## 4 Discussion  
This study analyzed how varying degrees of occlusion influence RFD kinetics during IMTP performance after fatiguing single-joint action in young women. Contrary to our initial hypothesis, RFD kinetics remained largely unaffected across conditions, with only modest time-dependent changes observed. Specifically, early-phase RFD (0-50 ms) and late-phase RFD (151-250 ms) kinetics demonstrated statistically significant main effects of time; however, post hoc analysis revealed only transient reductions at POST and 5 min, without consistent differences between occlusion groups. The mid-phase RFD (51-150 ms) showed no significant changes. Interestingly, the traditional force metrics, peak force (PF) and impulse (IP), declined significantly only in the control condition (0% LOP), whereas no significant reductions were observed under 40% or 80% LOP. These results suggest a protective trend under BFR conditions, potentially attenuating the magnitude of fatigue observed in the non-occluded condition. However, this interpretation remains speculative, as no physiological markers such as electromyography or muscle oxygenation were measured to confirm the mechanism. This nuanced outcome challenges assumptions about BFR's impact on explosive force performance and highlights the need for context-specific interpretation of BFR-induced fatigue. The analysis of RFD kinetics across distinct temporal windows revealed differential sensitivity to acute neuromuscular fatigue under blood flow restriction (BFR). Early-phase RFD (0-50 ms) kinetics appeared to be relatively stable, which may reflect a preserved capacity for rapid motor unit discharge during the initial contraction phase despite transient ischemia. This could indicate that the neuromuscular mechanisms responsible for immediate force generation are either less affected by metabolic stress or compensated for by an increased central drive. Similarly, the mid-phase RFD (51-150 ms) demonstrated minimal disruption across conditions, aligning with prior research suggesting that intermediate phases of force development are less responsive to acute fatigue, particularly in isometric contexts [7,34]. These intervals may represent a transition zone in which neither neural nor mechanical determinants are sufficiently challenged to elicit measurable decrements. Moreover, isometric tasks elicit less systemic and mechanical stress than dynamic movements, potentially blunting observable fatigue effects across intermediate timeframes [13]. Notably, the 151-250 ms window revealed a significant intragroup reduction in the 80% LOP condition, suggesting an acute fatigue response specific to this late phase of force production. Although 250 ms represents only a fraction of the 5-s maximal effort, the result likely reflects the neuromuscular consequences of high-pressure BFR rather than contraction duration per se. Elevated occlusion pressures have been shown to increase metabolite accumulation and restrict oxygen delivery, accelerating peripheral fatigue and impairing muscle contractility [35]. In parallel, high-pressure BFR may alter motor unit recruitment dynamics by increasing reliance on higher-threshold units and disrupting firing patterns [25]. These mechanisms can impair the rapid force output in the later phases of contraction, even without visible decrements in the peak force. Given that this was the only statistically significant comparison across all time windows, it underscores the importance of analyzing the RFD temporally and considering the distinct physiological responses elicited by high-pressure BFR. Together, these findings underscore the importance of considering the temporal dimension of the RFD when evaluating the acute effects of BFR, as not all phases respond uniformly to ischemic or neuromuscular perturbations. Our study employed a progressive single-joint knee extension protocol until failure, starting at 40% of the maximal voluntary isometric force (MVIF), with incremental 10% MVIF increases applied on each repetition until volitional failure.