Rh. Coker et al., SYMPATHETIC DRIVE TO LIVER AND NONHEPATIC SPLANCHNIC TISSUE DURING PROLONGED EXERCISE IS INCREASED IN DIABETES, Metabolism, clinical and experimental, 46(11), 1997, pp. 1327-1332
This study was conducted to assess whether nonhepatic splanchnic (NHS)
and hepatic tissues contribute to the increase in circulating norepin
ephrine during prolonged exercise, and to determine whether such a res
ponse is exaggerated during exercise in the poorly controlled diabetic
when the arterial norepinephrine response is excessive. Chronically c
atheterized (carotid artery, portal vein, and hepatic vein) and instru
mented (Doppler flow probes on hepatic artery and portal vein) normal
(n = 6) and alloxan-diabetic (n = 5) dogs were studied during rest (30
minutes) and moderate treadmill exercise (150 minutes), Basal plasma
glucose of diabetic dogs was threefold that of control dogs. Since epi
nephrine is not released by splanchnic tissues, NHS and hepatic epinep
hrine fractional extraction (FX) can be accurately measured. Because e
pinephrine FX = norepinephrine FX, norepinephrine spillover can be cal
culated. NHS and hepatic epinephrine FX remained stable during rest an
d exercise in both control and diabetic dogs. Although basal NHS norep
inephrine spillover was not different between the two groups, basal he
patic norepinephrine spillover was lower in the controls (1.1 +/- 0.3
ng/kg.min) compared with the diabetics (3.6 +/- 1.1 ng/kg.min). Althou
gh NHS norepinephrine spillover increased with exercise in the normal
dog (3.1 +/- 0.6 ng/kg.min at t = 150 minutes), there was no increase
in hepatic norepinephrine spillover (1.1 +/- 0.3 ng/kg.min at t = 150
minutes). In contrast, NHS (8.8 +/- 1.6 ng/kg.min at t = 150 minutes)
and hepatic (6.9 +/- 1.8 ng/kg min at t = 150 minutes) norepinephrine
spillover were both markedly increased in the diabetic dog to rates ap
proximately threefold and sixfold higher than in the normal dog. These
data show that an increase in NHS but not hepatic norepinephrine spil
lover is a component of the normal response to prolonged exercise. The
exaggerated increase in arterial norepinephrine during exercise in th
e diabetic state is due, in part, to both increased sympathetic drive
to the gut and liver. This increase in sympathetic drive to the splanc
hnic bed may contribute to the deleterious effects of exercise in poor
ly controlled diabetes. Copyright (C) 1997 by W.B. Saunders Company.