Peripheral chemoreceptor deactivation attenuates the sympathetic response to glucose ingestion

• Published in: Applied physiology, nutrition, and metabolism nutrition, and metabolism, 2019-04, Vol.44 (4), p.389-396
• Main Authors: Smorschok, Megan P, Sobierajski, Frances M, Purdy, Graeme M, Riske, Laurel A, Busch, Stephen A, Skow, Rachel J, Matenchuk, Brittany A, Pfoh, Jamie R, Vanden Berg, Emily R, Linares, Andrea, Borle, Kennedy, Lavoie, Lauren, Saran, Gurkarn, Dyck, Rebecca, Funk, Deanna R, Day, Trevor A, Boulé, Normand G, Davenport, Margie H, Steinback, Craig D
• Format: Article
• Language: English
• Subjects: apport alimentaire; autonomic nervous system; Blood glucose; Chemoreceptors; chimiorécepteurs périphériques; Diet; dietary intake; Glucose; glucose ingestion; Heart rate; Hyperglycemia; Hyperoxia; ingestion de glucose; Nervous system; Neuromuscular transmission; peripheral chemoreceptors; Peripheral nervous system; Physiological aspects; Physiological research; régulation sympathique; Sympathetic nervous system; sympathetic regulation; système nerveux autonome
• ISSN: 1715-5312; 1715-5320
• DOI: 10.1139/apnm-2018-0062

Acute increases in blood glucose are associated with heightened muscle sympathetic nerve activity (MSNA). Animal studies have implicated a role for peripheral chemoreceptors in this response, but this has not been examined in humans. Heart rate, cardiac output (CO), mean arterial pressure, total peripheral conductance, and blood glucose concentrations were collected in 11 participants. MSNA was recorded in a subset of 5 participants via microneurography. Participants came to the lab on 2 separate days (i.e., 1 control and 1 experimental day). On both days, participants ingested 75 g of glucose following baseline measurements. On the experimental day, participants breathed 100% oxygen for 3 min at baseline and again at 20, 40, and 60 min after glucose ingestion to deactivate peripheral chemoreceptors. Supplemental oxygen was not given to participants on the control day. There was a main effect of time on blood glucose (P < 0.001), heart rate (P < 0.001), CO (P < 0.001), sympathetic burst frequency (P < 0.001), burst incidence (P = 0.01), and total MSNA (P = 0.001) for both days. Blood glucose concentrations and burst frequency were positively correlated on the control day (r = 0.42; P = 0.03) and experimental day (r = 0.62; P = 0.003). There was a time × condition interaction (i.e., normoxia vs. hyperoxia) on burst frequency, in which hyperoxia significantly blunted burst frequency at 20 and 60 min after glucose ingestion only. Given that hyperoxia blunted burst frequency only during hyperglycemia, our results suggest that the peripheral chemoreceptors are involved in activating MSNA after glucose ingestion.