Effects of respiratory muscle work on cardiac output and its distribution during maximal exercise

1998 ◽  
Vol 85 (2) ◽  
pp. 609-618 ◽  
Author(s):  
Craig A. Harms ◽  
Thomas J. Wetter ◽  
Steven R. McClaran ◽  
David F. Pegelow ◽  
Glenn A. Nickele ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Respiratory Muscle ◽  
Maximal Exercise ◽  
Work Of Breathing ◽  
Venous Blood ◽  
Inspiratory Muscle ◽  
Mixed Venous Blood ◽  
Muscle Work ◽  
Mixed Venous

We have recently demonstrated that changes in the work of breathing during maximal exercise affect leg blood flow and leg vascular conductance (C. A. Harms, M. A. Babcock, S. R. McClaran, D. F. Pegelow, G. A. Nickele, W. B. Nelson, and J. A. Dempsey. J. Appl. Physiol. 82: 1573–1583, 1997). Our present study examined the effects of changes in the work of breathing on cardiac output (CO) during maximal exercise. Eight male cyclists [maximal O2 consumption (V˙o 2 max): 62 ± 5 ml ⋅ kg−1 ⋅ min−1] performed repeated 2.5-min bouts of cycle exercise atV˙o 2 max. Inspiratory muscle work was either 1) at control levels [inspiratory esophageal pressure (Pes): −27.8 ± 0.6 cmH2O], 2) reduced via a proportional-assist ventilator (Pes: −16.3 ± 0.5 cmH2O), or 3) increased via resistive loads (Pes: −35.6 ± 0.8 cmH2O). O2 contents measured in arterial and mixed venous blood were used to calculate CO via the direct Fick method. Stroke volume, CO, and pulmonary O2 consumption (V˙o 2) were not different ( P > 0.05) between control and loaded trials atV˙o 2 max but were lower (−8, −9, and −7%, respectively) than control with inspiratory muscle unloading atV˙o 2 max. The arterial-mixed venous O2difference was unchanged with unloading or loading. We combined these findings with our recent study to show that the respiratory muscle work normally expended during maximal exercise has two significant effects on the cardiovascular system: 1) up to 14–16% of the CO is directed to the respiratory muscles; and 2) local reflex vasoconstriction significantly compromises blood flow to leg locomotor muscles.

scholarly journals Respiratory muscle work compromises leg blood flow during maximal exercise

1997 ◽  
Vol 82 (5) ◽  
pp. 1573-1583 ◽  
Author(s):  
Craig A. Harms ◽  
Mark A. Babcock ◽  
Steven R. McClaran ◽  
David F. Pegelow ◽  
Glenn A. Nickele ◽  
...  
Keyword(s):  
Blood Flow ◽  
Respiratory Muscle ◽  
Maximal Exercise ◽  
Minute Ventilation ◽  
Muscle Blood Flow ◽  
Work Of Breathing ◽  
Esophageal Pressure ◽  
Leg Blood Flow ◽  
Muscle Work ◽  
Arterial Blood

Harms, Craig A., Mark A. Babcock, Steven R. McClaran, David F. Pegelow, Glenn A. Nickele, William B. Nelson, and Jerome A. Dempsey.Respiratory muscle work compromises leg blood flow during maximal exercise. J. Appl. Physiol.82(5): 1573–1583, 1997.—We hypothesized that during exercise at maximal O2 consumption (V˙o 2 max), high demand for respiratory muscle blood flow (Q˙) would elicit locomotor muscle vasoconstriction and compromise limb Q˙. Seven male cyclists (V˙o 2 max 64 ± 6 ml ⋅ kg−1 ⋅ min−1) each completed 14 exercise bouts of 2.5-min duration atV˙o 2 max on a cycle ergometer during two testing sessions. Inspiratory muscle work was either 1) reduced via a proportional-assist ventilator, 2) increased via graded resistive loads, or 3) was not manipulated (control). Arterial (brachial) and venous (femoral) blood samples, arterial blood pressure, leg Q˙ (Q˙legs; thermodilution), esophageal pressure, and O2 consumption (V˙o 2) were measured. Within each subject and across all subjects, at constant maximal work rate, significant correlations existed ( r = 0.74–0.90; P < 0.05) between work of breathing (Wb) and Q˙legs (inverse), leg vascular resistance (LVR), and leg V˙o 2(V˙o 2 legs; inverse), and between LVR and norepinephrine spillover. Mean arterial pressure did not change with changes in Wb nor did tidal volume or minute ventilation. For a ±50% change from control in Wb,Q˙legs changed 2 l/min or 11% of control, LVR changed 13% of control, and O2extraction did not change; thusV˙o 2 legschanged 0.4 l/min or 10% of control. TotalV˙o 2 max was unchanged with loading but fell 9.3% with unloading; thusV˙o 2 legsas a percentage of totalV˙o 2 max was 81% in control, increased to 89% with respiratory muscle unloading, and decreased to 71% with respiratory muscle loading. We conclude that Wb normally incurred during maximal exercise causes vasoconstriction in locomotor muscles and compromises locomotor muscle perfusion andV˙o 2.

Respiratory measurements of cardiac output: from elegant idea to useful test

2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo
Keyword(s):  
Cardiac Output ◽  
Human Subjects ◽  
Venous Blood ◽  
The Body ◽  
Mixed Venous Blood ◽  
Indirect Determination ◽  
Arterial Blood ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Mixed Venous

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.

Human respiratory muscle blood flow measured by near-infrared spectroscopy and indocyanine green

2008 ◽  
Vol 104 (4) ◽  
pp. 1202-1210 ◽  
Author(s):  
Jordan A. Guenette ◽  
Ioannis Vogiatzis ◽  
Spyros Zakynthinos ◽  
Dimitrios Athanasopoulos ◽  
Maria Koskolou ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Infrared Spectroscopy ◽  
Respiratory Muscle ◽  
Near Infrared ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Work Of Breathing ◽  
Dilution Method ◽  
Transdiaphragmatic Pressure

Measurement of respiratory muscle blood flow (RMBF) in humans has important implications for understanding patterns of blood flow distribution during exercise in healthy individuals and those with chronic disease. Previous studies examining RMBF in humans have required invasive methods on anesthetized subjects. To assess RMBF in awake subjects, we applied an indicator-dilution method using near-infrared spectroscopy (NIRS) and the light-absorbing tracer indocyanine green dye (ICG). NIRS optodes were placed on the left seventh intercostal space at the apposition of the costal diaphragm and on an inactive control muscle (vastus lateralis). The primary respiratory muscles within view of the NIRS optodes include the internal and external intercostals. Intravenous bolus injection of ICG allowed for cardiac output (by the conventional dye-dilution method with arterial sampling), RMBF, and vastus lateralis blood flow to be quantified simultaneously. Esophageal and gastric pressures were also measured to calculate the work of breathing and transdiaphragmatic pressure. Measurements were obtained in five conscious humans during both resting breathing and three separate 5-min bouts of constant isocapnic hyperpnea at 27.1 ± 3.2, 56.0 ± 6.1, and 75.9 ± 5.7% of maximum minute ventilation as determined on a previous maximal exercise test. RMBF progressively increased (9.9 ± 0.6, 14.8 ± 2.7, 29.9 ± 5.8, and 50.1 ± 12.5 ml·100 ml−1·min−1, respectively) with increasing levels of ventilation while blood flow to the inactive control muscle remained constant (10.4 ± 1.4, 8.7 ± 0.7, 12.9 ± 1.7, and 12.2 ± 1.8 ml·100 ml−1·min−1, respectively). As ventilation rose, RMBF was closely and significantly correlated with 1) cardiac output ( r = 0.994, P = 0.006), 2) the work of breathing ( r = 0.995, P = 0.005), and 3) transdiaphragmatic pressure ( r = 0.998, P = 0.002). These data suggest that the NIRS-ICG technique provides a feasible and sensitive index of RMBF at different levels of ventilation in humans.

Influence of changes in cardiac output on the acid-base status of arterial and mixed venous blood

1987 ◽  
Vol 410 (3) ◽  
pp. 257-262 ◽  
Author(s):  
Y. L. Hoogeveen ◽  
J. P. Zock ◽  
P. Rispens ◽  
W. G. Zijlstra
Keyword(s):  
Cardiac Output ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Acid Base ◽  
Acid Base Status ◽  
Mixed Venous

Lactate, pyruvate, glucose, and free fatty acid in mixed venous and arterial blood

1963 ◽  
Vol 18 (5) ◽  
pp. 933-936 ◽  
Author(s):  
P. Harris ◽  
T. Bailey ◽  
M. Bateman ◽  
M. G. Fitzgerald ◽  
J. Gloster ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cardiac Output ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Venous Blood ◽  
Average Concentration ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Acquired Heart Disease ◽  
Mixed Venous

The concentrations of lactic acid, pyruvic acid, glucose, and free fatty acids have been measured simultaneously in the blood from the pulmonary and brachial arteries at rest and during exercise in a group of patients with acquired heart disease. The arteriovenous differences in the concentration of lactate, pyruvate, and free fatty acid were such as could be attributed to chance. The average concentration of glucose was slightly but significantly higher in the brachial arterial blood than in the mixed venous blood. cardiac output; lung metabolism; exercise Submitted on January 15, 1963

Effects Of Respiratory Muscle Work On Cardiac Output And Its Distribution During Maximal Exercise.

1998 ◽  
Vol 9 (4) ◽  
pp. 11
Author(s):  
Craig A. Harms ◽  
Thomas J. Wetter ◽  
Steven R. McClaran ◽  
David F. Pegelow ◽  
Glenn A. Nickele ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Respiratory Muscle ◽  
Maximal Exercise ◽  
Muscle Work

Intrapulmonary arteriovenous shunts of >15 μm in diameter probably do not contribute to arterial hypoxemia in maximally exercising Thoroughbred horses

2005 ◽  
Vol 99 (1) ◽  
pp. 224-229 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz
Keyword(s):  
Maximal Exercise ◽  
Venous Blood ◽  
Blood Oxygenation ◽  
Mixed Venous Blood ◽  
Arteriovenous Shunting ◽  
Arterial Hypoxemia ◽  
Thoroughbred Horses ◽  
Arteriovenous Shunts ◽  
Exercise Induced ◽  
Mixed Venous

The present study examined whether Thoroughbred horses performing strenuous exercise exhibit intrapulmonary arteriovenous shunting that may contribute to the observed arterial hypoxemia. Experiments were carried out on seven healthy, exercise-trained Thoroughbreds at rest, maximal exercise (galloping at 14 m/s on a 3.5% uphill grade for 120 s), and submaximal exertion (8 m/s on a 3.5% uphill grade for 150 s). Along with blood gas/hemodynamic parameters, intrapulmonary arteriovenous shunting was studied by injecting 15-μm-diameter microspheres, labeled with different stable isotopes, into the right atrium while simultaneous blood samples were being withdrawn at a constant rate from the pulmonary artery and the aorta. Arterial hypoxemia was observed only during maximal exercise. Also, despite significant pulmonary arterial hypertension during submaximal and maximal exertion, 15-μm microspheres did not traverse the pulmonary microcirculation to appear in the aortic blood. Thus our findings did not support a role for intrapulmonary arteriovenous shunts of >15 μm in diameter in the exercise-induced arterial hypoxemia in racehorses. Interestingly, our observation that, in going from 30 to 120 s of maximal exertion, arterial O2 tension had remained unchanged despite significant reductions in mixed venous blood O2 tension, hemoglobin-O2 saturation, and O2 content also discounts the importance of intrapulmonary arteriovenous shunts in causing arterial hypoxemia. This is because, assuming that a constant fraction of total pulmonary blood flow bypasses the gas-exchange areas of the equine lungs via intrapulmonary arteriovenous shunts during 30–120 s of maximal exertion, the observed significant reductions in mixed venous blood oxygenation should cause a significant reduction in arterial O2 tension, which was not the case in our horses. Thus it is suggested that intrapulmonary arteriovenous shunting probably does not contribute to the exercise-induced arterial hypoxemia in racehorses.

NaHCO3 does not affect arterial O2 tension but attenuates desaturation of hemoglobin in maximally exercising Thoroughbreds

2004 ◽  
Vol 96 (4) ◽  
pp. 1349-1356 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
Maximal Exercise ◽  
Venous Blood ◽  
Pulmonary Hemorrhage ◽  
Physiological Saline ◽  
Mixed Venous Blood ◽  
Maximal Heart Rate ◽  
Arterial Hypoxemia ◽  
Arterial Blood ◽  
Exercise Induced ◽  
Mixed Venous

The objective of the present study was to examine the effects of preexercise NaHCO3 administration to induce metabolic alkalosis on the arterial oxygenation in racehorses performing maximal exercise. Two sets of experiments, intravenous physiological saline and NaHCO3 (250 mg/kg iv), were carried out on 13 healthy, sound Thoroughbred horses in random order, 7 days apart. Blood-gas variables were examined at rest and during incremental exercise, leading to 120 s of galloping at 14 m/s on a 3.5% uphill grade, which elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. NaHCO3 administration caused alkalosis and hemodilution in standing horses, but arterial O2 tension and hemoglobin-O2 saturation were unaffected. Thus NaHCO3 administration caused a reduction in arterial O2 content at rest, although the arterial-to-mixed venous blood O2 content gradient was unaffected. During maximal exercise in both treatments, arterial hypoxemia, desaturation, hypercapnia, acidosis, hyperthermia, and hemoconcentration developed. Although the extent of exercise-induced arterial hypoxemia was similar, there was an attenuation of the desaturation of arterial hemoglobin in the NaHCO3-treated horses, which had higher arterial pH. Despite these observations, the arterial blood O2 content of exercising horses was less in the NaHCO3 experiments because of the hemodilution, and an attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient was observed. It was concluded that preexercise NaHCO3 administration does not affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing short-term, high-intensity exercise.

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