The Effects of Aerobic Fitness on Blood Pressure Reactivity During Controlled Low and High Sodium Diets

Abstract

PurposeIncreased blood pressure (BP) reactivity to acute exercise is predictive of future cardiovascular events. Excess dietary sodium exaggerates centrally‐mediated BP reactivity in salt‐resistant rodents. Regular exercise attenuates BP reactivity in rodents, presumably through increased fitness. However, the influence of dietary sodium on BP reactivity has not been investigated in humans. Furthermore, the interaction between dietary sodium and aerobic fitness on neurovascular regulation has not been investigated in humans. Therefore, we sought to test the hypotheses that 1) high dietary sodium exaggerates BP reactivity to acute hand‐grip exercise in humans; and 2) high aerobic fitness modulates high dietary sodium‐induced alterations in BP reactivity in healthy, young adults.MethodsThirteen healthy, young adults (8F/5M, age: 28±2 yrs, BMI: 24.1±0.9 kg/m2; BP: 109±2/63±2mmHg; Mean±SEM) completed randomized, controlled 10‐day diets of high (7 g/day) and low (1 g/day) dietary sodium separated by ≥ four weeks. Beat‐to‐beat laboratory BP was measured via photoplethysmography on day 10 of both diets. BP reactivity was assessed as ΔBP (mmHg) during the final minute of a two‐minute static hand‐grip exercise trial at 40% maximal voluntary contraction compared to a preceding 10‐minute baseline. Aerobic fitness was assessed as VO2Peak using a progressive‐intensity treadmill exercise protocol and indirect calorimetry. Differences in high‐ vs. low‐sodium BP reactivity (high – low sodium ΔBP reactivity; using the final minute of hand‐grip exercise BP data) was compared by splitting the participants into two categories of fitness (low vs. high) and completing an independent‐samples t‐test. Low aerobic fitness was defined as a relative VO2Peak of ≤40 ml*kg−1*min−1. Using this criterion, seven participants were classified as having “low aerobic fitness” and six were classified as having “high aerobic fitness”. Twenty four‐hour urinary sodium excretion was measured to ensure dietary compliance.ResultsUrinary Na+ excretion increased on the high‐ vs. low‐sodium diet (259.7±18.4 vs. 33.2±6.6 mmol/24 hours; p < 0.01). There was no difference in 24‐hr mean arterial BP on the high‐ vs. low‐sodium diet (82.9±2.1 vs. 79.8±2.4 mmHg, p > 0.05). The high sodium diet augmented systolic (24.2±2.6 vs. 17.4±3.1; p = 0.03), but not diastolic (18.7±1.8 vs. 15.5±2.5; p = 0.19) BP reactivity during acute hand‐grip exercise in all participants. There was a trend (p = 0.06) for the low aerobic fitness participants to demonstrate greater Δ systolic BP reactivity compared to the high aerobic fitness participants (11.5±4.3 vs. 1.1±2.4 ΔBP reactivity). However, there was not a statistically significant difference (p = 0.32) between the low and high aerobic fitness participants regarding Δ diastolic BP reactivity between diets (5.5±3.5 vs. 0.7±2.9 ΔBP reactivity).ConclusionThese preliminary data suggest that 1) high dietary sodium exaggerates systolic BP reactivity to acute hand‐grip exercise in humans; and 2) high aerobic fitness may modulate some of the neurovascular effects of high dietary sodium in healthy young adults, although more data is needed.Support or Funding InformationNIH Grant 1RO1HL128388This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.