Neuromechanical features of the cardiac baroreflex after exercise.

A single bout of exercise is associated with postexercise hypotension, transient decreases in autonomic function, and changes in baroreflex sensitivity. The baroreflex is less sensitive to falling blood pressure than to rising blood pressure; we characterized the cardiac baroreflex in terms of hysteresis and its mechanical and neural components. We hypothesized that hysteresis would be exacerbated postexercise because of a greater relative decrease in falling blood pressure. In 10 healthy young humans (5 men), we used bolus injections of sodium nitroprusside and phenylephrine hydrochloride to drive transient decreases and increases in blood pressure, respectively, to quantify cardiac baroreflex sensitivity to falling and rising blood pressure. This was completed before and at 10, 30, and 60 minutes after 40 minutes of cycling at 60% estimated maximal oxygen consumption. Analyses of beat-to-beat blood pressure, R-R intervals and heart rate, and carotid artery diameter were used to determine the integrated cardiac baroreflex response; this was further quantified into a mechanical component (systolic blood pressure versus carotid diameter) and a neural component (carotid diameter versus R-R interval). There were 2 principle findings: after aerobic exercise baroreflex sensitivity is reduced and hysteresis manifests, and the reduction in sensitivity to falling blood pressure is mediated by decreased mechanical and neural gains, whereas the decreased baroreflex sensitivity to rising blood pressure is mediated by a reduced mechanical gain only. We suggest that impaired neural transduction of the cardiac baroreflex, and its influence on hysteresis, plays an important role in transient autonomic dysfunction after exercise.

Interactions between heart rate variability and pulmonary gas exchange efficiency in humans.

The respiratory component of heart rate variability (respiratory sinus arrhythmia, RSA) has been associated with improved pulmonary gas exchange efficiency in humans via the apparent clustering and scattering of heart beats in time with the inspiratory and expiratory phases of alveolar ventilation, respectively. However, since human RSA causes only marginal redistribution of heart beats to inspiration, we tested the hypothesis that any association between RSA amplitude and pulmonary gas exchange efficiency may be indirect. In 11 patients with fixed-rate cardiac pacemakers and 10 healthy control subjects, we recorded R-R intervals, respiratory flow, end-tidal gas tension and the ventilatory equivalents for carbon dioxide and oxygen during 'fast' (0.25 Hz) and 'slow' paced breathing (0.10 Hz). Mean heart rate, mean arterial blood pressure, mean arterial pressure fluctuations, tidal volume, end-tidal CO(2), and were similar between pacemaker and control groups in both the fast and slow breathing conditions. Although pacemaker patients had no RSA and slow breathing was associated with a 2.5-fold RSA amplitude increase in control subjects (39 +/- 21 versus 97 +/- 45 ms, P < 0.001), comparable (main effect for breathing frequency, F(1,19) = 76.54, P < 0.001) and reductions (main effect for breathing frequency, F(1,19) = 23.90, P < 0.001) were observed for both cohorts during slow breathing. In addition, the degree of (r = 0.36, P = 0.32) and reductions (r = 0.29, P = 0.43) from fast to slow breathing were not correlated to the degree of associated RSA amplitude enhancements in control subjects. These findings suggest that the association between RSA amplitude and pulmonary gas exchange efficiency during variable-frequency paced breathing observed in prior human work is not contingent on RSA being present. Therefore, whether RSA serves an intrinsic physiological function in optimizing pulmonary gas exchange efficiency in humans requires further experimental validation.