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.

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.

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.

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.

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.

Early postnatal overnutrition impairs VO2max gains with moderate exercise and increase post-exercise muscle damage in adult male rats

2021 ◽  
pp. 1-5
Author(s):  
Douglas Lopes Almeida ◽  
Gabriel Sergio Fabricio ◽  
Laize Peron Tófolo ◽  
Tatiane Aparecida Ribeiro ◽  
Camila Cristina Ianoni Matiusso ◽  
...  
Keyword(s):  
Early Life ◽  
Male Rats ◽  
Moderate Intensity ◽  
Moderate Exercise ◽  
Moderate Intensity Exercise ◽  
Post Exercise ◽  
Reduced Body ◽  
Male Wistar Rats ◽  
The Impact ◽  
Adaptation To Exercise

Abstract Exercise counteracts obesity effects, but information on how early-life obesity may affect long-term adaptation to exercise is lacking. This study investigates the impact of early-life postnatal overfeeding (PO) on animals’ adaptation to exercise. Only male Wistar rats were used. On postnatal day (PN) 30, rats from control (NL-9 pups) or PO (SL-3 pups) litters were separated into four groups: NL-sedentary (NL-Se), NL-exercised (NL-Ex), SL-sedentary (SL-Se), and SL-exercised (SL-Ex). Exercised groups performed moderate-intensity exercise, running on a treadmill, from PN30 to PN90. Further experiments were carried out between PN90 and PN92. PO promoted obesity in SL versus NL rats (P < 0.05). Exercise reduced body weight (P < 0.001), body fat (P < 0.01), and improved glucose homeostasis in SL-Ex versus SL-Se. SL-Ex presented lower VO2max (P < 0.01) and higher post-exercise LDH (P < 0.05) compared to NL-Ex rats. Although moderate exercise counteracted obesity in SL rats, early-life overnutrition restricts fitness gains in adulthood, indicating that early obesity may impair animals’ adaptation to exercise.

The acute effects of differential dietary fatty acids on human skeletal muscle pyruvate dehydrogenase activity

2008 ◽  
Vol 104 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Nicolette S. Bradley ◽  
George J. F. Heigenhauser ◽  
Brian D. Roy ◽  
Elizabeth M. Staples ◽  
J. Greig Inglis ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Pyruvate Dehydrogenase ◽  
Dietary Fatty Acids ◽  
Metabolic Effects ◽  
Moderate Intensity ◽  
Acute Effects ◽  
Moderate Intensity Exercise ◽  
Important Regulator ◽  
Male Subjects ◽  
Muscle Biopsies

Pyruvate dehydrogenase (PDH) is an important regulator of carbohydrate oxidation during exercise, and its activity can be downregulated by an increase in dietary fat. The purpose of this study was to determine the acute metabolic effects of differential dietary fatty acids on the activation of the PDH complex (PDHa activity) at rest and at the onset of moderate-intensity exercise. University-aged male subjects ( n = 7) underwent two fat-loading trials spaced at least 2 wk apart. Subjects consumed ∼300 g saturated (SFA) or n-6 polyunsaturated fatty acid (PUFA) fat over the course of 5 h. Following this, participants cycled at 65% of their maximum oxygen uptake for 15 min. Muscle biopsies were taken before and following fat loading and at 1 min exercise. Plasma free fatty acids increased from 0.15 ± 0.07 to 0.54 ± 0.19 mM over 5 h with SFA and from 0.11 ± 0.04 to 0.35 ± 0.13 mM with n-6 PUFA and were significantly lower throughout the n-6 PUFA trial. PDHa activity was unchanged following fat loading but increased at the onset of exercise in the SFA trial, from 1.18 ± 0.27 to 2.16 ± 0.37 mmol·min−1·kg wet wt−1. This effect was negated in the n-6 PUFA trial (1.04 ± 0.20 to 1.28 ± 0.36 mmol·min−1·kg wet wt−1). PDH kinase was unchanged in both trials, suggesting that the attenuation of PDHa activity with n-6 PUFA was a result of changes in the concentrations of intramitochondrial effectors, potentially intramitochondrial NADH or Ca2+. Our findings suggest that attenuated PDHa activity contributes to the preferential oxidation of n-6 PUFA during moderate-intensity exercise.

scholarly journals Growth hormone responses to repeated maximal cycle ergometer exercise at different pedaling rates

2002 ◽  
Vol 92 (2) ◽  
pp. 602-608 ◽  
Author(s):  
K. A. Stokes ◽  
M. E. Nevill ◽  
G. M. Hall ◽  
H. K. A. Lakomy
Keyword(s):  
Growth Hormone ◽  
Area Under The Curve ◽  
Cycle Ergometer ◽  
Mean Power ◽  
Ergometer Exercise ◽  
Hormone Responses ◽  
Sprint Cycling ◽  
Mean Power Output ◽  
Male Subjects ◽  
Serum Gh

The present study examined the growth hormone (GH) response to repeated bouts of maximal sprint cycling and the effect of cycling at different pedaling rates on postexercise serum GH concentrations. Ten male subjects completed two 30-s sprints, separated by 1 h of passive recovery on two occasions, against an applied resistance equal to 7.5% (fast trial) and 10% (slow trial) of their body mass, respectively. Blood samples were obtained at rest, between the two sprints, and for 1 h after the second sprint. Peak and mean pedal revolutions were greater in the fast than the slow trial, but there were no differences in peak or mean power output. Blood lactate and blood pH responses did not differ between trials or sprints. The first sprint in each trial elicited a serum GH response (fast: 40.8 ± 8.2 mU/l, slow: 20.8 ± 6.1 mU/l), and serum GH was still elevated 60 min after the first sprint. The second sprint in each trial did not elicit a serum GH response ( sprint 1 vs. sprint 2, P < 0.05). There was a trend for serum GH concentrations to be greater in the fast trial (mean GH area under the curve after sprint 1vs. after sprint 2: 1,697 ± 367 vs. 933 ± 306 min · mU−1 · l−1; P = 0.05). Repeated sprint cycling results in an attenuation of the GH response.

Measurement of gluconeogenesis in exercising men by mass isotopomer distribution analysis

2002 ◽  
Vol 93 (1) ◽  
pp. 233-241 ◽  
Author(s):  
Jeff K. Trimmer ◽  
Jean-Marc Schwarz ◽  
Gretchen A. Casazza ◽  
Michael A. Horning ◽  
Nestor Rodriguez ◽  
...  
Keyword(s):  
Rest Period ◽  
Glucose Production ◽  
Moderate Intensity ◽  
Dependent Manner ◽  
Distribution Analysis ◽  
Moderate Intensity Exercise ◽  
Isotopomer Distribution ◽  
Mass Isotopomer Distribution Analysis ◽  
The Difference ◽  
Mass Isotopomer

We evaluated the hypothesis that coordinated adjustments in absolute rates of gluconeogenesis (GNGab) and hepatic glycogenolysis (Gly) would maintain euglycemia and match glucose production (GP) to peripheral utilization during rest and exercise. Specifically, we evaluated the extent to which gradations in exercise power output would affect the contribution of GNGab to GP. For these purposes, we employed mass isotopomer distribution analysis (MIDA) and isotope-dilution techniques on eight postabsorptive (PA) endurance-trained men during 90 min of leg cycle ergometry at 45 and 65% peak O2 consumption (V˙o 2 peak; moderate and hard intensities, respectively) and the preceding rest period. GP was constant in resting subjects, whereas the fraction from GNG (fGNG) increased over time during rest (22.3 ± 0.9% at 11.25 h PA vs. 25.6 ± 0.9% at 12.0 h PA, P < 0.05). In the transition from rest to exercise, GP increased in an intensity-dependent manner (rest, 2.0 ± 0.1; 45%, 4.0 ± 0.4; 65%, 5.84 ± 0.64 mg · kg−1 · min−1, P < 0.05), although glucose rate of disappearance exceeded rate of appearance during the last 30 min of exercise at 65%V˙o 2 peak. Compared with rest, increases in GP were sustained by 92 and 135% increments in GNGab during moderate- and hard-intensity exercises, respectively. Correspondingly, Gly (calculated as the difference between GP and MIDA-measured GNGab) increased 100 and 203% over rest during the two exercise intensities. During moderate-intensity exercise, fGNG was the same as at rest; however, during the harder exercise fGNG decreased significantly to account for only 21% of GP. The highest sustained GNGab observed in these trials on PA men was 1.24 ± 0.3 mg · kg−1 · min−1. We conclude that, after an overnight fast, 1) absolute GNG rates increased with intensity of effort despite a reduced fGNG at 65% V˙o 2 peak, 2) during exercise Gly is more responsible than GNGab for maintaining GP, and 3) in 12-h fasted men, neither increased Gly or GNGab nor was their combination able to maintain euglycemia during prolonged hard (65%V˙o 2 peak) exercise.

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