Postexercise Intracranial Hypotension

Abstract

Arterial hypotension, minutes to hours after exercise, is a well described phenomenon. The drop in mean arterial blood pressure (MAP) likely results from a combination of sustained vasodilation of the previously active muscles, centrally mediated reduction in sympathetic nervous activity and resetting of thermo-, chemo-, and baroreceptors. Despite decreased MAP, cerebral blood flow is generally well maintained. PURPOSE: To characterize effects of moderate aerobic exercise on intracranial pressure (ICP) as a mechanism for maintaining cerebral perfusion pressure during and following exercise. METHODS: Sixteen healthy volunteers completed 30-min exercise at 70% estimated VO2-max on an upright ergonomic bicycle followed by a one-hour recovery phase in supine position. MAP, heart rate, stroke volume, and total peripheral resistance (TPR) were recorded continuously (Nexfin). In 15 subjects (8 female, 20±2 years, height 169±10 cm, weight 64±12 kg) ICP was estimated non-invasively by evoked tympanic membrane displacement (Cerebral Cochlea Fluid Pressure device). Invasive parenchymal ICP recordings were performed in one, cerebrally intact, former patient (male, 74 years, 176 cm, 80 kg) via a permanently implanted tip-transducer telemetric ICP-sensor (Neurovent-P-tele). RESULTS: 30 min moderate exercise did not increase ICP (-6.1mmHg during seated rest vs -6.8mmHg during exercise). Invasive (N=1) and non-invasive (N=15) ICP recordings followed the same trend, demonstrating a 52.8±22.9% (P<0.005) decrease immediately postexercise and graduate returned to baseline (fig). ICP was correlated to MAP (r2=0.8, P<0.05) and TPR (r2=0.9, P<0.005) DISCUSSION: Postexercise decrease in ICP is a potential factor for maintaining cerebral perfusion pressure during arterial hypotension. Future analysis and ongoing trials are stratifying these responses according to responsiveness, gender and age. Supported by Novo Nordic Foundation (NNF150C0019196)