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Skeletal Muscle And Exercise |
1 Department of Medicine, University of California, San Diego, La Jolla, CA 90293-0623, USA
2 Norwegian University of Science and Technology, Faculty of Medicine NO-7489 Trondheim, Norway
3 NMR Laboratory, AFM and CEA, IFR 14, Institut de Myologie, Pitié-Salpêtrière University Hospital, Paris, France
Intracellular oxygen (O2) availability and the impact of ambient hypoxia have far reaching ramifications in terms of cell signalling and homeostasis; however, in vivo cellular oxygenation has been an elusive variable to assess. Within skeletal muscle the extent to which myoglobin desaturates (deoxy-Mb) and the extent of this desaturation in relation to O2 availability provide an endogenous probe for intracellular O2 partial pressure (PiO2). By combining proton nuclear magnetic resonance spectroscopy (1H NMRS) at a high field strength (4 T), assessing a large muscle volume in a highly efficient coil, and extended signal averaging (30 min) we assessed the level of skeletal muscle deoxy-Mb in 10 healthy men (30 ± 4 years) at rest in both normoxia and hypoxia (10% O2). In normoxia there was an average deoxy-Mb signal of 9 ± 1%, which, when converted to PiO2 using an O2/Mb half-saturation (P50) of 3.2 mmHg, revealed an PiO2 of 34 ± 6 mmHg. In ambient hypoxia the deoxy-Mb signal rose to 13 ± 3% (PiO2= 23 ± 6 mmHg). However, intersubject variation in the defence of arterial oxygenation (SaO2) in hypoxia (SaO2 range: 86–67%) revealed a significant relationship between the changes in SaO2 and PiO2(r2= 0.5). These data are the first to document resting intracellular oxygenation in human skeletal muscle, highlighting the relatively high PiO2 values that contrast markedly with those previously recorded during exercise (
2–5 mmHg). Additionally, the impact of ambient hypoxia on PiO2 and the relationship between changes in SaO2 and PiO2 stress the importance of the O2 cascade from air to cell that ultimately effects O2 availability and O2 sensing at the cellular level.
(Received 23 November 2005;
accepted after revision 21 December 2005;
first published online 5 January 2006)
Corresponding author R. S. Richardson: Department of Medicine, Physiology Division, 9500 Gilman Drive, University of California San Diego, La Jolla, CA 92093-0623, USA. Email: rrichardson{at}ucsd.edu
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