Concurrent exercise from training to transcriptome

The principle of training specificity dictates that adaptations to exercise training are specific to the mode, frequency, and duration of exercise performed, and result in distinct and divergent skeletal muscle phenotypes. Strength-based training promotes skeletal muscle hypertrophy and maximal force-generating capacity while endurance-based training improves skeletal muscle oxidative capacity and cardiorespiratory fitness. Previous research has suggested the capacity of skeletal muscle to adapt to strength and endurance training when performed simultaneously (i.e., concurrent exercise training) appears to be limited and results in blunted resistance-based adaptations compared to resistance training alone – a phenomenon referred to as the ‘interference effect.’ The molecular basis of skeletal muscle adaptation to exercise training involves the propagation of numerous mechanical and chemical stimuli through signalling cascades that ultimately results in an increase in an array of exercise-induced proteins and increases in maximal enzyme activities. The nature of these alterations is specific to the frequency, intensity, volume, and type of metabolic demands placed upon the muscle during exercise. Given the divergent stimuli associated with endurance- and resistance-based exercise, it has been hypothesised that antagonistic molecular signals may underlie the adaptive interference observed with concurrent training. In order to circumvent this effect, strategies have focused on altering the proximity of training sessions (i.e., same day versus alternate day training) and training variables (i.e., frequency, volume, mode). Additionally, optimising post-exercise nutrition (i.e., dietary protein) has been proposed as a potential variable that may promote anabolic signalling and prevent the interference effect. To determine whether these training strategies in association with a high protein diet (2 g•kg-1•d-1) can attenuate the ‘interference effect,’ 32 recreationally active males (age: 25±5 y; body mass index: 24±3 kgm-2; mean ± standard deviation) performed 12 wk of either isolated resistance (RES; n=10) or endurance (END; n=10) training (3 sessions•wk-1), or concurrent resistance and endurance (CET; n=12) training (6 sessions•wk-1). Maximal strength, maximal aerobic capacity, peak power, body composition, and muscle architecture were assessed throughout the intervention. To explore molecular responses that may underpin any impaired adaptation after concurrent exercise training, satellite cells and myonuclei were assessed by immunohistochemistry from skeletal muscle biopsy samples. In addition, exploratory transcriptomics was performed from a subset of participants from each training condition. The results from the investigations undertaken for this thesis demonstrate that – despite efforts to circumvent the ‘interference effect’ by implementing recommended strategies of alternate day training, minimising exercise volume, and increasing dietary protein intake – maximal anaerobic power development was attenuated following 12 wk of concurrent exercise training. Myofibre hypertrophy increased to the same magnitude in all training modalities without changes to satellite cell content, suggesting that satellite cell content does not limit the magnitude of hypertrophy achieved during concurrent training. Conversely, myonuclear content displayed strong associations with the degree of myofibre hypertrophy. Transcriptome-wide analysis revealed that concurrent exercise training augments gene sets related to plasma membrane structures while suppressing those related to regulation of messenger ribonucleic acid (mRNA) processing and protein degradation, which may contribute to the ‘interference effect’ in myofibre hypertrophy. Additionally, considerable overlap of gene sets enriched for terms related to extracellular matrix remodelling were observed amongst concurrent exercise training and isolated endurance cycle training, which may underlie attenuations in maximal anaerobic power outputs observed following concurrent training. Collectively, these reveal that the current recommendations to maximise muscle hypertrophy with concurrent training do not result in augmented hypertrophic responses compared to single-mode training, and cannot be explained by satellite cell content or inhibition of anabolic gene programs. These findings underpin future investigations of molecular pathways that have not been considered in the context of concurrent training adaptations