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Extracellular ROS formation in contracting soleus muscle in mice with lung TNF‐α overexpression (1153.1)

Chronic obstructive pulmonary disease (COPD) commonly results in elevated levels of tumor necrosis factor‐alpha (TNF‐α). However, the mechanism of extracellular reactive oxygen species (ROS) formation in skeletal muscle isolated from pulmonary TNF‐α overexpression mice, has been overlooked. We hypothesized that ROS can be released from contracting skeletal muscle when there is increased TNF‐α formation in the lung and that this causes muscle early fatigue. Using wild type (WT) and pulmonary TNF‐α overexpression mice (Tg+), we performed a cytochrome c (cyt c) assay to measure extracellular superoxide (O2•–, one of the major types of ROS) production in isolated contracting soleus muscle. Our results showed that Tg+ soleus released higher levels of O2•– than WT during the contraction period (n = 5; P < 0.05). Tg+ soleus muscle also presented a reduced fatigue resistance compared to WT muscle. Perfusion of the contracting soleus with membrane‐impermeable superoxide dismutase, an extracellular O2•– scavenger, resulted in less cyt c reduction confirming that the type of ROS released from the Tg+ muscles was O2•–. We conclude that TNF‐α overexpression in the lung induces more O2•– release from Tg+ than WT muscle, and that the extracellular formation of O2•– markedly reduces the fatigue resistance in the Tg+ muscle. Thus, this study highlights O2•– as a potential mechanistic mediator in COPD induced muscle impairment.