Journal of Human Hypertension (2002) 16, 33–39  2002 Nature Publishing Group All rights reserved 0950-9240/02 $25.00 www.nature.com/jhh ORIGINAL ARTICLE Post exercise hypotension is not mediated by the serotonergic system in borderline hypertensive individuals JR MacDonald, JM Rosenfeld, MA Tarnopolsky, CD Hogben, CS Ballantyne and JD MacDougall Departments of Kinesiology and Medicine, McMaster University, Hamilton, Ontario, Canada Recent evidence from our laboratory and others have suggested that the mechanism for a decrease in resting blood pressure after an acute bout of exercise is a cen- trally mediated decrease in total peripheral resistance. This study examined the effect of the central sero- tonergic system on post exercise hypotension (PEH) in 11 borderline hypertensive individuals (nine male, two female) aged 24.5  5.1 years. Each subject completed two, 30-min cycling bouts at 70% of V ˙ O 2 Peak while under placebo or a selective serotonin re-uptake inhibitor (SSRI) treatment. Blood pressure was recorded directly from the radial artery, and treatments were randomised, double blinded and separated by at least 14 days. Base- line blood pressure was 145/72 mm Hg for systolic (SBP) and diastolic (DBP) respectively. Peripheral meas- ures of serotonin (5-HT) were lower under SSRI treat- ment, whereas the major 5-HT metabolite, 5-hydroxy- indoleacetic acid, was not significantly changed, Keywords: endurance exercise; indolamines; intra-arterial blood pressure; hypotension; human Introduction A growing body of literature has confirmed that an acute bout of exercise can cause a transient decrease in the normal resting blood pressure and may last up to several hours. 1–3 This phenomenon is particularly evident in hypertensive and borderline hypertensive individuals and has been termed post exercise hypo- tension (PEH). This decrease in blood pressure could be caused by a decreased cardiac output (Q ˙ c) or decreased total peripheral resistance (TPR) (or both). Since oxygen uptake (V ˙ O 2 ) and heart rate (HR) equal or exceed pre-exercise values during the post exercise hypotensive state 2 it is unlikely that there is a significant decrease in Q ˙ c. This suggests that PEH is a function of decreased TPR. Correspondence: JR MacDonald, Department of Medicine, Division of Neurology, McMaster University, Room 4U18, Hamil- ton, Ontario L8N 3Z5, Canada. E-mail: jaymacmcmaster.ca Received 12 May 2001, revised 27 July 2001, accepted 2 August 2001 indicating elevated central 5-HT levels. There was no dif- ference in any of the haemodynamic variables between trials. Despite an increased heart rate for the initial 75 min post exercise, SBP was decreased as much as 23 mm Hg during the initial 60 min post exercise, after which it had returned to normal. DBP was unchanged after exercise. Circulating adrenaline (0.60  0.14 ng/mL to 1.3  1.6 ng/ml) and noradrenaline (0.27  0.31 ng/ml to 4.5  2.1 ng/ml) were significantly elevated during exercise. Both returned to pre-exercise levels within 15 min post exercise. Unexpectedly, oxygen uptake was slightly (5%), but significantly increased over the entire duration of the SSRI trial. We conclude that the central serotonergic system is not responsible for PEH in our borderline hypertensive population. Journal of Human Hypertension (2002) 16, 33–39. DOI: 10.1038/sj/jhh/1001290 A decrease in TPR can be the result of centrally mediated mechanisms (eg, decreased efferent activity from the sympathetic nervous system (SNS)) or locally mediated vasodilation (eg, in response to locally released metabolites and compounds). The finding that the magnitude of the PEH is largely independent of exercise intensity, 4 exercise dur- ation 5 or the size of the exercising muscle group 6 argues against a local mechanism. In addition, PEH persists long after body temperature, circulating exercise metabolites or ionic imbalances have returned to normal. It has been shown that exercise induced alter- ations in the opioid system centrally affect blood pressure. 7 Although little is known about the mech- anics of the opioid system, it may moderate sym- pathetic activity. 7 Specifically, -endorphins are known to increase during exercise, and are often claimed to be responsible for the sensation of euphoria that accompanies moderate intensity endurance exercise. 8 Early work examining -endor- phins and blood pressure found that infusion of -