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
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.