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Blood Pressure Responsiveness to Muscle Metaboreflex Activation in Older Adults Following Dietary Nitrate Supplementation

There is an increased risk for adverse cardiac events in older individuals that exhibit exaggerated blood pressure (BP) responses to exercise. Evidence suggests that the exaggerated BP responses to exercise in older individuals are due in part to greater muscle metaboreflex activation. The vasoactive molecule nitric oxide (NO) contributes to the regulation of BP and may play a role in the metaboreflex. With aging, NO bioavailability is often reduced but can be improved through nitrate (NO3) supplementation via the nitrate‐nitrite‐NO pathway. Therefore, we sought to test the hypothesis that dietary NO3 supplementation would reduce the BP responses to muscle metaboreflex activation in healthy older adults. To test this hypothesis we utilized a randomized, double‐blind, placebo controlled crossover study design in 8 healthy older adults (67 ± 2 years; 5M/3F). Each subject was studied before and after 4 weeks of NO3 supplementation (beetroot powder) and placebo (beetroot powder devoid of NO3) for a total of 4 study days. The muscle metaboreflex test consisted of 2 min of isometric handgrip (IHG) at 30% of maximal voluntary contraction followed by 2 minutes and 15 seconds of post exercise forearm ischemia (PEI) to isolate muscle metaboreflex activation. PEI was achieved by inflation of a blood pressure cuff around the upper arm to 240 mmHg 3 seconds before the end of handgrip exercise. Beat‐to‐beat peripheral BP was measured via finger plethysmography) and heart rate via ECG throughout the muscle metaboreflex test. BP responses were analyzed as the change (Δ) from baseline to the end of the IHG and PEI periods. Both IHG and PEI increased systolic (SBP) and mean arterial pressure (MAP) relative to resting (baseline) measurements (P < 0.05 for both). No significant interaction (P = 0.39) was found for changes in ΔSBP when comparing 4‐weeks of NO3 supplementation (14 ± 4 vs. 11 ± 3 mmHg) vs. 4‐weeks of the placebo condition (12 ± 4 vs. 15 ± 3 mmHg). Likewise, the change in ΔMAP after 4 weeks did not differ between NO3 supplementation (10 ± 2 vs. 8 ± 2 mmHg) and the placebo condition (8 ± 1 vs. 8 ± 2 mmHg) during IHG (interaction, P = 0.29). Conversely, the ΔSBP (19 ± 3 vs. 13 ± 4 mmHg, P = 0.03) and ΔMAP (11 ± 2 vs. 7 ± 2 mmHg, P = 0.03) were reduced during PEI following 4‐weeks of NO3 supplementation, whereas placebo had no effect on ΔSBP (13 ± 2 vs. 15 ± 2, P = 0.31) or ΔMAP (7 ± 1 vs. 9 ± 1, P = 0.22) during PEI. The reduced BP during PEI suggests that dietary nitrate supplementation is capable of attenuating the muscle metaboreflex during exercise in older adults. Since the metabolic component of the exercise pressor reflex is augmented in older adults with hypertension, it may be possible that nitrate supplementation could have an even greater impact in this patient population.