Model of oxygen transport and metabolism predicts effect of hyperoxia on canine muscle oxygen uptake dynamics

2007 ◽  
Vol 103 (4) ◽  
pp. 1366-1378 ◽  
Author(s):  
Nicola Lai ◽  
Gerald M. Saidel ◽  
Bruno Grassi ◽  
L. Bruce Gladden ◽  
Marco E. Cabrera
Keyword(s):  
Experimental Data ◽  
Oxygen Uptake ◽  
Oxygen Content ◽  
Oxygen Transport ◽  
Mechanistic Model ◽  
Arterial Oxygen ◽  
Cellular Respiration ◽  
Arterial Oxygen Content ◽  
Muscle Oxygen ◽  
Muscle Oxygen Uptake

Previous studies have shown that increased oxygen delivery, via increased convection or arterial oxygen content, does not speed the dynamics of oxygen uptake, V̇o2m, in dog muscle electrically stimulated at a submaximal metabolic rate. However, the dynamics of transport and metabolic processes that occur within working muscle in situ is typically unavailable in this experimental setting. To investigate factors affecting V̇o2m dynamics at contraction onset, we combined dynamic experimental data across working muscle with a mechanistic model of oxygen transport and metabolism in muscle. The model is based on dynamic mass balances for O2, ATP, and PCr. Model equations account for changes in cellular ATPase, oxidative phosphorylation, and creatine kinase fluxes in skeletal muscle during exercise, and cellular respiration depends on [ADP] and [O2]. Model simulations were conducted at different levels of arterial oxygen content and blood flow to quantify the effects of convection and diffusion of oxygen on the regulation of cellular respiration during step transitions from rest to isometric contraction in dog gastrocnemius muscle. Simulations of arteriovenous O2 differences and V̇o2m dynamics were successfully compared with experimental data (Grassi B, Gladden LB, Samaja M, Stary CM, Hogan MC. J Appl Physiol 85: 1394–1403, 1998; and Grassi B, Gladden LB, Stary CM, Wagner PD, Hogan MC. J Appl Physiol 85: 1404–1412, 1998), thus demonstrating the validity of the model, as well as its predictive capability. The main findings of this study are: 1) the estimated dynamic response of oxygen utilization at contraction onset in muscle is faster than that of oxygen uptake; and 2) hyperoxia does not accelerate the dynamics of diffusion and consequently muscle oxygen uptake at contraction onset due to the hyperoxia-induced increase in oxygen stores. These in silico derived results cannot be obtained from experimental observations alone.

Heliox increases quadriceps muscle oxygen delivery during exercise in COPD patients with and without dynamic hyperinflation

2012 ◽  
Vol 113 (7) ◽  
pp. 1012-1023 ◽  
Author(s):  
Zafeiris Louvaris ◽  
Spyros Zakynthinos ◽  
Andrea Aliverti ◽  
Helmut Habazettl ◽  
Maroula Vasilopoulou ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Content ◽  
Oxygen Delivery ◽  
Quadriceps Muscle ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Muscle Oxygen ◽  
Peripheral Muscle ◽  
Copd Patients ◽  
Gastric Pressure

Some reports suggest that heliox breathing during exercise may improve peripheral muscle oxygen availability in patients with chronic obstructive pulmonary disease (COPD). Besides COPD patients who dynamically hyperinflate during exercise (hyperinflators), there are patients who do not hyperinflate (non-hyperinflators). As heliox breathing may differently affect cardiac output in hyperinflators (by increasing preload and decreasing afterload of both ventricles) and non-hyperinflators (by increasing venous return) during exercise, it was reasoned that heliox administration would improve peripheral muscle oxygen delivery possibly by different mechanisms in those two COPD categories. Chest wall volume and respiratory muscle activity were determined during constant-load exercise at 75% peak capacity to exhaustion, while breathing room air or normoxic heliox in 17 COPD patients: 9 hyperinflators (forced expiratory volume in 1 s = 39 ± 5% predicted), and 8 non-hyperinflators (forced expiratory volume in 1 s = 48 ± 5% predicted). Quadriceps muscle blood flow was measured by near-infrared spectroscopy using indocyanine green dye. Hyperinflators and non-hyperinflators demonstrated comparable improvements in endurance time during heliox (231 ± 23 and 257 ± 28 s, respectively). At exhaustion in room air, expiratory muscle activity (expressed by peak-expiratory gastric pressure) was lower in hyperinflators than in non-hyperinflators. In hyperinflators, heliox reduced end-expiratory chest wall volume and diaphragmatic activity, and increased arterial oxygen content (by 17.8 ± 2.5 ml/l), whereas, in non-hyperinflators, heliox reduced peak-expiratory gastric pressure and increased systemic vascular conductance (by 11.0 ± 2.8 ml·min−1·mmHg−1). Quadriceps muscle blood flow and oxygen delivery significantly improved during heliox compared with room air by a comparable magnitude (in hyperinflators by 6.1 ± 1.3 ml·min−1·100 g−1 and 1.3 ± 0.3 ml O2·min−1·100 g−1, and in non-hyperinflators by 7.2 ± 1.6 ml·min−1·100 g−1 and 1.6 ± 0.3 ml O2·min−1·100 g−1, respectively). Despite similar increase in locomotor muscle oxygen delivery with heliox in both groups, the mechanisms of such improvements were different: 1) in hyperinflators, heliox increased arterial oxygen content and quadriceps blood flow at similar cardiac output, whereas 2) in non-hyperinflators, heliox improved central hemodynamics and increased systemic vascular conductance and quadriceps blood flow at similar arterial oxygen content.

O2 Content and Pao2

PEDIATRICS ◽  
1974 ◽  
Vol 53 (5) ◽  
pp. 769-770
Author(s):  
Douglas D. Mair
Keyword(s):  
Oxygen Uptake ◽  
Oxygen Content ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Letter To The Editor ◽  
Oxygen Capacity ◽  
Fundamental Error

The April 1973 issue of Pediatrics contained a Letter to the Editor from Gerald B. Merenstein, M.D. In his letter, Dr. Merenstein was guilty of a fundamental error in the understanding of the mechanism of oxygen uptake by the tissues. Because this misconception is not uncommon, I believe that the topic deserves comment. Dr. Merenstein compared systemic arterial oxygen content of two neonates in a hypothetical example (he referred to oxygen content as oxygen capacity, but this error is relatively unimportant). His illustration was as follows:

Muscle oxygen kinetics at onset of intense dynamic exercise in humans

2000 ◽  
Vol 279 (3) ◽  
pp. R899-R906 ◽  
Author(s):  
J. Bangsbo ◽  
P. Krustrup ◽  
J. González-Alonso ◽  
R. Boushel ◽  
B. Saltin
Keyword(s):  
Oxygen Uptake ◽  
Initial Phase ◽  
Mean Transit Time ◽  
Oxygen Availability ◽  
Arterial Oxygen ◽  
Intense Exercise ◽  
Oxygen Utilization ◽  
Arterial Oxygen Content ◽  
Muscle Oxygen ◽  
Exercise In Humans

The present study examined the onset and the rate of rise of muscle oxidation during intense exercise in humans and whether oxygen availability limits muscle oxygen uptake in the initial phase of intense exercise. Six subjects performed 3 min of intense one-legged knee-extensor exercise [65.3 ± 3.7 (means ± SE) W]. The femoral arteriovenous blood mean transit time (MTT) and time from femoral artery to muscle microcirculation was determined to allow for an examination of the oxygen uptake at capillary level. MTT was 15.3 ± 1.8 s immediately before exercise, 10.4 ± 0.7 s after 6 s of exercise, and 4.7 ± 0.5 s at the end of exercise. Arterial venous O2 difference (a-vdiff O2) of 18 ± 5 ml/l before the exercise was unchanged after 2 s, but it increased ( P < 0.05) after 6 s of exercise to 43 ± 10 ml/l and reached 146 ± 4 ml/l at the end of exercise. Thigh oxygen uptake increased ( P < 0.05) from 32 ± 8 to 102 ± 28 ml/min after 6 s of exercise and to 789 ± 88 ml/min at the end of exercise. The time to reach half-peak a-vdiff O2 and thigh oxygen uptake was 13 ± 2 and 25 ± 3 s, respectively. The difference between thigh oxygen delivery (blood flow × arterial oxygen content) and thigh oxygen uptake increased ( P < 0.05) after 6 s and returned to preexercise level after 14 s. The present data suggest that, at the onset of exercise, oxygen uptake of the exercising muscles increases after a delay of only a few seconds, and oxygen extraction peaks after ∼50 s of exercise. The limited oxygen utilization in the initial phase of intense exercise is not caused by insufficient oxygen availability.

Effect of mild carboxy-hemoglobin on exercising skeletal muscle: intravascular and intracellular evidence

2002 ◽  
Vol 283 (5) ◽  
pp. R1131-R1139 ◽  
Author(s):  
R. S. Richardson ◽  
E. A. Noyszewski ◽  
B. Saltin ◽  
J. González-Alonso
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Muscle Oxygen ◽  
Progressive Exercise ◽  
Maximum Work ◽  
Young Subjects

We studied muscle blood flow, muscle oxygen uptake (V˙o 2), net muscle CO uptake, Mb saturation, and intracellular bioenergetics during incremental single leg knee-extensor exercise in five healthy young subjects in conditions of normoxia, hypoxia (H; 11% O2), normoxia + CO (COnorm), and 100% O2+ CO (COhyper). Maximum work rates and maximal oxygen uptake (V˙o 2 max) were equally reduced by ≈14% in H, COnorm, and COhyper. The reduction in arterial oxygen content (CaO2 ) (≈20%) resulted in an elevated blood flow (Q) in the CO and H trials. Net muscle CO uptake was attenuated in the CO trials. Suprasystolic cuff measurements of the deoxy-Mb signal were not different in terms of the rate of signal rise or maximum signal attained with and without CO. At maximal exercise, calculated mean capillary Po 2 was most reduced in H and resulted in the lowest Mb-associated Po 2. Reductions in ATP, PCr, and pH during H, COnorm, and COhyper occurred earlier during progressive exercise than in normoxia. Thus the effects of reduced CaO2 due to mild CO poisoning are similar to H.

Blood flow to fetal organs as a function of arterial oxygen content

1979 ◽  
Vol 135 (5) ◽  
pp. 637-646 ◽  
Author(s):  
Louis L.H. Peeters ◽  
Roger E. Sheldon ◽  
M. Douglas Jones ◽  
Edgar L. Makowski ◽  
Giacomo Meschia
Keyword(s):  
Blood Flow ◽  
Oxygen Content ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Fetal Organs

Cardiovascular and Respiratory Changes During Heat Stress in Rainbow Trout (Salmo Gairdneri)

1973 ◽  
Vol 59 (2) ◽  
pp. 323-338 ◽  
Author(s):  
ALAN G. HEATH ◽  
G. M. HUGHES
Keyword(s):  
Oxygen Content ◽  
Oxygen Demand ◽  
Heart Beat ◽  
Arterial Oxygen ◽  
Salmo Gairdneri ◽  
Steady Increase ◽  
Limiting Factor ◽  
Arterial Oxygen Content ◽  
Ventilatory Frequency ◽  
Increasing Temperature

1. Trout were subjected to a steady increase in water temperature (1.5 °C/h) from 15 °C until death occurred, while several respiratory and cardiovascular parameters were monitored. 2. Oxygen consumption increased during the warming (Q10 = 2.35 between 16 and 20 °C). At the higher temperatures the increase was more marked (Q10 =4.96 between 20 and 26 °C). 3. Ventilatory frequency increased during the rising temperature with a general levelling off observed above 23 °C. The amplitude of the pressure changes in the buccal and opercular cavities increased more than did the ventilatory frequency. Further analysis of the differential pressure across the gills suggests that the adjustment of respiratory pumping to the increased oxygen demand is predominantly in the volume pumped per stroke (cycle). 4. Heart rate rose steadily with the increasing temperature until about 24-25 °C, when a bradycardia usually became evident. Synchrony between the heart beat and the respiratory pumps was observed in some preparations at the higher temperatures. 5. Blood pressure increases during the warming were more marked in the ventral aorta than in the dorsal aorta. At the highest temperatures, abnormal cardiac cycles were frequently observed. 6. Arterial oxygen content declined slightly during warming and venous oxygen content dropped to zero above 23 °C. 7. It is suggested that cardiovascular adjustments may be a limiting factor in this type of stress.

scholarly journals Effects of Hematocrit Variations on Cerebral Blood Flow and Oxygen Transport in Ischemic Cerebrovascular Disease

1981 ◽  
Vol 1 (4) ◽  
pp. 413-417 ◽  
Author(s):  
Masahito Kusunoki ◽  
Kazufumi Kimura ◽  
Masaichi Nakamura ◽  
Yoshinari Isaka ◽  
Shotaro Yoneda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Disease ◽  
Oxygen Transport ◽  
Oxygen Delivery ◽  
Inverse Correlation ◽  
Arterial Oxygen ◽  
Brain Oxygenation ◽  
Arterial Oxygen Content ◽  
Ischemic Cerebrovascular Disease

The contribution of hematocrit (Ht) changes on cerebral blood flow (CBF) and brain oxygenation in ischemic cerebrovascular disease is still controversial. In the present study, effects of Ht variations on CBF and oxygen delivery were investigated in patients with ischemic cerebrovascular disease. CBF was measured by the Xe-133 intracarotid injection method in 27 patients, whose diagnoses included completed stroke, reversible ischemic neurological deficit, and transient ischemic attack. Ht values in the patients ranged from 31 to 53%. There was a significant inverse correlation between CBF and Ht in these Ht ranges. Oxygen delivery, i.e., the product of arterial oxygen content and CBF, increased with Ht elevation and reached the maximum level in the Ht range of 40–45% and then declined. The CBF-Ht and oxygen transport-Ht relations observed in our study were similar to those in the glass-tube model studies by other workers rather than to those in intact animal experiments. From these results, it is conceivable that in ischemic cerebrovascular disease, the vasomotor adjustment was impaired in such a manner that the relations among Ht, CBF, and oxygen delivery were different from those in healthy subjects. Further, an “optimal hematocrit” for brain oxygenation was also discussed.

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