title: Exaggerated Exercise Blood Pressure Response and Future Cardiovascular Disease.
abstract: Exaggerated blood pressure (BP) response to exercise predicts future hypertension. However, there is considerable lack of understanding regarding the mechanism of how this abnormal response is generated, and how it relates to the future establishment of cardiovascular disease. The authors studied 82 healthy male volunteers without cardiovascular risk factors. The participants were categorized into two age-matched groups depending on their exercise systolic BP (ExSBP) rise after 3 minutes of exercise using a submaximal step test: exaggerated ExSBP group (hyper-responders [peak SBP ≥ 180 mm Hg]) and low ExSBP responder group (hypo-responders [peak SBP <180 mm Hg]). Forearm venous occlusion plethysmography and intra-arterial infusions of acetylcholine (ACh), N(G)-monomethyl-L-arginine (L-NMMA), sodium nitroprusside (SNP), and norepinephrine (NE) were used to assess vascular reactivity. Proximal aortic compliance was assessed with ultrasound, and neurohormonal blood sampling was performed at rest and during peak exercise. The hyper-responder group exhibited a significantly lower increase in forearm blood flow (FBF) with ACh compared with the hypo-responder group (ΔFBF 215% [14] vs 332.3% [28], mean [standard error of the mean]; P<.001), as well as decreased proximal aortic compliance. The vasoconstrictive response to L-NMMA was significantly impaired in the hyper-responder group in comparison to the hypo-responder group (ΔFBF -40.2% [1.6] vs -50.2% [2.6]; P<.05). In contrast, the vascular response to SNP and NE were comparable in both groups. Peak exercise plasma angiotensin II levels were significantly higher in the hyper-responder group (31 [1] vs 23 [2] pg/mL, P=.01). An exaggerated BP response to exercise is related to endothelial dysfunction, decreased proximal aortic compliance, and increased exercise-related neurohormonal activation, the constellation of which may explain future cardiovascular disease.
authors.affiliation: Institute of Cardiovascular and Medical Sciences, British Heart Foundation, Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK.
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Tzemos
authors.affiliation: Hypertension Research Centre, Medical Research Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
authors.forename: Pitt O
authors.initials: PO
authors.lastname: Lim
authors.affiliation: Hypertension Research Centre, Medical Research Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
authors.forename: Isla S
authors.initials: IS
authors.lastname: Mackenzie
authors.affiliation: Hypertension Research Centre, Medical Research Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
authors.forename: Thomas M
authors.initials: TM
authors.lastname: MacDonald
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology*; D018660:Blood Pressure Monitoring, Ambulatory; D002318:Cardiovascular Diseases / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology*; D004452:Echocardiography; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test / Q000379:methods*; D006801:Humans; D008297:Male; D010991:Plethysmography / Q000379:methods; D011237:Predictive Value of Tests; D015203:Reproducibility of Results; D018570:Risk Assessment; D059289:Vascular Stiffness / Q000502:physiology