scholarly journals Effects of meal ingestion on blood pressure and regional hemodynamic responses after exercise

2016 ◽  
Vol 120 (11) ◽  
pp. 1343-1348 ◽  
Author(s):  
Masako Yamaoka Endo ◽  
Chizuko Fujihara ◽  
Akira Miura ◽  
Hideaki Kashima ◽  
Yoshiyuki Fukuba

This study investigated the combined effects of consuming a meal during postexercise hypotension (PEH) on hemodynamics. Nine healthy young male subjects performed each of three trials in random order: 1) cycling at 50% of heart rate reserve for 60 min, 2) oral ingestion of a carbohydrate liquid meal (75 g glucose), or 3) carbohydrate ingestion at 40 min after cycling exercise. Blood pressure, heart rate, cardiac output, and blood flow in the superior mesenteric (SMA), brachial, and popliteal arteries were measured continuously before and after each trial. Regional vascular conductance (VC) was calculated as blood flow/mean arterial pressure. Blood pressure decreased relative to baseline values ( P < 0.05) after exercise cessation. Blood flow and VC in the calf and arm increased after exercise, whereas blood flow and VC in the SMA did not. Blood pressure did not change after meal ingestion; however, blood flow and VC significantly decreased in the brachial and popliteal arteries and increased in the SMA for 120 min after the meal ( P < 0.05). When the meal was ingested during PEH, blood pressure decreased below PEH levels and remained decreased for 40 min before returning to postexercise levels. The sustained increase in blood flow and VC in the limbs after exercise was reduced to baseline resting levels immediately after the meal, postprandial cardiac output was unchanged by the increased blood flow in the SMA, and total VC and SMA VC increased. Healthy young subjects can suppress severe hypotension by vasoconstriction of the limbs even when carbohydrate is ingested during PEH.

1980 ◽  
Vol 48 (2) ◽  
pp. 281-283 ◽  
Author(s):  
L. E. Boerboom ◽  
J. N. Boelkins

Although man is being exposed to hyperbaric environments more frequently, the effects of these environments and the inert gases used are not clearly defined. We therefore designed an experiment to examine both the effects of helium and elevated pressure on the cardiovascular system in conscious rabbits exposed to normoxic levels of a helium-oxygen (He-O2) gas mixture at 1 and 11 atmospheres absolute (ATA) for 2 h. Variables studied included heart rate, blood pressure, cardiac output, systemic vascular resistance, organ blood flow, and resistance to flow. The only change observed was a decrease in heart rate from a control of 284 +/- 7 (mean +/- SE) to 246 +/- 12 beats/min after 2 h of breathing He-O2 at 1 ATA. We therefore conclude that the cardiovascular system is not adversely affected by helium or elevated pressure as used in this experiment.


Author(s):  
Dr Mark Harrison

2.1 Control of blood pressure and heart rate, 445 2.2 Control of heart rate, 446 2.3 Cardiac output (CO), 447 2.4 Measurement of cardiac output (CO), 450 2.5 Blood flow peripherally, 451 2.6 The cardiac cycle, 454 2.7 ECG, 458 2.8 Pharmacological manipulation of the heart and peripheral circulation, ...


1976 ◽  
Vol 50 (3) ◽  
pp. 177-184 ◽  
Author(s):  
J. Yudkin ◽  
R. D. Cohen ◽  
Barbara Slack

1. The effect of metabolic acidosis of 4–6 h duration on cardiac output, blood pressure, heart rate, and hepatic and renal blood flow has been studied in the rat. 2. In anaesthetized rats, blood pressure and heart rate fell linearly with blood pH in both sham-operated and nephrectomized rats. There was no significant difference between the two groups in the effect of acidosis on either variable. 3. Cardiac output showed a significant fall with increasing acidosis in the conscious rat. 4. Estimated hepatic blood flow in conscious rats showed a significant positive correlation with blood pH in both sham-operated and nephrectomized animals. There was no significant difference in estimated hepatic blood flow between the two groups of animals at any blood pH. 5. In conscious rats, increasing acidosis caused a progressive decrease in estimated renal blood flow. 6. It is concluded that the increase in the previously described apparent renal contribution to lactate removal in the acidotic rat cannot be explained by any circulatory effect mediated by the kidney. The possible relevance of the findings to lactate homeostasis is discussed.


1989 ◽  
Vol 257 (2) ◽  
pp. H540-H552 ◽  
Author(s):  
S. E. Spencer ◽  
W. B. Sawyer ◽  
A. D. Loewy

L-Glutamate microinjections into the tuberal region of the lateral hypothalamic area (LHAt) caused a fall in blood pressure and heart rate in pentobarbital-anesthetized rats. The bradycardia was mediated by both beta-adrenergic and muscarinic mechanisms as demonstrated with pharmacological blockade. The hypotension was due to a decrease in cardiac output, not a decrease in total peripheral resistance. In addition, there was a reduction in coronary blood flow. If heart rate was held constant by pharmacological blockade or by electrical cardiac pacing, L-glutamate stimulation of the LHAt still caused a fall in blood pressure. When the electrically paced model was used, this hypotension was due to a fall in cardiac output. In contrast, with the pharmacological blockade of the heart, the hypotension was due to a decrease in the total peripheral resistance. The cardiac output reduction in the paced condition was not mediated solely by either beta-sympathetic or parasympathetic mechanisms as determined by pharmacological blockade. With heart rate held constant by either drugs or pacing, LHAt stimulation did not alter regional blood flow or resistance in any vascular bed, including the coronary circulation. We conclude that L-glutamate stimulation of the LHAt lowers the cardiac output and heart rate by both parasympathetic and beta-adrenergic mechanisms and elicits hypotension by lowering cardiac output in the naive and electrically paced model.


1993 ◽  
Vol 84 (3) ◽  
pp. 263-270 ◽  
Author(s):  
M. B. Sidery ◽  
A. J. Cowley ◽  
I. A. MacDonald

1. The cardiovascular responses to high-fat and high-carbohydrate meals (2.5 MJ) were compared in healthy, non-obese elderly subjects (mean age 68 years, range 63–74 years). 2. Measurements of cardiac output, blood pressure, heart rate, calf blood flow and superior mesenteric artery blood flow were made before and for 60 min after the two meals. 3. Systolic blood pressure only fell after the high-carbohydrate meal, reaching a nadir 13 mmHg below baseline values (95% confidence interval of the change, −2 to −25 mmHg). Diastolic blood pressure fell by 8 mmHg at 30 min after the high-carbohydrate meal (95% confidence interval of the change, −1 to −15 mmHg) and by 5 mmHg 45 min after the high-fat meal (95% confidence interval of the change, −1 to −8 mmHg). 4. Superior mesenteric artery blood flow rose by 70% after the high-carbohydrate meal (95% confidence interval of the change, +105 to +297 ml/min) and by 42% after the high-fat meal (95% confidence interval of the change, +35 to +256 ml/min, P <0.0001, analysis of variance). Calf blood flow reached a nadir 30 min after the high-carbohydrate meal (95% confidence interval of the change, −0.14 to −0.96ml min−1 100 ml−1) and 15min after the high-fat meal (95% confidence interval of the change, −0.1 to −0.92ml min−1 100ml−1P <0.01). There was no significant change in heart rate or cardiac output over the experimental period. 5. In elderly subjects the gut hyperaemia associated with food ingestion is not accompanied by concomitant increases in cardiac output and heart rate. This failure of cardiovascular adjustment to the vascular demands by the gut is likely to contribute to the fall in blood pressure seen in these healthy elderly subjects.


1986 ◽  
Vol 70 (2) ◽  
pp. 199-206 ◽  
Author(s):  
U. Freyschuss ◽  
P. Hjemdahl ◽  
A. Juhlin-Dannfelt ◽  
B. Linde

1. Cardiovascular and metabolic responses to intravenous infusions of adrenaline (ADR), which raised arterial plasma ADR in a stepwise fashion from 0.3 to 1.3, 2.3 and 6.0 nmol/l, were studied in 11 healthy volunteers. 2. ADR evoked marked and concentration-dependent increases in stroke volume and cardiac output (thermodilution), as well as decreases in the vascular resistances of the systemic circulation, calf and adipose tissue. These changes were significant from 1.3 nmol/l ADR. Less marked effects were found on blood pressure and heart rate. 3. Significant arterial ADR concentration-effect relationships were found for cyclic AMP, glycerol, glucose, lactate and noradrenaline, but not for insulin. Cyclic AMP and glycerol were significantly elevated at 1.3, glucose at 2.3, but lactate not below 6.0 nmol/l ADR. Increases in adipose tissue blood flow and arterial glycerol levels were correlated (P < 0.001), suggesting a metabolic component in the blood flow response of adipose tissue. 4. Invasive haemodynamic measurements revealed that ADR at arterial concentrations within the lower physiological range had considerable effects on cardiac output and vascular resistances, despite moderate changes in the conventional non-invasive haemodynamic variables blood pressure and heart rate. 5. ADR elicited clear-cut responses at arterial plasma concentrations attained during various kinds of mild to moderate stress.


1964 ◽  
Vol 207 (6) ◽  
pp. 1349-1353 ◽  
Author(s):  
G. C. Whittow ◽  
P. D. Sturkie ◽  
G. Stein

The effect of hyperthermia on the respiratory rate, cardiac output, blood pressure, arterial hematocrit, and the skin temperatures of the extremities of unanesthetized hens has been investigated. During hyperthermia, the respiratory rate increased to a maximal value and then declined. There was also an increase in cardiac output, followed by a decrease, but the peak cardiac output occurred at a rectal temperature which was significantly higher than that at which the peak respiratory rate was recorded. The increase in cardiac output was the result of an increase in both stroke volume and heart rate. The diminution of cardiac output seemed to be related to a decrease in the stroke volume at high levels of heart rate. The decrease in blood pressure and total peripheral resistance was attributed partly to an increased blood flow through the extremities.


2021 ◽  
pp. 187-215
Author(s):  
Graham Mitchell

As discussed in this chapter, giraffes have, compared with any other mammal, a very high mean blood pressure of ~250 mmHg. Human blood pressure is ~90 mmHg. Its size is determined by the length of the neck, the height of the head above the heart, by hydrostatic pressure generated by gravity acting on the column of blood in the carotid artery, and contractions of the heart muscles: blood pressure must be high enough to ensure that blood reaches the brain. Uniquely in giraffes blood pressure is regulated by receptors that are located in both the carotid and occipital arteries. Once thought to be ~2.5% of body mass the heart is smaller (~0.5% of body mass) but its muscle walls, especially of the interventricular wall and left ventricle wall, are exceptionally thick (up to 8 cm). The relative cardiac output is the same as in other mammals (~5 L 100 kg–1 of body mass) through a combination of a higher than predicted heart rate (70 b min–1 vs 50 b min–1) and smaller than predicted stroke volume (~0.7 ml kg–1 body mass vs 1.2 ml kg–1). Stroke volume is small because the left ventricle muscle wall is thick. The origin of high blood pressure is the resistance to blood flow, which is about twice what it is in other mammals. The higher resistance results from a combination of the thick muscular walls and narrow lumens of a giraffe’s blood vessels and unique mechanisms that regulate blood flow to the brain.


1977 ◽  
Vol 232 (3) ◽  
pp. H231-H235 ◽  
Author(s):  
C. R. Rosenfeld

Cardiac output and organ blood flows were measured in 6 nonpregnant and 24 pregnant ewes from 38 to 141 days of gestation employing radionuclide-labeled microspheres. From the nonpregnant state to term increases in cardiac output, from 73.7 +/- 4.6 ml/min-kg of maternal weight to 148 +/- 2.4 ml/min-kg, and heart rate, from 88.5 +/- 10.3 to 106 +/- 4.6 beats/min, were noted, while mean arterial blood pressure was unchanged. Near term, the blood flows to the uterus and mammary gland represented approximately 18% of cardiac output. The blood flow to nonreproductive organs increased from 76.6 +/- 6.8 ml/min-kg of nonreproductive tissue in the nonpregnant state to 132 +/- 3.5 ml/min-kg at 130-140 days' gestation (P less than 0.01). No significant changes in renal blood flow were detected.


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