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Quantification of myoglobin deoxygenation and intracellular partial pressure of O 2 during muscle contraction during haemoglobin‐free medium perfusion
Author(s) -
Takakura Hisashi,
Masuda Kazumi,
Hashimoto Takeshi,
Iwase Satoshi,
Jue Thomas
Publication year - 2010
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2009.050344
Subject(s) - myoglobin , perfusion , contraction (grammar) , deoxygenation , chemistry , intracellular , oxygenation , oxygen , biophysics , hindlimb , medicine , myocyte , muscle contraction , anatomy , biochemistry , biology , organic chemistry , catalysis
Although the O 2 gradient regulates O 2 flux from the capillary into the myocyte to meet the energy demands of contracting muscle, intracellular O 2 dynamics during muscle contraction remain unclear. Our hindlimb perfusion model allows the determination of intracellular myoglobin (Mb) saturation () and intracellular oxygen tension of myoglobin () in contracting muscle using near infrared spectroscopy (NIRS). The hindlimb of male Wistar rats was perfused from the abdominal aorta with a well‐oxygenated haemoglobin‐free Krebs–Henseleit buffer. The deoxygenated Mb (Δ[deoxy‐Mb]) signal was monitored by NIRS. Based on the value of Δ[deoxy‐Mb], and were calculated, and the time course was evaluated by an exponential function model. Both and started to decrease immediately after the onset of contraction. The steady‐state values of and progressively decreased with relative work intensity or muscle oxygen consumption. At the maximal twitch rate, and were 49% and 2.4 mmHg, respectively. Moreover, the rate of release of O 2 from Mb at the onset of contraction increased with muscle oxygen consumption. These results suggest that at the onset of muscle contraction, Mb supplies O 2 during the steep decline in , which expands the O 2 gradient to increase the O 2 flux to meet the increased energy demands.