Hypoxia in skeletal muscle at rest and during the transition to steady work
| Autor: | Carl R. Honig |
|---|---|
| Rok vydání: | 1977 |
| Předmět: |
medicine.medical_specialty
Partial Pressure Rest Physical Exertion Respiratory chain Vasodilation Mitochondrion Biology Biochemistry Microcirculation Internal medicine medicine Animals Myoglobin Muscles Skeletal muscle Cell Biology Blood flow Hypoxia (medical) NAD Rats Oxygen Endocrinology medicine.anatomical_structure Regional Blood Flow Cats Lactates Biophysics medicine.symptom Cardiology and Cardiovascular Medicine NADP Intracellular Muscle Contraction |
| Zdroj: | Microvascular Research. 13:377-398 |
| ISSN: | 0026-2862 |
| DOI: | 10.1016/0026-2862(77)90105-4 |
| Popis: | This paper reviews O2 transport to skeletal muscle at rest and during the transition to steady work. In animals whose surface area is large relative to volume, mean intracellular PO2 is about 5 mm Hg, and V O 2 increases if flow increases. However, coupled V O 2 of mitochondria in vitro and in vivo is maximal when intracellular PO2 exceeds about 0.1 mm Hg. The 50-fold difference between the critical PO2 for V O 2 of mitochondria and V O 2 of whole muscle is accounted for, at least in part, by nonuniformities in the muscle microcirculation. These nonuniformities cause focal anoxia, even though mean intracellular PO2 greatly exceeds critical mitochondrial PO2. It remains to be determined whether biochemical pathways to O2 parallel and/or, alternative to the classical respiratory chain, contribute to the flow dependence of muscle V O 2 . Most of the O2 debt in phasic contraction is acquired during the first 30–60 sec. while blood flow is increasing rapidly. This initial phase of vasodilation is entirely due to short neurones intrinsic to skeletal muscle arterioles. A minor component of the O2 debt is acquired after maximum flow is attained. This may be accounted for by slow recruitment of capillaries, which are under metabolic rather than neural control. |
| Databáze: | OpenAIRE |
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