2. Abstract
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; V̇O2peak, 44 ± 11 mL-kg−1min−1) underwent 8 wk (3 sessions-wk−1) 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.
Table of contents category: Muscle
Key points summary
Ribosome biogenesis is an important process linked with human skeletal muscle growth following resistance training (RT); however, whether concurrent training alters skeletal muscle ribosome biogenesis compared with RT alone in unknown
In agreement with previous studies, concurrent training blunted the RT-induced increase in type I, but not type II, muscle fibre size
Despite the attenuated muscle hypertrophy with concurrent training, changes in markers of skeletal muscle ribosome biogenesis were generally more favourable with concurrent training vs. RT performed alone
Conversely, a single session of resistance exercise (RE) performed post-training was more potent for inducing signalling responses in skeletal muscle related to both ribosome biogenesis and the mTORC1 pathway, vs. concurrent exercise
Ribosome biogenesis is therefore not compromised following short-term concurrent training; however, both mTORC1 and ribosome biogenesis-related signalling are attenuated in skeletal muscle following a single session of concurrent exercise performed in a training-accustomed state
- 1-RM
- one-repetition maximum
- 4E-BP1
- eukaryotic initiation factor 4E binding protein 1
- AMPK
- 5’ adenosine monophosphate-activated protein kinase
- β2M
- beta-2 microglobulin
- CDK
- cyclin-dependent kinase
- DXA
- dual-energy x-ray absorptiometry
- Fox-O1
- forkhead box-O1
- GAPDH
- glyceraldehyde 3-phosphate dehydrogenase
- HIT
- high-intensity interval training cycling
- LT
- lactate threshold
- MICT
- moderate-intensity continuous cycling
- MPS
- muscle protein synthesis
- mRNA
- messenger RNA
- mTORC1
- mechanistic target or rapamycin complex 1
- MuRF-1
- muscle RING-finger 1
- p70S6K1
- 70 kilodalton ribosomal protein subunit kinase 1
- PGC-1α
- peroxisome proliferator activated receptor gamma co-activator 1 alpha
- POLR1B
- polymerase (RNA) 1 polypeptide B
- RE
- resistance exercise
- RPE
- rating of perceived exertion
- rRNA
- ribosomal ribonucleic acid
- RT
- resistance training
- SL-1
- selectivity factor-1
- TBP
- TATA binding protein
- TIF-1A
- RRN3 polymerase 1 transcription factor
- UBF
- upstream binding factor
- V̇O2peak
- peak volume of oxygen uptake
- Wpeak
- peak aerobic power.