Postexercise orthostatic intolerance: influence of exercise intensity.

NEW FINDINGS: What is the central question of this study? Following exercise, hypotension is often reported and syncope is more likely. It is unresolved whether the postexercise hypotension associated with different exercise intensities contributes to the rate at which syncope develops. What is the main finding and its importance? The physiological events that induce presyncope are the same both before and after exercise; however, more intense exercise accelerated the development of hypocapnia, hypotension and, ultimately, syncope. These data indicate that higher intensity exercise induces a postexercise hypotension that reduces cardiovascular reserve, an earlier development of hypocapnia and, ultimately, cerebral hypoperfusion. After exercise, a reduction in mean arterial pressure is often experienced and is referred to as postexercise hypotension. Whilst syncope is more likely following exercise, it is unknown whether orthostatic tolerance is impacted by any exercise intensity-mediated effect on postexercise hypotension. We examined the effect of exercise intensity on time to presyncope, induced via combined head-up tilt and lower body negative pressure following 1 h of cycling at 30 and 70% of heart rate range. Healthy participants (n = 8; mean ± SD, 28 ± 5 years old) completed orthostatic testing to presyncope before and after exercise. Beat-to-beat middle cerebral artery blood flow velocity (MCAv), mean arterial pressure and cerebral oxygenation (measured by near-infrared spectroscopy) were recorded continuously throughout orthostatic testing. During exercise, heart rates were 95 ± 6 and 147 ± 5 beats min(-1) for 30 and 70% heart rate range, respectively, with average power outputs of 103 ± 22 and 221 ± 45 W, respectively. Time to presyncope occurred 32% sooner after the 70% heart rate range trial (952 ± 484 versus 1418 ± 435 s; P = 0.004). Both before and after exercise, presyncope occurred at the same reduction in MCAv (grouped mean, -30 ± 11 cm s(-1) ), mean arterial pressure (-18 ± 13 mmHg), total oxygenation index (-6 ± 2%) and partial pressure of end-tidal CO2 (-16 ± 8 mmHg; all P > 0.1). At presyncope following exercise, the MCAv response was related more to the change in partial pressure of end-tidal CO2 from the baseline preceding orthostatic testing (r(2)  = 0.50, P = 0.01) than to the hypotension (r(2)  = 0.12, P = 0.17). Presyncope both before and after exercise occurred as a result of the same physiological perturbations, albeit greatly accelerated following more intense exercise.

Slow breathing as a means to improve orthostatic tolerance: a randomized sham-controlled trial.

Endogenous oscillations in blood pressure (BP) and cerebral blood flow have been associated with improved orthostatic tolerance. Although slow breathing induces such responses, it has not been tested as a therapeutic strategy to improve orthostatic tolerance. With the use of a randomized, crossover sham-controlled design, we tested the hypothesis that breathing at six breaths/min (vs. spontaneous breathing) would improve orthostatic tolerance via inducing oscillations in mean arterial BP (MAP) and cerebral blood flow. Sixteen healthy participants (aged 25 ± 4 yr; mean ± SD) had continuous beat-to-beat measurements of middle cerebral artery blood velocity (MCAv), BP (finometer), heart rate (ECG), and end-tidal carbon dioxide partial pressure during an incremental orthostatic stress test to presyncope by combining head-up tilt with incremental lower-body negative pressure. Tolerance time to presyncope was improved (+15%) with slow breathing compared with spontaneous breathing (29.2 ± 5.4 vs. 33.7 ± 6.0 min; P < 0.01). The improved tolerance was reflected in elevations in low-frequency (LF; 0.07-0.2 Hz) oscillations of MAP and mean MCAv, improved metrics of dynamic cerebrovascular control (increased LF phase and reduced LF gain), and a reduced rate of decline for MCAv (-0.60 ± 0.27 vs. -0.99 ± 0.51 cm·s(-1)·min(-1); P < 0.01) and MAP (-0.50 ± 0.37 vs. -1.03 ± 0.80 mmHg/min; P = 0.01 vs. spontaneous breathing) across time from baseline to presyncope. Our findings show that orthostatic tolerance can be improved within healthy individuals with a simple, nonpharmacological breathing strategy. The mechanisms underlying this improvement are likely mediated via the generation of negative intrathoracic pressure during slow and deep breathing and the related beneficial impact on cerebrovascular and autonomic function.