SUBMAXIMAL DYNAMIC EXERCISE DOES NOT IMPAIR CEREBRAL AUTOREGULATION

Abstract

875 Current static methods of assessing cerebral autoregulation are unable to determine if autoregulation is impaired during steady state exercise. The purpose of this study was to use beat-by-beat changes in both mean flow velocities (MFV) of the middle cerebral artery (MCA) and the anterior cerebral artery (ACA) as well as mean arterial pressure (MAP) to determine if changes in autoregulation had occurred during steady state submaximal exercise. Subjects were asked to ride a cycle ergometer for 5 minutes of loadless pedaling, followed by a 5 min constant workload determined to be at either 50%, 85%, or 115% of ventilatory threshold (VT) or 90% of the difference between VT and max (d90), followed by 5 min loadless pedaling. All subjects completed the full or part of the five minutes at each workload on two separate days. Cerebral autoregulation was assessed by comparing the gain between the MAP and the MFV in both arteries. High values indicate that cerebral autoregulation was not dampening out swings in MAP. Results found no change in autoregulation during any of the workrates in the MCA (Gain: 0W - 0.0827±0.012, step - 0.109±0.032, 0W - 0.118±0.050) or the ACA (Gain: 0W - 0.0613±0.005, step - 0.0876±0.020, 0W - 0.110±0.050). There was a significant increase in MFV in the MCA (p<0.001) during the three lower workrates, 14% at 50% TV, 13% at 85% TV, and 24% at 115% TV, however, MFV slightly decreased at d90, likely due to the extreme hyperventilation at this workrate. The ACA demonstrated a similar pattern of increases (p<0.001), 10% at 50% TV, 9% at 85% TV, and 23% at 115% TV, and again a slight decrease at d90. These changes in MFV correspond with a significant increase in BP at the three lower workrates (p<0.03) with no change in cerebrovascular resistance in either the MCA or ACA bed. These data indicate that while autoregulation is still intact during submaximal dynamic exercise, there is still a slight increase in MFV, possibly due to increased cerebral metabolism. Supported by NSERC, MRC and the CSA.