The roles of the mode of contraction (i.e., dynamic or static) and the active muscle mass as determinants of the cardiovascular responses to exercise were studied. Six healthy men performed static handgrip (SHG), dynamic handgrip (DHG), static two-knee extension (SKE), and dynamic two-knee extension (DKE) to local muscular fatigue in approximately 6 min. Increases in mean arterial pressure were similar for each mode of contraction, 29 +/- 5 and 30 +/- 3 mmHg in SHG and DHG and 56 +/- 2 and 48 +/- 2 mmHg in SKE and DKE (P greater than 0.05) but larger for KE than HG (P less than 0.001). Cardiac output increased more for dynamic than for static exercise and for each mode more for KE than HG (P less than 0.001). Systemic resistance was lower for dynamic than static exercise and fell from resting levels by approximately 1/3 during DKE. The magnitude of the pressor response was related to the active muscle mass but independent of the contraction mode. However, the mode of contraction affected the circulatory changes contributing to the pressor response. Equalization of the pressor responses was achieved by proportionately larger increases in cardiac output during dynamic exercise.
The roles of absolute and relative oxygen uptake (VO2 and percent of muscle group specific VO2 max) as determinants of the cardiovascular and ventilatory responses to exercise over a wide range of active muscle mass have not previously been defined. Six healthy men performed four types of dynamic exercise--one-arm curl, one-arm cranking, and one- and two-leg cycling at four different relative work loads--25, 50, 75, and 100% of VO2 max for the corresponding muscle group. VO2 during maximal one-arm curl, one-arm cranking, and one-leg cycling averaged 20, 50, and 75%, respectively, of that for maximal two-leg cycling. Cardiac output was linearly related to VO2 with a similar slope and intercept for each type of exercise. Heart rate at a given %VO2 max was higher with larger active muscle mass. In relation to %VO2 max, systemic resistance was lower and plasma catecholamine levels were higher with larger active muscle mass. The cardiovascular responses to exercise are determined to a large extent by the active muscle mass and the absolute oxygen uptake, with the principal feature appearing to be the tight linkage between systemic oxygen transport and utilization.
SUMMARY We studied the blood pressure responses to infused norepinephrine in 34 normotensive and 21 unmedicated subjects with essential hypertension. The two groups were similar in age, relative body weight, and urinary electrolyte excretion. Patients were studied on two extremes of dietary salt (200 mEq Na and 10 mEq Na per day). The dose-response curves were highly linear (p<0.00001) for both systolic and diastolic blood pressures. There was no evidence for an increased sensitivity to infused norepinephrine among the hypertensive subjects. On the other hand, older subjects had steeper slopes ( p < 0.005). Subjects on a high salt diet had steeper slopes than those on low salt diets (p<0.0025); this trend was especially apparent among blacks (p<0.005). Black and white hypertensive subjects responded to the high salt diet in opposite fashion: The blacks showed an increased pressor sensitivity (p<0.05), whereas the whites demonstrated a nonsignificant decreased pressor sensitivity. These results indicate that age, race, and salt effects must be meticulously controlled in studies of sympathetic nervous system physiology. 1 made the intriguing observation that hypertensive patients seemed unusually sensitive to the blood pressure (BP)-elevating effects of infused norepinephrine (NE). Since then, many investigators have studied the slope of this relationship, comparing hypertensive and normotensive subjects. Since BP is elevated in many essential hypertensive patients because of increased peripheral resistance, many researchers have expected that hypertensive patients would demonstrate an increased vascular sensitivity (or steeper dose-response slopes) to infused NE.2 Over the years, however, this hypothesized increased sensitivity has not been replicated consistently. Although no one has reported that hypertensive subjects are less sensitive than normotensive subjects to infused NE, the findings are mixed,
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