Patrice Nault and Josée Paradis
University of Ottawa, Gatineau, PQ, Canada
Background:High altitudes trigger the carotid bodies to increase blood pressure and heart rate to counteract the low atmospheric O2 pressure(hypoxemia) during the first week above 4000m. It is not known if there is a differential increase in blood pressure in arms vs legs in healthy subjects at 4000m. High blood pressure is a cause of peripheral artery disease (PAD), which is 20 times more common in the legs than arms, suggesting potential differences in regulation between arms and legs. We wanted to see if high altitude cause blood pressure differences in arms vs. legs in healthy subjects.
Objectives:The objectives of this study were twofold:
1. to determine the effects of altitude (4000 m) on ABI
2. to determine the relationship between high altitude ABIs with previously measured health variables.
Methods:Twenty climbers (17 males, 3 females) from the same Canadian region (sea level, T1) were recruited. Age, BMI, waist circumference and VO2 max were assessed by registered kinesiologist prior to ascension. ABI at T1 were performed in a vascular laboratory.
All ABIs at 4000 m (T2) were performed by the same vascular surgeon (RVT) who was blinded to baseline data. ABI, O2 saturation and pulse rate were measured at the end of the day after 1-hour of rest
SPSS 14.0 was used for statistical analysis.
Results :ABIs measured at T2 (mean = 1.19) were greater than those at T1 (mean = 0.97) (t = - 6.23; 95% CI: -0.32 to - 0.17; p < .001). T2 ABIs were positively related to oxygen saturation measured at T2 (N = 19; r = .45; p = .02). T2 ABIs were positively related to VO2 max at T1 (n = 19; r = 0.436; p = .03). ABIs at T2 were inversely related to T1 resting heart rate (n = 19; r = -.47; p = .04). Overall blood pressure was increased at T2.
Conclusions: ABIs at T2 were greater than those at T1 and highest T2 ABIs were related to higher oxygen saturation. This finding shows that the blood pressure in legs can be different than that in the arms under physiologic stresses in subjects who did not demonstrate differences at baseline