Comparison of Intracellular PO2 and Conditions for Blood-Tissue O2 Transport in Heart and Working Red Skeletal Muscle

1987 ◽  
pp. 309-321 ◽  
Author(s):  
C. R. Honig ◽  
T. E. J. Gayeski
Keyword(s):  
Skeletal Muscle ◽  
O2 Transport

O2 transport during two forms of stagnant hypoxia following acid and base infusions

1983 ◽  
Vol 54 (6) ◽  
pp. 1518-1524 ◽  
Author(s):  
S. M. Cain ◽  
R. P. Adams
Keyword(s):  
Skeletal Muscle ◽  
Control Period ◽  
Pericardial Tamponade ◽  
The Other ◽  
Whole Body ◽  
O2 Uptake ◽  
Volume Depletion ◽  
O2 Transport ◽  
Organ Systems ◽  
Acid And Base

Cardiac output and mean arterial pressure were decreased in two groups of 16 anesthetized paralyzed dogs ventilated by pump. Pericardial tamponade was used in one group, and hemorrhagic hypotension was used in the other. After a 30-min control period and 30 min of circulatory shock by either method, 0.3N HCl was infused into half the dogs in each group and 1.0N NaHCO3 into the other half so that pH was separated by 0.3–0.4 units. The slope of the line relating O2 uptake to total O2 transport (blood flow X arterial O2 concentration) was used to evaluate how well the tissues extracted O2 relative to O2 supply. During the initial shock period before infusion, the slope of the line relating O2 uptake of left hindlimb skeletal muscle to total O2 transport in the limb was almost twice as great as that for the whole body. Acid infusion increased the slope of the whole-body line but did not alter that for the hindlimb. Base infusion, on the other hand, decreased the slope of the line for the limb during hemorrhagic shock but had no other effect. We concluded that acid either improved the distribution of a limiting blood supply to nonmuscle organ systems, or increased tissue capillary PO2 and O2 diffusion by decreasing hemoglobin O2 affinity (HOA), or both. The effect of an increased HOA with base infusion was noticeable in hindlimb skeletal muscle only when volume depletion by hemorrhage presumably greatly increased the normally short intercapillary diffusion distance in muscle.

Adaptation of Skeletal Muscle O2 Transport and Utilization in Rats with Right Heart Failure

2010 ◽  
Vol 42 ◽  
pp. 376
Author(s):  
Rob C.I. Wüst ◽  
David Benoist ◽  
Rachel Stones ◽  
T Scott Bowen ◽  
Ed White ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Right Heart Failure ◽  
Right Heart ◽  
O2 Transport

Does myoglobin contribute significantly to diffusion of oxygen in red skeletal muscle?

1987 ◽  
Vol 252 (2) ◽  
pp. R341-R347 ◽  
Author(s):  
D. G. Covell ◽  
J. A. Jacquez
Keyword(s):  
Skeletal Muscle ◽  
Computer Simulation ◽  
O2 Consumption ◽  
Simulation Experiments ◽  
One Dimensional ◽  
O2 Transport ◽  
O2 Diffusion ◽  
O2 Delivery ◽  
And Diffusion

We have examined the role of myoglobin to facilitate O2 diffusion to active mitochondria in skeletal muscle by constructing computer-simulation experiments. Steady-state mitochondrial O2 consumption under different conditions of supply partial pressure of O2 (PO2) in a system with and without myoglobin were examined for a one-dimensional slab of tissue. O2 consumption by mitochondria was saturable with the mitochondria located in bands at uniform intervals throughout the tissue. Under these conditions, myoglobin provides a measurable increase in O2 transport for supply PO2 below 10 Torr and diffusion lengths expected for skeletal muscle fibers. We conclude that under circumstances where hypoxia lowers PO2 below 10 Torr that myoglobin begins to provide a measurable increase in O2 delivery to mitochondria.

The pathophysiology of McArdle's disease: clues to regulation in exercise and fatigue

1986 ◽  
Vol 61 (2) ◽  
pp. 391-401 ◽  
Author(s):  
S. F. Lewis ◽  
R. G. Haller
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fatigue ◽  
Muscle Afferents ◽  
Common Denominator ◽  
Circulatory Response ◽  
Mcardle's Disease ◽  
O2 Transport ◽  
Mcardle’S Disease ◽  
Muscle Phosphorylase ◽  
Response To Exercise

Muscle phosphorylase deficiency (McArdle's disease) has conventionally been considered a disorder of glycogenolysis, and the associated impairment in oxidative metabolism has been largely overlooked. Muscle glycogen normally is the primary oxidative fuel at exercise work loads requiring more than 75–80% of maximal O2 uptake (VO2max). Evidence is presented to support the hypothesis that a limited flux through the Embden-Myerhof pathway in McArdle's disease reduces the capacity to generate NADH required to support a normal VO2max. The extent of the oxidative defect is substrate dependent; i.e., it can be partially corrected by increasing the availability of alternative oxidative substrates (e.g., glucose, free fatty acids) to working muscle. Experiments employing modification of substrate availability closely link the hyperkinetic circulatory response to exercise (i.e., an abnormally large increase in O2 transport to skeletal muscle) and the premature muscle fatigue and cramping of McArdle patients with their oxidative impairment and suggest that a metabolic common denominator in these abnormal responses may be a pronounced decline in the muscle phosphorylation potential ([ATP]/[ADP][Pi]). The hyperkinetic circulation likely is mediated by the local effects on metabolically sensitive skeletal muscle afferents and vascular smooth muscle of K+, Pi, or adenosine or a combination of these substances released excessively from working skeletal muscle. The premature muscle fatigue and cramping of McArdle patients does not appear to be due to depletion of ATP but is associated with an increased accumulation of Pi and probably ADP in skeletal muscle. Accumulations of Pi and ADP are known to inhibit the myofibrillar, Ca2+, and Na+-K+-ATPase reactions.

Hydroxymalonate inhibits lactate uptake by the rabbit hindlimb

1994 ◽  
Vol 76 (6) ◽  
pp. 2735-2741 ◽  
Author(s):  
G. Gutierrez ◽  
E. Fernandez ◽  
F. J. Hurtado ◽  
R. Kiiski ◽  
S. Chakravarthy ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Normal Saline ◽  
Mechanically Ventilated ◽  
O2 Transport ◽  
Femoral Blood Flow ◽  
Net Uptake ◽  
Femoral Blood ◽  
Lactate Uptake ◽  
Resting Muscle ◽  
Arterial Po2

Lactate uptake by skeletal muscle occurs under diverse conditions, including hypoxia and electrical stimulation. A possible metabolic fate of lactate in resting muscle is its conversion to pyruvate followed by carboxylation to malate in the cytosolic malic reaction. To test this hypothesis, we measured hindlimb lactate uptake in hypoxic mechanically ventilated rabbits. Rabbits were given intravenous infusions of hydroxymalonate, an inhibitor of the malic reaction (200 mM; n = 7), or normal saline (n = 7) at 1.1 ml/min. Hindlimb lactate uptake/release was calculated as femoral blood flow times the arteriovenous lactate difference. Saline or hydroxymalonate was infused continuously during sequential 30-min periods of normoxia (arterial PO2 approximately 150 Torr), hypoxemia (arterial PO2 approximately 30 Torr), and reoxygenation (arterial PO2 approximately 150 Torr). Hindlimb O2 transport decreased with hypoxemia, but O2 consumption remained unchanged in both groups. During hypoxemia there was net uptake of lactate by the hindlimb of the group given normal saline [4.5 +/- 0.9 (SE) mumol/min]. The hindlimb of the hydroxymalonate group continued to release lactate (-0.5 +/- 1.0 mumol/min). The inhibition of lactate uptake by hydroxymalonate supports the hypothesis that the malic reaction plays a major role in the metabolism of lactate by resting rabbit skeletal muscle.

Metabolic control of cardiac output response to exercise in McArdle's disease

1984 ◽  
Vol 57 (6) ◽  
pp. 1749-1753 ◽  
Author(s):  
S. F. Lewis ◽  
R. G. Haller ◽  
J. D. Cook ◽  
C. G. Blomqvist
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Output ◽  
Nicotinic Acid ◽  
Plasma Free Fatty Acid ◽  
Muscle Afferents ◽  
Tight Coupling ◽  
Metabolic State ◽  
Mcardle's Disease ◽  
O2 Transport ◽  
Mcardle’S Disease

During dynamic exercise cardiac output (Q) normally increases approximately 5 liters per liter of increase in O2 uptake (Vo2) (i.e., delta Q/delta Vo2 approximately equal to 5), indicative of a tight coupling between systemic O2 transport and utilization. We studied four patients with muscle phosphorylase deficiency (McArdle's disease) in whom Q was normal at rest, but delta Q/delta Vo2 was 14.1 +/- 1.3 during bicycle exercise. Procedures designed to alter the availability of substrates were employed to test the hypothesis that the increased delta Q/delta Vo2 is linked to the abnormal metabolic state of skeletal muscle. Fasting plus prolonged moderate exercise was used to increase the availability of plasma free fatty acid (FFA) and resulted in a normalization of delta Q/delta Vo2 (5.3 +/- 0.4). Hyperglycemia (70% above control levels) partially normalized delta Q/delta Vo2. Nicotinic acid lowered plasma FFA concentration and dramatically increased delta Q/delta Vo2 (4.6 to 13.7) when administered after fasting plus prolonged exercise in one patient. Glucose infusion after nicotinic acid administration markedly lowered delta Q/delta Vo2. The results support the hypothesis and suggest that the metabolic state of skeletal muscle, possibly via activation of muscle afferents, participates in the regulation of systemic O2 transport.

Regional blood flow and O2 transport during hypoxic and CO hypoxia in neonatal and adult sheep

1985 ◽  
Vol 248 (1) ◽  
pp. H118-H124 ◽  
Author(s):  
R. C. Koehler ◽  
R. J. Traystman ◽  
M. D. Jones
Keyword(s):  
Skeletal Muscle ◽  
Carbon Monoxide ◽  
Blood Flow ◽  
Small Intestine ◽  
Regional Blood Flow ◽  
Hypoxic Hypoxia ◽  
Age Group ◽  
Lung Inflation ◽  
Adult Sheep ◽  
O2 Transport

We compared regional blood flow in unanesthetized newborn lambs with that in adult sheep during acute, isocapnic hypoxic hypoxia [HH, 40-50% reduction of arterial O2 content (CaO2)]. The HH response in lambs and adults was qualitatively similar in heart, brain, and skeletal muscle, where flow increased; and in spleen, where it decreased. The response differed in skin and kidney, where flow decreased in lambs and was unchanged in adults, and in small intestine, where it was unchanged in lambs and increased in adults. Thus vasoconstriction during HH was less prominent in skin, kidney, and small intestine in adults. However, the trend toward lesser vasoconstriction in the adult cannot be attributed to a diminishing carotid chemoreflex and/or a more prominent vasodilatory lung inflation reflex because the same trend occurred during carbon monoxide hypoxia (COH). COH reduces CaO2 but stimulates neither the carotid chemoreflex nor, since hyperpnea is absent, the lung inflation reflex. Within each age group the responses to COH and HH were qualitatively the same. These data therefore provide no evidence for an active carotid chemoreflex in unanesthetized postnatal sheep. This is either because the peripheral circulatory effect of the chemoreflex is suppressed by the lung inflation reflex or, less likely, because the chemoreflex does not operate in the sheep at this level of HH.

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