Abstract
PURPOSE: Increased blood pressure (BP) reactivity and variability are predictive of future cardiovascular events. Excess dietary salt exaggerates neurally-mediated BP reactivity, and BP variability in salt-resistant rodents. Regular physical activity (PA) blunts BP reactivity in rodents. However, the interaction of salt and PA on neurovascular regulation has not been investigated in humans. Therefore, we sought to test the hypothesis that high habitual PA mitigates high dietary salt-induced increases in BP reactivity and BP variability in healthy, young adults. METHODS: Nine participants (5F/4M, 27±2 yrs, BMI: 23.3±0.9 kg/m2) completed randomized, controlled 10-day diets of low (2.6 g/day), and high (18 g/day) salt. Beat-to-beat laboratory BP was measured via photoplethysmography on day 10 of each diet. BP reactivity was assessed as ΔBP (mmHg) during the final minute of a 2-min hand grip exercise at 40% maximal voluntary contraction compared to a preceding baseline. Average real variability (ARV) index was used to assess BP variability derived from 24-hour ambulatory BP monitoring. Habitual PA was assessed via accelerometry (Actigraph GT3X). Differences in high vs. low salt BP reactivity (ΔBP reactivity) and ambulatory BP variability (ΔBP ARV) were correlated against PA. Twenty four-hour urinary sodium excretion was measured. RESULTS: There were no differences in 24-hr mean arterial BP on the high vs. low salt diet (82.9±2.1 vs. 79.8±2.4 mmHg; p > 0.10). Urinary Na+ excretion increased on the high vs. low salt diet (256.9±20.5 vs. 39.5±11.2 mmol/24 hours; p < 0.05). There was a trend for the high salt diet to augment systolic (p = 0.08), but not diastolic BP reactivity during hand grip exercise. Habitual PA was inversely correlated to Δ systolic BP reactivity (r = -0.74, p = 0.03), and there was a trend for an inverse correlation with Δ diastolic BP reactivity (r = -0.68, p = 0.06) during hand grip exercise. There was a trend for higher 24-hr systolic BP ARV on the high salt diet (10.6±0.8 vs. 8.9±0.6 mmHg; p = 0.09), but there was no correlation between PA with Δ systolic BP ARV (r = -0.29, p = 0.48) on the high vs. low salt diet. CONCLUSION: These preliminary data suggest that high habitual physical activity may offset some of the adverse neurovascular effects of high dietary salt in young, healthy, salt-resistant humans.
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