After effects of chronic hypoxia on cardiac output and muscle blood flow at rest and exercise

The distribution of cardiac output (CO) between compliant and noncompliant organs is an important determinant of the slope of the relationship predicted between CO and right atrial pressure (RAP). However, curves relating CO to RAP at rest are shifted rightward (higher CO) and upward (higher RAP) by exercise with no change in slope, despite a large rise in the fraction of CO directed to noncompliant muscle vasculature, which is predicted to decrease the slope. We sought to test whether reductions in CO imposed during rest and exercise are accompanied by changes in its distribution that would favor constant slopes. Six dogs had atrioventricular block produced surgically and had blood flow transducers implanted on the ascending aorta and the terminal aorta. Total muscle blood flow (MBF) was estimated from terminal aortic flow by assuming that all of the increase in CO in mild dynamic exercise is directed to muscle. CO was reduced by lowering ventricular pacing rate at rest and during graded treadmill exercise (2 and 4 miles/h at 0% grade). Exercise increased the fraction of CO directed to muscle (MBF/CO) (P < 0.001). The effect of changes in CO on MBF/CO depended on exercise intensity (P < 0.01). At rest, MBF/CO fell from 0.53 to 0.45 when CO was reduced; this is expected to reduce the slope of the measured relationship between CO and RAP. During exercise at 2 miles/h, MBF/CO changed little when CO was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.01160.2007 ◽

2008 ◽

Vol 104 (4) ◽

pp. 1202-1210 ◽

Cited By ~ 50

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.

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Costal vs. crural diaphragmatic blood flow during submaximal and near-maximal exercise in ponies

Journal of Applied Physiology ◽

10.1152/jappl.1988.65.4.1514 ◽

1988 ◽

Vol 65 (4) ◽

pp. 1514-1519 ◽

Cited By ~ 32

Author(s):

M. Manohar

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Left Atrium ◽

Maximal Exercise ◽

Muscle Blood Flow ◽

Intercostal Muscle ◽

Quiet Breathing ◽

Blood Flows ◽

Graded Exercise ◽

Crural Diaphragm

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)

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Reduced submaximal leg blood flow after high-intensity aerobic training

Journal of Applied Physiology ◽

10.1152/jappl.2001.91.6.2619 ◽

2001 ◽

Vol 91 (6) ◽

pp. 2619-2627 ◽

Cited By ~ 37

Author(s):

David N. Proctor ◽

Jordan D. Miller ◽

Niki M. Dietz ◽

Christopher T. Minson ◽

Michael J. Joyner

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Power Output ◽

High Intensity ◽

Aerobic Training ◽

Muscle Blood Flow ◽

Splanchnic Blood Flow ◽

Active Muscle ◽

Leg Blood Flow ◽

Power Outputs

This study evaluated the hypothesis that active muscle blood flow is lower during exercise at a given submaximal power output after aerobic conditioning as a result of unchanged cardiac output and blunted splanchnic vasoconstriction. Eight untrained subjects (4 men, 4 women, 23–31 yr) performed high-intensity aerobic training for 9–12 wk. Leg blood flow (femoral vein thermodilution), splanchnic blood flow (indocyanine green clearance), cardiac output (acetylene rebreathing), whole body O2 uptake (V˙o 2), and arterial-venous blood gases were measured before and after training at identical submaximal power outputs (70 and 140 W; upright 2-leg cycling). Training increased ( P < 0.05) peak V˙o 2(12–36%) but did not significantly change submaximalV˙o 2 or cardiac output. Leg blood flow during both submaximal power outputs averaged 18% lower after training ( P = 0.001; n = 7), but these reductions were not correlated with changes in splanchnic vasoconstriction. Submaximal leg V˙o 2 was also lower after training. These findings support the hypothesis that aerobic training reduces active muscle blood flow at a given submaximal power output. However, changes in leg and splanchnic blood flow resulting from high-intensity training may not be causally linked.

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Comment on Point:Counterpoint "In health and in a normoxic environment, V̇o2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow"

Journal of Applied Physiology ◽

10.1152/japplphysiol.00018.2006 ◽

2006 ◽

Vol 100 (5) ◽

pp. 1742-1742

Author(s):

Timothy David Noakes

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Muscle Blood Flow

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Effects of epinephrine on cardiovascular and metabolic responses to leg exercise in man

Journal of Applied Physiology ◽

10.1152/jappl.1963.18.6.1118 ◽

1963 ◽

Vol 18 (6) ◽

pp. 1118-1122 ◽

Cited By ~ 4

Author(s):

Robert J. Marshall ◽

John T. Shepherd

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Oxygen Content ◽

Muscle Blood Flow ◽

Venous Blood ◽

Metabolic Responses ◽

Leg Muscles ◽

Leg Exercise ◽

The Subject ◽

The Mean

In studies on six experienced subjects lying supine, cardiac output and oxygen content of femoral venous blood were measured with the subject at rest, during the increase in muscle blood flow caused by intravenous infusion of epinephrine, during mild leg exercise, and during identical exercise combined with an infusion. The oxygen content of the blood from the exercising limb was much higher (average, 50%) during an infusion than when no infusion was given (average, 32%). The mean increase in cardiac output during the combined maneuver (8.2 liters/min) almost equaled the sum of the increases during the separate infusion (3.7 liters) and during exercise (4.7 liters). All individual studies showed approximately this same result. Thus, the additional blood supplied to the leg muscles by the infusion did not appear to be used for metabolic purposes during exercise. cardiac output; muscle blood flow Submitted on March 22, 1963

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Regional hemodynamic responses to hypoxia in polycythemic dogs

Journal of Applied Physiology ◽

10.1152/jappl.1988.65.5.2069 ◽

1988 ◽

Vol 65 (5) ◽

pp. 2069-2074 ◽

Cited By ~ 1

Author(s):

R. L. Stork ◽

D. L. Bredle ◽

C. K. Chapler ◽

S. M. Cain

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Muscle Blood Flow ◽

Regional Distribution ◽

Experimental Conditions ◽

Hypoxic Vasoconstriction ◽

O2 Extraction ◽

Anesthetized Dogs ◽

O2 Delivery ◽

Resting Muscle

Polycythemia increases blood viscosity so that systemic O2 delivery (QO2) decreases and its regional distribution changes. We examined whether hypoxia, by promoting local vasodilation, further modified these effects in resting skeletal muscle and gut in anesthetized dogs after hematocrit had been raised to 65%. One group (CON, n = 7) served as normoxic controls while another (HH, n = 6) was ventilated with 9% O2--91% N2 for 30 min between periods of normoxia. Polycythemia decreased cardiac output so that QO2 to both regions decreased approximately 50% in both groups. In compensation, O2 extraction fraction increased to 65% in muscle and to 50% in gut. When QO2 was reduced further during hypoxia, blood flow increased in muscle but not in gut. Unlike previously published normocythemic studies, there was no initial hypoxic vasoconstriction in muscle. Metabolic vasodilation during hypoxia was enhanced in muscle when blood O2 reserves were first lowered by increased extraction with polycythemia alone. The increase in resting muscle blood flow during hypoxia with no change in cardiac output may have decreased O2 availability to other more vital tissues. In that sense and under these experimental conditions, polycythemia caused a maladaptive response during hypoxic hypoxia.

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The role of α-adrenergic receptors in carbon monoxide hypoxia

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y86-244 ◽

1986 ◽

Vol 64 (11) ◽

pp. 1442-1446 ◽

Cited By ~ 4

Author(s):

S. M. Villeneuve ◽

C. K. Chapler ◽

C. E. King ◽

S. M. Cain

Keyword(s):

Carbon Monoxide ◽

Blood Flow ◽

Cardiac Output ◽

Adrenergic Receptors ◽

Muscle Blood Flow ◽

Control Period ◽

Arterial Oxygen ◽

Adrenergic Blockade ◽

Limb Blood Flow ◽

Arterial Oxygen Content

The importance of α-adrenergic receptors in the cardiac output and peripheral circulatory responses to carbon monoxide (CO) hypoxia was studied in anesthetized dogs. Phenoxybenzamine (3 mg/kg i.v.) was injected to block α-receptor activity and the data obtained were then compared with those from a previous study of CO hypoxia in unblocked animals. Values for cardiac output, hindlimb blood flow, vascular resistance, and oxygen uptake were obtained prior to and at 30 and 60 min of CO hypoxia which reduced arterial oxygen content by approximately 50%. α-Adrenergic blockade resulted in a lower (p < 0.05) control value for cardiac output than observed in unblocked animals, but no differences were present between the two groups at 30 or 60 min of CO hypoxia. Similarly, limb blood flow was lower (p < 0.05) during the control period in the α-blocked group but rose to the same level as that in the unblocked animals at 60 min of COH. No change in limb blood flow occurred during CO hypoxia in the unblocked group. These findings demonstrated that during CO hypoxia (i) α-receptor mediated venoconstriction does not contribute to the cardiac output response and (ii) α-receptor mediated vasoconstriction probably does prevent a rise in hindlimb skeletal muscle blood flow.

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Ideas about control of skeletal and cardiac muscle blood flow (1876–2003): cycles of revision and new vision

Journal of Applied Physiology ◽

10.1152/japplphysiol.01220.2003 ◽

2004 ◽

Vol 97 (1) ◽

pp. 384-392 ◽

Cited By ~ 73

Author(s):

Loring B. Rowell

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Cardiac Muscle ◽

Neural Control ◽

Muscle Blood Flow ◽

Dynamic Exercise ◽

Vascular Conductance ◽

Site Of Action ◽

New Vision ◽

Muscle Chemoreflex

This perspective examines origins of some key ideas central to major issues to be addressed in five subsequent mini-reviews related to Skeletal and Cardiac Muscle Blood Flow. The questions discussed are as follows. 1) What causes vasodilation in skeletal and cardiac muscle and 2) might the mechanisms be the same in both? 3) How important is muscle's mechanical contribution (via muscle pumping) to muscle blood flow, including its effect on cardiac output? 4) Is neural (vasoconstrictor) control of muscle vascular conductance and muscle blood flow significantly blunted in exercise by muscle metabolites and what might be a dominant site of action? 5) What reflexes initiate neural control of muscle vascular conductance so as to maintain arterial pressure at its baroreflex operating point during dynamic exercise, or is muscle blood flow regulated so as to prevent accumulation of metabolites and an ensuing muscle chemoreflex or both?

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