Dynamic response of cerebral perfusion during low-intensity cycling exercise: A study using transcranial Doppler ultrasound
<p><tt>We investigated the changes in cerebral perfusion during constant low-intensity exercise and the effect of a late increase in workload. Eleven healthy males participated in this study. Four subjects performed 15 min of constant low-intensity exercise on a cycle ergometer, while seven subjects performed 20 min of exercise consisting of 17 min of low-intensity exercise, which was incremented to moderate-intensity for the final 3 min. As an index for cerebral perfusion, the time-averaged mean velocity of flow in the middle cerebral artery (MCAV<sub>mean</sub>) was measured using transcranial Doppler ultrasound. During the 15-min of low-intensity exercise (78 ± 3 Watts), pulmonary oxygen consumption (<em>V</em>O<sub>2</sub>) increased to 19.1 ± 2.5 ml/min/kg within 3-6 min, while </tt>end-tidal pressure of carbon dioxide (P<sub>ET</sub>CO<sub>2</sub>) increased to <tt>42.0 ± 3.2 mmHg, and MCAV<sub>mean</sub> increased to a peak 19.2 ± 9.1 % above the pre-exercise resting level then gradually decreased back toward the resting level. During the 20-min exercise at low and then moderate intensity </tt>(77 <tt>± 4 and </tt>111 <tt>± 7 Watts for low and moderate intensity, respectively), <em>V</em>O<sub>2</sub> increased from 19.1 ± 2.8 to 24.2 ± 3.6 ml/min/kg after the late increment in exercise intensity, while</tt> P<sub>ET</sub>CO<sub>2</sub> remained unchanged (<tt>p = 0.48, Tukey’s post hoc test</tt>), and <tt>MCAV<sub>mean</sub> tended to increase but did not change significantly. K</tt>inetic analysis of <em>V</em>O<sub>2</sub> and <tt>MCAV<sub>mean</sub></tt> at low and moderate exercise intensities <tt>using a monoexponential model revealed that the </tt>time constant (τ) for <em>V</em>O<sub>2</sub> was significantly related to the τ for <tt>MCAV<sub>mean</sub></tt> at low (n=9) (R<sup>2 </sup>=0.52, P =0.03) and moderate intensity (n=6) (R<sup>2</sup> = 0.69, P =0.04). These findings imply that cardiac output exerts an indirect effect to alter cerebral perfusion and that cerebral autoregulation likely operates to stabilize cerebral blood flow during prolonged exercise at a constant workload.</p>