Research

Dietary calcium intake and Renin Angiotensin System polymorphisms alter the blood pressure response to aerobic exercise: a randomized control design

Linda S Pescatello¹ , Debbie Turner² , Nancy Rodriguez³ , Bruce E Blanchard^1,4 , Gregory J Tsongalis⁵ , Carl M Maresh¹ , Valerie Duffy² and Paul D Thompson⁶

¹Department of Kinesiology, University of CT, Storrs, CT, USA

²Department of Allied Health Sciences, University of CT, Storrs, CT, USA

³Department of Nutritional Sciences, University of CT, Storrs, CT, USA

⁴Department of Pathology, Hartford Hospital, Hartford, CT, USA

⁵Department of Pathology, Dartmouth-Hitchcock Medical Center, Lebanon, NH, USA

⁶Division of Cardiology, Hartford Hospital, Hartford, CT, USA

author email corresponding author email

Nutrition & Metabolism 2007, 4:1doi:10.1186/1743-7075-4-1

Published:	4 January 2007

Abstract

Background

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. Thus, we examined the effect of dietary calcium intake and selected RAS polymorphisms on postexercise hypotension.

Methods

Subjects 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.

Results

Systolic 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).

Conclusion

SBP 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.