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

Abstract

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 (S_mbO₂) and decreased muscle oxygen uptake (mVO₂) due to elevated intracellular oxygen tension (P_mbO₂) 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 S_mbO₂ was higher during muscle contraction in the IM group, resulting in elevated P_mbO₂ (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.