Submitted on September 12, 2008
Revised on December 9, 2008
Accepted on December 9, 2008
Hypercapnic versus hypoxic control of cardiovascular, cardiovagal and sympathetic function
Craig D Steinback1, Deborah Salzer, Philip J. Medeiros2, John M. Kowalchuk3, and J. Kevin Shoemaker2*
1 The University of Western Ontario
2 University of Western Ontario
3 The University Western Ontario
* To whom correspondence should be addressed. E-mail: kshoemak{at}uwo.ca.
We compared the integrated cardiovascular and autonomic responses to hypercapnia (HC) and hypoxia (HX) to test the hypothesis that these stimuli differentially affect muscle sympathetic nerve activity (MSNA) discharge patterns and cardiovagal and sympathetic baroreflex function in a manner related to ventilatory chemoreflex sensitivity. Six males and six females underwent 5 min of HX (end-tidal PO2=45 Torr) and 5 min of HC (end-tidal PCO2=+8 Torr from baseline) causing similar ventilatory responses. A downward-right shift in cardiovagal set-point was observed during both conditions which was strongly related to the change in inspiratory time (Ti) from baseline to HC (r2 = 0.67, P=0.007) and HX (r2 = 0.79, p<0.001). Cardiovagal baroreflex gain was decreased during HX (20.1 ± 6.9 vs. 8.9 ± 5.1 ms/mmHg, P<0.001) but not HC (26.7 ± 12.7 vs. 23.0 ± 9.1 ms/mmHg). Both HX and HC increased MSNA burst amplitude whereas HX, but not HC, also increased in MSNA burst frequency (21 ± 9 vs. 28 ± 7 bursts/min, P = 0.03) and total MSNA (4.56 ± 3.07 vs. 7.37 ± 3.26 mV/min, P = 0.002). However, neither HC nor HX affected sympathetic burst probability or baroreflex gain. HX also caused a greater reduction in total peripheral resistance (TPR) (P = 0.04), a greater increase in HR (P = 0.002) and a trend for a greater cardiac output (Q) response (P = 0.06) compared to HC. Nonetheless, central venous pressure remained unchanged during either condition. These results suggest that HC and HX exert differential effects on cardiovagal, but not sympathetic, baroreflex gain and set point in a manner not related to ventilatory chemoreflex sensitivity. Further, the data suggest that the individual's respiratory pattern to HX or HC, as reflected in the inspiratory time, was a strong determinant of BRS rather than the total ventilatory chemoreflex gain per se.
