Background: This exploratory study examined associations between Angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism (ACE I/D) and aerobic and strength responses to concurrent training in high-level football players. Methods: Twenty-five male players completed six weeks of concurrent training (DD, n = 8; ID, n = 10; II, n = 7). Outcomes were peak oxygen uptake (VO₂peak), squat one-repetition maximum (1RM), and bench press 1RM. Primary analyses assessed genotype × time interactions using mixed-design repeated-measures analysis of variance (ANOVA), with Benjamini–Hochberg correction across outcomes and Holm-adjusted pairwise comparisons of changes. Supplementary analyses included baseline-adjusted analysis of covariance (ANCOVA)and change-score regressions adjusted for age and body mass index, with HC3 robust standard errors. Results: All three outcomes improved significantly within each genotype group. Genotype × time interactions were significant for VO₂peak, squat 1RM, and bench press 1RM (Benjamini–Hochberg-adjusted p = 0.0015, 0.0015, and 0.0028, respectively). Holm-adjusted comparisons showed greater VO₂peak gains in ID and II than in DD (adjusted p ≤ 0.006). DD showed greater squat and bench press gains than ID and II (adjusted p ≤ 0.026). No outcome differed significantly between ID and II after Holm adjustment. However, the ID versus DD difference in VO₂peak change was not significant in age- and BMI-adjusted regression with HC3 standard errors (p = 0.063). Conclusions: ACE I/D genotype was associated with differences in aerobic and strength adaptations following concurrent training in this small cohort. Support for individual comparisons varied across analyses. These exploratory findings require replication in larger independent cohorts before genotype-based training prescriptions can be justified.

Background/Objectives: Whether caffeine provides additional benefit when superimposed on individualized plyometric conditioning remains unclear. We examined whether 3 mg·kg⁻¹ caffeine altered the temporal countermovement jump (CMJ) response following reactive strength index (RSI)-derived individualized drop-jump (DJ) conditioning and explored moderation by habitual caffeine exposure. Methods: Thirty Chinese Han male basketball players (median age, 22.0 years [IQR, 21.0–27.75]) entered a randomized, double-blind, placebo-controlled crossover trial; 17 reported no caffeine exposure and 13 reported exposure during the preceding 4 weeks. After caffeine (CAF; 3 mg·kg⁻¹) or placebo (PLA), a 60-min absorption period, and warm-up, participants performed a post-supplement, pre-conditioning CMJ followed by 3 × 5 DJs. CMJ was assessed at 15 s, 3, 6, 9, and 12 min. The primary outcome was the Condition × Time effect on CMJ. All 30 randomized participants contributed data; three did not complete Period 2 because readiness criteria were not met, but Period 1 data were retained (57 participant-period observations). Results: CMJ varied across time (p < 0.001), but Condition × Time was not significant (p = 0.305). CAF–PLA differences at 15 s, 3, 6, 9, and 12 min were 0.89 cm (95% CI, −0.11 to 1.88), 0.39 (−0.61 to 1.38), 0.21 (−0.79 to 1.21), 0.84 (−0.15 to 1.84), and 0.71 (−0.29 to 1.71), respectively (all Holm-adjusted p ≥ 0.399). Habitual caffeine exposure showed no global moderation continuously (p = 0.158) or categorically (p = 0.116). An isolated 9-min contrast at zero reported exposure favored CAF by 1.83 cm (95% CI, 0.74–2.92; Holm-adjusted p = 0.031) but was exploratory. RPE showed no Condition × Time interaction (p = 0.253); at 15 s, CAF–PLA was −0.60 points (95% CI, −1.09 to −0.12; Holm-adjusted p = 0.088). Conclusions: This study did not obtain clear evidence that 3 mg·kg⁻¹ caffeine provided additional CMJ improvement following this specific RSI-derived individualized DJ protocol. Habitual caffeine exposure did not systematically moderate the temporal response; the isolated signal was exploratory.