A I Hirasawa1, Kohei Sato, Marina Yoneya, Tomoko Sadamoto, Damian M Bailey, Shigehiko Ogoh. 1. 1Advanced Triage Team, Kyorin University, Mitaka-shi, Tokyo, JAPAN; 2Research Institute of Physical Fitness, Japan Women's College of Physical Education, Setagaya-Ku, Tokyo, JAPAN; 3Neurovascular Research Laboratory, Faculty of Life Sciences and Education, University of South Wales, Wales, UNITED KINGDOM; 4Department of Biomedical Engineering, Faculty of Science and Engineering, Toyo University, Kawagoe-shi, Saitama, JAPAN.
Abstract
PURPOSE: The present study was designed to explore to what extent low-intensity resistance exercise-induced acute hypertension influences intracranial cerebral perfusion. METHODS: Twelve healthy participants performed one-legged static knee extension exercise at 30% maximal voluntary contraction for 2 min. Blood flow to the internal and external carotid arteries (ICA/ECA) were evaluated by duplex ultrasonography. RESULTS: ICA blood flow increased and reached a plateau before stabilizing 60 s into exercise despite continued increases in cardiac output and arterial blood pressure. ICA conductance significantly decreased by -14.4% ±13.8% at the end of exercise (P < 0.01), whereas in contrast, ECA blood flow (P < 0.01) and conductance were shown to increase (P < 0.05). CONCLUSIONS: The present findings demonstrate that low-intensity resistance exercise was associated with vasodilation of the ECA that was accompanied by vasoconstriction of the ICA. We propose that the heterogeneity and reciprocal regulation of intracranial cerebral blood flow reflect an adaptive neuroprotective mechanism that serves to protect the brain and associated vasculature against the structural damage associated with resistance exercise-induced hypertension.
PURPOSE: The present study was designed to explore to what extent low-intensity resistance exercise-induced acute hypertension influences intracranial cerebral perfusion. METHODS: Twelve healthy participants performed one-legged static knee extension exercise at 30% maximal voluntary contraction for 2 min. Blood flow to the internal and external carotid arteries (ICA/ECA) were evaluated by duplex ultrasonography. RESULTS:ICA blood flow increased and reached a plateau before stabilizing 60 s into exercise despite continued increases in cardiac output and arterial blood pressure. ICA conductance significantly decreased by -14.4% ±13.8% at the end of exercise (P < 0.01), whereas in contrast, ECA blood flow (P < 0.01) and conductance were shown to increase (P < 0.05). CONCLUSIONS: The present findings demonstrate that low-intensity resistance exercise was associated with vasodilation of the ECA that was accompanied by vasoconstriction of the ICA. We propose that the heterogeneity and reciprocal regulation of intracranial cerebral blood flow reflect an adaptive neuroprotective mechanism that serves to protect the brain and associated vasculature against the structural damage associated with resistance exercise-induced hypertension.