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Review
. 2014 Nov;44 Suppl 2(Suppl 2):S117-25.
doi: 10.1007/s40279-014-0252-0.

Using molecular biology to maximize concurrent training

Affiliations
Review

Using molecular biology to maximize concurrent training

Keith Baar. Sports Med. 2014 Nov.

Abstract

Very few sports use only endurance or strength. Outside of running long distances on a flat surface and power-lifting, practically all sports require some combination of endurance and strength. Endurance and strength can be developed simultaneously to some degree. However, the development of a high level of endurance seems to prohibit the development or maintenance of muscle mass and strength. This interaction between endurance and strength is called the concurrent training effect. This review specifically defines the concurrent training effect, discusses the potential molecular mechanisms underlying this effect, and proposes strategies to maximize strength and endurance in the high-level athlete.

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Figures

Fig. 1
Fig. 1
The concurrent training effect on strength. The figure shows the increase in one repetition maximum in the squat in subjects who participated in 10 weeks of high-intensity resistance exercise alone (resistance), endurance exercise alone (endurance), and both types of training (concurrent). Also, note that the strength and concurrent groups both increased their strength together up to 7 weeks, when the strength group started making greater gains than the concurrent group (adapted from Hickson [1], with permission). 1RM one repetition maximum
Fig. 2
Fig. 2
The activation of the mechanistic target of rapamycin complex 1 (mTORC1, mTOR, and raptor complex) following resistance exercise and feeding. Lifting a heavy weight to failure stimulates a mechanoreceptor that in turn activates an RxRxxS*/T* kinase (depicted by ??? at the membrane) that phosphorylates and moves the TSC2 away from the lysosome allowing Rheb to remain in the GTP bound state. Simultaneously, amino acid uptake and intracellular amino acid levels increase. The extra amino acids stimulate the LRS to act as a GAP towards RagC/D and GATOR2 blocks GATOR1 (the GAP of RagA/B) and the Ragulator GTP loads RagA/B and activates the complex. The active Rag complex then binds to raptor and positions mTOR beside its activator: GTP bound Rheb. The resulting elevation of mTORC1 activity drives myofibrillar protein synthesis and eventually leads to an increase in muscle mass and strength. DEPTOR DEP (Dishevelled, Egl-10 and Pleckstrin) domain-containing mTOR-interacting protein, GβL G-protein beta subunit-like protein, GAP GTPase activating protein, GATOR GAP Activity Towards Rags, GDP guanosine diphosphate, GTP guanosine triphosphate, LAMP2 lysosome-associated membrane protein 2, LAT1 L-type amino acid transporter, LRS leucyl transfer RNA synthase, mTOR mammalian target of rapamycin, mTORC1 mTOR complex 1 P phosphorylation, PRAS40 proline-rich Akt substrate of 40 kDa, Rab7 Ras-related protein 7, raptor the regulatory-associated protein of mTOR, Rheb Ras homolog enriched in brain, TSC2 tublerosclerosis complex

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References

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