Difference between revisions of "Richardson 1999 J Appl Physiol (1985)"
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{{Publication | {{Publication | ||
|title=Richardson RS, Leigh JS, Wagner PD, Noyszewski EA (1999) Cellular | |title=Richardson RS, Leigh JS, Wagner PD, Noyszewski EA (1999) Cellular ''P''<sub>O<sub>2</sub></sub> as a determinant of maximal mitochondrial O<sub>2</sub> consumption in trained human skeletal muscle. https://doi.org/10.1152/jappl.1999.87.1.325 | ||
|info=[https://pubmed.ncbi.nlm.nih.gov/10409591/ PMID: 10409591 Open Access] | |info=J Appl Physiol (1985) 87:325-31. [https://pubmed.ncbi.nlm.nih.gov/10409591/ PMID: 10409591 Open Access] | ||
|authors=Richardson RS, Leigh JS, Wagner PD, Noyszewski EA | |authors=Richardson RS, Leigh JS, Wagner PD, Noyszewski EA | ||
|year=1999 | |year=1999 | ||
|journal=J Appl Physiol (1985) | |journal=J Appl Physiol (1985) | ||
|abstract=Previously, by measuring myoglobin-associated | |abstract=Previously, by measuring myoglobin-associated ''P''<sub>O<sub>2</sub></sub> (''P''<sub><sub>Mb</sub></sub><sub>O<sub>2</sub></sub>) during maximal exercise, we have demonstrated that 1) intracellular ''P''<sub>O<sub>2</sub></sub> is 10-fold less than calculated mean capillary ''P''<sub>O<sub>2</sub></sub> and 2) intracellular ''P''<sub>O<sub>2</sub></sub> and maximum O<sub>2</sub> uptake (''V''<sub>O<sub>2</sub>max</sub>) fall proportionately in hypoxia. To further elucidate this relationship, five trained subjects performed maximum knee-extensor exercise under conditions of normoxia (21 % O<sub>2</sub>), hypoxia (12 % O<sub>2</sub>), and hyperoxia (100 % O<sub>2</sub>) in balanced order. Quadriceps O<sub>2</sub> uptake (''V''<sub>O<sub>2</sub></sub>) was calculated from arterial and venous blood O<sub>2</sub> concentrations and thermodilution blood flow measurements. Magnetic resonance spectroscopy was used to determine myoglobin desaturation, and an O<sub>2</sub> half-saturation pressure of 3.2 Torr was used to calculate ''P''<sub><sub>Mb</sub></sub><sub>O<sub>2</sub></sub> from saturation. Skeletal muscle ''V''<sub>O<sub>2</sub>max</sub> at 12, 21, and 100 % O<sub>2</sub> was 0.86 ± 0.1, 1.08 ± 0.2, and 1.28 ± 0.2 mL.min<sup>-1</sup>.mL<sup>-1</sup>, respectively. The 100 % O<sub>2</sub> values approached twice that previously reported in human skeletal muscle. ''P''<sub><sub>Mb</sub></sub><sub>O<sub>2</sub></sub> values were 2.3 ± 0.5, 3.0 ± 0.7, and 4.1 ± 0.7 Torr while the subjects breathed 12, 21, and 100 % O<sub>2</sub>, respectively. From 12 to 21 % O<sub>2</sub>, ''V''<sub>O<sub>2</sub></sub> and ''P''<sub><sub>Mb</sub></sub><sub>O<sub>2</sub></sub> were again proportionately related. However, 100 % O<sub>2</sub> increased ''V''<sub>O<sub>2</sub>max</sub> relatively less than ''P''<sub><sub>Mb</sub></sub><sub>O<sub>2</sub></sub>, suggesting an approach to maximal mitochondrial capacity with 100 % O<sub>2</sub>. These data 1) again demonstrate very low cytoplasmic ''P''<sub>O<sub>2</sub></sub> at ''V''<sub>O<sub>2</sub>max</sub>, 2) are consistent with supply limitation of ''V''<sub>O<sub>2</sub>max</sub> of trained skeletal muscle, even in hyperoxia, and 3) reveal a disproportionate increase in intracellular ''P''<sub>O<sub>2</sub></sub> in hyperoxia, which may be interpreted as evidence that, in trained skeletal muscle, very high mitochondrial metabolic limits to muscle ''V''<sub>O<sub>2</sub></sub> are being approached. | ||
|editor=Gnaiger E | |editor=Gnaiger E | ||
}} | }} | ||
Latest revision as of 23:15, 15 July 2022
| Richardson RS, Leigh JS, Wagner PD, Noyszewski EA (1999) Cellular PO2 as a determinant of maximal mitochondrial O2 consumption in trained human skeletal muscle. https://doi.org/10.1152/jappl.1999.87.1.325 |
» J Appl Physiol (1985) 87:325-31. PMID: 10409591 Open Access
Richardson RS, Leigh JS, Wagner PD, Noyszewski EA (1999) J Appl Physiol (1985)
Abstract: Previously, by measuring myoglobin-associated PO2 (PMbO2) during maximal exercise, we have demonstrated that 1) intracellular PO2 is 10-fold less than calculated mean capillary PO2 and 2) intracellular PO2 and maximum O2 uptake (VO2max) fall proportionately in hypoxia. To further elucidate this relationship, five trained subjects performed maximum knee-extensor exercise under conditions of normoxia (21 % O2), hypoxia (12 % O2), and hyperoxia (100 % O2) in balanced order. Quadriceps O2 uptake (VO2) was calculated from arterial and venous blood O2 concentrations and thermodilution blood flow measurements. Magnetic resonance spectroscopy was used to determine myoglobin desaturation, and an O2 half-saturation pressure of 3.2 Torr was used to calculate PMbO2 from saturation. Skeletal muscle VO2max at 12, 21, and 100 % O2 was 0.86 ± 0.1, 1.08 ± 0.2, and 1.28 ± 0.2 mL.min-1.mL-1, respectively. The 100 % O2 values approached twice that previously reported in human skeletal muscle. PMbO2 values were 2.3 ± 0.5, 3.0 ± 0.7, and 4.1 ± 0.7 Torr while the subjects breathed 12, 21, and 100 % O2, respectively. From 12 to 21 % O2, VO2 and PMbO2 were again proportionately related. However, 100 % O2 increased VO2max relatively less than PMbO2, suggesting an approach to maximal mitochondrial capacity with 100 % O2. These data 1) again demonstrate very low cytoplasmic PO2 at VO2max, 2) are consistent with supply limitation of VO2max of trained skeletal muscle, even in hyperoxia, and 3) reveal a disproportionate increase in intracellular PO2 in hyperoxia, which may be interpreted as evidence that, in trained skeletal muscle, very high mitochondrial metabolic limits to muscle VO2 are being approached.
• Bioblast editor: Gnaiger E
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Stress:Hypoxia Organism: Human Tissue;cell: Skeletal muscle
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