Muscle immobilization delays abrupt change in myoglobin saturation at onset of muscle contraction

Hindlimb immobilization (IM) produces a decrease in functional oxidative capacity as well as morphological changes in muscles. However, the effect of IM on the mechanism of O2 supply to mitochondria in muscle tissue during muscle contraction is unknown, especially the contribution of myoglobin (Mb)...

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Hauptverfasser: Hisashi Takakura (VerfasserIn), Tatsuya Yamada (VerfasserIn), Yasuro Furuichi (VerfasserIn), Takeshi Hashimoto (VerfasserIn), Satoshi Iwase (VerfasserIn), Thomas Jue (VerfasserIn), Kazumi Masuda (VerfasserIn)
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Veröffentlicht: Japanese Society of Physical Fitness and Sports Medicine, 2022-03-01T00:00:00Z.
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042 |a dc 
100 1 0 |a Hisashi Takakura  |e author 
700 1 0 |a Tatsuya Yamada  |e author 
700 1 0 |a Yasuro Furuichi  |e author 
700 1 0 |a Takeshi Hashimoto  |e author 
700 1 0 |a Satoshi Iwase  |e author 
700 1 0 |a Thomas Jue  |e author 
700 1 0 |a Kazumi Masuda  |e author 
245 0 0 |a Muscle immobilization delays abrupt change in myoglobin saturation at onset of muscle contraction 
260 |b Japanese Society of Physical Fitness and Sports Medicine,   |c 2022-03-01T00:00:00Z. 
500 |a 2186-8131 
500 |a 2186-8123 
500 |a 10.7600/jpfsm.11.87 
520 |a Hindlimb immobilization (IM) produces a decrease in functional oxidative capacity as well as morphological changes in muscles. However, the effect of IM on the mechanism of O2 supply to mitochondria in muscle tissue during muscle contraction is unknown, especially the contribution of myoglobin (Mb) to mitochondrial respiration. This study investigated whether IM causes a delayed response of intracellular Mb saturation (SmbO2) and decreased muscle oxygen uptake (mVO2) due to elevated intracellular oxygen tension (PmbO2) in contracting muscles using a rat hindlimb perfusion model. Three-week IM decreased the O2 release rate from Mb at the onset of muscle contraction (IM: 3.2 ± 0.9 vs. control (Con): 7.5 ± 2.9 10-2 µmol g-1 min-1; p < 0.05) and state 3 of mitochondrial respiration in muscle tissue (IM: 0.021 ± 0.006 vs. Con: 0.030 ± 0.009 10-3 µM g-1 sec-1; p < 0.05). Despite the increase in mVO2, the steady-state level of SmbO2 was higher during muscle contraction in the IM group, resulting in elevated PmbO2 (IM: 4.2 ± 1.0 vs. Con: 2.1 ± 1.0 mmHg; p < 0.05). In conclusion, IM decreased the O2 release rate from Mb; this alteration could be associated with mitochondrial dysfunction. These changes within muscle cells may be related to the delayed tissue response seen with near-infrared spectroscopy at the onset of muscle contraction. 
546 |a EN 
690 |a hindlimb perfusion 
690 |a myoglobin 
690 |a immobilization 
690 |a mitochondrial respiration 
690 |a Sports medicine 
690 |a RC1200-1245 
690 |a Physiology 
690 |a QP1-981 
655 7 |a article  |2 local 
786 0 |n Journal of Physical Fitness and Sports Medicine, Vol 11, Iss 2, Pp 87-96 (2022) 
787 0 |n https://www.jstage.jst.go.jp/article/jpfsm/11/2/11_87/_pdf/-char/en 
787 0 |n https://doaj.org/toc/2186-8131 
787 0 |n https://doaj.org/toc/2186-8123 
856 4 1 |u https://doaj.org/article/5c0f4c0ea96b40f2847a1d29ac3fcbb5  |z Connect to this object online.