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Concurrent training further enhances markers of skeletal muscle ribosome biogenesis, but not associated signalling responses, versus single-mode resistance training

J.J. Fyfe,1,2 D.J. Bishop,2 J.D. Bartlett,2 E.D. Hanson,2,3 M.J. Anderson,2 A.P. Garnham1,2 and N.K. Stepto,2 1School of Exercise and Nutrition Sciences, Deakin University, Burwood, VIC 3125, Australia, 2Institute of Sport, Exercise and Active Living (ISEAL), Victoria University, Footscray, VIC 3011, Australia and 3Department of Exercise and Sport Science, University of North Carolina, Chapel Hill, NC 27514, USA.

Previous work (Apro et al., 2013; Fyfe et al., 2016) suggests attenuated skeletal muscle hypertrophy with concurrent training is not mediated via blunted post-exercise increases in translational efficiency (i.e. mTORC1 signalling or rates of muscle protein synthesis). Whether increased translational capacity (i.e. ribosome biogenesis), which occurs following resistance training (RT) in humans (Figueiredo et al., 2015), is instead attenuated with concurrent training is unclear. We therefore examined markers of ribosome biogenesis in human skeletal muscle after concurrent training [incorporating either high-intensity interval training (HIT) or moderate-intensity continuous training (MICT)], versus RT performed alone.

Recreationally-active men (n = 23; VO2peak, 44 ± 11 mL·kg-1·min-1; mean ± SD) underwent 8 wk (3 sessions/wk) of either 1) HIT cycling and RT (HIT+RT group, n=8), 2) MICT cycling and RT (MICT+RT group, n=7) or 3) RT only (RT group, n=8). Vastus lateralis biopsies were obtained at rest both pre- and post-training to evaluate basal training-induced responses, and 1 h and 3 h after the final training bout to examine post-exercise skeletal muscle molecular responses in a training-accustomed state.

Basal training-induced changes in markers of ribosome biogenesis in skeletal muscle, including expression of the 45S rRNA (ribosomal RNA) precursor (∼75%), and mature rRNA species 5.8S (∼125%) and 28S (∼75%) were greater for both MICT+RT and HIT+RT versus RT alone, mirroring the larger increases in total RNA content (∼27-47%). During the final training session, RT further increased the phosphorylation of p70S6K1Thr389 (∼50%) and regulators of 45S rRNA transcription [TIF-1ASer649 (∼52-75%) and UBFSer388 (∼49-64%)] versus concurrent exercise. Training-induced increases in type I muscle fibre cross-sectional area were attenuated following HIT+RT versus RT alone (∼34%).

Training-induced changes in mature rRNA expression and total RNA content in skeletal muscle were greater with concurrent training versus RT alone, suggesting enhanced ribosome biogenesis. This occurred despite RT further inducing both mTORC1 and ribosome biogenesis-related signalling responses following the final training bout. Attenuated changes in skeletal muscle translational capacity therefore do not appear to mediate interference to RT adaptations with short-term concurrent training; however, blunted mTORC1 and ribosome biogenesis-related signalling may play a role following longer-term training.

Apro W, Wang L, Ponten M, Blomstrand E & Sahlin K. (2013) Am J Physiol Endocrinol Metab 305: E22-32.

Figueiredo VC, Caldow MK, Massie V, Markworth JF, Cameron-Smith D & Blazevich AJ. (2015) Am J Physiol Endocrinol Metab 309: E72-83.

Fyfe JJ, Bishop DJ, Zacharewicz E, Russell AP & Stepto NK. (2016) Am J Physiol Regul Integr Comp Physiol 310: R1297-1311.