Received January 15, 2004
Revised February 11, 2004
Accepted after revision April 28, 2004
THE EFFECTS OF BREATHING 5% CO2 ON HUMAN CARDIOVASCULAR RESPONSES AND TOLERANCE TO ORTHOSTATIC STRESS
Reuben Howden 1*,
J. Timothy Lightfoot 2,
Stephen J Brown 3,
Ian L Swaine 4
1 NIEHS
2 University of North Carolina
3 De Montfort University
4 Canterbury Christ Church University College
* To whom correspondence should be addressed. E-mail: howden{at}niehs.nih.gov.
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Abstract |
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Breathing carbon dioxide (CO2) is known to induce hypercapnic acidosis and to affect chemoreceptor regulation of the cardiovascular system. However, there is limited information in the literature regarding the effects of breathing CO2 upon tolerance to orthostatic stress where cardiovascular regulation is challenged. The purpose of this study was to investigate the effect of breathing 5% CO2 on pre-syncopal tolerance to lower body negative pressure (LBNP). Nine subjects [5 males and 4 females; average± SD, age 21.9 ± 0.9 years, height 172.4 ±9.7 cm, mass 70.3 ± 7.1 Kg] volunteered to participate in this study. Orthostatic tolerance was determined by exposing subjects to LBNP until the onset of pre-syncopal signs and symptoms on two occasions each separated by approximately one week. On one occasion investigations were carried out while subjects were breathing room air and on the other, subjects were breathing air containing 5% carbon dioxide (CO2) inducing hypercapnia thus stimulating the systemic chemoreceptors. During hypercapnic conditions, when compared to normocapnia, there were significant increases (P<0.05) in minute ventilation, end-tidal CO2 and estimated arterial PCO2. Furthermore, under hypercapnic conditions there was an increase in orthostatic tolerance, peak heart rate and time to peak heart rate during LBNP. The LBNP induced increase in calf circumference was significantly attenuated at -50 mmHg of LBNP in addition to a further 22.3% reduction in stroke volume under hypercapnic conditions. In conclusion, these results suggest that the possible protective element of presyncope was delayed during hypercapnia at the expense of further reductions in stroke volume. This delayed presyncopal response may have been associated with increases in cerebral blood flow induced by the increased arterial PCO2.
Key Words:
Blood pressure, Cardiovascular, Chemoreceptor
