Sympathetic drive to liver and nonhepatic splanchnic tissue during heavy exercise

Abstract

Coker, Robert H., Mahesh G. Krishna, D. Brooks Lacy, Eric J. Allen, and David H. Wasserman. Sympathetic drive to liver and nonhepatic splanchnic tissue during heavy exercise. J. Appl. Physiol. 82(4): 1244–1249, 1997.—The contribution of sympathetic drive and vascular catecholamine delivery to the splanchnic bed during heavy exercise was studied in dogs that underwent a laparotomy during which flow probes were implanted onto the portal vein and hepatic artery and catheters were inserted into the carotid artery, portal vein, and hepatic vein. At least 16 days after surgery, dogs completed a 20-min heavy exercise protocol (mean work rate of 5.7 ± 1 miles/h, 20 ± 2% grade). Arterial epinephrine (Epi) and norepinephrine (NE) increased by ∼500 and ∼900 pg/ml, respectively, after 20 min of heavy exercise. Because Epi is not released from the splanchnic bed and because Epi fractional extraction (FX) = NE FX, NE uptake by splanchnic tissue can be calculated despite simultaneous release of NE. Basal nonhepatic splanchnic (NHS) FX increased from a basal rate of 0.52 ± 0.09 to a peak of 0.64 ± 0.05 at 10 min of exercise. Hepatic Epi FX increased from a basal rate of 0.68 ± 0.10 to 0.81 ± 0.09 at 20 min of exercise. Even though NHS extraction of Epi reduced portal vein Epi levels by ∼60%, the release of NE from NHS tissue maintained portal vein NE at levels similar to those in arterial blood. NHS NE spillover increased from a basal rate of 5.7 ± 1.4 to 11.7 ± 2.8 ng ⋅ kg−1 ⋅ min−1at 20 min of exercise. Hepatic NE spillover increased from a basal rate of 5.0 ± 1.2 ng ⋅ kg−1 ⋅ min−1to a peak of 14.2 ± 2.8 ng ⋅ kg−1 ⋅ min−1at 15 min of exercise. These results show that 1) approximately two- and threefold increases in NHS and hepatic NE spillover occur during heavy exercise, demonstrating that sympathetic drive to these tissues contributes to the increase in circulating NE; 2) the high catecholamine FX by the NHS tissues results in an Epi level at the liver that is considerably lower than that in the arterial blood; and 3) circulating NE delivery to the liver is sustained despite high catecholamine FX due to simultaneous NHS NE release.