On the basis of measurement techniques that require steady-state hemodynamic conditions when the measurement of cerebral blood flow (CBF) is being obtained, cerebral autoregulation (CA) maintains CBF stable over a wide range of cerebral perfusion pressures. When an acute (or dynamic) change in cerebral perfusion pressure (seconds) is imposed, CBF is not maintained. For example, after thigh cuff occlusion, its release induces an acute drop in arterial blood pressure (ABP). The sharp decrease in CBF indicates that CA was unable to respond to the dynamic (or rapid) changes in cerebral perfusion pressure. Therefore, control mechanisms of arterial pressure with short time constants must contribute importantly to CBF regulation. In order for CA to be effective, the cerebral perfusion pressure must lie within an autoregulatory range of perfusion pressures. The traditional thinking is that changes in sympathetic tone have a limited effect on CBF at rest. However, moderate- to heavy-intensity exercise causes only moderate increases in CBF despite large increases in sympathetic activity and ABP. Animal studies demonstrate that increases in sympathetic nerve activity cause cerebral vasoconstriction and protection against disruption of the blood-brain barrier. These findings suggest that the regulation of CBF during exercise is modulated not only by CA but also by autonomic nervous system and the arterial baroreflex-mediated control of the systemic circulation.
