Postexercise hypotension differs between white and black women.

BACKGROUND: Because data are lacking, we examined the acute effect of exercise on ambulatory blood pressure (BP) in premenopausal white women (n = 18) and black women (n = 15) with normal (n = 21) and high (n = 12) BP. METHODS: Women performed 40 minutes of control and moderate-intensity exercise. BP and hormones were measured before, during, and after the control and exercise periods. By means of RMANCOVA (repeated measures analysis of covarience), we tested whether BP and hormones differed with time and between ethnic, BP, and experimental groups. Multiple regression analysis was used to examine hormonal mediators of the postexercise BP response. RESULTS: Among white women with hypertension, average daytime systolic (S) and diastolic (D) BP decreased 11.0 +/- 3.3 mm Hg (-2.9, -19.1; P =.017) and 8.2 +/- 2.8 mm Hg (-1.2, -13.9; P =.000), from 142.6 +/- 5.8 mm Hg and 96.1 +/- 2.8 mm Hg, respectively, after exercise. Among black women with high BP, mean daytime SBP rose 12.5 +/- 5.2 mm Hg (-2.0, 27.1; P =.000) after exercise, from 121.8 +/- 6.1 mm Hg, whereas DBP was similar before and after exercise (81.4 +/- 4.3 mm Hg and 82.8 +/- 4.7 mm Hg, respectively). In white women without hypertension, daytime SBP and DBP were similar before and after exercise. In black women without hypertension, mean daytime SBP increased 6.3 +/- 2.6 mm Hg (0.4, 12.1; P =.000) after exercise from 103.6 +/- 1.4 mm Hg, and DBP did not change. In black women, hypertension (P = 0.000) and exercise-mediated insulin decreases (P =.005) explained 85.6% of the postexercise SBP response (P =.000). In white women, hypertension (P =.003) and baseline plasma renin (P =.049) accounted for 53.3% of the postexercise SBP response (P =.001). Exercise acutely reduced daytime BP in white women, but not in black women with high BP. CONCLUSION: Endurance exercise may adversely affect the BP of black women.

Exercise training alters skeletal muscle mitochondrial morphometry in heart failure patients.

BACKGROUND: Previous research has demonstrated that exercise intolerance in heart failure patients is associated with significant alterations in skeletal muscle ultrastructure and oxidative metabolism that may be more consequential than cardiac output. DESIGN: To examine the effect of exercise training on skeletal muscle mitochondrial size in chronic heart failure patients. METHODS: Six heart failure patients participated in 16-weeks of supervised upper and lower extremity exercise training. At the conclusion of training, percutaneous needle biopsies of the vastus lateralis were taken and electron microscopy was used to assess mitochondrial sizes. RESULTS: The exercise programme resulted in a significant increase in peak maximal oxygen consumption ( P< 0.05) and anaerobic threshold (P < 0.04). Knee extension muscle force increased following training ( P< 0.02). After exercise training, the average size of the mitochondria increased by 23.4% (0.036 to 0.046 mu(2), P< 0.015) and the average shape was unaltered. CONCLUSION: Exercise training with heart failure patients alters skeletal muscle morphology by increasing mitochondrial size, with no change in shape. This may enhance oxidative metabolism resulting in an increased exercise tolerance.

Reduction of abdominal obesity in lipodystrophy associated with human immunodeficiency virus infection by means of diet and exercise: case report and proof of principle.

Lipodystrophy associated with human immunodeficiency virus infection causes abdominal fat gain, peripheral subcutaneous fat atrophy, insulin resistance, low levels of high-density lipoprotein cholesterol, and hypertriglyceridemia. An exercise program combined with a moderate-fat, low-glycemic-index, high-fiber diet can reverse several aspects of lipodystrophy, and, until specific treatment is available, should be considered for treatment of lipodystrophy.