Effects of hyperoxia on leg blood flow and metabolism during exercise

1977 ◽  
Vol 42 (3) ◽  
pp. 385-390 ◽  
Author(s):  
H. G. Welch ◽  
F. Bonde-Petersen ◽  
T. Graham ◽  
K. Klausen ◽  
N. Secher
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Aerobic Capacity ◽  
Power Output ◽  
Limb Blood Flow ◽  
O2 Uptake ◽  
Maximal Aerobic Capacity ◽  
Leg Blood Flow ◽  
O2 Delivery

These experiments were designed to investigate the effects of O2 breathing on limb blood flow and metabolism during exercise. Six subjects took part in the study. Four subjects breathed air or 100% O2 while pedaling a Krogh bicycle at 150 W (55–70% of maximal aerobic capacity). Two subjects breathed either 60% or 100% O2 while working at a power output at or slightly in excess of their maximal aerobic capacities. The major findings of the study were 1) leg blood flow is reduced during exercise when comparing hyperoxia with normoxia; 2) VO2 of the exercising limb is not different during hyperoxia; 3) O2 delivery to the leg (the product of blood flow and arteriovenous O2 difference) is not significantly different in the two conditions; and 4) blood pressure is not markedly affected in the experiments at 150 W. Since BP was not different during hyperoxia, at a time when flow was reduced by 11%, this suggests an increased resistance to flow in the exercising limb. In general, these findings are consistent with those reported for the in situ dog muscle but are at variance with results of experiments with humans, especially the reports indicating substantial increases in O2 uptake during hypertoxic conditions.

Muscle maximal O2 uptake at constant O2 delivery with and without CO in the blood

1990 ◽  
Vol 69 (3) ◽  
pp. 830-836 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
A. T. Gray ◽  
P. D. Wagner ◽  
J. B. West ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Hemoglobin Concentration ◽  
O2 Uptake ◽  
Isometric Twitch ◽  
O2 Delivery ◽  
Arterial Po2 ◽  
O2 Dissociation Curve ◽  
Total Hemoglobin Concentration

In the present study we investigated the effects of carboxyhemoglobinemia (HbCO) on muscle maximal O2 uptake (VO2max) during hypoxia. O2 uptake (VO2) was measured in isolated in situ canine gastrocnemius (n = 12) working maximally (isometric twitch contractions at 5 Hz for 3 min). The muscles were pump perfused at identical blood flow, arterial PO2 (PaO2) and total hemoglobin concentration [( Hb]) with blood containing either 1% (control) or 30% HbCO. In both conditions PaO2 was set at 30 Torr, which produced the same arterial O2 contents, and muscle blood flow was set at 120 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. To minimize CO diffusion into the tissues, perfusion with HbCO-containing blood was limited to the time of the contraction period. VO2max was 8.8 +/- 0.6 (SE) ml.min-1.100 g-1 (n = 12) with hypoxemia alone and was reduced by 26% to 6.5 +/- 0.4 ml.min-1.100 g-1 when HbCO was present (n = 12; P less than 0.01). In both cases, mean muscle effluent venous PO2 (PVO2) was the same (16 +/- 1 Torr). Because PaO2 and PVO2 were the same for both conditions, the mean capillary PO2 (estimate of mean O2 driving pressure) was probably not much different for the two conditions, even though the O2 dissociation curve was shifted to the left by HbCO. Consequently the blood-to-mitochondria O2 diffusive conductance was likely reduced by HbCO.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of [Hb] on blood flow distribution and O2 transport in maximally working skeletal muscle

1995 ◽  
Vol 79 (5) ◽  
pp. 1729-1735 ◽  
Author(s):  
S. S. Kurdak ◽  
B. Grassi ◽  
P. D. Wagner ◽  
M. C. Hogan
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Flow Distribution ◽  
Hemoglobin Concentration ◽  
Related Factor ◽  
Blood Flow Distribution ◽  
O2 Uptake ◽  
Cell Spacing ◽  
O2 Delivery

We investigated whether the reduction in calculated muscle diffusion capacity for O2 (DmO2) previously shown to occur with lowered hemoglobin concentration ([Hb]) perfusion of maximally working muscle is related to changes in the blood flow distribution. If blood flow distribution is altered during low [Hb] conditions, the reduction in the calculated DmO2 may in fact be due to increasing heterogeneity and not to some other hemoglobin-related factor. Color-stained (15-microns-diam) microspheres were injected into the artery supplying maximally working isolated in situ dog gastrocnemius muscle (n = 6) while it was being perfused (flow controlled by pump perfusion) with whole blood at three different levels of [Hb] (14.1 +/- 0.5, 8.9 +/- 0.4, and 5.7 +/- 0.4 (SE) g/100 ml] in a blocked-order design. Muscle blood flow and arterial PO2 were not changed as [Hb] was altered. Maximal O2 uptake (11.8 +/- 1.3, 8.2 +/- 0.8, and 6.0 +/- 0.9 ml.100 g-1 min-1 for those [Hb] values, respectively) and the associated estimate of DmO2 (0.25 +/- 0.03, 0.18 +/- 0.03, and 0.15 +/- 0.03 ml.100 g-1.min-1.Torr-1) declined significantly (P < 0.05) with [Hb]. However, the dispersion of the blood flow distribution did not change significantly and, if anything, indicated less heterogeneity at lower [Hb] (coefficient of variation - 0.52 +/- 0.06, 0.46 +/- 0.05, and 0.43 +/- 0.03). These results suggest that in maximally working canine muscle in situ, when O2 delivery is reduced by lowering [Hb] (at constant blood flow), changes in blood flow distribution play no significant role in the reduction of maximal O2 uptake and calculated DmO2. The apparent increase in the resistance to O2 diffusion (i.e., reduction in the DmO2) during anemia may therefore be a result of increased red blood cell spacing in the capillary, slow chemical off-loading kinetics of O2 from Hb, or some other effect that remains to be determined.

Analysis of oxygen delivery and uptake relationships in the Krogh tissue model

1989 ◽  
Vol 67 (3) ◽  
pp. 1234-1244 ◽  
Author(s):  
P. T. Schumacker ◽  
R. W. Samsel
Keyword(s):  
Blood Flow ◽  
Critical Point ◽  
Real Data ◽  
Whole Body ◽  
O2 Uptake ◽  
Highly Sensitive ◽  
O2 Extraction ◽  
O2 Supply ◽  
Experimental Findings ◽  
O2 Delivery

Normally, tissue O2 uptake (VO2) is set by metabolic activity rather than O2 delivery (QO2 = blood flow X arterial O2 content). However, when QO2 is reduced below a critical level, VO2 becomes limited by O2 supply. Experiments have shown that a similar critical QO2 exists, regardless of whether O2 supply is reduced by progressive anemia, hypoxemia, or reduction in blood flow. This appears inconsistent with the hypothesis that O2 supply limitation must occur by diffusion limitation, since very different mixed venous PO2 values have been seen at the critical point with hypoxic vs. anemic hypoxia. The present study sought to begin clarifying this paradox by studying the theoretical relationship between tissue O2 supply and uptake in the Krogh tissue cylinder model. Steady-state O2 uptake was computed as O2 delivery to tissue representative of whole body was gradually lowered by anemic, hypoxic, or stagnant hypoxia. As diffusion began to limit uptake, the fall in VO2 was computed numerically, yielding a relationship between QO2 and VO2 in both supply-independent and O2 supply-dependent regions. This analysis predicted a similar biphasic relationship between QO2 and VO2 and a linear fall in VO2 at O2 deliveries below a critical point for all three forms of hypoxia, as long as intercapillary distances were less than or equal to 80 microns. However, the analysis also predicted that O2 extraction at the critical point should exceed 90%, whereas real tissues typically extract only 65–75% at that point. When intercapillary distances were larger than approximately 80 microns, critical O2 extraction ratios in the range of 65–75% could be predicted, but the critical point became highly sensitive to the type of hypoxia imposed, contrary to experimental findings. Predicted gas exchange in accord with real data could only be simulated when a postulated 30% functional peripheral O2 shunt (arterial admixture) was combined with a tissue composed of Krogh cylinders with intercapillary distances of less than or equal to 80 microns. The unrealistic efficacy of tissue O2 extraction predicted by the Krogh model (in the absence of postulated shunt) may be a consequence of the assumed homogeneity of tissues, because real tissues exhibit many forms of heterogeneity among capillary units. Alternatively, the failure of the original Krogh model to fully predict tissue O2 supply dependency may arise from basic limitations in the assumptions of that model.

Gastrointestinal blood flow and oxygen consumption in awake newborn piglets: effect of feeding

1983 ◽  
Vol 245 (5) ◽  
pp. G697-G702 ◽  
Author(s):  
P. T. Nowicki ◽  
B. S. Stonestreet ◽  
N. B. Hansen ◽  
A. C. Yao ◽  
W. Oh
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
O2 Consumption ◽  
Gi Tract ◽  
Local Blood Flow ◽  
O2 Uptake ◽  
O2 Extraction ◽  
Gastrointestinal Blood Flow ◽  
O2 Delivery ◽  
Effect Of Feeding

Regional and total gastrointestinal (GI) blood flow, O2 delivery, and whole-gut O2 extraction and O2 consumption were measured before and 30, 60, and 120 min after feeding in nonanesthetized, awake 2-day-old piglets. Cardiac output and blood flow to kidneys, heart, brain, and liver were also determined. Blood flow was measured using the radiolabeled microsphere technique. In the preprandial condition, total GI blood flow was 106 +/- 9 ml X min-1 X 100 g-1, while O2 extraction was 17.2 +/- 0.9% and O2 consumption was 1.99 +/- 0.19 ml O2 X min-1 X 100 g-1. Thirty minutes after slow gavage feeding with 30 ml/kg artificial pig milk, O2 delivery to the GI tract and O2 extraction rose significantly (P less than 0.05) by 35 +/- 2 and 33 +/- 2%, respectively. The increase in O2 delivery was effected by a significant increase in GI blood flow, which was localized to the mucosal-submucosal layer of the small intestine. O2 uptake by the GI tract increased 72 +/- 4% 30 min after feeding. Cardiac output and blood flow to non-GI organs did not change significantly with feeding, whereas arterial hepatic blood flow decreased significantly 60 and 120 min after feeding. The piglet GI tract thus meets the oxidative demands of digestion and absorption by increasing local blood flow and tissue O2 extraction.

Oxygen transport to exercising leg in chronic hypoxia

1988 ◽  
Vol 65 (6) ◽  
pp. 2592-2597 ◽  
Author(s):  
P. R. Bender ◽  
B. M. Groves ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
S. Y. Huang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sea Level ◽  
Chronic Hypoxia ◽  
Peripheral Resistance ◽  
Hemoglobin Concentration ◽  
Barometric Pressure ◽  
Ambient Air ◽  
Leg Blood Flow ◽  
State Cycle ◽  
O2 Delivery

Residence at high altitude could be accompanied by adaptations that alter the mechanisms of O2 delivery to exercising muscle. Seven sea level resident males, aged 22 +/- 1 yr, performed moderate to near-maximal steady-state cycle exercise at sea level in normoxia [inspired PO2 (PIO2) 150 Torr] and acute hypobaric hypoxia (barometric pressure, 445 Torr; PIO2, 83 Torr), and after 18 days' residence on Pikes Peak (4,300 m) while breathing ambient air (PIO2, 86 Torr) and air similar to that at sea level (35% O2, PIO2, 144 Torr). In both hypoxia and normoxia, after acclimatization the femoral arterial-iliac venous O2 content difference, hemoglobin concentration, and arterial O2 content, were higher than before acclimatization, but the venous PO2 (PVO2) was unchanged. Thermodilution leg blood flow was lower but calculated arterial O2 delivery and leg VO2 similar in hypoxia after vs. before acclimatization. Mean arterial pressure (MAP) and total peripheral resistance in hypoxia were greater after, than before, acclimatization. We concluded that acclimatization did not increase O2 delivery but rather maintained delivery via increased arterial oxygenation and decreased leg blood flow. The maintenance of PVO2 and the higher MAP after acclimatization suggested matching of O2 delivery to tissue O2 demands, with vasoconstriction possibly contributing to the decreased flow.

Right and left ventricular O2 uptake during hemodilution and beta-adrenergic stimulation

1993 ◽  
Vol 265 (5) ◽  
pp. H1769-H1777 ◽  
Author(s):  
G. J. Crystal ◽  
S. J. Kim ◽  
M. R. Salem
Keyword(s):  
Blood Flow ◽  
Blood Cells ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
O2 Uptake ◽  
Isovolemic Hemodilution ◽  
Content Difference ◽  
O2 Extraction ◽  
In Series ◽  
O2 Delivery

Myocardial O2 uptake (MVO2) and related variables were compared in right and left ventricles (RV and LV, respectively) during isovolemic hemodilution (HD) alone and combined with isoproterenol (Iso) infusion in 13 isoflurane-anesthetized open-chest dogs. Measurements of myocardial blood flow (MBF) obtained with radioactive microspheres were used to calculate MVO2. Lactate extraction (Lacext) was determined. The study consisted of two experimental series: 1) graded HD (dextran) to hematocrit (Hct) of 10% and 2) Iso (0.1 microgram.kg-1.min-1 iv) during moderate HD (Hct = 18 +/- 1%). In series 1, arteriovenous O2 content difference in both ventricles decreased in parallel with reduced arterial O2 content caused by HD, i.e., percent O2 extraction was constant; MVO2 was maintained by proportional increases in MBF. In series 2, Iso during moderate HD raised MVO2 (RV, +156%; LV, +80%). Higher MVO2 was satisfied by combination of increased MBF and O2 extraction in RV and by increased MBF alone in LV. Lacext remained consistent with adequate myocardial O2 delivery throughout study. Conclusions were that 1) both RV and LV tolerated extreme HD (Hct = 10%) because blood flow reserves were sufficient to fully compensate for reduced arterial O2 content; 2) significant cardiac reserve was evident during HD, which could be recruited Iso; and 3) because increase in MVO2 in RV caused by Iso in presence of HD was partially satisfied by increased O2 extraction, the absence of augmented O2 extraction during HD alone was not due to impaired release of O2 from diluted red blood cells.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Reduced submaximal leg blood flow after high-intensity aerobic training

2001 ◽  
Vol 91 (6) ◽  
pp. 2619-2627 ◽  
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.

Blood flow elevation increases VO2 maximum during repetitive tetanic contractions of dog muscle in situ

1993 ◽  
Vol 74 (4) ◽  
pp. 1499-1503 ◽  
Author(s):  
W. F. Brechue ◽  
B. T. Ameredes ◽  
G. M. Andrew ◽  
W. N. Stainsby
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Power Production ◽  
Arterial Supply ◽  
O2 Uptake ◽  
Plantaris Muscle ◽  
Control Series ◽  
Flow Through ◽  
Series Of Experiments

Blood flow through the gastrocnemius-plantaris muscle of the dog in situ was increased by a pump in the arterial supply during a 30-min period of 1/s isotonic tetanic contractions. Compared with a control series of experiments with normoxemia and spontaneous flow, the pump increased flow 84%, from 1.51 +/- 0.08 to 2.78 +/- 0.15 ml.g-1.min-1. The perfusion pressure was increased from 125 to 196 mmHg. The pump hyperemia increased maximal O2 uptake (VO2) at 5 min of contractions by 31%, from 8.97 +/- 0.44 to 12.89 +/- 0.30 mumol.g-1.min-1. The extraction was decreased, and venous PO2 (PVO2) was increased. Fatigue, measured as a drop in power production from the highest level at 10 s to 30 min, was 49% during pump hyperemia and 54% in the control conditions. VO2 decreased 30% from the 5-min value to the 30-min value with pump hyperemia and 28% over the same time in the control conditions. At maximal VO2, the ratio VO2/PVO2 was increased by pump hyperemia compared with control conditions, suggesting an increased O2 diffusing conductance of the muscles. We conclude that the elevated perfusion pressure of pump hyperemia increased flow to raise maximal VO2 mainly in areas of the muscle that had restricted flow under control conditions.

Maximal O2 uptake of in situ dog muscle during acute hypoxemia with constant perfusion

1990 ◽  
Vol 69 (2) ◽  
pp. 570-576 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
P. D. Wagner ◽  
J. B. West
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Peripheral Tissue ◽  
Diffusing Capacity ◽  
O2 Uptake ◽  
Lactate Output ◽  
O2 Diffusion ◽  
Arterial Po2 ◽  
Different Levels

We investigated the relationships among maximal O2 uptake (VO2max), effluent venous PO2 (PvO2), and calculated mean capillary PO2 (PCO2) in isolated dog gastrocnemius in situ as arterial PO2 (PaO2) was progressively reduced with muscle blood flow held constant. The hypothesis that VO2max is determined in part by peripheral tissue O2 diffusion predicts proportional declines in VO2max and PCO2 if the diffusing capacity of the muscle remains constant. The inspired O2 fraction was altered in each of six dogs to produce four different levels of PaO2 [22 +/- 2, 29 +/- 1, 38 +/- 1, and 79 +/- 4 (SE) Torr]. Muscle blood flow, with the circulation isolated, was held constant at 122 +/- 15 ml.100 g-1.min-1 while the muscle worked maximally (isometric twitches at 5-7 Hz) at each of the four different values of PaO2. Arterial and venous samples were taken to measure lactate, pH, PO2, PCO2, and muscle VO2. PCO2 was calculated using Fick's law of diffusion and a Bohr integration procedure. VO2max fell progressively (P less than 0.01) with decreasing PaO2. The decline in VO2max was proportional (R = 0.99) to the fall in both muscle PvO2 and calculated PCO2 while the calculated muscle diffusing capacity was not different among the four conditions. Fatigue developed more rapidly with lower PaO2, although lactate output from the muscle was not different among conditions. These results are consistent with the hypothesis that resistance to O2 diffusion in the peripheral tissue may be a principal determinant of VO2max.

O2 delivery to contracting muscle during hypoxic or CO hypoxia

1987 ◽  
Vol 63 (2) ◽  
pp. 726-732 ◽  
Author(s):  
C. E. King ◽  
S. L. Dodd ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Gastrocnemius Muscle ◽  
Dissociation Curve ◽  
Muscle Preparation ◽  
O2 Uptake ◽  
Oxyhemoglobin Dissociation Curve ◽  
O2 Extraction ◽  
O2 Supply ◽  
O2 Delivery ◽  
Oxyhemoglobin Dissociation

The consequences of a decreased O2 supply to a contracting canine gastrocnemius muscle preparation were investigated during two forms of hypoxia: hypoxic hypoxia (HH) (n = 6) and CO hypoxia (COH) (n = 6). Muscle O2 uptake, blood flow, O2 extraction, and developed tension were measured at rest and at 1 twitch/s isometric contractions in normoxia and in hypoxia. No differences were observed between the two groups at rest. During contractions and hypoxia, however, O2 uptake decreased from the normoxic level in the COH group but not in the HH group. Blood flow increased in both groups during hypoxia, but more so in the COH group. O2 extraction increased further with hypoxia (P less than 0.05) during concentrations in the HH group but actually fell (P less than 0.05) in the COH group. The O2 uptake limitation during COH and contractions was associated with a lesser O2 extraction. The leftward shift in the oxyhemoglobin dissociation curve during COH may have impeded tissue O2 extraction. Other factors, however, such as decreased myoglobin function or perfusion heterogeneity must have contributed to the inability to utilize the O2 reserve more fully.

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