Cardiovascular responses to high-fat and high-carbohydrate meals in young subjects.

We compared the cardiovascular, glucose, insulin, and catecholamine responses to high-fat (F) and high-carbohydrate (C) meals in healthy young subjects (mean age 23 yr, range 19-39). Cardiac output rose 30 min after C by 32% [95% confidence interval (CI) of the increase +0.32 to +1.64 l/min] and after F by 22% [95% CI +0.30 to +1.96 l/min; P = 0.03, analysis of variance (ANOVA)]. Superior mesenteric artery blood flow rose by 87% 15 min after C (95% CI +119 to +258 ml/min) and by 122% (95% CI +138 to +392 ml/min) 45 min after F, with significantly different patterns of response (interaction effect P less than 0.05, ANOVA). Calf blood flow fell and remained low for 60 min after F but only fell 15 min after C, with a return to fasting levels thereafter (interaction effect P less than 0.03, ANOVA). Thirty minutes postprandially the change of calf blood flow from baseline after C was significantly different than after F (95% CI of differences +0.1 to +2.04 ml.100 ml-1.min-1). Glucose, insulin, and norepinephrine levels increased more after C than after F. Thus there are different regional vascular responses to C and F despite similar cardiac output increases.

Post-prandial worsening of angina: all due to changes in cardiac output?

BACKGROUND: The precise mechanism leading to the post-prandial worsening of angina has yet to be adequately defined. It has been attributed to an increase in double product but is perhaps more likely to be related to an increase in cardiac output after food. This study was designed to evaluate the effects of food on patients' exercise tolerance and compare these with changes in haemodynamic variables. METHODS: 23 patients with chronic stable angina who had post-prandial worsening of their angina were studied. The patients were evaluated on two occasions and at each visit they underwent two symptom limited treadmill exercise tests. They remained fasting on the first visit and were given a 1400 kcal meal 60 minutes before the second exercise test on the second visit. Time to onset of 1 mm ST segment depression, heart rate, systemic arterial blood pressure, and cardiac output were measured at rest and during exercise. RESULTS: There were no differences in any of the variables during the two exercise tests on the day the patients remained fasting. After the meal exercise tolerance fell significantly by 136 seconds and the stage at which 1 mm ST segment depression was first seen was also significantly reduced. Resting cardiac output increased significantly by 0.86 1/min with the patients sitting and by 0.89 1/min standing. The exercise times after food were significantly related to cardiac output even when fasting times were taken into account. Resting heart rate increased significantly by 8.3 beats per minute sitting and 10.4 beats per minute standing. There was little change in blood pressure and no evidence that the double product predicted the post-prandial exercise time. CONCLUSIONS: Worsening of angina was related to the increase in cardiac output after a meal and successful treatment will depend upon the prevention of this increase.

Exercise capability in heart failure: is cardiac output important after all?

The exercise capability of 39 patients with severe chronic heart failure was assessed in several ways and compared with measurements of cardiac output. The relation between cardiac index and exercise tolerance measured on a treadmill was poor (r = 0.191, p = 0.245). However, exercise tolerance measured with a series of self-paced corridor walk tests showed moderate correlations with cardiac index (r = -0.404, p = 0.015 to r = -0.516, p = 0.001) and customary activity assessed by step counting correlated better with cardiac index (r = 0.537, p less than 0.001). Cardiac output therefore seems to be a factor determining patients' exercise capability when they choose their own walking speed but not when they undergo formal treadmill tests in the laboratory.