Microvascular O2 delivery and O2 utilization during metabolic transitions in skeletal muscle. One-hundred years after the pioneering work by August Krogh

2021 ◽  
Vol 252 ◽  
pp. 110842 ◽  
Author(s):  
Bruno Grassi ◽  
Michael C. Hogan ◽  
L. Bruce Gladden
Keyword(s):  
Skeletal Muscle ◽  
O2 Delivery

Continued divergence in V̇o2 max of rats artificially selected for running endurance is mediated by greater convective blood O2 delivery

2006 ◽  
Vol 101 (5) ◽  
pp. 1288-1296 ◽  
Author(s):  
Norberto C. Gonzalez ◽  
Scott D. Kirkton ◽  
Richard A. Howlett ◽  
Steven L. Britton ◽  
Lauren G. Koch ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Stroke Volume ◽  
High Capacity ◽  
Female Rats ◽  
O2 Delivery ◽  
Seven Generations ◽  
Cardiopulmonary System ◽  
Hypoxic Exercise ◽  
Selection Of

We previously showed that after seven generations of artificial selection of rats for running capacity, maximal O2 uptake (V̇o2 max) was 12% greater in high-capacity (HCR) than in low-capacity runners (LCR). This difference was due exclusively to a greater O2 uptake and utilization by skeletal muscle of HCR, without differences between lines in convective O2 delivery to muscle by the cardiopulmonary system (Q̇o2 max). The present study in generation 15 (G15) female rats tested the hypothesis that continuing improvement in skeletal muscle O2 transfer must be accompanied by augmentation in Q̇o2 max to support V̇o2 max of HCR. Systemic O2 transport was studied during maximal normoxic and hypoxic exercise (inspired Po2 ∼70 Torr). V̇o2 max divergence between lines increased because of both improvement in HCR and deterioration in LCR: normoxic V̇o2 max was 50% higher in HCR than LCR. The greater V̇o2 max in HCR was accompanied by a 41% increase in Q̇o2 max: 96.1 ± 4.0 in HCR vs. 68.1 ± 2.5 ml stpd O2·min−1·kg−1 in LCR ( P < 0.01) during normoxia. The greater G15 Q̇o2 max of HCR was due to a 48% greater stroke volume than LCR. Although tissue O2 diffusive conductance continued to increase in HCR, tissue O2 extraction was not significantly different from LCR at G15, because of the offsetting effect of greater HCR blood flow on tissue O2 extraction. These results indicate that continuing divergence in V̇o2 max between lines occurs largely as a consequence of changes in the capacity to deliver O2 to the exercising muscle.

MUSCLE METABOREFLEX INCREASES O2 DELIVERY TO ISCHEMIC ACTIVE SKELETAL MUSCLE.

1999 ◽  
Vol 31 (Supplement) ◽  
pp. S225
Author(s):  
D. S. O'Leary ◽  
R. A. Augustyniak ◽  
E. J. Ansorge ◽  
H. L. Collins
Keyword(s):  
Skeletal Muscle ◽  
Muscle Metaboreflex ◽  
O2 Delivery

HYPOVOLEMIC HYPOTENSION ALTERS THE DYNAMIC BALANCE BETWEEN O2 DELIVERY AND UTILIZATION IN CONTRACTING SKELETAL MUSCLE

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S309 ◽  
Author(s):  
K D. Ross ◽  
L A. Abbo ◽  
B J. Behnke ◽  
D J. Padilla ◽  
T I. Musch ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Dynamic Balance ◽  
O2 Delivery ◽  
Hypovolemic Hypotension

Skeletal muscle metabolic recovery following submaximal exercise in chronic heart failure is limited more by O2 delivery than O2 utilization

2010 ◽  
Vol 118 (3) ◽  
pp. 203-210 ◽  
Author(s):  
Hareld M.C. Kemps ◽  
Jeanine J. Prompers ◽  
Bart Wessels ◽  
Wouter R. De Vries ◽  
Maria L. Zonderland ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Submaximal Exercise ◽  
Daily Activities ◽  
Control Group ◽  
Resonance Spectroscopy ◽  
Post Exercise ◽  
Metabolic Recovery ◽  
O2 Delivery

CHF (chronic heart failure) is associated with a prolonged recovery of skeletal muscle energy stores following submaximal exercise, limiting the ability to perform repetitive daily activities. However, the pathophysiological background of this impairment is not well established. The aim of the present study was to investigate whether muscle metabolic recovery following submaximal exercise in patients with CHF is limited by O2 delivery or O2 utilization. A total of 13 stable CHF patients (New York Heart Association classes II–III) and eight healthy subjects, matched for age and BMI (body mass index), were included. All subjects performed repetitive submaximal dynamic single leg extensions in the supine position. Post-exercise PCr (phosphocreatine) resynthesis was assessed by 31P-MRS (magnetic resonance spectroscopy). NIRS (near-IR spectroscopy) was applied simultaneously, using the rate of decrease in HHb (deoxygenated haemoglobin) as an index of post-exercise muscle re-oxygenation. As expected, PCr recovery was slower in CHF patients than in control subjects (time constant, 47±10 compared with 35±12 s respectively; P=0.04). HHb recovery kinetics were also prolonged in CHF patients (mean response time, 74±41 compared with 44±17 s respectively; P=0.04). In the patient group, HHb recovery kinetics were slower than PCr recovery kinetics (P=0.02), whereas no difference existed in the control group (P=0.32). In conclusion, prolonged metabolic recovery in CHF patients is associated with an even slower muscle tissue re-oxygenation, indicating a lower O2 delivery relative to metabolic demands. Therefore we postulate that the impaired ability to perform repetitive daily activities in these patients depends more on a reduced muscle blood flow than on limitations in O2 utilization.

scholarly journals Distinguishing the effects of convective and diffusive O2 delivery on V̇o2 on-kinetics in skeletal muscle contracting at moderate intensity

2013 ◽  
Vol 305 (5) ◽  
pp. R512-R521 ◽  
Author(s):  
Jessica Spires ◽  
L. Bruce Gladden ◽  
Bruno Grassi ◽  
Matthew L. Goodwin ◽  
Gerald M. Saidel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Demand ◽  
Experimental Studies ◽  
Moderate Intensity ◽  
Oxygen Utilization ◽  
Muscle Oxygen ◽  
Mean Response Time ◽  
Convective Oxygen Delivery ◽  
Dynamics Simulations ◽  
O2 Delivery

With current techniques, experimental measurements alone cannot characterize the effects of oxygen blood-tissue diffusion on muscle oxygen uptake (V̇o2) kinetics in contracting skeletal muscle. To complement experimental studies, a computational model is used to quantitatively distinguish the contributions of convective oxygen delivery, diffusion into cells, and oxygen utilization to V̇o2 kinetics. The model is validated using previously published experimental V̇o2 kinetics in response to slowed blood flow (Q) on-kinetics in canine muscle (τQ = 20 s, 46 s, and 64 s) [Goodwin ML, Hernández A, Lai N, Cabrera ME, Gladden LB. J Appl Physiol. 112:9–19, 2012]. Distinctive effects of permeability-surface area or diffusive conductance ( PS) and Q on V̇o2 kinetics are investigated. Model simulations quantify the relationship between PS and Q, as well as the effects of diffusion associated with PS and Q dynamics on the mean response time of V̇o2. The model indicates that PS and Q are linearly related and that PS increases more with Q when convective delivery is limited by slower Q dynamics. Simulations predict that neither oxygen convective nor diffusive delivery are limiting V̇o2 kinetics in the isolated canine gastrocnemius preparation under normal spontaneous conditions during transitions from rest to moderate (submaximal) energy demand, although both operate close to the tipping point.

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.

Critical O2 delivery to skeletal muscle at high and low PO2 in endotoxemic dogs

1989 ◽  
Vol 66 (6) ◽  
pp. 2553-2558 ◽  
Author(s):  
D. L. Bredle ◽  
R. W. Samsel ◽  
P. T. Schumacker ◽  
S. M. Cain
Keyword(s):  
Skeletal Muscle ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Adult Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
The Body ◽  
O2 Uptake ◽  
O2 Extraction ◽  
O2 Delivery ◽  
Arterial Po2

An ischemic canine limb model was used to determine whether endotoxin reduces the ability of resting skeletal muscle to extract O2 and whether increasing the arterial PO2 would increase its O2 extraction. Isolated limbs were pump perfused via an extracorporeal circuit with membrane oxygenator at three progressively lower flows and PO2 of both 60 and 200 Torr, whereas the rest of the body remained normoxic and normotensive. Six anesthetized, paralyzed dogs were injected with endotoxin (4 mg/kg, ENDO), and another six were controls (CONT). Limb critical O2 delivery was higher (P less than 0.05) in ENDO than CONT (8.3 vs. 6.1 ml.kg-1.min-1). Critical venous PO2 was also higher (P less than 0.05) in ENDO than CONT (38 vs. 30 Torr). Critical O2 extraction ratio was lower (P less than 0.05) in ENDO than CONT (0.60 vs. 0.73). There were no differences in these variables between low and high arterial PO2. We concluded that 1) endotoxin can cause a small but significant O2 extraction defect in skeletal muscle, 2) increasing arterial PO2 did not correct such a defect, nor did it improve O2 uptake in ischemic, but otherwise healthy, muscle, and 3) skeletal muscle may contribute to the peripheral O2 extraction defect in adult respiratory distress syndrome insofar as endotoxin effects model those found in adult respiratory distress syndrome.

Effect of gradual reduction in O2 delivery on intracellular homeostasis in contracting skeletal muscle

1996 ◽  
Vol 80 (4) ◽  
pp. 1313-1321 ◽  
Author(s):  
M. C. Hogan ◽  
S. S. Kurdak ◽  
P. G. Arthur
Keyword(s):  
Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Force Production ◽  
Tight Coupling ◽  
Gradual Reduction ◽  
Force Development ◽  
Atp Supply ◽  
O2 Delivery ◽  
Arterial Po2

This study was designed to investigate 1) whether a protocol employing a gradual reduction in O2 availability to submaximally contracting muscle results in relatively minor disturbances in intracellular homeostasis and 2) the interaction between tissue oxygenation and the proposed regulators of muscle respiration, metabolism, and force production. O2 delivery to isolated submaximally contracting [isometric contractions at 3 Hz; approximately 50% of peak O2 uptake (VO2)] in situ canine gastrocnemius (n = 6) was manipulated by decreasing arterial PO2 (hypoxemia; H) or muscle blood flow (ischemia; I) during three separate periods in each muscle [control (C), H, or I; each separated by 45 min of rest]. O2 delivery was reduced gradually in small steps every 3 min by H or I during two of the contraction periods (6 steps for a total of 21 min; O2 delivery reduced by 67% by the end of 21 min), whereas C was at normal O2 delivery for a 15-min period. Muscle VO2 was maintained at control levels for the first two O2 delivery reduction steps for the H and I conditions and then fell proportionally with O2 delivery to approximately 35% of the initial value by the end of the 21-min contraction period. Muscle force development generally fell in parallel with VO2. There was no significant changes from the values obtained during C contractions in intracellular concentrations of ATP, phosphocreatine, NH3, calculated free ADP, lactate, and redox state ratios as the O2 delivery was reduced, even with the severe decline in VO2 and developed force. These results demonstrated that when O2 availability was reduced gradually to contracting skeletal muscle, 1) developed force (ATP utilization) was reduced through a tight coupling with aerobic ATP supply, such that there was little additional disruption of intracellular homeostasis, and 2) there was an apparent dissociation of some of the proposed regulators of cell respiration and force development from the control of these processes.

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