Cerebrovascular Responses to Varying Handgrip Exercise Paradigms

Abstract

Although the brain constitutes only ∼ 2% of body mass, it accounts for ∼ 20% of total energy expenditure, highlighting the importance of understanding local cerebral blood flow (CBF) regulation. Exercise can be used as a stressor to induce changes in CBF. Acute handgrip exercise (HGE) elevates cerebrovascular hemodynamics, yet it remains unclear if CBF is differentially regulated across varying HGE types and intensities commonly used in HGE experiments. This study investigates middle cerebral artery blood velocity (MCAv) and internal carotid artery (ICA) diameter responses during static and rhythmic HGE at different intensities (i.e., %maximum voluntary contraction; MVC). Thirty-four healthy volunteers (17 females; age range: 22{27 years) completed four randomized HGE protocols (5 minutes each, 15 minutes rest in between): rhythmic HGE (RHGE) at 60% and 30% MVC, and static HGE (SHGE) at 30% and 15% MVC. Independent of intensity, RHGE and high-intensity HGE elicited a greater MCAv response (p<0.01) compared to SHGE and low-intensity HGE in the first minute of exercise. Additionally, high-intensity RHGE induced greater changes (p<0.05), independent of time, while no significant differences were observed between low-intensity RHGE, low-intensity SHGE, and high-intensity SHGE. No significant interaction effects were found for ICA diameter. Mean arterial pressure, heart rate, and systolic blood pressure showed significant time*intensity interactions, with high-intensity exercise eliciting greater responses compared to lower intensity during the exercise duration (p<0.05). A time*intensity interaction was also found for PETCO2, with high-intensity exercise resulting in significantly lower PETCO2 than lower-intensity exercise at minute 5 of HGE, independent of type. These findings suggest that cerebral hemodynamic responses are greater in RHGE when compared to SHGE and greater in higher intensity in RHGE only. We speculate that differences in local CBF regulatory mechanisms such as cerebral sympathetic nervous activity, may influence changes in MCAv.