Concurrent resistance and aerobic exercise stimulates both myofibrillar and mitochondrial protein synthesis in sedentary middle-aged men

Donges, Cheyne E.; Burd, Nicholas A.; Duffield, Rob; Smith, Greg; West, Daniel W. D.; Short, Michael; Mackenzie, Richard W.A.; Plank, Lindsay D.; Shepherd, Peter R.; Phillips, Stuart M.; Edge, Johann

doi:10.1152/japplphysiol.00166.2012

Cited by 85 publications

(110 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interference to mTORC1 signaling has been investigated as a mechanism contributing to attenuated RE adaptations during concurrent training in humans (1,29,57). However, whether higher endurance exercise intensities, previously shown to further increase AMPK activity in skeletal muscle compared with lower intensity endurance exercise (70), are associated with greater interference to mTORC1 signaling following concurrent exercise has not been examined.…”

Section: Discussionmentioning

confidence: 99%

“…Biopsies were obtained immediately before RE (REST), after a preceding bout of HIT or work-matched MICT (POST), and 1 h (RE ϩ 1 h) and 3 h (RE ϩ 3 h) after RE. To minimize the number of biopsy samples taken from participants, the initial resting biopsy obtained from the RE trial was used as a basal reference for changes in signaling responses and gene expression for each trial (29). This allowed insight into the influence of prior HIT and MICT on responses within skeletal muscle before subsequent RE.…”

Section: Experimental Trial Overviewmentioning

confidence: 99%

“…Given that AMPK, acting primarily through the peroxisome proliferator-activated ␥-receptor coactivator 1␣ (PGC-1␣), has been associated with many skeletal muscle adaptations to chronic endurance training (67), the interference effect with concurrent training may be partly explained by AMPK-mediated inhibition of the mTORC1 signaling pathway. However, several human studies have shown that concurrent exercise does not compromise either postexercise mTORC1 signaling or rates of MPS (1,2,17,29,69), or even potentiates these responses (57), relative to RE performed alone. Whether these putative interference mechanisms explain the attenuated skeletal muscle adaptations reported following concurrent training in humans (10,53,84) remains unclear.…”

mentioning

confidence: 99%

“…Recent evidence suggests that high-intensity interval training (HIT) is more effective in improving V O 2 max (41,42,79,85) and metabolic health markers (79,85), compared with moderate-intensity continuous training (MICT), while also being more enjoyable (7). However, most studies investigating the early molecular responses to concurrent exercise in humans have employed MICT (e.g., 30 -90 min at 65-70% V O 2 max or 55-70% W max ) (17,22,29,57,81). Whether the intensity of endurance exercise, when performed concurrently with RE, is important in mediating any potential interference effect on postexercise anabolic responses in skeletal muscle is unknown.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle

Fyfe

Bishop

Zacharewicz

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Fyfe JJ, Bishop DJ, Zacharewicz E, Russell AP, Stepto NK. Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle. Am J Physiol Regul Integr Comp Physiol 310: R1297-R1311, 2016. First published April 13, 2016 doi:10.1152/ajpregu.00479.2015.-We compared the effects of concurrent exercise, incorporating either high-intensity interval training (HIT) or moderate-intensity continuous training (MICT), on mechanistic target of rapamycin complex 1 (mTORC1) signaling and microRNA expression in skeletal muscle, relative to resistance exercise (RE) alone. Eight males (mean Ϯ SD: age, 27 Ϯ 4 yr; V O2 peak, 45.7 Ϯ 9 ml·kg Ϫ1 ·min Ϫ1 ) performed three experimental trials in a randomized order: 1) RE (8 ϫ 5 leg press repetitions at 80% 1-repetition maximum) performed alone and RE preceded by either 2) HIT cycling [10 ϫ 2 min at 120% lactate threshold (LT); HIT ϩ RE] or 3) work-matched MICT cycling (30 min at 80% LT; MICT ϩ RE). Vastus lateralis muscle biopsies were obtained immediately before RE, either without (REST) or with (POST) preceding endurance exercise and ϩ1 h (RE ϩ 1 h) and ϩ3 h (RE ϩ 3 h) after RE. Prior HIT and MICT similarly reduced muscle glycogen content and increased ACC Ser79 and p70S6K Thr389 phosphorylation before subsequent RE (i.e., at POST). Compared with MICT, HIT induced greater mTOR Ser2448 and rps6 Ser235/236 phosphorylation at POST. REinduced increases in p70S6K and rps6 phosphorylation were not influenced by prior HIT or MICT; however, mTOR phosphorylation was reduced at RE ϩ 1 h for MICT ϩ RE vs. both HIT ϩ RE and RE. Expression of miR-133a, miR-378, and miR-486 was reduced at RE ϩ 1 h for HIT ϩ RE vs. both MICT ϩ RE and RE. Postexercise mTORC1 signaling following RE is therefore not compromised by prior HIT or MICT, and concurrent exercise incorporating HIT, but not MICT, reduces postexercise expression of miRNAs implicated in skeletal muscle adaptation to RE. concurrent training; interference; exercise intensity; high-intensity interval training; continuous training INCORPORATING BOTH RESISTANCE (RE) and endurance exercise into a periodized training program is termed concurrent training (56). Compared with undertaking RE alone, concurrent training attenuates skeletal muscle hypertrophy and maximal strength development in some (10,19,33,48,53), but not all (5,58,63,75,76), studies. Given that skeletal muscle mass plays an important role in overall metabolic health (87), and many athletes require elements of strength and muscle hypertrophy, concomitantly with a high aerobic capacity (47), minimizing interference during concurrent training has implications for optimizing both health and performance outcomes.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Experimental Trial Overviewmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle

Fyfe

Bishop

Zacharewicz

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…Our results do not preclude PGC-1α4 to be required for muscle hypertrophy in other contexts. Accordingly, some studies show no changes in PGC-1α expression in human skeletal muscle after resistance exercise (33)(34)(35), whereas others have reported opposite results (17,36).…”

Section: Discussionmentioning

confidence: 99%

The transcriptional coactivator PGC-1α is dispensable for chronic overload-induced skeletal muscle hypertrophy and metabolic remodeling

Pérez-Schindler

Summermatter

Santos

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Skeletal muscle mass loss and dysfunction have been linked to many diseases. Conversely, resistance exercise, mainly by activating mammalian target of rapamycin complex 1 (mTORC1), promotes skeletal muscle hypertrophy and exerts several therapeutic effects. Moreover, mTORC1, along with peroxisome proliferatoractivated receptor γ coactivator 1α (PGC-1α), regulates skeletal muscle metabolism. However, it is unclear whether PGC-1α is required for skeletal muscle adaptations after overload. Here we show that although chronic overload of skeletal muscle via synergist ablation (SA) strongly induces hypertrophy and a switch toward a slow-contractile phenotype, these effects were independent of PGC-1α. In fact, SA down-regulated PGC-1α expression and led to a repression of energy metabolism. Interestingly, however, PGC-1α deletion preserved peak force after SA. Taken together, our data suggest that PGC-1α is not involved in skeletal muscle remodeling induced by SA.muscle overload | transcriptional regulation | resistance training S keletal muscle size exhibits drastic changes throughout life, mainly dependent on mechanical load and nutritional supply (1). For example, loss of muscle mass is observed during immobilization and starvation, but also under pathological conditions like heart failure and cancer (2). To date, resistance exercise is considered as one of the most efficient ways to induce skeletal muscle hypertrophy and to revert the adverse effects of muscle wasting (2, 3). However, because pharmacological interventions are scarce, identification of the molecular regulation of muscle remodeling via resistance exercise is of great therapeutic interest.Activation of mammalian target of rapamycin complex 1 (mTORC1) is the main regulatory step by which resistance exercise enhances protein synthesis and skeletal muscle size (4). In fact, inhibition of mTORC1 drastically abrogates plantaris hypertrophy via chronic overload (5), even though muscle size is not affected uniformly by muscle knockout of the mTORC1 inhibitor tuberous sclerosis complex 1 (6). Interestingly, the activity of the mTORC1 protein kinase complex positively correlates with oxidative capacity (7,8). Moreover, mTORC1 is recruited to the promoter of a wide range of metabolism-related genes to regulate their expression (9-11). In skeletal muscle, mTORC1 regulates oxidative metabolism by facilitating the activation of Yin Yang 1 by the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) (10, 12). The physiological context in which the mTORC1-PGC-1α axis regulates energy metabolism, however, is unknown.Protein degradation is an important limiting factor of skeletal muscle hypertrophy. This process is fine-tuned by the transcription factor forkhead box O3 (FOXO3), which regulates the expression of the E3 ubiquitin ligases muscle ring finger protein 1 (MuRF1) and F-box protein 32 (Fbxo32/atrogin-1) (13). Interestingly, PGC-1α represses FOXO3 activity and consequently ameliorates skeletal muscle mass loss during denervation and aging (14-16)...

show abstract

Exercise and the Mitochondria

Gidlund

2019

Cardiorespiratory Fitness in Cardiometabolic Diseases

View full text Add to dashboard Cite

Concurrent resistance and aerobic exercise stimulates both myofibrillar and mitochondrial protein synthesis in sedentary middle-aged men

Cited by 85 publications

References 45 publications

Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle

Concurrent exercise incorporating high-intensity interval or continuous training modulates mTORC1 signaling and microRNA expression in human skeletal muscle

The transcriptional coactivator PGC-1α is dispensable for chronic overload-induced skeletal muscle hypertrophy and metabolic remodeling

Exercise and the Mitochondria

Contact Info

Product

Resources

About