Skeletal Muscle Force Is Preserved In Nox4 Deficient Mice

NADPH oxidase levels are elevated in various cardiovascular diseases. The NOX4 isoform of NADPH oxidase generates reactive oxygen species that promotes calcium release in skeletal muscle. NOX4 knockdown depresses maximal tetanic force in mouse EDL muscle. We tested the hypotheses that NOX4 deficient mice would have decreased muscle force, rightward shift in the force‐frequency relationship, and accelerated fatigue in vitro. We studied intact soleus muscle from genetic control (C57BL/6J) and NOX 4 knockout mice (n = 7/group; 2 males/group) at 95%O2 and 37°C. Our initial experiments suggest no difference in maximal soleus tetanic force (Po) between groups (in N/cm2; Control 32 ± 6, NOX 4−/− 36 ± 4). Neither the stimulus frequency that elicited 50% Po (Control 53 ± 3 Hz; NOX4−/− 53 ± 8 Hz) nor muscle fatigue (not shown) was affected by NOX4 deficiency. Our study suggests that skeletal muscle force is preserved in mice lacking NOX4 isoform of NADPH oxidase.