Purpose: Inorganic nitrate (NO3–) supplementation has been reported to improve, whilst caffeine consumption has been reported to increase strain on, various aspects of cardiovascular function. Since it has been suggested that the efficacy of NO3– supplementation to improve cardiovascular function may be enhanced with increased cardiovascular strain, the purpose of this study was to test the hypotheses that dietary NO3– ingestion would blunt the acute perturbations to cardiovascular function following caffeine ingestion, and that such effects would be greater than the improvement in cardiovascular function with NO3– ingestion compared to placebo in the absence of caffeine-induced cardiovascular strain.
Methods: Twenty-four (17 males, 7 females; mean ± SD: age 24 ± 3 yr, BMI 24 ± 3 kg/m2, systolic BP 109 ± 10 mmHg) healthy participants completed four experimental conditions in a double-blind, randomized, crossover design. The experimental conditions were NO3–-rich (400 mg NO3–) and NO3–-depleted (92 mg NO3–) beetroot powder consumed acutely, with (BR-CAF and CAF) and without (BR and PL) 6 mg/kg caffeine. Post-supplement assessments were conducted 2.5 h post NO3–-rich and NO3–-depleted beetroot ingestion and 1 h post caffeine and placebo capsules. Brachial and central blood pressure (BP) and arterial stiffness variables were measured pre- and post-supplementation with macrovascular endothelial function assessed via flow mediated dilation (FMD) post-supplementation. Venous blood was also sampled post-supplementation for the assessment of plasma concentrations of nitrite ([NO2–]) and cyclic guanosine monophosphate ([cGMP]). Data were assessed using linear mixed models, with Holm Bonferroni post-hoc analyses and statistical significance accepted as P < 0.05.
Results: Augmentation pressure and index were higher after CAF (3 ± 2 mmHg and 10 ± 9%) than PL (1 ± 3 mmHg and 4 ± 11%) and BR (0 ± 3 mmHg and 1 ± 11%; P < 0.001-0.007), with no difference between BR-CAF (1 ± 3 mmHg and 3 ± 10%) and PL or BR (P = 0.505-0.689). Compared to PL, brachial BP, central BP and macrovascular endothelial function were not altered with BR or CAF (P = 0.067-0.359). Plasma [nitrite] was higher in BR and BR-CAF than PL and CAF (P < 0.001), with no differences between BR and BR-CAF (P = 1.000). There were no between-group differences in plasma [cGMP] (P = 0.370).
Conclusion: Caffeine ingestion adversely impacted augmentation pressure and index compared to PL, with this effect attenuated after NO3– and caffeine co-ingestion such that augmentation pressure and index were not different between PL and BR-CAF. Acute NO3– ingestion did not independently improve arterial stiffness variables compared to PL. Neither acute caffeine nor NO3– ingestion altered central or brachial BP or FMD compared to PL. These findings suggest that NO3– supplementation can attenuate arterial stiffness elicited by caffeine consumption, but that NO3– supplementation did not improve cardiovascular function variables independently and when caffeine did not invoke strain on a given cardiovascular function variable. These data improve our understanding of the cardiovascular health benefits of dietary NO3– supplementation and support the notion that the efficacy of NO3– supplementation to improve cardiovascular health appears to be linked to baseline cardiovascular strain.