Calculated intra- and extracellular PO2 gradients in heavily working red muscle

Abstract

A recently introduced three-dimensional analytical model of O2 diffusion to heavily working muscle that considers myoglobin-facilitated O2 diffusion inside the muscle fiber and a carrier-free layer separating erythrocytes and fiber is able to furnish the following new insights in O2 supply to red muscle at high performance. 1) Fiber PO2 profiles are essentially flat, and the major PO2 gradients are located in the perierythrocytic region, in good agreement with experimental findings [T. E. J. Gayeski and C. R. Honig, Am. J. Physiol. 251 (Heart Circ. Physiol. 20): H789-H799, 1986]. No specialized anatomical pericapillary barrier structure is required to explain these results. 2) A functional barrier to O2 diffusion has been identified that consists of the carrier-free layer and of the pericapillary muscle fiber portions. There are three reasons that make these structures act as a diffusion barrier: a "geometric reason," a "diffusivity-related reason," and a "myoglobin-related reason." 3) PO2 fields of adjacent red blood cells (RBCs) practically do not interact. 4) Small scale heterogeneities in capillary and RBC spacing are compensated for by high myoglobin-facilitated fiber diffusivity. Limiting factor for diffusional O2 transport is the number of RBCs present on the fiber surface.

Influence of blood flow occlusion on muscle oxygenation characteristics and the parameters of the power-duration relationship

“…In the present study, fractional O 2 extraction was significantly greater for occlusion than for control. This is consistent with previous reports of alterations in the fractional O 2 extraction with varying inspired O 2 concentrations (41,46,51 (16,24,29,33). The similar peak plateaus in microvascular hematocrit (i.e., total-[HbϩMb]) in the present study for control exercise suggest that the peak microvascular hematocrit, and, therefore, Ḋ o 2 , is constrained for a given condition.…”

Does intracellular metabolite diffusion limit post-contractile recovery in burst locomotor muscle?

“…This leads to relatively shallow P O ∑ gradients across the sarcolemma that, when coupled to the low SA:V of large fibers, would be expected to promote very low rates of O 2 flux into the fiber. The lack of myoglobin (Mb) in the light levator muscle amplifies this effect, since Mb-less fibers require a higher extracellular P O ∑ to support a given rate of O 2 consumption compared with muscles with Mb (Groebe and Thews, 1990). This view is consistent with recent observations in isolated Xenopus laevis skeletal muscle fibers, which are also relatively large and lack Mb, that low intracellular P O ∑ limits the rate of NAD(P)H oxidation by the electron transport system during steady-state contraction (Hogan et al, 2005).…”

Estimated contribution of hemoglobin and myoglobin to near infrared spectroscopy

“…In contrast, other studies and analyses suggest that Mb may contribute more to the NIRS signal than previously thought, possibly even more than Hb. Due to the potentially significant role of Mb in oxygen transport from capillary to mitochondria (Richardson et al, 2006, Richardson et al, 2001, Groebe and Thews, 1990, Garry et al, 1998) the contribution of Mb to the NIRS signal needs to be re-examined.…”

“…Due to a) the potentially significant role of Mb in oxygen transport from capillary to mitochondria (Richardson et al, 2006, Richardson et al, 2001, Groebe and Thews, 1990)(but see also Ordway and Garry, 2004), and b) the assumption in the above methodologies that Hb is the primary/exclusive source of the NIRS signal, the contribution of Mb to the NIRS signal needs to be re-examined. Therefore, the purposes of this study were to a) using the relative concentrations of [Mb] and [Hb] in mammalian skeletal muscle based on published chemical and morphometric data, estimate the resulting potential contributions of Hb and Mb to the NIRS signal (expressed as light absorbing potential (LAP)) (Part 1), and b) use the information in a) to interpret changes in total [Hb+Mb] by NIRS during exercise (Part 2).…”