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Intracellular Critical PO2 Measured in Human Skeletal Muscle In Vivo
Author(s) -
Lanza Ian R,
Befroy Douglas E,
Tevald Michael A,
KentBraun Jane A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.962.24
Subject(s) - phosphocreatine , skeletal muscle , myoglobin , inflection point , chemistry , in vivo , ischemia , oxygen , respiration , biophysics , medicine , anatomy , biochemistry , biology , energy metabolism , geometry , mathematics , microbiology and biotechnology , organic chemistry
Under some conditions, intracellular oxygen tension (PO2) may decrease to the point where oxygen availability limits respiration. Information about this critical PO2 and its determinants in vivo is sparse. PURPOSE: To determine the critical PO2 of human skeletal muscle, and its relationship to cellular energy consumption. METHODS: Interleaved proton and phosphorus magnetic resonance spectroscopy were used to quantify deoxymyoglobin and phosphorous metabolites in the tibialis anterior muscle of 6 subjects during 15 minutes of leg ischemia. Critical PO2 was determined as the PO2 at the phosphocreatine inflection point during ischemia. The rate of ATP consumption was determined from the linear slope of PCr depletion following the inflection point. RESULTS: The time to PCr inflection point was 282 ± 112 s (mean±SE). The corresponding critical PO2 was 0.47±0.27 torr, with a range of 0.21–0.96. PO2crit was not associated with the resting rate of ATP consumption (r =0.17), but was directly correlated to the rate of myoglobin desaturation (r =0.93) and inversely correlated to the time required to reach the PCr inflection point (r = −0.74). CONCLUSION: These data suggest that the relatively wide range of PO2crit in these subjects is attributable to inter‐subject differences in the ability of the muscle to maintain ATP production in the face of an ischemic insult. Support NIH AG21094, K02 AG023582