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Linking pulmonary oxygen uptake, muscle oxygen utilization and cellular metabolism during exercise
No full textVO2 on-kinetics in isolated canine muscle in situ during slowed convective O2 delivery
No full textThe purpose of this study was to examine O(2) uptake (Vo(2)) on-kinetics when the spontaneous blood flow (and therefore O(2) delivery) on-response was slowed by 25 and 50 s. The isolated gastrocnemius muscle complex (GS) in situ was studied in six anesthetized dogs during transitions from rest to a submaximal metabolic rate (≈50-70% of peak Vo(2)). Four trials were performed: 1) a pretrial in which resting and steady-state blood flows were established, 2) a control trial in which the blood flow on-kinetics mean response time (MRT) was set at 20 s (CT20), 3) an experimental trial in which the blood flow on-kinetics MRT was set at 45 s (EX45), and 4) an experimental trial in which the blood flow on-kinetics MRT was set at 70 s (EX70). Slowing O(2) delivery via slowing blood flow on-kinetics resulted in a linear slowing of the Vo(2) on-kinetics response (R = 0.96). Average MRT values for CT20, EX45, and EX70 Vo(2) on-kinetics were (means ± SD) 17 ± 2, 23 ± 4, and 26 ± 3 s, respectively (P < 0.05 among all). During these transitions, slowing blood flow resulted in greater muscle deoxygenation (as indicated by near-infrared spectroscopy), suggesting that lower intracellular Po(2) values were reached. In this oxidative muscle, Vo(2) and O(2) delivery were closely matched during the transition period from rest to steady-state contractions. In conjunction with our previous work showing that speeding O(2) delivery did not alter Vo(2) on-kinetics under similar conditions, it appears that spontaneously perfused skeletal muscle operates at the nexus of sufficient and insufficient O(2) delivery in the transition from rest to contractions
Model of oxygen transport and metabolism predicts effect of hyperoxia on canine muscle oxygen uptake dynamics
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Models of muscle contraction and energetics
No full textHow does skeletal muscle manage to regulate the pathways of ATP synthesis during large-scale changes in work rate while maintaining metabolic homeostasis remains unknown. The classic model of metabolic regulation during muscle contraction states that accelerating ATP utilization leads to increasing concentrations of ADP and Pi, which serve as substrates for oxidative phosphorylation and thus accelerate ATP synthesis. An alternative model states that both the ATP demand and ATP supply pathways are simultaneously activated. Here, we review experimental and computational models of muscle contraction and energetics at various organizational levels and compare them with respect to their pros and cons in facilitating understanding of the regulation of energy metabolism during exercise in the intact organism
Multiscale Modeling of Respiration Linking External to Cellular Respiration During Exercise
No full textA multiscale mathematical model was developed to distinguish responses of external and cellular respiration to exercise of moderate intensity. The simulation shows that the characteristic MRTs of external and cellular respiration are similar even when a transit delay exists between the tissue cells and the lungs. The results of our model show that the O 2 transport processes from lungs to muscle are tightly coupled to provide sufficient O 2 for working skeletal muscle during exercise in normal subjects. Under abnormal conditions, the effect of O 2 transport limitation, occurring at a different scale of the body, on internal and external respiration can be examined. Such results can be used for comparative quantitative analysis of the regulation of respiration in subjects suffering from abnormal function associated with disease states (for example, chronic obstructive pulmonary disease, diabetes, and congenital heart disease)
Relating pulmonary oxygen uptake to muscle oxygen consumption at exercise onset: in vivo and in silico studies
No full textMuscle oxygen uptake differs from consumption dynamics during transients in exercise
No full textRelating external to internal respiration during exercise requires quantitative modeling analysis for reliable inferences with respect to metabolic rate. Often, oxygen transport and metabolism based on steady-state mass balances (Fick principle) and passive diffusion between blood and tissue are applied to link pulmonary to cellular respiration. Indeed, when the work rate does not change rapidly, a quasi-steady-state analysis based on the Fick principle is sufficient to estimate the rate of O2 consumption in working muscle. During exercise when the work rate changes quickly, however, non-invasive in vivo measurements to estimate muscle O2 consumption are not sufficient to characterize cellular respiration of working muscle. To interpret transient changes of venous O2 concentration, blood flow, and O2 consumption in working muscle, a mathematical model of O 2 transport and consumption based on dynamic mass balances is required. In this study, a comparison is made of the differences between simulations of O2 uptake and O2 consumption within working skeletal muscle based on a dynamic model and quasi-steady-state approximations. The conditions are specified under which the quasi-steadystate approximation becomes invalid
Non-invasive estimation of metabolic flux and blood flow in working muscle: Effect of blood-tissue distribution
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