Purpose <p>Muscle oxygen availability influences contractile performance and neuromuscular control, yet it remains unclear whether graded reductions in oxygen saturation at rest elicit proportional impairments in neuromuscular function. This study tested whether progressive decreases in muscle tissue saturation (S_tO₂) alter neuromuscular efficiency (NME) and force complexity during submaximal voluntary contractions.</p> Methods <p>Twenty-nine healthy adults (12&#xa0;M, 17&#xa0;F) performed dorsiflexion contractions at 50% of maximal voluntary contraction under four conditions: Control (<i>n</i> = 29) and arterial occlusion targeting 70% (<i>n</i> = 26), 60% (<i>n</i> = 25), and 50% (<i>n</i> = 9) S_tO₂. During each condition, electromyography and force output were collected to assess normalized root mean square, NME, and measures of force variability and complexity.</p> Results <p>Reductions in S_tO₂ progressively increased neural excitation requirements and decreased NME (both <i>p</i> &lt; 0.001), with greater desaturation associated with greater impairments. Force output became more variable and less complex with declining S_tO₂, as reflected by increased coefficient of variation and detrended fluctuation analysis α, and reduced approximate and sample entropy (all <i>p</i> &lt; 0.05). These effects were evident during contractions initiated after minimal prior exertion, i.e., without fatigue, and followed a dose-responsive pattern.</p> Conclusion <p>These findings demonstrate that muscle oxygenation at rest influences excitation efficiency and disrupts the temporal structure of motor output at the onset of contractions. As S_tO₂ declined, greater neural drive was required to maintain force, and force signals became less complex, suggesting a loss of adaptability in motor unit control. This work highlights the role of oxygen availability in preserving excitation efficiency and maintaining adaptable motor output, with potential clinical relevance for populations with impaired muscle oxygenation.</p>