Abstract
BackgroundDietary calcium intake and the renin angiotensin system (RAS) regulate blood pressure (BP) by modulating calcium homeostasis. Despite similar BP regulatory effects, the influence of dietary calcium intake alone and combined with RAS polymorphisms on the BP response following acute aerobic exercise (i.e., postexercise hypotension) has not been studied. Thus, we examined the effect of dietary calcium intake and selected RAS polymorphisms on postexercise hypotension.MethodsSubjects were men (n = 50, 43.8 ± 1.3 yr) with high BP (145.3 ± 1.5/85.9 ± 1.1 mm Hg). They completed three experiments: non-exercise control and two cycle bouts at 40% and 60% of maximal oxygen consumption (VO2max). Subjects provided 3 d food records on five protocol-specific occasions. Dietary calcium intake was averaged and categorized as low (<880 mg/d = LowCa) or high (≥ 880 mg/d = HighCa). RAS polymorphisms (angiotensin converting enzyme insertion/deletion, ACE I/D; angiotensin II type 1 receptor, AT1R A/C) were analyzed with molecular methods. Genotypes were reduced from three to two: ACE II/ID and ACE DD; or AT1R AA and AT1R CC/AC. Repeated measure ANCOVA tested if BP differed among experiments, dietary calcium intake level and RAS polymorphisms.ResultsSystolic BP (SBP) decreased 6 mm Hg after 40% and 60% VO2max compared to non-exercise control for 10 h with LowCa (p < 0.01), but not with HighCa (p ≥ 0.05). Under these conditions, diastolic BP (DBP) did not differ between dietary calcium intake levels (p ≥ 0.05). With LowCa, SBP decreased after 60% VO2max versus non-exercise control for 10 h among ACE II/ID (6 mm Hg) and AT1R AA (8 mm Hg); and by 8 mm Hg after 40% VO2max among ACE DD and AT1R CC/CA (p < 0.01). With HighCa, SBP (8 mm Hg) and DBP (4 mm Hg) decreased after 60% VO2max compared to non-exercise control for 10 h (p < 0.05), but not after 40% VO2max (p ≥ 0.05).ConclusionSBP decreased after exercise compared to non-exercise control among men with low but not high dietary calcium intake. Dietary calcium intake interacted with the ACE I/D and AT1R A/C polymorphisms to further modulate postexercise hypotension. Interactions among dietary calcium intake, exercise intensity and RAS polymorphisms account for some of the variability in the BP response to exercise.
Highlights
Dietary calcium intake and the renin angiotensin system (RAS) regulate blood pressure (BP) by modulating calcium homeostasis
BP response by dietary calcium level and RAS polymorphisms Low calcium dietary intake Angiotensin converting enzyme (ACE) I/D polymorphism Among carriers of the ACE I allele (i.e., ACE II/ID), systolic BP (SBP) was reduced by 5.7 mm Hg from a pre-experiment baseline SBP of 126.6 ± 3.5 mm Hg after 60% VO2max compared to non-exercise control for 10 h (p < 0.01) (Table 3)
Among ACE DD homozygotes, SBP was reduced by about 7.5 mm Hg from a baseline SBP of 125.1 ± 3.2 mm Hg and diastolic BP (DBP) was lower by 4.5 mm Hg from a baseline DBP of 88.9 ± 2.6 mm Hg after 60% VO2max compared to non-exercise control for 10 h (p < 0.05)
Summary
Dietary calcium intake and the renin angiotensin system (RAS) regulate blood pressure (BP) by modulating calcium homeostasis. Despite similar BP regulatory effects, the influence of dietary calcium intake alone and combined with RAS polymorphisms on the BP response following acute aerobic exercise (i.e., postexercise hypotension) has not been studied. We examined the effect of dietary calcium intake and selected RAS polymorphisms on postexercise hypotension. The blood pressure (BP) lowering effects of dietary interventions are greater than those resulting from exercise [2,3]. Low calcium dietary intake has been linked to higher BP and the development of hypertension, whereas calcium supplementation lowers BP. Ruidavets et al [11] recently found significant and independent associations among higher dairy product and dietary calcium intakes and lower BP among 912 middle aged men [systolic BP (SBP) more so than diastolic BP (DBP)]. Dietary calcium intake is hypothesized to regulate BP by its influence on calcitrophic hormones, intracellular calcium concentration and vasculature reactivity [8,9,10,11,12,13]
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