Association between carotid-femoral pulse wave velocity and VO2peak in individuals with chronic kidney disease

Cardiovascular disease (CVD) is the leading cause of mortality in chronic kidney disease (CKD). Vascular dysfunction and a decline in exercise capacity are hallmarks of CKD that contribute to CVD burden. Reduced exercise capacity leads to lower levels of physical activity further exacerbating the risk for CVD. Arterial stiffness is a nontraditional risk factor for CVD in CKD and increases with the progression of disease. Compliant central arteries are important during exercise to accommodate the associated increase in cardiac output. Therefore, increased arterial stiffness may play a role in impairing exercise capacity in CKD patients by altering ventricular-vascular coupling. The purpose of the present study was to investigate the relation between arterial stiffness and exercise capacity in patients with stages 3 to 4 CKD. We hypothesized that carotid-femoral pulse wave velocity (cfPWV), a measure of aortic stiffness, would be associated with VO2peak in CKD. We studied 35 non-dialysis patients with CKD (11F/24M) aged 59±12 years with a mean estimated glomerular filtration rate of 43.3±12.9 mL/min/1.73m2. cfPWV was assessed by simultaneous recording of carotid (applanation tonometry) and femoral pressure (oscillometric) waves. Central pressure and augmentation index (AI, a measure of wave reflection) were assessed via radial applanation tonometry and a generalized transfer function. VO2peak was assessed via cardiopulmonary exercise testing on a cycle ergometer with workload increased by 15W/min. cfPWV averaged (±SD) 9.6±1.9 m/s, central pulse pressure (PP) 51±19 mmHg, AI 29±13%, and VO2peak 17.5±5.5 mL/kg/min. cfPWV, PP, and AI were all inversely associated with VO2peak. Multiple linear regression revealed that only cfPWV was a significant predictor of VO2peak (R2 = 0.28, p = 0.001). An increase in cfPWV of 1 m/s predicted a 1.50mL/kg/min lower VO2peak. These findings suggest that arterial stiffness may impair exercise capacity and contribute to exercise intolerance and subsequent reduction in physical activity in patients with CKD. This work was supported by National Institutes of Health Grants R01HL113514 and P20GM113125. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.