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Abstract

Insulin sensitivity, part of the mosaic of factors in the etiology or hypertension, has profound effects on the cardiovascular system. This study examined hemodynamic reactivity to a laboratory stressor in subjects receiving a high carbohydrate (CHO) or low CHO diet.

Fifty subjects were studied on two occasions, four weeks apart. They were randomly assigned to receive a high CHO (75% of Calories) or low CHO (35% of Calories) diet. Subjects were white (16), black (34), male (34), female (16), normotensive (33), or hypertensive (17). Subjects were further classified to high (23) or low (27) insulin sensitivity using a median split on the insulin sensitivity index (ISI120). Dependent measures were systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR). BP was determined with a Dinamap monitor, HR by ECG, and SV via impedance cardiography. CO and TPR were calculated. Reactivity is reported as the percent change in the dependent measures in response to speech stressor. Data were analyzed using a 2 (race) X 2(gender) X 2 (hypertension diagnosis) X 2 (insulin sensitivity) X 2 (diet) MANOVA.

The analysis revealed a significant diagnosis X insulin sensitivity X diet interaction (p = .002). No significant effects were observed for race or gender. The subsequent analyses found no significant difference on the low CHO diet. On the high CHO diet the following were observed: SBP, no difference; DBP, normotensives had a larger response than hypertensives (p = .042); HR, SV, CO bigger response in the insulin sensitive subjects (p's < .02); TPR responses were smaller in the insulin sensitive normotensives, unchanged in the insulin sensitive hypertensives, and larger in the insulin resistant subjects.

These findings indicate that under a normal to high glucose load, individuals who are insulin sensitive will respond to stress with increased cardiac responses. On the other hand insulin resistant subjects with hypertension meet the same challenge by increasing vascular resistance.

Insulin Resistance, Stress, Cardiovasucular Reactivity
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© American Journal of Hypertension, Ltd. 2001
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