No abstract

The response of cerebral vasculature to exercise is different from other peripheral vasculature; it has a small vascular bed and is strongly regulated by cerebral autoregulation and the partial pressure of arterial carbon dioxide (Pa(CO(2))). In contrast to other organs, the traditional thinking is that total cerebral blood flow (CBF) remains relatively constant and is largely unaffected by a variety of conditions, including those imposed during exercise. Recent research, however, indicates that cerebral neuronal activity and metabolism drive an increase in CBF during exercise. Increases in exercise intensity up to approximately 60% of maximal oxygen uptake produce elevations in CBF, after which CBF decreases toward baseline values because of lower Pa(CO(2)) via hyperventilation-induced cerebral vasoconstriction. This finding indicates that, during heavy exercise, CBF decreases despite the cerebral metabolic demand. In contrast, this reduced CBF during heavy exercise lowers cerebral oxygenation and therefore may act as an independent influence on central fatigue. In this review, we highlight methodological considerations relevant for the assessment of CBF and then summarize the integrative mechanisms underlying the regulation of CBF at rest and during exercise. In addition, we examine how CBF regulation during exercise is altered by exercise training, hypoxia, and aging and suggest avenues for future research.

Non-technical summary The mechanism underlying the plateau or relative decrease in cerebral blood flow during maximal incremental dynamic exercise remains unclear. We show that during graded dynamic exercise, the regulation of internal carotid artery blood flow was limited by a large increase in external carotid artery blood flow, one function of which is thermoregulation during heavy exercise. The mechanism of the plateau or decrease in internal carotid artery blood flow appears to be partly due to exercise-induced redistribution of arterial blood flow to the head and brain. AbstractThe mechanism underlying the plateau or relative decrease in cerebral blood flow (CBF) during maximal incremental dynamic exercise remains unclear. We hypothesized that cerebral perfusion is limited during high-intensity dynamic exercise due to a redistribution of carotid artery blood flow. To identify the distribution of blood flow among the arteries supplying the head and brain, we evaluated common carotid artery (CCA), internal carotid artery (ICA), external carotid artery (ECA) and vertebral artery (VA) blood flow during dynamic exercise using Doppler ultrasound. Ten subjects performed graded cycling exercise in a semi-supine position at 40, 60 and 80% of peak oxygen uptake (V O 2 peak ) for 5 min at each workload. The ICA blood flow increased by 23.0 ± 4.6% (mean ± SE) from rest to exercise at 60%V O 2 peak . However, at 80% V O 2 peak , ICA blood flow returned towards near resting levels (9.6 ± 4.7% vs. rest). In contrast, ECA, CCA and VA blood flow increased proportionally with workload. The change in ICA blood flow during graded exercise was correlated with end-tidal partial pressure of CO 2 (r = 0.72). The change in ICA blood flow from 60%V O 2 peak to 80%V O 2 peak was negatively correlated with the change in ECA blood flow (r = −0.77). Moreover, there was a significant correlation between forehead cutaneous vascular conductance and ECA blood flow during exercise (r = 0.79). These results suggest that during high-intensity dynamic exercise the plateau or decrease in ICA blood flow is partly due to a large increase in ECA blood flow, which is selectively increased to prioritize thermoregulation.

We examined the relationship between changes in cardiac output (Q) and middle cerebral artery mean blood velocity (MCA V mean ) in seven healthy volunteer men at rest and during 50% maximal oxygen uptake steady-state submaximal cycling exercise. Reductions inQ were accomplished using lower body negative pressure (LBNP), while increases inQ were accomplished using infusions of 25% human serum albumin. Heart rate (HR), arterial blood pressure and MCA V mean were continuously recorded. At each stage of LBNP and albumin infusionQ was measured using an acetylene rebreathing technique. Arterial blood samples were analysed for partial pressure of carbon dioxide tension (P a,CO 2 ). During exercise HR andQ were increased above rest (P < 0.001), while neither MCA V mean nor P a,CO 2 was altered (P > 0.05). The MCA V mean andQ were linearly related at rest (P < 0.001) and during exercise (P = 0.035). The slope of the regression relationship between MCA V mean andQ at rest was greater (P = 0.035) than during exercise. In addition, the phase and gain between MCA V mean and mean arterial pressure in the low frequency range were not altered from rest to exercise indicating that the cerebral autoregulation was maintained. These data suggest that theQ associated with the changes in central blood volume influence the MCA V mean at rest and during exercise and its regulation is independent of cerebral autoregulation. It appears that the exercise induced sympathoexcitation and the change in the distribution ofQ between the cerebral and the systemic circulation modifies the relationship between MCA V mean andQ.