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1 Division on Aging, Gerontology Division, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA, USA
2 Department of Kinesiology, The University of Waterloo, Waterloo, ON, Canada
3 Canadian Centre for Activity and Aging, School of Kinesiology and Department of Physiology and Pharmacology, The University of Western Ontario, London, ON, Canada
4 Sunnybrook and Womens Health Sciences Centre, Toronto, ON, Canada
5 Department of Anaesthesia, University of California, San Francisco, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: serrador{at}hms.harvard.edu.
Reductions in end-tidal CO2 during upright posture have been suggested to be the result of hyperventilation and the cause of decreases in cerebral blood flow. The goal of this study was to determine if decreases in end-tidal CO2 reflected decreases in arterial CO2 and their relation to increases in alveolar ventilation and decreases in cerebral blood flow. Fifteen (10 women, 5 men) healthy subjects experienced a 10 min head-up tilt protocol. Arterial PCO2 (arterial blood samples), alveolar ventilation and cerebral flow velocity in the middle and anterior cerebral arteries were examined. Twelve subjects who completed the tilt demonstrated reductions in both end-tidal and arterial PCO2 (-1.7±0.5 & -1.1±0.4 mmHg, P<0.05) during the first minute of tilt that was associated with a significant increase in alveolar ventilation (+0.7±0.3 L/min, P<0.05). However, further decreases in arterial PCO2 (-0.5±0.5 mmHg, P<0.05), from first to last minute of tilt, occurred even though alveolar ventilation did not change significantly (-0.2±0.3 L/min, P=NS). Similarly, decreases in cerebral flow velocity from first to last minute of tilt occurred in both the middle and anterior cerebral arteries (-7±2 % & -8±2 %, P<0.05) even though arterial PCO2 changes were minimal. These data suggest that decreases in end tidal and arterial PCO2 during upright posture are not solely due to increased alveolar ventilation but could be due to ventilation-perfusion mismatch or a redistribution of CO2 stores. Furthermore, the reduction in arterial PCO2 did not fully explain the decrease in cerebral flow velocity throughout head-up tilt. These data suggest that factors in addition to a reduction in arterial CO2 play a role in the cerebral blood flow response to orthostatic stress.
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