Combining RT with endurance training (i.e., concurrent training) may attenuate skeletal muscle hypertrophy consequent to RT; however, the underlying mechanisms are unclear. We investigated whether markers of ribosome biogenesis, a process linked with skeletal muscle hypertrophy, are attenuated following concurrent training vs. RT alone. Twenty-three males (mean ± SD: age, 29.6 ± 5.5 y; VO2peak, 44 ± 11 mL/kg/min) underwent 8 wk (3 sessions/wk) of either: 1) HIT (high-intensity interval training) combined with RT (HIT+RT group, n=8), 2) work-matched MICT (moderate-intensity continuous training) combined with RT (MICT+RT group, n=7), or 3) RT alone (RT group, n=8). Vastus lateralis biopsies were obtained before training, and immediately before, 1 h and 3 h after the final training session. Type I muscle fibre cross-sectional area (CSA) was further increased by RT vs. HIT+RT (34 ±22%; ES, 1.03 ±0.80), but not vs. MICT+RT (15 ±54%; ES, 0.39 ±1.45). Basal training-induced changes in expression of the 45S ribosomal RNA (rRNA) precursor, and 5.8S and 28S mature rRNAs were greater for concurrent exercise vs. RT, largely because of trends for reduced rRNA expression following RT. During the final training session, RT further increased skeletal muscle mTORC1 signalling (p70S6K1 and rps6 phosphorylation) and signalling related to 45S rRNA transcription (TIF-1A and UBF phosphorylation) vs. concurrent exercise. Thus, when performed in a training-accustomed state, RT preferentially induces mTORC1 and ribosome biogenesis-related signalling in human skeletal muscle vs. concurrent exercise. However, changes in markers of skeletal muscle ribosome biogenesis were more favourable with concurrent training vs. RT.