Regulation of the Circulation During Exercise

1956 ◽  
Vol 184 (3) ◽  
pp. 613-623 ◽  
Author(s):  
A. C. Barger ◽  
V. Richards ◽  
J. Metcalfe ◽  
B. Günther

Oxygen consumption and cardiac output (direct Fick) have been measured in normal dogs at rest and during graded exercise on the treadmill up to a work intensity of 5 mph and 10°. Systemic and pulmonary artery pressures have also been recorded. The changes in cardiac output produced ‘at rest’ by excitement were frequently as large as those induced by moderate exercise. A short bout of exercise followed by a rest period was far more efficacious in producing lower and more uniform results during rest and subsequent exercise than a prolonged rest period alone. Under such conditions the ‘steady state’ was reached in 3 minutes or less of exercise. The linear relation between oxygen consumption and cardiac output during exercise in the dog is similar to that observed in man, and in the horse. The possible significance of this similarity is discussed and it is suggested that the data are consistent with the hypothesis that the increase in blood flow during exercise is largely the increase in muscle flow with a constant arteriovenous oxygen difference of approximately 14 vol. %.

1976 ◽  
Vol 231 (5) ◽  
pp. 1515-1519 ◽  
Author(s):  
DE Fixler ◽  
JM Atkins ◽  
JH Mitchell ◽  
LD Horwitz

The distribution of cardiac output was analyzed in six dogs, with the animals at rest and running on a level treadmill for 3 min at 3-4 mph (mild exercise) and 3 min at 6-8 mph (moderate exercise). Organ flows were measured using 25-mug-diam radioactive microspheres. Cardiac output averaged 2.5, 4.6, and 5.7 liters/min, for rest, mild exercise, and moderate exercise, respectively. The greatest change was in diaphragmatic flow which increased by 275% with mild exercise and 500% with moderate exercise. Flow to intercostal muscles increased by 160 and 186%, to the exercising gastrocnemius muscle by 153 and 224%, and to cardiac muscle by 57 and 109% during mild and moderate exercise, respectively. Renal and cerebral flows did not change significantly. Significant decreases in flow occurred in the small and large intestines during moderate exercise. It is concluded that the increase in cardiac output during submaximal exercise was redistributed in a manner which limited flow to the brain, intestines, and kidneys and increased flow flow to the diaphragm, heart, and limb muscles.


1963 ◽  
Vol 204 (2) ◽  
pp. 291-296 ◽  
Author(s):  
Edmundo Ashkar ◽  
William F. Hamilton

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.


1962 ◽  
Vol 17 (6) ◽  
pp. 922-926 ◽  
Author(s):  
H. Duke Thomas ◽  
Carlos Gaos ◽  
T. J. Reeves

Measurements of the cardiac output utilizing the classical Fick method were carried out in 38 cardiac patients at rest and during exercise. The predicted cardiac output during exercise was calculated by the regression equation derived by Donald et al. ( Clin. Sci. 14: 37, 1955), relating cardiac output to oxygen consumption during the steady state of exercise in normal subjects (cardiac index = 3.708 + 0.00534 x O2 consumption, ml/min m2). The resting arteriovenous oxygen difference was found to correlate much better with the calculated percentage of predicted cardiac index during exercise (γ = 0.547) than did the resting cardiac index (γ = 0.304). The finding of an arteriovenous oxygen difference greater than 5.16 ml/100 cc indicated a strong probability of subnormal cardiac index during exercise relative to the oxygen consumption. Submitted on June 18, 1962


1988 ◽  
Vol 65 (4) ◽  
pp. 1514-1519 ◽  
Author(s):  
M. Manohar

The present study was carried out 1) to compare blood flow in the costal and crural regions of the equine diaphragm during quiet breathing at rest and during graded exercise and 2) to determine the fraction of cardiac output needed to perfuse the diaphragm during near-maximal exercise. By the use of radionuclide-labeled 15-micron-diam microspheres injected into the left atrium, diaphragmatic and intercostal muscle blood flow was studied in 10 healthy ponies at rest and during three levels of exercise (moderate: 12 mph, heavy: 15 mph, and near-maximal: 19-20 mph) performed on a treadmill. At rest, in eucapnic ponies, costal (13 +/- 3 ml.min-1.100 g-1) and crural (13 +/- 2 ml.min-1.100 g-1) phrenic blood flows were similar, but the costal diaphragm received a much larger percentage of cardiac output (0.51 +/- 0.12% vs. 0.15 +/- 0.03% for crural diaphragm). Intercostal muscle perfusion at rest was significantly less than in either phrenic region. Graded exercise resulted in significant progressive increments in perfusion to these tissues. Although during exercise, crural diaphragmatic blood flow was not different from intercostal muscle blood flow, these values remained significantly less (P less than 0.01) than in the costal diaphragm. At moderate, heavy, and near-maximal exercise, costal diaphragmatic blood flow (123 +/- 12, 190 +/- 12, and 245 +/- 18 ml.min-1.100 g-1) was 143%, 162%, and 162%, respectively, of that for the crural diaphragm (86 +/- 10, 117 +/- 8, and 151 +/- 14 ml.min-1.100 g-1).(ABSTRACT TRUNCATED AT 250 WORDS)


1959 ◽  
Vol 197 (5) ◽  
pp. 1111-1114 ◽  
Author(s):  
Matthew N. Levy

Temperature was diminished in a stepwise fashion in the isolated kidney of the dog perfused from a peripheral artery of the original, normothermic animal. Decreased temperature resulted in an appreciable reduction of renal blood flow at constant arterial blood pressure. Increased blood viscosity and vasoconstriction were both responsible for this reduction of flow. Hypothermia also resulted in a reduction in arteriovenous oxygen difference which was roughly proportional to the centigrade temperature. Furthermore, hypothermia exerted a marked but reversible depression of the rate of oxidative metabolism. This effect was relatively more severe than the changes for the body as a whole at equivalent temperatures reported by other investigators.


1976 ◽  
Vol 4 (6) ◽  
pp. 402-409 ◽  
Author(s):  
Attilio Maseri ◽  
Antonio Pesola ◽  
Antonio L'Abbate ◽  
Carlo Contini ◽  
Glauco Magini

The acute systemic and coronary haemodynamic effects of a new hypotensive drug L 6150 (3-hydrazino-6-[N,N-bis(2-hydroxyethyl)amino]pyridazine) have been studied in six patients with renal or essential hypertension. The drug, administered intravenously at a dose of 2-9 mg, caused a marked hypotension and increase of cardiac output in five cases. Though left ventricular work was reduced or unchanged after the drug, myocardial blood flow increased markedly, coronary resistance decreased and coronary A-V oxygen difference decreased by about 50% indicating coronary vasodilation. When compared with the available data on the effects of hydrazinophthalazine, L 6150 appeared to have qualitatively similar effects, but a somewhat greater direct coronary vasodilator effect.


1957 ◽  
Vol 188 (3) ◽  
pp. 473-476 ◽  
Author(s):  
Bernard Fisher ◽  
Clem Russ ◽  
E. J. Fedor

The changes occurring in cardiac output and oxygen consumption in short periods of hypothermia are the same when either ether or pentobarbital sodium is used as the anesthetic agent during the induction of hypothermia. Following an initial decrease in oxygen consumption, no further change occurred as long as the body temperature was maintained at a constant level. Cardiac output, arterial-venous oxygen difference, and coefficient of oxygen utilization remain unchanged for longer periods of time than most physiologic parameters studied during prolonged hypothermia at constant temperatures. After about 14 hours they also begin to alter so that by 24 hours the changes are profound. Stagnant anoxemia and marked increased in the coefficient of O2 utilization resulting from the markedly lowered cardiac output, which was 5% of the precooled controls, occurred.


1969 ◽  
Vol 47 (9) ◽  
pp. 771-780 ◽  
Author(s):  
E. Don Stevens

The effect of moderate exercise on cardiac output and its distribution was studied in the rat. During moderate exercise blood flow to the skeletal and heart muscle increased. The decrease in the flow fraction of the cardiac output to the splanchnic bed and kidneys was offset by the increase in cardiac output so that blood flow to these organs was maintained during exercise. Blood flow decreased to the spleen and to that area of skin overlying the tail during moderate exercise. Thus, the tissues associated with the increased oxygen demand during exercise profited most from the increased cardiac output.


1959 ◽  
Vol 197 (1) ◽  
pp. 190-192 ◽  
Author(s):  
Lloyd R. Yonce ◽  
W. F. Hamilton

The surgical technique of isolation of the blood supply of the gracilis muscle of the dog has been developed for analysis of the oxygen consumption during reactive hyperemia. The time course of the blood flow, A-V oxygen difference and the oxygen consumption follow the same pattern. Immediately after the release of the arterial occlusion, there is an increase in all three values which decay and go below the control level that existed just prior to the occlusion. The increased oxygen consumption during reactive hyperemia is possible primarily by the increased blood flow, although the A-V oxygen difference is increased also. A theoretical oxygen deficit is overpaid by the oxygen consumption during the period of increased blood flow but essentially repaid if the period of decreased blood flow is included.


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