Effects of intravenous low-dose dopamine infusion on glucose regulation during prolonged aerobic exercise

Blair D. Johnson, Ana B. Peinado, Sushant M. Ranadive, Timothy B Curry, Michael Joseph Joyner

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The carotid body chemoreceptors are activated during hypoglycemia and contribute to glucoregulation during prolonged exercise in dogs. Low-dose intravenous infusions of dopamine have been shown to blunt the activation of the carotid body chemoreceptors during hypoxia. Therefore, we tested the hypotheses that dopamine would blunt glucoregulatory responses and attenuate plasma glucose during prolonged aerobic exercise in healthy participants. Twelve healthy participants completed two randomized exercise sessions at 65% peak oxygen consumption for up to 120 min. Saline was infused during one exercise session, and dopamine (2 μg·kg-1·min-1) was infused during the other session. Arterial plasma glucose, growth hormone, glucagon, cortisol, norepinephrine, and epinephrine were measured every 10 min. Exercise duration during dopamine infusion was 107 ± 6 and 119 ± 0.8 min during saline infusion. Glucose area under the curve during exercise was lower during dopamine (9,821 ± 686 vs. 11,194 ± 395 arbitrary units; P = 0.016). The ratio of circulating growth hormone to glucose and the ratio of glucagon to glucose were greater during dopamine (P = 0.045 and 0.037, respectively). These results indicate that the infusion of dopamine during aerobic exercise impairs glucoregulation. This suggests that the carotid body chemoreceptors contribute to glucoregulation during prolonged exercise in healthy exercise-trained humans.

Original languageEnglish (US)
Pages (from-to)R49-R57
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume314
Issue number1
DOIs
StatePublished - Jan 1 2018

Fingerprint

Dopamine
Exercise
Glucose
Carotid Body
Glucagon
Growth Hormone
Healthy Volunteers
Hypoglycemia
Intravenous Infusions
Oxygen Consumption
Epinephrine
Area Under Curve
Hydrocortisone
Norepinephrine
Dogs

Keywords

  • Cortisol
  • Epinephrine
  • Glucagon
  • Growth hormone
  • Norepinephrine

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Effects of intravenous low-dose dopamine infusion on glucose regulation during prolonged aerobic exercise. / Johnson, Blair D.; Peinado, Ana B.; Ranadive, Sushant M.; Curry, Timothy B; Joyner, Michael Joseph.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 314, No. 1, 01.01.2018, p. R49-R57.

Research output: Contribution to journalArticle

@article{b1c54d509c6c4a068aeb9c6e816a1d11,
title = "Effects of intravenous low-dose dopamine infusion on glucose regulation during prolonged aerobic exercise",
abstract = "The carotid body chemoreceptors are activated during hypoglycemia and contribute to glucoregulation during prolonged exercise in dogs. Low-dose intravenous infusions of dopamine have been shown to blunt the activation of the carotid body chemoreceptors during hypoxia. Therefore, we tested the hypotheses that dopamine would blunt glucoregulatory responses and attenuate plasma glucose during prolonged aerobic exercise in healthy participants. Twelve healthy participants completed two randomized exercise sessions at 65{\%} peak oxygen consumption for up to 120 min. Saline was infused during one exercise session, and dopamine (2 μg·kg-1·min-1) was infused during the other session. Arterial plasma glucose, growth hormone, glucagon, cortisol, norepinephrine, and epinephrine were measured every 10 min. Exercise duration during dopamine infusion was 107 ± 6 and 119 ± 0.8 min during saline infusion. Glucose area under the curve during exercise was lower during dopamine (9,821 ± 686 vs. 11,194 ± 395 arbitrary units; P = 0.016). The ratio of circulating growth hormone to glucose and the ratio of glucagon to glucose were greater during dopamine (P = 0.045 and 0.037, respectively). These results indicate that the infusion of dopamine during aerobic exercise impairs glucoregulation. This suggests that the carotid body chemoreceptors contribute to glucoregulation during prolonged exercise in healthy exercise-trained humans.",
keywords = "Cortisol, Epinephrine, Glucagon, Growth hormone, Norepinephrine",
author = "Johnson, {Blair D.} and Peinado, {Ana B.} and Ranadive, {Sushant M.} and Curry, {Timothy B} and Joyner, {Michael Joseph}",
year = "2018",
month = "1",
day = "1",
doi = "10.1152/ajpregu.00030.2017",
language = "English (US)",
volume = "314",
pages = "R49--R57",
journal = "American Journal of Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "1",

}

TY - JOUR

T1 - Effects of intravenous low-dose dopamine infusion on glucose regulation during prolonged aerobic exercise

AU - Johnson, Blair D.

AU - Peinado, Ana B.

AU - Ranadive, Sushant M.

AU - Curry, Timothy B

AU - Joyner, Michael Joseph

PY - 2018/1/1

Y1 - 2018/1/1

N2 - The carotid body chemoreceptors are activated during hypoglycemia and contribute to glucoregulation during prolonged exercise in dogs. Low-dose intravenous infusions of dopamine have been shown to blunt the activation of the carotid body chemoreceptors during hypoxia. Therefore, we tested the hypotheses that dopamine would blunt glucoregulatory responses and attenuate plasma glucose during prolonged aerobic exercise in healthy participants. Twelve healthy participants completed two randomized exercise sessions at 65% peak oxygen consumption for up to 120 min. Saline was infused during one exercise session, and dopamine (2 μg·kg-1·min-1) was infused during the other session. Arterial plasma glucose, growth hormone, glucagon, cortisol, norepinephrine, and epinephrine were measured every 10 min. Exercise duration during dopamine infusion was 107 ± 6 and 119 ± 0.8 min during saline infusion. Glucose area under the curve during exercise was lower during dopamine (9,821 ± 686 vs. 11,194 ± 395 arbitrary units; P = 0.016). The ratio of circulating growth hormone to glucose and the ratio of glucagon to glucose were greater during dopamine (P = 0.045 and 0.037, respectively). These results indicate that the infusion of dopamine during aerobic exercise impairs glucoregulation. This suggests that the carotid body chemoreceptors contribute to glucoregulation during prolonged exercise in healthy exercise-trained humans.

AB - The carotid body chemoreceptors are activated during hypoglycemia and contribute to glucoregulation during prolonged exercise in dogs. Low-dose intravenous infusions of dopamine have been shown to blunt the activation of the carotid body chemoreceptors during hypoxia. Therefore, we tested the hypotheses that dopamine would blunt glucoregulatory responses and attenuate plasma glucose during prolonged aerobic exercise in healthy participants. Twelve healthy participants completed two randomized exercise sessions at 65% peak oxygen consumption for up to 120 min. Saline was infused during one exercise session, and dopamine (2 μg·kg-1·min-1) was infused during the other session. Arterial plasma glucose, growth hormone, glucagon, cortisol, norepinephrine, and epinephrine were measured every 10 min. Exercise duration during dopamine infusion was 107 ± 6 and 119 ± 0.8 min during saline infusion. Glucose area under the curve during exercise was lower during dopamine (9,821 ± 686 vs. 11,194 ± 395 arbitrary units; P = 0.016). The ratio of circulating growth hormone to glucose and the ratio of glucagon to glucose were greater during dopamine (P = 0.045 and 0.037, respectively). These results indicate that the infusion of dopamine during aerobic exercise impairs glucoregulation. This suggests that the carotid body chemoreceptors contribute to glucoregulation during prolonged exercise in healthy exercise-trained humans.

KW - Cortisol

KW - Epinephrine

KW - Glucagon

KW - Growth hormone

KW - Norepinephrine

UR - http://www.scopus.com/inward/record.url?scp=85043573313&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85043573313&partnerID=8YFLogxK

U2 - 10.1152/ajpregu.00030.2017

DO - 10.1152/ajpregu.00030.2017

M3 - Article

VL - 314

SP - R49-R57

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6119

IS - 1

ER -