Normally, central elastic arteries (e.g., aorta and common carotid artery) effectively buffer cardiac pulsation-induced flow/pressure fluctuations. With advancing age, arterial stiffening deteriorates this function and produces the greater cerebral hemodynamic pulsatility that impacts vulnerable brain tissue. It is well known that the buffering function of the central artery is improved by regular aerobic exercise, but the influence of endurance training on the pulsatile component of cerebral hemodynamics remains poorly understood. To characterize the functional role of the central artery at the heart-brain hemodynamic connection comprehensively, we assessed relations among the endurance training-induced changes in the left ventricle (LV), carotid arterial compliance, and cerebral hemodynamics. Thirteen collegiate tennis players (20 ±1 yr) underwent a 16-wk endurance training intervention designed for improving cardiovascular function. Expectedly, maximal oxygen uptake (V? O2peak ), LV ejection velocity (via Doppler ultrasound), and the maximal rate of pressure increase of estimated aortic pressure waveform (via general transfer function) improved after the training intervention, whereas middle cerebral arterial (MCA) hemodynamics (via transcranial Doppler), such as mean and pulsatile flow velocities, remained unchanged. Carotid arterial compliance (via ultrasound and applanation tonometry) increased after the training intervention, and a larger increase in carotid arterial compliance was significantly associated with the greater attenuations of pulsatile MCA velocity (r =-0.621) normalized by mean MCA velocity. These results suggest that the training-induced improvement of carotid artery Windkessel function might offset the expected increase in the pulsatile component of cerebral perfusion induced by the enhanced LV systolic function.
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