Aerobic fitness may be associated with reduced orthostatic tolerance. To investigate whether trained individuals have less effective regulation of cerebral vascular resistance, we studied the middle cerebral artery blood velocity (MCA Vmean) response to a sudden drop in mean arterial pressure (MAP) following 2.5 min of leg ischemia in endurance athletes and untrained subjects (maximal oxygen uptake: 69±7 vs. 42±5 ml O2.min-1.kg-1; n=9 for both; mean ± SE). Following cuff release when seated, the athletes had larger drops in MAP (94±6 to 62±5 mmHg; -39% vs. 99±5 to 73±4 mmHg; -26%) and MCA Vmean (53±3 to 37±2 cm.s-1; -30% vs. 58±3 to 43±2 cm.s-1; -25%). The athletes also had slower recovery to baseline of both MAP (25±2 vs. 16±1 s; P<0.01) and MCA Vmean (15±1 vs. 11±1 s; P<0.05). The onset of autoregulation, determined by the timepoint of increase in cerebrovascular conductance index (CVCi=MCAVmean/MAP) appeared later in the athletes (3.9±0.4 vs. 2.7± 0.4s; P=0.01). Spectral analysis revealed a normal MAP-to-MCA Vmean phase in both groups but ~40% higher normalized MAP to MCA Vmean LF transfer function gain in the trained subjects. No significant differences were detected in the rates of recovery of MAP, MCA Vmean and the rate of CVCi regulation (18±4 vs. 24±7 %.s-1; P=0.2). In highly-trained endurance athletes, a drop in blood pressure following release of resting leg ischemia was more pronounced than in untrained subjects and associated with parallel changes in indices of cerebral blood flow. Once initiated, the autoregulatory response was similar between the groups. A delayed onset of autoregulation with a larger normalized transfer gain conforms to a less effective dampening of MAP oscillations, indicating that athletes may be more prone to instances of symptomatic cerebral hypoperfusion when MAP declines.
- cerebral blood flow
- frequency analysis
- leg ischemia
- Copyright © 2011, Journal of Applied Physiology