Role of carotid bodies in control of the neuroendocrine response to exercise

This study was aimed at assessing the role of carotid body function in neur oendocrine and glucoregulatory responses to exercise. The carotid bodies an d associated nerves were removed (CBR, n = 6), or left intact (Sham, n = 6) in anesthetized dogs > 16 clays before experiments, and infusion and sampl ing catheters were implanted. Conscious dogs were studied at rest and durin g 150 min of exercise. Isotopic dilution was used to Assess glucose product ion (R-a) and disappearance (R-d). Arterial glucagon was reduced in CBR com pared with Sham at rest (29 +/- 3 vs. 47 +/- 3 pg/ml). During exercise, glu cagon increased more in Sham than in CBR (47 +/- 9 vs. 15 +/- 2 pg(ml). Cor tisol and epinephrine levels were similar in the two groups at rest and dur ing exercise. Basal norepinephrine was similar in CBR and Sham. During exer cise, norepinephrine increased by 432 +/- 124 pg/ml in Sham, but by only 20 1 +/- 28 pg(ml. in CBR. Basal arterial plasma glucose was 108 +/- 2 and 105 +/- 2 mg/dl in CBR and Sham, respectively. Arterial glucose dropped by 10 +/- 3 mg/dl at onset of exercise in CBR (P < 0.01), but was unchanged in Sh am (decrease of 3 2 mg/dl, not significant). Basal glucose kinetics were eq ual in Sham and CBR. At onset of exercise, R-a and R-d were transiently unc oupled in CBR (i.e., R-d > R-a) but were closely matched in Sham. In steady -state exercise, R-a and R-d were closely matched in both groups. Insulin w as equal in the basal period and decreased similarly during exercise. These studies, suggest. that input from the carotid bodies, or receptors anatomi cally close to them, 1) is important in control of basal glucagon and the e xercise-induced increment in glucagon, 2) is involved in the sympathetic re sponse to exercise, and 3) participates in., the non-steady-state coupling of R-a to R-d, but 4) is not essential to glucoregulation during sustained exercise.