Ten days of exercise training reduces glucose production and utilization during moderate-intensity exercise

1994 ◽  
Vol 266 (1) ◽  
pp. E136-E143 ◽  
Author(s):  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
D. L. Habash ◽  
A. R. Coggan
Keyword(s):  
Endurance Training ◽  
Time Course ◽  
Plasma Concentrations ◽  
Glucose Production ◽  
Peak Oxygen Uptake ◽  
Cycle Ergometer ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Ergometer Exercise ◽  
Exercise Induced

We have previously shown that 12 wk of endurance training reduces the rate of glucose appearance (Ra) during submaximal exercise (Coggan, A. R., W. M. Kohrt, R. J. Spina, D. M. Bier, and J. O. Holloszy. J. Appl. Physiol. 68: 990-996, 1990). The purpose of the present study was to examine the time course of and relationship between training-induced alterations in glucose kinetics and endocrine responses during prolonged exercise. Accordingly, seven men were studied during 2 h of cycle ergometer exercise at approximately 60% of pretraining peak oxygen uptake on three occasions: before, after 10 days, and after 12 wk of endurance training. Ra was determined using a primed, continuous infusion of [6,6-2H]glucose. Ten days of training reduced mean Ra during exercise from 36.9 +/- 3.3 (SE) to 28.5 +/- 3.4 mumol.min-1.kg-1 (P < 0.001). Exercise-induced changes in insulin, C-peptide, glucagon, norepinephrine, and epinephrine were also significantly blunted. After 12 wk of training, Ra during exercise was further reduced to 21.5 +/- 3.1 mumol.min-1.kg-1 (P < 0.001 vs. 10 days), but hormone concentrations were not significantly different from 10-day values. The lower glucose Ra during exercise after short-term (10 days) training is accompanied by, and may be due to, altered plasma concentrations of the major glucoregulatory hormones. However, other adaptations must be responsible for the further reduction in Ra with more prolonged training.

Epinephrine infusion during moderate intensity exercise increases glucose production and uptake

2000 ◽  
Vol 278 (5) ◽  
pp. E949-E957 ◽  
Author(s):  
Stuart H. Kreisman ◽  
Nicholas Ah Mew ◽  
Mylène Arsenault ◽  
Sharon J. Nessim ◽  
Jeffrey B. Halter ◽  
...  
Keyword(s):  
Plasma Catecholamines ◽  
Glucose Production ◽  
Cycle Ergometer ◽  
Moderate Intensity ◽  
Metabolic Clearance ◽  
Moderate Exercise ◽  
Moderate Intensity Exercise ◽  
Epinephrine Infusion ◽  
Ergometer Exercise ◽  
Male Subjects

The glucoregulatory response to intense exercise [IE, >80% maximum O2 uptake (V˙o 2 max)] comprises a marked increment in glucose production (Ra) and a lesser increment in glucose uptake (Rd), resulting in hyperglycemia. The Ra correlates with plasma catecholamines but not with the glucagon-to-insulin (IRG/IRI) ratio. If epinephrine (Epi) infusion during moderate exercise were able to markedly stimulate Ra, this would support an important role for the catecholamines' response in IE. Seven fit male subjects (26 ± 2 yr, body mass index 23 ± 0.5 kg/m2,V˙o 2 max 65 ± 5 ml ⋅ kg− 1 ⋅ min− 1) underwent 40 min of postabsorptive cycle ergometer exercise (145 ± 14 W) once without [control (CON)] and once with Epi infusion [EPI (0.1 μg ⋅ kg− 1 ⋅ min− 1)] from 30 to 40 min. Epi levels reached 9.4 ± 0.8 nM (20× rest, 10× CON). Ra increased ∼70% to 3.75 ± 0.53 in CON but to 8.57 ± 0.58 mg ⋅ kg− 1 ⋅ min− 1in EPI ( P < 0.001). Increments in Ra and Epi correlated ( r 2 = 0.923, P ≤ 0.01). In EPI, peak Rd (5.55 ± 0.54 vs. 3.38 ± 0.46 mg ⋅ kg− 1 ⋅ min− 1, P = 0.006) and glucose metabolic clearance rate (MCR, P= 0.018) were higher. The Ra-to-Rdimbalance in EPI caused hyperglycemia (7.12 ± 0.22 vs. 5.59 ± 0.22 mM, P = 0.001) until minute 60 of recovery. A small and late IRG/IRI increase ( P = 0.015 vs. CON) could not account for the Ra increase. Norepinephrine (∼4× increase at peak) did not differ between EPI and CON. Thus Epi infusion during moderate exercise led to increments in Ra and Rd and caused rises of plasma glucose, lactate, and respiratory exchange ratio in fit individuals, supporting a regulatory role for Epi in IE. Epi's effects on Rd and MCR during exercise may differ from its effects at rest.

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.

Peripheral Chemoreflex Drive in Moderate-Intensity Exercise

1996 ◽  
Vol 21 (4) ◽  
pp. 285-300 ◽  
Author(s):  
Claudette M. St. Croix ◽  
David A. Cunningham ◽  
Donald H. Paterson ◽  
John M. Kowalchuk
Keyword(s):  
Peak Level ◽  
Cycle Ergometer ◽  
Open Loop ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Peripheral Chemoreceptor ◽  
Carotid Bodies ◽  
Ergometer Exercise ◽  
End Tidal ◽  
Peripheral Chemoreflex

The purpose of this study was to measure the contribution of the peripheral chemoreceptor (pRc) to [Formula: see text] during the steady-state of moderate-intensity cycle ergometer exercise using continuous hyperoxic suppression of pRc drive, while stabilizing the drive from the central chemoreceptor by clamping end-tidal PCO2 (PETCO2) at the peak level attained during the hyperoxic period of a poikilocapnic ride. In the isocapnic protocol, the PETCO2 was maintained at a constant level by a negative feedback, open loop system. Five subjects completed four repetitions of each of the poikilocapnic and isocapnic protocols. In the poikilocapnic protocol, [Formula: see text] declined following the step into hyperoxia and then began to increase, whereas the decline in [Formula: see text] was maintained in the isocapnic protocol. However, the mean decrease in [Formula: see text] was not significantly different between the poikilocapnic (16.1 ± 5.0%) and isocapnic (14.9 ± 4.4%) protocols. These results suggest that the declining phase of [Formula: see text] is fully complete before the secondary central stimulating actions of hyperoxia on [Formula: see text] and that the pRc contributes about 15% of the drive to breathe in moderate intensity exercise. Key words: ventilatory control, carotid bodies, hyperoxia

scholarly journals Oxygen Cost of Recreational Horse-Riding in Females

2015 ◽  
Vol 12 (6) ◽  
pp. 808-813 ◽  
Author(s):  
Louisa Beale ◽  
Neil S Maxwell ◽  
Oliver R Gibson ◽  
Rosemary Twomey ◽  
Becky Taylor ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Cycle Ergometer ◽  
Peak Oxygen Consumption ◽  
Moderate Intensity ◽  
Oxygen Cost ◽  
Metabolic Demand ◽  
Moderate Intensity Exercise ◽  
The Public ◽  
Horse Riding ◽  
Ergometer Exercise

Background:The purpose of this study was to characterize the physiological demands of a riding session comprising different types of recreational horse riding in females.Methods:Sixteen female recreational riders (aged 17 to 54 years) completed an incremental cycle ergometer exercise test to determine peak oxygen consumption (VO2peak) and a 45-minute riding session based upon a British Horse Society Stage 2 riding lesson (including walking, trotting, cantering and work without stirrups). Oxygen consumption (VO2), from which metabolic equivalent (MET) and energy expenditure values were derived, was measured throughout.Results:The mean VO2 requirement for trotting/cantering (18.4 ± 5.1 ml·kg-1·min-1; 52 ± 12% VO2peak; 5.3 ± 1.1 METs) was similar to walking/trotting (17.4 ± 5.1 ml·kg-1·min-1; 48 ± 13% VO2peak; 5.0 ± 1.5 METs) and significantly higher than for work without stirrups (14.2 ± 2.9 ml·kg-1·min-1; 41 ± 12% VO2peak; 4.2 ± 0.8 METs) (P = .001).Conclusion:The oxygen cost of different activities typically performed in a recreational horse riding session meets the criteria for moderate intensity exercise (3-6 METs) in females, and trotting combined with cantering imposes the highest metabolic demand. Regular riding could contribute to the achievement of the public health recommendations for physical activity in this population.

Effects of sleep deprivation on thermoregulation during exercise

1984 ◽  
Vol 246 (1) ◽  
pp. R72-R77 ◽  
Author(s):  
M. N. Sawka ◽  
R. R. Gonzalez ◽  
K. B. Pandolf
Keyword(s):  
Sleep Deprivation ◽  
Sweat Rate ◽  
Thermal Conductance ◽  
Cycle Ergometer ◽  
Moderate Intensity ◽  
Control Test ◽  
Moderate Intensity Exercise ◽  
Ergometer Exercise ◽  
Total Body ◽  
And Control

Five fit men completed a practice, control, and sleep deprivation exercise test. Two nights of normal sleep preceded the control test, and 33 h of wakefulness preceded the sleep deprivation test. These tests consisted of 20 min of rest followed by 40 min of cycle-ergometer exercise (50% of peak O2 uptake, VO2) in a temperate (ambient temperature, 28 degrees C; relative humidity, 30%)-environment. Esophageal temperature (Tes), local sweat rate (mds), and chest thermal conductance (kch) were continuously measured. During exercise a 0.7 and 0.5 degrees C rise in Tes was found for the sleep deprivation and control tests, respectively. This increase in Tes values from rest to the end of exercise was greater (P = 0.08) for the sleep deprivation than control test. Total body sweat rate, calculated from Potter balance measurements, was 27% less (P less than 0.01) for the sleep deprivation than the control test. Both mds and kch values were lower (P less than 0.05) during the final 20 min of exercise for the sleep deprivation than control test. Final exercise mds values were 19% lower (P less than 0.05) for the sleep deprivation than control test. An asynchronous rather than a normal synchronous mds pattern was frequently observed during the sleep deprivation test. During the sleep deprivation test, the mds sensitivity (delta mds X delta Tes-1) was 38% lower (P less than 0.01) and kch sensitivity (delta kch X delta Tes-1) was 42% lower (P less than 0.05) than during the control test. These data indicate that sleep deprivation decreases evaporative and dry heat loss during moderate-intensity exercise.

Exercise-induced changes in blood zinc and related proteins in humans

1985 ◽  
Vol 58 (5) ◽  
pp. 1453-1458 ◽  
Author(s):  
H. Ohno ◽  
K. Yamashita ◽  
R. Doi ◽  
K. Yamamura ◽  
T. Kondo ◽  
...  
Keyword(s):  
Carbonic Anhydrase ◽  
Zinc Concentration ◽  
Plasma Concentrations ◽  
Cycle Ergometer ◽  
Male Students ◽  
Ergometer Exercise ◽  
Exercise Induced ◽  
Induced Changes ◽  
Related Proteins ◽  
Blood Zinc

Effects of cycle ergometer exercise (approximately 75% maximum ventilatory O2 consumption for 30 min) on the concentrations of zinc and related proteins in erythrocytes and/or plasma were studied on 11 sedentary male students. Lower concentrations of total zinc and of zinc derived from carbonic anhydrase I type (CA-I) in erythrocytes were observed immediately after exercise, but they disappeared after 30 min of rest. The change in total zinc concentration in erythrocytes correlated well with that in CA-I concentration immediately after exercise, as well as after rest. The concentration of carbonic anhydrase II type (CA-II)-derived zinc did not vary substantially at any time. On the other hand, there were significant increases in the plasma concentrations of total zinc and of alpha 2-macroglobulin (alpha 2-MG)-bound zinc immediately after exercise, whereas no such effect was noted in albumin-bound zinc. A positive correlation was found between total zinc and alpha 2-MG concentrations in plasma immediately after exercise. In addition, the change in the activity of alkaline phosphatase, a zinc metalloenzyme, correlated well with that in the total zinc concentration in plasma. These results suggest that a brief physical exercise induces the movement of zinc into plasma.

scholarly journals Acute Effects of Energy Deficit Induced by Moderate-Intensity Exercise or Energy-Intake Restriction on Postprandial Lipemia in Healthy Girls

2015 ◽  
Vol 27 (2) ◽  
pp. 192-202 ◽  
Author(s):  
Alice Emily Thackray ◽  
Laura Ann Barrett ◽  
Keith Tolfrey
Keyword(s):  
Energy Intake ◽  
Postprandial Lipemia ◽  
Peak Oxygen Uptake ◽  
Energy Deficit ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Time Curve ◽  
Fasting Plasma ◽  
Exercise Effect ◽  
Exercise Induced

Eleven healthy girls (mean ± SD: age 12.1 ± 0.6 years) completed three 2-day conditions in a counterbalanced, crossover design. On day 1, participants either walked at 60 (2)% peak oxygen uptake (energy deficit 1.55[0.20] MJ), restricted food energy intake (energy deficit 1.51[0.25] MJ) or rested. On day 2, capillary blood samples were taken at predetermined intervals throughout the 6.5 hr postprandial period before, and following, the ingestion of standardized breakfast and lunch meals. Fasting plasma triacylglycerol concentrations (TAG) was 29% and 13% lower than rest control in moderate-intensity exercise (effect size [ES] = 1.39, p = .01) and energy-intake restriction (ES = 0.57, p = .02) respectively; moderate-intensity exercise was 19% lower than energy-intake restriction (ES = 0.82, p = .06). The moderate-intensity exercise total area under the TAG versus time curve was 21% and 13% lower than rest control (ES = 0.71, p = .004) and energy-intake restriction (ES = 0.39, p = .06) respectively; energy-intake restriction was marginally lower than rest control (-10%; ES = 0.32, p = .12). An exercise-induced energy deficit elicited a greater reduction in fasting plasma TAG with a trend for a larger attenuation in postprandial plasma TAG than an isoenergetic diet-induced energy deficit in healthy girls.

scholarly journals Carotid chemoreceptors have a limited role in mediating the hyperthermia-induced hyperventilation in exercising humans

2019 ◽  
Vol 126 (2) ◽  
pp. 305-313
Author(s):  
Naoto Fujii ◽  
Miki Kashihara ◽  
Glen P. Kenny ◽  
Yasushi Honda ◽  
Tomomi Fujimoto ◽  
...  
Keyword(s):  
Young Men ◽  
Progressive Increase ◽  
Peak Oxygen Uptake ◽  
Body Core Temperature ◽  
Moderate Intensity ◽  
Esophageal Temperature ◽  
Moderate Intensity Exercise ◽  
Carotid Chemoreceptors ◽  
Exercise Induced ◽  
Induced Changes

Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young men (23 ± 2 yr) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual’s predetermined peak oxygen uptake (moderate intensity). To suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P ≤ 0.05), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (−9 to −13 l/min) than at rest (−2 ± 1 l/min); however, the magnitude of reduction during exercise did not differ at low (0.5°C) to severe (2.0°C) increases in esophageal temperature (all P > 0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by percent change from prehyperoxic levels were not different at all levels of hyperthermia (~15–20%, all P > 0.05). We show that in young men carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat. NEW & NOTEWORTHY Exercise-induced increases in hyperthermia cause a progressive increase in ventilation in humans. However, the mechanisms underpinning this response remain unresolved. We showed that in young men hyperventilation associated with exercise-induced hyperthermia is not predominantly mediated by carotid chemoreceptors. This study provides important new insights into the mechanism(s) underpinning the regulation of hyperthermia-induced hyperventilation in humans and suggests that factor(s) other than carotid chemoreceptors play a more important role in mediating this response.

Acid-base regulation during exercise and recovery in humans

1992 ◽  
Vol 72 (3) ◽  
pp. 954-961 ◽  
Author(s):  
W. Stringer ◽  
R. Casaburi ◽  
K. Wasserman
Keyword(s):  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Exercise Tests ◽  
Cycle Ergometer Exercise ◽  
Arterial Ph ◽  
Ergometer Exercise ◽  
Exercise In Humans

Arterial pH, PCO2, standard bicarbonate, lactate, and ventilation were measured with a high sampling density during rest, exercise, and recovery in normal subjects performing upright cycle ergometer exercise. Three 6-min constant-work exercise tests (moderate, heavy, and very heavy) were performed by each subject. We found a small respiratory acidosis during the moderate-intensity exercise and an early respiratory acidosis followed by a metabolic acidosis for the heavy- and very-heavy-intensity exercise. During recovery, arterial pH rapidly returned to the preexercise value for the moderate-intensity work. However, arterial pH decreased further during the first 2 min of recovery for the heavy- and very-heavy-intensity work, before a slower return toward the resting values. We conclude that arterial acidosis is the consistent arterial pH reaction for moderate-, heavy-, and very-heavy-intensity cycle ergometer exercise in humans and that this acidosis is blunted but not eliminated by the ventilatory response. During recovery, the return to resting arterial pH and PCO2 and standard bicarbonate appears to be determined by the rate of lactate decline.

Hepatic nerves are not essential to the increase in hepatic glucose production during muscular work

1990 ◽  
Vol 259 (2) ◽  
pp. E195-E203 ◽  
Author(s):  
D. H. Wasserman ◽  
P. E. Williams ◽  
D. B. Lacy ◽  
D. Bracy ◽  
A. D. Cherrington
Keyword(s):  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Moderate Intensity ◽  
Moderate Intensity Exercise ◽  
Hepatic Glucose ◽  
Exercise Induced ◽  
Glucagon And Insulin ◽  
Induced Changes ◽  
Hepatic Nerves ◽  
Rest And Exercise

To establish the role of hepatic nerves in hepatic glycogenolytic and gluconeogenic regulation during exercise, dogs underwent a laparotomy during which the hepatic nerves were either left intact (C; n = 8) or cut (DN; n = 5). At least 17 days after surgery, dogs were studied during 150 min of treadmill exercise (12% grade, 100 m/min). Glucose production (Ra) and gluconeogenesis (GNG) were assessed by combining [3-3H]glucose, [U-14C]alanine, and indocyanine green infusions with arterial, portal vein, and hepatic vein sampling. Glucagon and insulin were similar at rest and exercise in both groups. Norepinephrine rose from 145 +/- 10 to 242 +/- 32 pg/ml by 150 min of exercise in C and from 150 +/- 25 to 333 +/- 83 pg/ml in DN. Epinephrine rose from 66 +/- 7 pg/ml at rest to 108 +/- 10 and 148 +/- 24 pg/ml after 30 and 150 min of exercise in C and from 90 +/- 15 pg/ml at rest to 185 +/- 33 (P less than 0.05 compared with C) and 194 +/- 36 pg/ml after 30 and 150 min of exercise in DN. Plasma glucose fell gradually from 108 +/- 2 and 106 +/- 3 mg/dl at rest to 96 +/- 4 and 92 +/- 8 by the end of exercise in C and DN, respectively. Ra was similar in C and DN rising from 3.2 +/- 0.2 to 8.7 +/- 0.6 and 2.6 +/- 0.2 to 7.5 +/- 1.1 mg.kg-1.min-1, respectively, by the end of exercise. Minimum and maximum rates of GNG from alanine, glycerol, and lactate were elevated in DN compared with C during rest and exercise. However, the exercise-induced changes in GNG were similar in both groups. In conclusion, nerves to the liver are not essential to the increased Ra and glucose homeostasis during moderate-intensity exercise.

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