Relationship between body and leg VO2 during maximal cycle ergometry

1992 ◽  
Vol 73 (3) ◽  
pp. 1114-1121 ◽  
Author(s):  
D. R. Knight ◽  
D. C. Poole ◽  
W. Schaffartzik ◽  
H. J. Guy ◽  
R. Prediletto ◽  
...  

It is not known whether the asymptotic behavior of whole body O2 consumption (VO2) at maximal work rates (WR) is explained by similar behavior of VO2 in the exercising legs. To resolve this question, simultaneous measurements of body and leg VO2 were made at submaximal and maximal levels of effort breathing normoxic and hypoxic gases in seven trained male cyclists (maximal VO2, 64.7 +/- 2.7 ml O2.min-1.kg-1), each of whom demonstrated a reproducible VO2-WR asymptote during fatiguing incremental cycle ergometry. Left leg blood flow was measured by constant-infusion thermodilution, and total leg VO2 was calculated as the product of twice leg flow and radial arterial-femoral venous O2 concentration difference. The VO2-WR relationships determined at submaximal WR′s were extrapolated to maximal WR as a basis for assessing the body and leg VO2 responses. The differences between measured and extrapolated maximal VO2 were 235 +/- 45 (body) and 203 +/- 70 (leg) ml O2/min (not significantly different). Plateauing of leg VO2 was associated with, and explained by, plateauing of both leg blood flow and O2 extraction and hence of leg VO2. We conclude that the asymptotic behavior of whole body VO2 at maximal WRs is a direct reflection of the VO2 profile at the exercising legs.

1978 ◽  
Vol 45 (6) ◽  
pp. 966-970 ◽  
Author(s):  
S. M. Cain ◽  
C. K. Chapler

The ability of the hind limb to obtain oxygen and maintain its O2 uptake in relation to the whole body during isovolemic hemodilution with dextran was measured in eight anesthetized, paralyzed dogs kept at constant ventilation. Hind limb venous outflow (ankle to upper thigh) was restricted by tourniquets to femoral vein. Hind limb blood flow, O2 uptake (VO2), cardiac output, and total VO2 were measured at normal hematocrit, at hematocrits just above (16%, stage 2) and just below (10%, stage II) that at which total VO2 could be maintained at the control level, and following isovolemic reinfusion of recovered red blood cells (Hct = 23%). VO2 was maintained at the control level in whole body and hind limb during stage I. Total VO2 decreased significantly in stage II (P less than 0.05), whereas limb VO2 did not. Hind limb had a consistently greater extraction ratio for O2 (P less than 0.01) and lower venous oxygen partial pressure than the body as a whole (P less than 0.01). In spite of limitations of O2 delivery by anemia to the point that total O2 demand was not met, there was no redistribution of blood flow away from or decreased demand for O2 by the hind limb, which was mostly skeletal muscle.


1974 ◽  
Vol 82 (1) ◽  
pp. 87-95 ◽  
Author(s):  
E. F. Annison ◽  
R. Bickerstaffe ◽  
J. L. Linzell

SUMMARYThe effects of changing to a high starch: low roughage diet have been studied in two Friesian and two Jersey cows, surgically prepared for the simultaneous study of udder metabolism (arteriovenous difference x udder blood flow) and whole body turnover of milk precursors (isotope dilution).In the Friesian cows milk fat concentration was lower on the high starch diet but in the Jerseys fell only slightly in one animal. In both Friesians and in the one Jersey these changes were accompanied by an increase in total rumen VFA concentration. Rumen acetate concentration did not change but propionate doubled. Thus this confirms that the usually reported fall in ‘acetate:propionate ratio’ is due to a rise in propionate production rather than due to a fall in acetate production.There were significant falls in the blood concentrations of acetate and β-hydroxy-butyrate. The rate of extraction by the udder of acetate and β-hydroxybutyrate did not change but triglyceride extraction fell. Therefore since udder blood flow did not alter the uptake of all three fat precursors fell.The entry rate of glucose into the circulation and its contribution to total body CO2 increased. The entry rate and contribution to CO2 of acetate decreased but this was probably mainly due to a fall in endogenous acetate production by the body tissues. Plasma FFA concentration showed little change but the entry rate of palmitate fell on the high starch diet. There was also an increased proportion of unsaturated and trans fatty acids in the plasma and milk triglycerides.


1989 ◽  
Vol 67 (3) ◽  
pp. 1234-1244 ◽  
Author(s):  
P. T. Schumacker ◽  
R. W. Samsel

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.


2020 ◽  
Author(s):  
Ada Admin ◽  
Solvejg L. Hansen ◽  
Kirstine N. Bojsen-Møller ◽  
Anne-Marie Lundsgaard ◽  
Frederikke L. Hendrich ◽  
...  

Women with polycystic ovary syndrome (PCOS) have been shown to be less insulin sensitive compared with control women, independent of BMI. Training is associated with molecular adaptations in skeletal muscle improving glucose uptake and metabolism in both healthy and type 2 diabetic individuals. In the present study, lean, hyperandrogenic women with PCOS (n=9) and healthy controls (CON, n=9) completed 14 weeks of controlled and supervised exercise training. In CON, the training intervention increased whole body insulin action by 26% and insulin-stimulated leg glucose uptake by 53%, together with increased insulin-stimulated leg blood flow and a more oxidative muscle fiber type distribution. In PCOS, no such changes were found, despite similar training intensity and improvements in maximal oxygen uptake. In skeletal muscle of CON, but not PCOS, training increased GLUT4 and HKII mRNA and protein expressions. These data suggest that the impaired increase in whole body insulin action in women with PCOS with training is caused by an impaired ability to upregulate key glucose handling proteins for insulin-stimulated glucose uptake in skeletal muscle, and insulin-stimulated leg blood flow. Still, other important benefits of exercise training appeared in women with PCOS, including an improvement of the hyperandrogenic state.


1989 ◽  
Vol 257 (6) ◽  
pp. H1812-H1818 ◽  
Author(s):  
G. K. Savard ◽  
E. A. Richter ◽  
S. Strange ◽  
B. Kiens ◽  
N. J. Christensen ◽  
...  

The purpose of this study was to determine the effect of increasing muscle mass involvement in dynamic exercise on both sympathetic nervous activation and local hemodynamic variables of individual active and inactive skeletal muscle groups. Six male subjects performed 15-min bouts of one-legged knee extension either alone or in combination with the knee extensors of the other leg and/or with the arms. The range of work intensities varied between 24 and 71% (mean) of subjects' maximal aerobic capacity (% VO2max). Leg blood flow, measured in the femoral vein by thermodilution, was determined in both legs. Arterial and venous plasma concentrations of norepinephrine (NE) and epinephrine were analyzed, and the calculated NE spillover was used as an index of sympathetic nervous activity to the limb. NE spillover increased gradually both in the resting, and to a larger extent in the exercising legs, with a steeper rise occurring approximately 70% VO2max. These increases were not associated with any significant changes in leg blood flow or leg vascular conductance at the exercise intensities examined. These results suggest that, as the total active muscle mass increases, the rise in sympathetic nervous activity to skeletal muscle, either resting or working at a constant load, is not associated with any significant neurogenic vasoconstriction and reduction in flow or conductance through the muscle vascular bed, during whole body exercise demanding up to 71% VO2max.


1984 ◽  
Vol 62 (7) ◽  
pp. 769-774 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain ◽  
C. K. Chapler

To compare with earlier studies of anemic hypoxia obtained by hemodilution, O2 carring capacity was decreased by carbon monoxide (CO) hypoxia. Arterial O2 content was reduced either 50% (moderate CO) or 65% (severe CO). In two groups of anesthetized dogs (moderate and severe CO) hindlimb innervation remained intact while in a third group (moderate CO) the hindlimb was denervated. Measurements were obtained prior to and at 30 and 60 min of CO hypoxia. Cardiac output was elevated at 30 min of CO hypoxia in all groups (p < 0.01) and in the severe CO group at 60 min (p < 0.01). Hindlimb blood flow remained unchanged during CO hypoxia in the intact groups. In the denervated group, hindlimb blood flow was greater (p < 0.05) than that in the intact groups throughout the experiment. A decrease in mean arterial pressure (p < 0.01) in all groups was associated with a fall in total resistance (p < 0.01). Hindlimb resistance remained unchanged during moderate CO hypoxia in the intact group but increased (p < 0.05) in the denervated group. In the severe CO group hindlimb resistance was decreased (p < 0.05) at 60 min. The results indicate that the increase in cardiac output during CO hypoxia was directed to nonmuscle areas of the body and that intact sympathetic innervation was required to achieve this redistribution.


2016 ◽  
Vol 48 ◽  
pp. 1010
Author(s):  
Salvador J. Jaime ◽  
Stacey Alvarez-Alvarado ◽  
Joy L. Post ◽  
Arturo Figueroa

1994 ◽  
Vol 77 (2) ◽  
pp. 653-659 ◽  
Author(s):  
M. E. Ward ◽  
H. Chang ◽  
F. Erice ◽  
S. N. Hussain

When tissue O2 delivery falls below a critical threshold, tissue O2 uptake (VO2) becomes limited. We compared critical O2 delivery and critical and maximum O2 extraction ratios of the resting and contracting left hemidiaphragm with those of nondiaphragmatic tissues in seven dogs. The left hemidiaphragm was perfused through the left inferior phrenic artery with blood from the left femoral artery. Phrenic venous blood was sampled through a catheter in the inferior phrenic vein. Systemic O2 delivery was reduced in stages by controlled hemorrhage. Left diaphragmatic VO2 during rest and during 3 min of continuous stimulation (3 Hz) of the left phrenic nerve and VO2 of the remaining nonleft hemidiaphragmatic tissues were measured at each stage. Critical diaphragmatic O2 delivery for the resting diaphragm averaged 0.8 +/- 0.16 ml.min-1.100 g-1 with a critical O2 extraction ratio of 65.5 +/- 6%. In the contracting diaphragm, they averaged 5.1 +/- 0.9 ml.min-1.100 g-1 and 81 +/- 5%, respectively. Whole body O2 delivery at which resting diaphragmatic VO2 became supply limited was similar to that for nondiaphragmatic tissues. By comparison, supply limitation of VO2 occurred at a higher systemic O2 delivery in the contracting diaphragm than in the rest of the body despite the increase in critical diaphragmatic extraction ratio. Thus, oxygenation of the isolated diaphragm does not appear to be preferentially preserved during generalized reductions in O2 delivery. These results suggest that, in diseases associated with increased work of breathing and decreased O2 delivery, the diaphragm may become metabolically impaired before limitation of VO2 is observed systemically.


1986 ◽  
Vol 64 (1) ◽  
pp. 7-12 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain

The mechanisms by which the body attempts to avoid tissue hypoxia when total body oxygen delivery is compromised during acute anemia are reviewed. When the hematocrit is reduced by isovolemic hemodilution the compensatory adjustments include an increase in cardiac output, redistribution of blood flow to some tissues, and an increase in the whole body oxygen extraction ratio. These responses permit whole body oxygen uptake to be maintained until the hematocrit has been lowered to about 10%. Several factors are discussed which contribute to the increase in cardiac output during acute anemia including the reduction in blood viscosity, sympathetic innervation of the heart, and increased venomotor tone. The latter has been shown to be dependent on intact aortic chemoreceptors. With respect to peripheral vascular responses, the rise in coronary and cerebral blood flows which occur following hemodilution is proportionally greater than the increase in cardiac output while the opposite is true for kidney, liver, spleen, and intestine. Skeletal muscle does not contribute to a redistribution of blood flow to more vital areas during acute anemia despite its relatively large anaerobic capacity. Overall, peripheral compensatory adjustments result in an increased oxygen extraction ratio during acute anemia which reflects a better matching of the limited oxygen supply to tissue oxygen demands. However, some areas such as muscle are relatively overperfused which limits an even more efficient utilization of the reduced oxygen supply. Studies of the response of the microcirculation and the extent to which sympathetic vascular controls are involved in peripheral blood flow regulation are necessary to further appreciate the complex pattern of physiological responses which help ensure survival of the organism during acute anemia.


1986 ◽  
Vol 251 (5) ◽  
pp. H1038-H1044 ◽  
Author(s):  
L. B. Rowell ◽  
B. Saltin ◽  
B. Kiens ◽  
N. J. Christensen

Blood flow (Q) to quadriceps muscles was measured by thermal dilution in six men during rest and dynamic exercise [20, 38, and 42.5-60 W (peak load)] restricted to quadriceps of one leg in normoxia (N) and hypoxemia (H; 10-11% O2). Without exception Q and quadriceps vascular conductance were higher in H. Arterial mean pressure, lactate, norepinephrine, and epinephrine all rose when work exceeded 20 W. Q in N was 0.25, 3.28, 4.27, and 5.81 l/min (rest to peak exercise) and in H was 0.25, 4.08, 5.24, and 6.58 l/min. Peak Q per 100 grams of muscle (quadriceps mass = 2.2 kg) was 273.3 (N) and 308.8 ml/min (H). Quadriceps VO2 (Q X femoral A-VO2 difference) was 25, 388, 556, and 771 ml/min (N) and 25, 390, 556, and 743 (lower peak load in H)-net mechanical efficiency was 23%. Muscle O2 delivery (Q X arterial O2 content) was unaffected by H; O2 extraction fell in H but femoral venous O2 content remained near 6 (N) and 5 ml/100 ml (H) at all workloads, in contrast to much lower values in whole body exercise. In H muscle Q can rise to even higher peak values, without apparent limit, when the mass of active muscle is too small to overwhelm the pumping capacity of the heart.


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