Differences in Peak VO2 Among Healthy Andean Highlanders and Males with Chronic Mountain Sickness Before and After Isovolemic Hemodilution at 4350m

Abstract

Excessive erythrocytosis is the hallmark of Chronic Mountain Sickness (CMS), a maladaptive clinical syndrome common in Andeans that is thought to negatively impact oxygen transport and exercise capacity. We performed cardiopulmonary exercise testing at 4350m in both healthy males (controls) and those with CMS pre‐ and post‐isovolemic hemodilution (n = 8 controls, n = 6 CMS) to determine whether they differed in exercise capacity as a function of hematocrit (Hct). Hct differed significantly between control (Hct=51.6±4.0) and pre‐hemodilution CMS subjects and between pre‐ and post‐hemodilution (Hct=66.7±4.1, 53.2±1.8, respectively; all p<0.0005), and Hct showed a negative trend with exercise capacity in CMS subjects. Anaerobic threshold was lower in CMS subjects compared to controls (p<0.01) but normalized after hemodilution. While peak VO2/kg was similar pre‐ and post‐hemodilution in CMS subjects, it was significantly different between control and CMS subjects with or without hemodilution (p<0.05). Cardiac output (QT/kg) during maximal exercise was lower in pre‐ and post‐hemodilution CMS compared to controls (p<0.02) and was relatively lower in pre‐ versus post‐hemodilution CMS subjects (p<0.05). The slopes of the QT‐VO2 relationship indicate that decreased QT response to exercise in CMS subjects is partially normalized post hemodilution (p<0.04), while the intercept is not statistically different. While QT is reduced in CMS and can be partially recovered by hemodilution, VO2 max did not increase in CMS individuals post hemodilution, suggesting this reduction of Hct does not influence exercise capacity. How the differences between CMS and non‐CMS individuals relate to other components of oxygen transport and the presence and absence of adaptive genetic factors remains to be determined.Support or Funding InformationThis study was supported by an NIH NRSA Individual Postdoctoral Fellowship (Parent F32) to ECH (F32HL131218), a Wellcome Trust PHTM grant (107544/Z/15/Z) to FCV, and an NIH R00HL118215 and American Physiological Society Giles F. Filley Memorial Award to TSS.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.