Spina ◽  
W. M. Kohrt ◽  
J. O. Holloszy
Keyword(s):  
Endurance Training ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Cycle Ergometer ◽  
Vastus Lateralis Muscle ◽  
Carbohydrate Utilization ◽  
Citrate Concentration ◽  
P Concentration ◽  
Ergometer Exercise ◽  
Before And After

It has been hypothesized that endurance training reduces carbohydrate utilization during exercise via citrate-mediated inhibition of phosphofructokinase (PFK). To test this hypothesis, vastus lateralis muscle biopsy samples were obtained from eight men before and immediately (approximately 10 s) after 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake, both before and after 12 wk of endurance exercise training (3 days/wk running, 3 days/wk interval cycling). Training increased muscle citrate synthase (CS) activity from 3.69 +/- 0.48 (SE) to 5.30 +/- 0.42 mol.h-1.kg protein-1 and decreased the mean respiratory exchange ratio during exercise from 0.92 +/- 0.01 to 0.88 +/- 0.01 (both P < 0.001). Muscle citrate concentration at the end of exercise correlated significantly with CS activity (r = 0.70; P < 0.005) and was slightly but not significantly higher after training (0.80 +/- 0.19 vs. 0.54 +/- 0.19 mmol/kg dry wt; P = 0.16). Muscle glucose 6-phosphate (G-6-P) concentration at the end of exercise, however, was 31% lower in the trained state (1.17 +/- 0.10 vs. 1.66 +/- 0.27 mmol/kg dry wt; P < 0.05), in keeping with a 36% decrease in the amount of muscle glycogen utilized (133 +/- 22 vs. 209 +/- 19 mmol.kg dry wt-1.2 h-1; P < 0.01). The lower G-6-P concentration after training suggests that the training-induced reduction in carbohydrate utilization results from attenuation of flux before the PFK step in glycolysis and is not due to citrate-mediated inhibition of PFK.

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.

Effect of endurance training on hepatic glycogenolysis and gluconeogenesis during prolonged exercise in men

1995 ◽  
Vol 268 (3) ◽  
pp. E375-E383 ◽  
Author(s):  
A. R. Coggan ◽  
S. C. Swanson ◽  
L. A. Mendenhall ◽  
D. L. Habash ◽  
C. L. Kien
Keyword(s):  
Endurance Training ◽  
Prolonged Exercise ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Cycle Ergometer ◽  
Hepatic Glucose Metabolism ◽  
Ergometer Exercise ◽  
Hepatic Glucose ◽  
Before And After ◽  
Response To Exercise

In humans, endurance training markedly reduces the rate of hepatic glucose production during exercise. To determine whether this is due to a reduction in glycogenolysis, in gluconeogenesis, or in both processes, six men were studied at rest and during 2 h of cycle ergometer exercise at 60% pretraining peak O2 consumption (VO2peak), both before and after completion of a strenuous endurance training program (cycling at 75-100% VO2peak for 45-90 min/day, 6 days/wk for 12 wk). The overall rate of glucose appearance (Ra) was determined using a primed continuous infusion of [6,6-2H]glucose, whereas the rate of gluconeogenesis (Rgng) was estimated from the incorporation of 13C into glucose (via pyruvate carboxylase) from simultaneously infused [13C]bicarbonate. Training did not affect glucose kinetics at rest but reduced the average Ra during exercise by 42% [from 36.8 +/- 3.8 to 21.5 +/- 3.6 (SE) mumol.min-1.kg-1; P < 0.001]. This decrease appeared to be mostly due to a reduction in hepatic glycogenolysis. However, the estimated Rgng during exercise also decreased significantly (P < 0.001) with training, falling from 7.5 +/- 1.6 mumol.min-1.kg-1 (23 +/- 3% of total Ra) before training to 3.1 +/- 0.6 mumol.min-1.kg-1 (14 +/- 3% of total Ra) after training. These training-induced adaptations in hepatic glucose metabolism were associated with an attenuated hormonal response to exercise (i.e., higher insulin and lower glucagon, norepinephrine, and epinephrine concentrations) as well as a reduced availability of gluconeogenic precursors (i.e., lower lactate and glycerol concentrations). We conclude that endurance training reduces both hepatic glycogenolysis and gluconeogenesis during prolonged exercise in men.

Central and peripheral adaptations of the gas transport system to one-leg training

1981 ◽  
Vol 59 (11) ◽  
pp. 1146-1154 ◽  
Author(s):  
S. G. Thomas ◽  
D. A. Cunningham ◽  
M. J. Plyley ◽  
D. R. Boughner ◽  
R. A. Cook
Keyword(s):  
Cardiac Output ◽  
Oxygen Uptake ◽  
Endurance Training ◽  
Maximal Oxygen Uptake ◽  
Enzyme Activities ◽  
Cardiovascular Responses ◽  
Cycle Ergometer ◽  
Left Ventricular ◽  
Enzyme Analysis ◽  
Ergometer Exercise

The role of central and peripheral adaptations in the response to endurance training was examined. Changes in cardiac structure and function, oxygen extraction, and muscle enzyme activities following one-leg training were studied.Eleven subjects (eight females, three males) trained on a cycle ergometer 4 weeks with one leg (leg 1), then 4 weeks with the second leg (leg 2). Cardiovascular responses to exercise with both legs and each leg separately were evaluated at entry (T1), after 4 weeks of training (T2), and after a second 4 weeks of training (T3). Peak oxygen uptake ([Formula: see text] peak) during exercise with leg 1 (T1 to T2 increased 19.8% (P < 0.05) and during exercise with leg 2 (T2 to T3 increased 16.9% (P < 0.05). Maximal oxygen uptake with both legs increased 7.9% from T1 to T2 and 9.4% from T2 to T3 (P < 0.05). During exercise at 60% of [Formula: see text] peak, cardiac output [Formula: see text] was increased significantly only when the trained leg was exercised. [Formula: see text] increased 12.2% for leg 1 between T1 and T2 and 13.0% for leg 2 between T2 and T3 (P < 0.05). M-mode echocardiographic assessment of left ventricular internal diameter at diastole and peak velocity of circumferential fibre shortening at rest or during supine cycle ergometer exercise at T1 and T3 revealed no training induced changes in cardiac dimensions or function. Enzyme analysis of muscle biopsy samples from the vastus lateralis (At T1, T2, T3) revealed no consistent pattern of change in aerobic (malate dehydrogenase and 3-hydroxyacyl-CoA dehydrogenase) or anaerobic (phosphofructokinase, lactate dehydroginase, and creatine kinase) enzyme activities. Increases in cardiac output and maximal oxygen uptake which result from short duration endurance training can be achieved, therefore, without measurable central cardiac adaptation. The absence of echocardio-graphically determined changes in cardiac dimensions and contractility and the absence of an increase in cardiac output during exercise with the nontrained leg following training of the contralateral limb support this conclusion.

The relationship between human skeletal muscle pyruvate dehydrogenase phosphatase activity and muscle aerobic capacity

2011 ◽  
Vol 111 (2) ◽  
pp. 427-434 ◽  
Author(s):  
Lorenzo K. Love ◽  
Paul J. LeBlanc ◽  
J. Greig Inglis ◽  
Nicolette S. Bradley ◽  
Jon Choptiany ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Endurance Training ◽  
Aerobic Capacity ◽  
Pyruvate Dehydrogenase ◽  
Human Skeletal Muscle ◽  
Citrate Synthase ◽  
Tricarboxylic Acid Cycle ◽  
Carbohydrate Oxidation ◽  
Pyruvate Dehydrogenase Phosphatase

Pyruvate dehydrogenase (PDH) is a mitochondrial enzyme responsible for regulating the conversion of pyruvate to acetyl-CoA for use in the tricarboxylic acid cycle. PDH is regulated through phosphorylation and inactivation by PDH kinase (PDK) and dephosphorylation and activation by PDH phosphatase (PDP). The effect of endurance training on PDK in humans has been investigated; however, to date no study has examined the effect of endurance training on PDP in humans. Therefore, the purpose of this study was to examine differences in PDP activity and PDP1 protein content in human skeletal muscle across a range of muscle aerobic capacities. This association is important as higher PDP activity and protein content will allow for increased activation of PDH, and carbohydrate oxidation. The main findings of this study were that 1) PDP activity ( r2 = 0.399, P = 0.001) and PDP1 protein expression ( r2 = 0.153, P = 0.039) were positively correlated with citrate synthase (CS) activity as a marker for muscle aerobic capacity; 2) E1α ( r2 = 0.310, P = 0.002) and PDK2 protein ( r2 = 0.229, P =0.012) are positively correlated with muscle CS activity; and 3) although it is the most abundant isoform, PDP1 protein content only explained ∼18% of the variance in PDP activity ( r2 = 0.184, P = 0.033). In addition, PDP1 in combination with E1α explained ∼38% of the variance in PDP activity ( r2 = 0.383, P = 0.005), suggesting that there may be alternative regulatory mechanisms of this enzyme other than protein content. These data suggest that with higher muscle aerobic capacity (CS activity) there is a greater capacity for carbohydrate oxidation (E1α), in concert with higher potential for PDH activation (PDP activity).

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.

scholarly journals Effects of 30 min of aerobic exercise on gene expression in human neutrophils

2008 ◽  
Vol 104 (1) ◽  
pp. 236-243 ◽  
Author(s):  
Shlomit Radom-Aizik ◽  
Frank Zaldivar ◽  
Szu-Yun Leu ◽  
Pietro Galassetti ◽  
Dan M. Cooper
Keyword(s):  
Gene Expression ◽  
Mononuclear Cells ◽  
Cycle Ergometer ◽  
Human Neutrophils ◽  
Peripheral Blood Mononuclear ◽  
False Discovery ◽  
Ergometer Exercise ◽  
Before And After ◽  
Ease Score ◽  
Repair Genes

Relatively brief bouts of exercise alter gene expression in peripheral blood mononuclear cells (PBMCs), but whether exercise changes gene expression in circulating neutrophils (whose numbers, like PBMCs, increase) is not known. We hypothesized that exercise would activate neutrophil genes involved in apoptosis, inflammation, and cell growth and repair, since these functions in leukocytes are known to be influenced by exercise. Blood was sampled before and immediately after 30 min of constant, heavy (∼80% peak O2uptake) cycle ergometer exercise in 12 healthy men (19–29 yr old) of average fitness. Neutrophils were isolated using density gradients; RNA was hybridized to Affymetrix U133+2 Genechip arrays. With false discovery rate (FDR) <0.05 with 95% confidence, a total of 526 genes were differentially expressed between before and after exercise. Three hundred and sixteen genes had higher expression after exercise. The Jak/STAT pathway, known to inhibit apoptosis, was significantly activated (EASE score, P < 0.005), but 14 genes were altered in a way likely to accelerate apoptosis as well. Similarly, both proinflammatory (e.g., IL-32, TNFSF8, and CCR5) and anti-inflammatory (e.g., ANXA1) were affected. Growth and repair genes like AREG and FGF2 receptor genes (involved in angiogenesis) were also activated. Finally, a number of neutrophil genes known to be involved in pathological conditions like asthma and arthritis were altered by exercise, suggesting novel links between physical activity and disease or its prevention. In summary, brief heavy exercise leads to a previously unknown substantial and significant alteration in neutrophil gene expression.

Effect of carbohydrate ingestion on exercise metabolism

1988 ◽  
Vol 65 (4) ◽  
pp. 1553-1555 ◽  
Author(s):  
M. Hargreaves ◽  
C. A. Briggs
Keyword(s):  
Muscle Glycogen ◽  
Venous Blood ◽  
Cycle Ergometer ◽  
Strenuous Exercise ◽  
Carbohydrate Ingestion ◽  
Ergometer Exercise ◽  
Glucose Polymer ◽  
Before And After ◽  
Plasma Insulin Levels ◽  
Glycogen Utilization

Five male cyclists were studied during 2 h of cycle ergometer exercise (70% VO2 max) on two occasions to examine the effect of carbohydrate ingestion on muscle glycogen utilization. In the experimental trial (CHO) subjects ingested 250 ml of a glucose polymer solution containing 30 g of carbohydrate at 0, 30, 60, and 90 min of exercise; in the control trial (CON) they received an equal volume of a sweet placebo. No differences between trials were seen in O2 uptake or heart rate during exercise. Venous blood glucose was similar before exercise in both trials, but, on average, was higher during exercise in CHO [5.2 +/- 0.2 (SE) mmol/l] compared with CON (4.8 +/- 0.1, P less than 0.05). Plasma insulin levels were similar in both trials. Muscle glycogen levels were also similar in CHO and CON both before and after exercise; accordingly, there was no difference between trials in the amount of glycogen used during the 2 h of exercise (CHO = 62.8 +/- 10.1 mmol/kg wet wt, CON = 56.9 +/- 10.1). The results of this study indicate that carbohydrate ingestion does not influence the utilization of muscle glycogen during prolonged strenuous exercise.

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