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(Hypertension. 1995;25:391-398.)
© 1995 American Heart Association, Inc.
Articles |
From the Hypertension Research Unit, Centre Hospitalier de l'Université Laval Research Center, Laval University, Québec, Canada.
Abstract We recently reported that ambulatory blood pressure decreased during the awake period after training at low intensity but not after training at moderate intensity in subjects with mild to moderate hypertension. The reasons for the failure of moderate-intensity training to reduce blood pressure are not clear. In the present article, we report the effects of different training intensities on cardiopulmonary baroreflex control of forearm vascular resistance, left ventricular function, vascular reactivity, and resistive vessel structure. After moderate-intensity training, the cardiopulmonary baroreflex control of forearm vascular resistance was significantly attenuated, left ventricular performance was enhanced, and vascular reactivity and resistive vessel wall thickness in the calf were reduced compared with values after the control sedentary period. No significant changes in these indexes were found after low-intensity training compared with sedentary values. These results indicate that attenuation of the cardiopulmonary baroreflex control of skeletal muscle vascular resistance after training at moderate intensity may contribute to the lack of antihypertensive effects, as seen from unchanged ambulatory blood pressure levels during the awake period, after training at this intensity. A decreased vascular smooth muscle response to sympathetic nervous stimulation appears to be partly involved in the alteration in the baroreflex control of forearm vascular resistance after moderate-intensity training. Although these findings should be confirmed in a greater number of subjects, the present results point to a key mechanism that might explain why moderate endurance exercise training fails to lower arterial blood pressure in hypertensive subjects.
Key Words: exercise muscles vascular resistance ventricular function, left norepinephrine vasodilation
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