## 1 Introduction  
During a swimming training session, various sets of repetitions may be included and applied at different exercise-intensity domains [1]. Maintaining performance in these training sets relies on the effectiveness of optimal limb coordination, which must remain consistent across consecutive stroke cycles [2]. Since 85% of the propulsive force in swimming is derived from the upper limbs [3], the effectiveness of upper limb coordination can be assessed through stroke rate (SR) and stroke length (SL) [4]. The aforementioned biomechanical variables are considered useful for monitoring swimming techniques [4], along with the stroke index (SI: the product of SL multiplied by swimming speed), which is strongly associated with low energy cost [5]. A decrease in SL and an increase in SR have been observed as swimming intensity increases [6, 7]. Such modifications in biomechanical parameters are suggested to occur alongside changes in blood lactate concentration (BL) during incremental swimming [8, 9]. Significant alterations in SR and SL have notably been observed around the maximal lactate steady state [7] or lactate threshold (LT) intensity [10]. The metabolic imbalance that occurs when swimming above LT (which delineates the transition between moderate and heavy intensity exercise [11]) is proposed as a key factor contributing to adjustments in SRand SL [7; 12], likely serving as a compensatory mechanism to counteract hydrodynamic drag [13]. Specifically, swimming at a speed 2.5% above the maximal lactate steady state forced swimmers to adopt a higher SR to compensate for the loss of SL. In comparison, no difference was observed at intensity 2.5% lower than the maximal lactate steady state [7]. The decrease in SL as a function of speed resulted in a decrease in SI, indicating the importance of the ability to maintain technical efficiency as exercise intensity increases [7]. The abovementioned reports are in accordance with other studies at imposed pages [6; 14; 15]. Although no difference was observed over time in biomechanical parameters while swimming at the maximal lactate steady state intensity [6], a 3.3% decrease in SL and a 3.6% increase in SR may be meaningful. The latter was confirmed by [PERSON] and colleagues [7], who highlighted an increase in SR and a decline in SL and SI at the end of continuous swimming compared to the very start of the trial. These biomechanical adaptations may also be influenced by the physiological impact of localized muscle fatigue [6]. A metabolic imbalance may arise not only due to increasing swimming intensity but also as a consequence of a preceding high-intensity training set [16; 17]. Specifically, repeated sprints performed as the initial set in a training session may alter the metabolic environment, subsequently affecting an aerobic-dominated training set conducted at intensities around the LT and the maximal aerobic speed (MAS) [16; 17]. Such a substantial alteration in metabolic conditions may trigger neural feedback mediated by thin-fiber muscle afferents, leading to an inhibitory response in central motor drive [18]. This response is expressed as increased perceived exertion, enabling swimmers to sustain the required speed. Regardless of the underlying mechanism, swimmers naturally self-optimize their movement patterns to maintain performance levels while experiencing fatigue [12]. This optimization process can be observed through adjustments in SR and SL [2]. Furthermore, swimming efficiency and fatigue-induced modifications can be evaluated using the SI, where a decline in SI reflects reduced efficiency, whereas an increase indicates improved efficiency [5]. The purpose of this study was to compare the biomechanical responses (SR, SL, SI) during aerobic-dominated training sets when performed following repeated sprints versus when conducted as the initial set of a training session.