## 4 Discussion
These adaptations may enhance upper-body oxidative capacity [67; 68], facilitating improved oxygen extraction and utilization of Type I muscle fibers, delaying the recruitment of Type II fibers [69]. Additionally, increased upper-body strength might reduce muscle activation during prolonged submaximal exercise [69; 70], leading to improved perfusion conditions [8; 15; 16] and muscle oxygen saturation [71]. Strong correlations between resistance-training-induced strength gains (1 RM) and changes in VO2 peak-DP underscore the role of resistance training in mitigating peripheral limitations, explaining 23-41% of the observed variance. However, existing literature presents varying outcomes regarding the relationship between resistance training and VO2 peak-DP [15; 16; 17; 18; 19; 20]. While some studies reported increases in absolute terms that became non-significant when normalized for body mass [19; 20], others showed no effect at all [15; 16; 17; 18], emphasizing the need for a comprehensive understanding of contributing factors. Studies have shown that an increase in VO2 peak is often accompanied by a rise in muscle-mass-related parameters such as body mass, fat-free mass, and upper-extremity circumference [19; 20]. This supports the hypothesis that, up to a certain threshold, VO2 peak-DP is primarily constrained by the amount of muscle mass that can be utilized to produce propulsion and/or peripheral factors within the working muscles. This limitation persists until a critical level of active muscle mass is attained. At this point, central factors, such as stroke volume, assume a more prominent role in limiting VO2 peak and VO2 max [24]. Therefore, the current body of evidence on the impact of resistance training on VO2 peak-DP may be biased due to the focus on neuromuscular adaptations in previous studies, potentially neglecting hypertrophic or other physiological responses [15; 16; 17]. In this study, the somewhat lower response rate for VO2 peak-DP compared to dynamic strength (Figure 5) could be attributed to potential neural adaptations resulting from resistance training, underscoring the greater impact of structural changes over neural adaptations on VO2 peak-DP development. Additionally, the performance level and gender of the investigated populations are crucial variables that need consideration. For instance, [PERSON] et al. [18] reported no significant effect of resistance training on VO2 peak-DP standardized to body mass (from 68.5 \(\pm\) 5.3 mL-min-1.kg-1 to 68.3 \(\pm\) 5.4 mL-min-1.kg-1), despite a regimen involving three exercises for three sets in the 4 to 12 RM range. Although VO2 max data were not provided, the reported values suggest a smaller ratio between VO2 peak and VO2 max compared to the population in this study, indicating limited potential for performance improvement by peripheral factors. This may elucidate why resistance training failed to influence VO2 peak-DP despite a notable increase in upper-body lean body mass. Moreover, [PERSON] et al. [20] observed significant enhancements in VO2 peak-DP among female athletes but noted non-significant changes in men. [PERSON] et al. [28] linked gender differences in DP performance to significantly higher muscle mass in the upper body of male athletes compared to that of their female counterparts. These sex-specific nuances underscore the importance of considering the diverse physiological responses to resistance training based on sex, further contributing to the complexity of understanding its impact on VO2 peak-DP. The observed increase in VO2 peak-DP corresponded to substantial improvements in peak power during the DP peak oxygen uptake test, particularly evident in the HL group (14.6% absolute; 14.8% relative) compared to LL (10.3% absolute; 8.1% relative) and CON (0.2% absolute; \(-\)1.6% relative). These outcomes align with existing studies demonstrating the positive effect of resistance training on various aspects of DP performance.