Submaximal Cardiovascular Responses to Exercise in Children: Treadmill versus Cycle Ergometer

1997 ◽  
Vol 9 (4) ◽  
pp. 331-341
Author(s):  
Kenneth R. Turley ◽  
Jack H. Wilmore
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Regression Analysis ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Cycle Ergometer ◽  
Individual Values ◽  
Oxygen Difference

This study investigated whether cardiovascular responses at a given submaximal oxygen consumption (V̇O2, L · min-1) are different between the treadmill (TM) and cycle ergometer (CE). Submaximal cardiovascular measurements were obtained at three work rates on both the TM and CE in 7- to 9-year-old children (12 males and 12 females). Using regression analysis, it was determined that there were no differences between the TM and CE in cardiac output (L · min-1), stroke volume (SV, ml · beat-1) or heart rate (beats · min-1) at a given V̇O2 (L · min-1). There were differences in the total peripheral resistance (TPR, units) and arterial-venous oxygen difference (a-vO2 diff, ml · 100 ml-1) to V̇O2 (L · min-1) relationship. While there were statistically significant differences in TPR and a-vO2 diff between the two modalities, there was substantial overlap of individual values at any given submaximal V̇O2, thus the physiological significance is questionable. Hence, we conclude that in 7- to 9-yearold children there are no differences in submaximal cardiovascular responses between the CE and TM.

Cardiovascular response to graded exercise in the sympathectomized-vagotomized dog

1963 ◽  
Vol 204 (2) ◽  
pp. 291-296 ◽  
Author(s):  
Edmundo Ashkar ◽  
William F. Hamilton
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Stroke Volume ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Graded Exercise ◽  
Oxygen Difference

Seven dogs who ran well on a motor-driven treadmill were completely sympathectomized (including adrenal denervation) and subjected to unilateral vagotomy below the recurrent laryngeal branch. After recovery and retraining, a terminal experiment was performed in which, after completing the vagotomy, direct Fick determinations of cardiac output and continuous recordings of mean arterial pressure, heart rate, and oxygen consumption were made at rest and during increasing exercise The results were compared with those described by Barger et al. ( Am. J. Physiol. 184: 613, 1956) for normal dogs running at smaller speeds and grades. The heart rate of the operated dogs increased from 117 to 134. Barger's normal dogs doubled their heart rate. The A-V oxygen difference increased with work slightly less than Barger's normal dogs but the scatter in both groups was wide, as was the case with the stroke volume. The resting cardiac output was nearly normal in the operated dogs but increased only 34% with exercise, as against 200–300% in Barger's normals. Oxygen consumption increased about twofold as against the expected normal of three- to sevenfold. Peripheral resistance in both groups went down about 40%. The blood pressure in the normal increased substantially while that in the operated dogs fell about 20% to an average of 60 mm Hg.

CARDIAC OUTPUT IN ACUTE EXPERIMENTAL METHEMOGLOBINEMIA

1960 ◽  
Vol 38 (12) ◽  
pp. 1411-1416 ◽  
Author(s):  
C. W. Gowdey
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Viscosity ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Hematocrit Level ◽  
Arterial Oxygen Content ◽  
Anesthetized Dogs ◽  
Oxygen Difference

Methemoglobinemia induced in normal anesthetized dogs by intravenous infusions of aniline resulted in a decreased arterial oxygen content and a marked increase in cardiac output. Heart rate, arterial pressure, blood viscosity, and oxygen consumption increased, while total peripheral resistance and arteriovenous oxygen difference decreased. The elevation of cardiac output occurred in spite of the fact that the hematocrit level and blood viscosity increased. Ganglion-blocking doses of pentolinium bitartrate did not significantly alter the cardiovascular responses to the methemoglobinemia.

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

CARDIOVASCULAR EFFECTS OF PRONETHALOL IN THE DOG

1965 ◽  
Vol 43 (3) ◽  
pp. 411-420 ◽  
Author(s):  
M. A. Chiong ◽  
P. F. Binnion ◽  
J. D. Hatcher
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Cardiovascular Effects ◽  
Stroke Work ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure

The cardiovascular effects of an intravenous injection of pronethalol (2.5 mg/kg) and the effect of this agent on the cardiovascular changes induced by an infusion of adrenaline (0.2 μg/kg per minute) were investigated in intact anaesthetized dogs. Fifteen minutes after the administration of pronethalol, significant increases were observed in oxygen consumption, right ventricular systolic pressure, and haematocrit, and decreases in arterial blood pressure and total peripheral resistance. Arterial hypotension and a fall in stroke work were the only changes noted at 30 minutes. There was considerable variability in cardiac output, stroke volume, and heart rate but, on the average, no significant change was observed. Pretreatment with pronethalol abolished or significantly reduced the adrenaline-induced rises in cardiac output, heart rate, stroke volume, stroke work, oxygen consumption, right ventricular systolic pressure, and arterial haematocrit, and reversed the changes in diastolic arterial pressure and peripheral resistance. It is concluded that pronethalol is not devoid of sympathomimetic activity and that it effectively blocks the adrenaline responses mediated by β-receptors.

CARDIAC OUTPUT IN ACUTE EXPERIMENTAL METHEMOGLOBINEMIA

1960 ◽  
Vol 38 (1) ◽  
pp. 1411-1416 ◽  
Author(s):  
C. W. Gowdey
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Viscosity ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Hematocrit Level ◽  
Arterial Oxygen Content ◽  
Anesthetized Dogs ◽  
Oxygen Difference

Methemoglobinemia induced in normal anesthetized dogs by intravenous infusions of aniline resulted in a decreased arterial oxygen content and a marked increase in cardiac output. Heart rate, arterial pressure, blood viscosity, and oxygen consumption increased, while total peripheral resistance and arteriovenous oxygen difference decreased. The elevation of cardiac output occurred in spite of the fact that the hematocrit level and blood viscosity increased. Ganglion-blocking doses of pentolinium bitartrate did not significantly alter the cardiovascular responses to the methemoglobinemia.

scholarly journals Development of cardiovascular responses to hypoxia in larvae of the frog Xenopus laevis

1996 ◽  
Vol 271 (4) ◽  
pp. R912-R917 ◽  
Author(s):  
R. Fritsche ◽  
W. Burggren
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Xenopus Laevis ◽  
Stroke Volume ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Inhibitory Effect ◽  
Show Evidence

Cardiovascular responses (blood pressure, heart rate, stroke volume, cardiac output, and peripheral vascular resistance) to acute hypoxia (Po2 = 70 mmHg) in developing larvae of Xenopus laevis from Nieuwkoop-Faber (NF) stage 45 and up to newly metamorphosed froglets were investigated. The results revealed two distinct response patterns to acute hypoxia in "early" (NF stages 45-48 and 49-51) and "late" (NF stages 52-53, 54-57, and 58-62) larval Xenopus. The early larvae responded to acute hypoxia with a significantly decreased stroke volume, cardiac output, and blood pressure. Peripheral resistance increased, whereas no change in heart rate occurred. In late larvae, stroke volume and blood pressure increased during acute hypoxia, but an offsetting bradycardia prevented major changes in cardiac output. We conclude that, up to stage 51 of development, hypoxia exerts a direct inhibitory effect on the heart and smooth muscle of the blood vessels, with no Frank-Starling relationship apparent. Older larvae show evidence of both intrinsic and extrinsic regulation of the cardiovascular system in response to acute hypoxia, suggesting that there is a specific point in larval development when cardiovascular regulation during hypoxia is expressed.

Cardiovascular changes in the exercising emu

1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Oxygen Content ◽  
Body Mass ◽  
Fold Increase ◽  
Exercise Heart Rate ◽  
Rate Of Oxygen Consumption ◽  
Cardiovascular Variables

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

Cardiopulmonary effects of continuous pressure breathing in hypothermic dogs

1965 ◽  
Vol 20 (4) ◽  
pp. 669-674 ◽  
Author(s):  
J. Salzano ◽  
F. G. Hall
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Negative Pressure Breathing ◽  
Continuous Positive Pressure ◽  
Respiratory Dead Space

Continuous pressure breathing was studied in hypothermic anesthetized dogs. Alveolar ventilation decreased during continuous positive-pressure breathing and increased during continuous negative-pressure breathing. The changes in alveolar ventilation were due to changes in respiratory rate as well as in respiratory dead space. Cardiac output fell significantly during continuous positive-pressure breathing due to a reduction in heart rate and stroke volume. During continuous negative-pressure breathing cardiac output was only slightly greater than during control as a result of a fall in heart rate and an increase in stroke volume. Oxygen consumption was reduced to 60% of control during continuous positive-pressure breathing of 16 cm H2O but was 25% greater than control during continuous negative-pressure breathing. Qualitatively, CO2 production changed as did O2 consumption but was different quantitatively during continuous negative-pressure breathing indicating hyperventilation due to increased respiratory rate. Mean pulmonary artery pressures and pulmonary resistance varied directly with the applied intratracheal pressure. The results indicate that the hypothermic animal can tolerate an imposed stress such as continuous pressure breathing and can increase its oxygen consumption during continuous negative-pressure breathing as does the normothermic animal. hypothermia; respiratory dead space; metabolic rate; cardiac output Submitted on December 8, 1964

Role of vasopressin in the cardiovascular response to hypoxia in the conscious rat

1986 ◽  
Vol 251 (6) ◽  
pp. H1316-H1323 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Hypoxic Exposure ◽  
Conscious Rat ◽  
Time Control ◽  
Hemodynamic Variables

Previous experiments have demonstrated that hypoxia stimulates the release of arginine vasopressin in conscious animals including the rat. The present study was designed to test whether AVP may exert a vasoconstrictor influence during hypoxia at varying levels of CO2. Systemic hemodynamics were assessed in conscious rats for 30 min under hypocapnic hypoxic, isocapnic hypoxic, hypercapnic hypoxic, and room air conditions. Progressive effects on heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were observed with varying CO2 under hypoxic conditions. Hypocapnic hypoxia [arterial PO2 (PaO2) = 32 Torr; arterial PCO2 (PaCO2) = 22 Torr] caused HR and CO to rise and TPR to fall. Isocapnic hypoxia (PaO2 = 36 Torr; PaCO2 = 35 Torr) was associated with no significant changes in HR and CO or TPR, whereas hypercapnic hypoxia (PaO2 = 35 Torr; PaCO2 = 51 Torr) caused HR and CO to fall and TPR to rise. Room air time control experiments were associated with no change in measured hemodynamic variables. To determine the possible role of circulating AVP on these cardiovascular responses, additional experiments were performed where the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (10 micrograms/kg iv) was administered at the midpoint of hypoxic exposure. Antagonist administration had no effect on hypocapnic hypoxic animals or animals breathing room air; however, blood pressure and TPR were significantly reduced by d(CH2)5Tyr(Me)AVP in both isocapnic and hypercapnic hypoxic animals. The heart rate response to hypoxia at the various CO2 levels was unaffected; however, cardiac output and stroke volume were increased after V1-antagonism in the isocapnic and hypercapnic hypoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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