The Effects of Sodium Loading on Pulsatile Arterial Load Are Not Associated With Aerobic Capacity

High sodium diets blunt vascular function when compared to low sodium diets, providing evidence that the vasculature is an early contributor to the increased cardiovascular disease (CVD) risk associated with high sodium intake. In contrast, increased aerobic capacity is associated with decreased CVD risk. It is unclear whether the effects of dietary sodium on pulsatile arterial load are influenced by aerobic capacity. Therefore, we tested the hypothesis that the effects of short-term sodium loading on measures of pulsatile arterial load are inversely associated with aerobic capacity (VO 2 peak). Thirty-one healthy young adults were studied (17M / 14F; 25 ± 4 yr; 24.1 ± 3.0 kg/m 2 ; 112 ± 11 / 68 ± 13 mmHg). VO 2 peak was determined via cardiopulmonary exercise testing on a cycle ergometer and expressed as percent of predicted peak VO 2 (Hansen/Wasserman equation) to account for the influence of sex, age, and body size. Participants consumed capsules containing either table salt (~3.4 g of sodium/day) or a placebo for 10 days in a randomized cross-over design. Participants were instructed to maintain their usual diet throughout the study. Urine was collected for 24 hrs prior to each visit and sodium excretion was used as an index of daily sodium intake. Pulsatile arterial load was assessed at rest on day 11 of both sodium and placebo conditions via pressure-flow analyses using time-aligned left ventricular outflow waveforms (echocardiography) and aortic pressure waveforms derived via radial artery applanation tonometry and a generalized transfer function. The primary arterial hemodynamic variables of interest were reflected wave amplitude (Pb), reflected wave transit time (RWTT), and wasted pressure effort (WPE). Aortic pressure waveform morphology was used to determine augmentation index (AIx), a surrogate marker of wave reflection. Mean VO 2 peak was 39.2 ± 12.0 ml/kg/min and 101 ± 30% of equation predicted peak VO 2 (range: 64 to 191%). Total 24 hr urinary sodium excretion was higher following sodium compared to placebo (310 ± 94 vs. 170 ± 68 mmol/24 hr, p<0.001). Sodium increased AIx (6 ± 14 vs. 2 ± 15%, P=0.02), but did not change Pb (P=0.71) or RWTT (P=0.98). WPE was also not different between conditions (sodium: 2158 ± 768, placebo: 2052 ± 906 mmHg·ms, P=0.41). Percent of predicted peak VO 2 was not associated with ΔAIx (r=-0.09, P=0.63), ΔPb (r=0.04, P=0.83), ΔRWTT (r=0.08, P=0.70), or ΔWPE (r=-0.20, P=0.31).Contrary to our hypothesis, sodium loading-induced changes in pulsatile arterial load were not associated with aerobic capacity. There was no effect of excess sodium intake on Pb, RWTT, or WPE. However, our sample habitually consumed a high sodium diet as shown by the high urinary sodium excretion during the placebo condition. Future studies should include a low sodium condition to ensure that any potential negative effects of high sodium are not masked by the habitual sodium intake of the participants. Supported by NIH 5R01HL104106 and 5P20GM113125; AHA 20POST35080171 This abstract was presented at the American Physiology Summit 2025 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.