Relationships between vascular resistance and energy deficiency, nutritional status and oxidative stress in oestrogen deficient physically active women

Oestrogen deficiency contributes to altered cardiovascular function in premenopausal amenorrheic physically active women. We investigated whether other energy deficiency-associated factors might also be associated with altered cardiovascular function in these women. A prospective observational study was completed at a research facility at the University of Toronto. Thirty-two healthy premenopausal women (18-35 years old) were studied; 9 sedentary and ovulatory; 14 physically active and ovulatory; and 8 physically active and amenorrheic. We measured calf vascular resistance, resting heart rate, dietary energy intake, resting energy expenditure and serum measures of homocysteine, high-sensitivity C-reactive protein, oxidized low-density lipoproteins, total T-3, ghrelin, leptin and insulin. Groups were similar (P > 0.05) in age (25.1 +/- 0.8 years; mean +/- SEM), weight (57.3 +/- 1.1 kg), and BMI (21.4 +/- 0.3 kg/m(2)). Resting vascular resistance and ghrelin were highest (P < 0.05, main effect), and total T-3 and energy expenditure adjusted for fat free mass lowest (P < 0.05, main effect) in oestrogen deficient women. Using pooled data for stepwise multiple regression modelling: ghrelin and resting energy expenditure adjusted for fat free mass were associated with resting vascular resistance (R-2 = 0.398, P = 0.018); adjusted dietary energy intake was associated with peak-ischaemic vascular resistance (R-2 = 0.231, P = 0.015). Adjusted resting energy expenditure (r = 0.624, P < 0.001) and total T-3 correlated (r = 0.427, P = 0.019) with resting heart rate. Homocysteine, high-sensitivity C-reactive protein and oxidized low-density lipoproteins were similar (P > 0.05, main effect) among the groups, and were unrelated to cardiovascular measures. Altered resting vascular resistance in premenopausal oestrogen deficient physically active amenorrheic women is not associated with vascular inflammation or oxidative stress, but rather with parameters that reflect metabolic allostasis and dietary intake, suggesting a potential role for chronic energy deficiency in vascular regulation.