Sympathetic Response to Resistance Breathing During Simulated Hemorrhage in Humans

Background: Resistance breathing increases venous return and stroke volume by amplifying the respiratory pump during inspiration. Breathing with resistance devices augments reflex compensatory mechanisms to improve tolerance to hypovolemic stress, such as hemorrhage. We tested the hypothesis that protection of arterial pressure with resistance breathing during simulated hemorrhage is due to the mechanical effect of the respiratory pump, and not due to increases in sympathetic nervous system activity. Methods: Lower body negative pressure (LBNP) was used to simulate hemorrhage in eight human subjects (4M, 3F; 27.5±1.6 y). Two experiments were conducted (randomized order): 1) a control condition in which ramp LBNP was applied at 3 mmHg/min until the onset of presyncope, and 2) a resistance breathing condition in which the same LBNP protocol was used, but subjects breathed through a resistance device during the final stages of the protocol. Mean arterial pressure and stroke volume were monitored continuously, and blood samples were collected every 5-min for measurement of plasma norepinephrine and epinephrine. Results: There were no differences in the reduction in stroke volume (control, -36.9±13.8% vs. resistance breathing, -33.5±17.1%, P=0.31) or mean arterial pressure (control, -5.5±4.2% vs. resistance breathing, -6.3±7.4%, P=0.63) between conditions. LBNP induced increases in both norepinephrine (P=0.03) and epinephrine (P=0.003), but there was no main effect of resistance breathing on these responses (norepinephrine, P=0.8; epinephrine, P=0.48). Conclusion: These data support the hypothesis that, based on circulating catecholamine responses, resistance breathing has no direct effect on sympathetic drive to compensate for central hypovolemia.