ACE GENE POLYMORPHISM AND EXERCISE TRAINING-INDUCED CHANGES IN SODIUM EXCRETION IN AFRICAN AMERICAN HYPERTENSIVES

Abstract

We sought to determine whether the changes in urinary NA+ excretion in response to shortterm exercise training were associated with the angiotensin converting enzyme (ACE) gene polymorphism. Subjects (n = 13; age 51 ± 8 yrs) were obese (body fat > 35%), sedentary (VO2max 21.8 ± 4.8 ml/kg/min), hypertensive (BP 143 ± 3 / 91 ± 2 mmHg) male and female African Americans. The insertion/deletion ACE gene (II, n = 5; ID, n = 4; DD, n = 4) polymorphism was determined using standard PCR procedures. Exercise consisted of 7 consecutive days of treadmill walking and stationary cycling for 50 min/d at 65% of heart rate reserve. Na+ excretion was determined by 24-hour urine collection at baseline and beginning 14–18 hours after the last exercise session. Subjects consumed diets identical in macronutrient and Na+ content during the testing periods. Baseline Na+ excretion, fasting insulin and glucose levels, percent body fat, VO2max, and casual mean blood pressure (MBP) were similar in the ACE genotype groups. After seven days of exercise training, Na+ excretion was significantly increased in the II (119 ± 26 vs 186 ± 42 mmol/d, p = 0.03), ID (102 ± 16 vs 125 ± 13 mmol/d, p = 0.043), and DD (138 ± 11 vs 160 ± 12 mmol/d, p = 0.024) genotype groups. The increase in Na+ excretion in response to short-term exercise training tended to be higher in the II (57%) genotype group compared to the ID (23%) and DD (16%) genotype groups (p = 0.079). Fasting insulin levels were significantly decreased in the II (8 ± 1 vs 5 ± 1 uU/ml, p = 0.018) genotype group but not in the ID (10 ± 3 vs 6 ± 1 uU/ml, p = 0.134) and DD (12 ± 3 vs 11 ± 3 uU/ml, p = 0.608) genotype groups. MBP was significantly reduced only in the DD genotype group (113 ± 1 vs 110 ± 2 mmHg, p = 0.016). These preliminary results suggest that the ACE gene polymorphism is associated with short-term exercise training-induced Na+ excretion and this effect may be related to changes in fasting insulin levels. Supported by NIH NCRR/GCRC 01RR00056, NIA AG 12781, and NHLBI HL54526