Cerebral autoregulation dynamics in endurance-trained individuals

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Abstract
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 (MCA) mean blood velocity ( Vmean) response to a sudden drop in mean arterial pressure (MAP) after 2.5 min of leg ischemia in endurance athletes and untrained subjects (maximal O2uptake: 69 ± 7 vs. 42 ± 5 ml O2·min−1·kg−1; n = 9 for both, means ± SE). After cuff release when seated, endurance 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, −30%, vs. 58 ± 3 to 43 ± 2 cm/s, −25%). The athletes also had a 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 time point of increase in the cerebrovascular conductance index (CVCi = MCA Vmean/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 Vmeanphase in both groups but ∼40% higher normalized MAP to MCA Vmeanlow-frequency transfer function gain in the trained subjects. No significant differences were detected in the rates of recovery of MAP and MCA Vmeanand the rate of CVCi regulation (18 ± 4 vs. 24 ± 7%/s, P = 0.2). In highly trained endurance athletes, a drop in blood pressure after the release of resting leg ischemia was more pronounced than in untrained subjects and was associated with parallel changes in indexes 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 with a less effective dampening of MAP oscillations, indicating that athletes may be more prone to instances of symptomatic cerebral hypoperfusion when MAP declines.

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