MIDDLE CEREBRAL-ARTERY FLOW VELOCITY AND BLOOD-FLOW DURING EXERCISE AND MUSCLE ISCHEMIA IN HUMANS

Changes in middle cerebral artery flow velocity (V(mean)), measured by transcranial Doppler ultrasound, were used to determine whether increases in mean arterial pressure (MAP) or brain activation enhance cerebral perfusion during exercise. We also evaluated the role of "central command," mechanoreceptors, and/or muscle "metaboreceptors" on cerebral perfusion. Ten healthy subjects performed two levels of dynamic exercise corresponding to a heart rate of 110 (range 89-134) and 148 (129-170) beats/min, respectively, and exhaustive one-legged static knee extension. Measurements were continued during 2-2.5 min of muscle ischemia. MAP increased similarly during static [114 (102-133) mmHg] and heavy dynamic exercise [121 (104-136) mmHg] and increased during muscle ischemia after dynamic exercise. During heavy dynamic exercise, V(mean) increased 24% (10-47%; P < 0.01) over approximately 3 min despite constant arterial carbon dioxide tension. In contrast, static exercise with a higher rate of perceived exertion [18 (13-20) vs. 15 (12-18) units; P < 0.01] was associated with no significant change in V(mean). Muscle ischemia after exercise was not associated with an elevation in V(mean), and it did not provoke an increase in V(mean) after static exercise. Changes in V(mean) during exercise were similar to those recorded with the initial slope index of the Xe-133 clearance method. The data show that middle cerebral artery mean flow velocity reflects changes in cerebral perfusion during exercise. Furthermore, they support the hypothesis that cerebral perfusion during exercise reflects an increase in brain activation that is independent of MAP, central command, and muscle metaboreceptors but is likely to depend on influence of mechanoreceptors.