Analysis of alteration of blood pressure response to exercise through baroreflex.

BACKGROUND: The baroreflex has been reported to play an important role in hemodynamic regulation during exercise. Therefore, impairment of baroreflex function can induce an abnormal response of systolic blood pressure (SBP) to exercise, including exercise-induced hypertension. To clarify whether baroreflex function alters SBP response, we examined the relationship of baroreflex sensitivity (BRS) with SBP response to exercise. METHODS: In 22 subjects without cardiac dysfunction, BRS (ms/mmHg) was measured by the phenylephrine method, and a treadmill exercise test was administered according to Bruce's protocol. RESULTS: 1) The chronotropic response to exercise was higher in the normal BRS group than in the reduced BRS group (p<0.01). The SBP at the initial phase of exercise (1 min after the start of exercise) showed a smaller increase in the normal BRS group than in the reduced BRS group (p<0.01). During the initial phase of exercise, BRS had negative correlation with the SBP increment from rest (r=-0.408, p<0.05). During submaximal exercise (6 min after the start of exercise), a positive correlation between BRS and SBP response (r=0.422, p<0.05) was shown. 2) Subjects were divided into 2 groups: 12 subjects with normal BRS (> or =5 ms/mmHg) and 10 subjects with reduced BRS (<5 ms/mmHg). During the initial exercise phase, the negative correlation between BRS and SBP response was stronger in the normal BRS group (r=-0.398) than in the reduced BRS group (r= -0.126). During submaximal exercise, BRS had a positive correlation with BP response to exercise in subjects with normal BRS (r=0.462). CONCLUSION: Preserved baroreflex function is thought to be related to the pressor response to submaximal exercise, although the baroreflex is thought to be associated with the stabilization of blood pressure change during the initial exercise phase. These findings suggest that exercise-induced hypertension develops through the baroreflex mechanism.

Improvement of sympathetic response to exercise by oral administration of ascorbic acid in patients after myocardial infarction.

BACKGROUND: Recent studies indicated that excessive oxidative stress in an animal heart failure model injures both the sympathetic nerve endings and receptors, resulting in disturbance of norepinephrine release and sensitivity to norepinephrine. However, it has not been clarified whether this phenomenon is expressed clinically in patients with heart disease. Therefore, we examined the efficacy of ascorbic acid administration as an antioxidant vitamin in relation to the heart rate and norepinephrine response to exercise in patients after myocardial infarction. METHODS: In this randomized crossover trial, 21 male patients who had had myocardial infarction underwent symptom-limited ergometer cardiopulmonary exercise testing twice, that is, without and with ascorbic acid (2 g) administration. Plasma norepinephrine concentrations were assessed at rest and at peak exercise, and heart rate responsiveness to the norepinephrine increment from rest to peak exercise (DeltaHR/logDeltaNE) was calculated. RESULTS: In the exercise test after ascorbic acid administration, peak oxygen consumption (VO(2)) improved over baseline. Ascorbic acid administration significantly increased the change in heart rate and norepinephrine from rest to peak exercise and DeltaHR/logDeltaNE. The increment in heart rate was significantly correlated with peak VO(2) in each test. CONCLUSION: Ascorbic acid intake before exercise improved exercise capacity through enhancement of the heart rate and norepinephrine response to exercise in patients after myocardial infarction. These findings suggest that ascorbic acid intake improves sympathetic dysfunction resulting from injury by excessive oxidative stress after myocardial infarction.

Impaired baroreflex as a cause of chronotropic incompetence during exercise via autonomic mechanism in patients with heart disease.

PURPOSE: It is thought that the mechanisms responsible for impaired chronotropic response to exercise are related to disturbance of cardiovascular autonomic regulation such as the baroreflex. However, it is still unclear whether the baroreflex mechanisms modulate heart rate (HR) responses to exercise via vagal and/or sympathetic alteration. We therefore investigated the effects of baroreflex sensitivity (BRS) on the exercise HR response in the early phase of vagal deactivation and in the later phase of sympathetic excitation via metabolic stimulation. METHODS: Twenty-four patients (18 males and 6 females, age 59+/-9 years) with heart disease underwent symptom-limited treadmill exercise testing according to the Bruce protocol, and BRS was measured utilizing the phenylephrine method. Subjects were grouped by their resting BRS value: 12 with normal BRS (> or =6 ms/mmHg) and 12 with depressed BRS (<6 ms/mmHg). The HR response to exercise was assessed using two parameters: the increment in HR during exercise and the ratio of HR response to the metabolic reserve (chronotropic index). RESULTS: (1) In the patients with depressed BRS, the HR responses within 1 min after the start of exercise and from 1 min to peak exercise were attenuated compared with those having a normal BRS (15+/-8 vs. 24+/-8 bpm and 36+/-9 vs. 47+/-15 bpm, respectively). (2) The chronotropic index in the patients with depressed BRS was lower than in those with normal BRS (0.50+/-0.14 vs. 0.64+/-0.08). CONCLUSION: These findings suggest that impaired BRS modulates both the parasympathetic influence in early exercise and sympathetic effects in the later phase on HR response to exercise.