The role of neuronal regulation of human cardiovascular function remains incompletely elucidated, especially during exercise. Here we, by positron emission tomography, monitored tissue-specific blood flow (BF) changes in nine healthy young men during femoral arterial infusions of norepinephrine (NE) and phentolamine. At rest, the α-adrenoceptor agonist NE reduced BF by ~40%, similarly in muscles (from 3.2 ± 1.9 to 1.4 ± 0.3 ml·min-1·100 g-1 in quadriceps femoris muscle), bone (from 1.1 ± 0.4 to 0.5 ± 0.2 ml·min-1·100 g-1) and adipose tissue (AT) (from 1.2 ± 0.7 to 0.7 ± 0.3 ml·min-1·100 g-1). During exercise, NE reduced exercising muscle BF by ~16%. BF in AT was reduced similarly as rest. The α-adrenoceptor antagonist phentolamine increased BF similarly in the different muscles and other tissues of the limb at rest. During exercise, BF in inactive muscle was increased 3.4-fold by phentolamine compared with exercise without drug, but BF in exercising muscles was not influenced. Bone and AT (P = 0.055) BF were also increased by phentolamine in the exercise condition. NE increased and phentolamine decreased oxygen extraction in the limb during exercise. We conclude that inhibition of α-adrenergic tone markedly disturbs the distribution of BF and oxygen extraction in the exercising human limb by increasing BF especially around inactive muscle fibers. Moreover, although marked functional sympatholysis also occurs during exercise, the arterial NE infusion that mimics the exaggerated sympathetic nerve activity commonly seen in patients with cardiovascular disease was still capable of directly limiting BF in the exercising leg muscles.

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Keywords α-adrenergic regulation, Blood flow, Humans
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Journal American Journal of Physiology - Heart and Circulatory Physiology
Heinonen, I.H.A, Wendelin-Saarenhovi, M, Kaskinoro, K, Knuuti, J, Scheinin, M, & Kalliokoski, K.K. (2013). Inhibition of α-adrenergic tone disturbs the distribution of blood flow in the exercising human limb. American Journal of Physiology - Heart and Circulatory Physiology, 305(2). doi:10.1152/ajpheart.00925.2012