Cellular Po-2 as a determinant of maximal mitochondrial O-2 consumption intrained human skeletal muscle

Citation
Rs. Richardson et al., Cellular Po-2 as a determinant of maximal mitochondrial O-2 consumption intrained human skeletal muscle, J APP PHYSL, 87(1), 1999, pp. 325-331
Citations number
32
Categorie Soggetti
Physiology
Journal title
JOURNAL OF APPLIED PHYSIOLOGY
ISSN journal
87507587 → ACNP
Volume
87
Issue
1
Year of publication
1999
Pages
325 - 331
Database
ISI
SICI code
8750-7587(199907)87:1<325:CPAADO>2.0.ZU;2-1
Abstract
Cellular Po-2 as a determinant of maximal mitochondrial O-2 consumption in trained human skeletal muscle. J. Appl. Physiol. 87(1): 325-331, 1999.-Prev iously, by measuring myoglobin-associated Po-2 (P-MbO2) during maximal exer cise, we have demonstrated that 1) intracellular Po, is 10-fold less than c alculated mean capillary Po-2 and 2) intracellular Po-2 anti maximum O-2 up take (V overdot o(2max)) fall proportionately in hypoxia. To further elucid ate this relationship, five trained subjects performed maximum knee-extenso r exercise under conditions of normoxia (21% Ga), hypoxia (125 O-2), and hy peroxia (100% O-2) in balanced order. Quadriceps O-2 uptake (Vo(2)) was cal culated from arterial and venous blood O-2 concentrations and thermodilutio n blood flow measurements. Magnetic resonance spectroscopy was used to dete rmine myoglobin desaturation, and an O-2 half-saturation pressure of 3.2 To rr was used to calculate P(Mb)o(2) from saturation. Skeletal muscle V overd ot o(2max) at 12, 21, and 100% O-2 was 0.86 +/- 0.1, 1.08 +/- 0.2, and 1.28 +/- 0.2 ml.min(-1) ml-l, respectively The 100% O-2 values approached twice that previously reported in human skeletal muscle. P(Mb)o(2) values were 2 .3 +/- 0.5, 3.0 +/- 0.7, and 4.1 +/- 0.7 Torr while the subjects breathed 1 2, 21, and 300% 0.2, respectively. From 12 to 21% O-2,V overdot o(2) and P( Mb)o(2) were again proportionately related. However, 100% O-2 increased V o verdot o(2max) relatively less than P(Mb)o(2), suggesting an approach to ma ximal mitochondrial capacity with 100% O-2. These data 1) again demonstrate very low cytoplasmic Po-2 at V overdot o(2max), 2) are consistent with sup ply limitation of V overdot o(2max), of trained skeletal muscle, even in hy peroxia, and 3) reveal a disproportionate increase in intracellular Po-2 in hyperoxia, which may be interpreted as evidence that, in trained skeletal muscle, very high mitochondrial metabolic limits to muscle V overdot o(2) a re being approached.