## 4 Discussion
Furthermore, \(\mathrm{VL}_{\mathrm{MT}}\), a surrogate of quadriceps--one of the main muscles involved in force production during jumping--muscle mass, is another variable that is notably affected by strength training [34]. Although many other manifestations of neuromuscular performance and morphology exist and are affected by strength training, our data--obtained from untrained persons, which present greater heterogeneity in these markers compared to trained persons--suggest that lower-limb muscle performance and mass are not associated with changes in powerful actions following pre-activation. It could be speculated that the mechanisms underpinning greater responsiveness to PAPE in trained populations are related not to increased musclestrength, power and mass, but rather to other cellular and neural mechanisms that are affected by strength training. As in many other physiological processes, PAPE is a multifactorial phenomenon that relies on several adaptive mechanisms triggered by the stress imposed by pre-activation [35]. Therefore, it is reasonable to assume that no neuromuscular variable should explain PAPE in isolation. Considering this, linear stepwise multiple regression models were applied to screen for the possibility that some of the investigated variables could conjunctively predict responsiveness to PAPE. However, none of the tested models--which were proposed hierarchically, according to the coefficients of correlation between each predictor and \(\Delta\)CMJ--were found to be significant. Hence, we present evidence that the investigated neuromuscular variables might not predict responsiveness to PAPE in untrained males, even when analyzed in conjunction. Improvements in maximal and explosive force and muscle mass are some of the many functional and morphological adaptations to strength training. Other adaptations, such as increased muscle-tendon stiffness [36], skeletal muscle angiogenesis [37], intramuscular glycogen and phosphocreatine content [38; 39], selective type II fiber hypertrophy [40], and a shift towards greater expression of type II myosin heavy chain [13; 14], are observed following strength training interventions. Some of these adaptations, which are not directly translated into changes in the independent variables investigated in the present study, might be more closely related to responsiveness to PAPE. For instance, myosin head phosphorylation--especially type IIx--has been frequently observed following pre-activation protocols, resulting in a transient increase in evoked force [41]. Whether or not this phenomenon impacts voluntary performance is still in debate [35; 42; 43], but trained individuals are known to express greater amounts of type IIx myosin heads [44], which could explain the greater responsiveness to PAPE (or at least post-activation potentiation) observed in this population. It is also proposed that transient increases in intramuscular water content and temperature might underpin improvements in neuromuscular performance following pre-activation [9; 10], while the greater capillary bed promoted by strength training might facilitate these mechanisms. Finally, strength training-induced increases in glycogen and, especially, phosphocreatine content within the muscle might favor the balance between fatigue and recovery following pre-activation, promoting a wider and/or larger PAPE window. This is supported by data showing that creatine supplementation improves responsiveness to PAPE [45]. Although speculative, these considerations should be considered when designing future studies to investigate the mechanisms underpinning responsiveness to PAPE. The present study has limitations that should be mentioned. The first is the lack of responsiveness to PAPE. However, although this might have indicated that the adopted protocol was not ideal to induced PAPE, the occurrence of responsive, unresponsive, and negatively responsive individuals might have enriched the analyses performed in this study.