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European Journal of Applied Physiology

, Volume 117, Issue 11, pp 2125–2135 | Cite as

Do metabolites that are produced during resistance exercise enhance muscle hypertrophy?

  • Scott J. Dankel
  • Kevin T. Mattocks
  • Matthew B. Jessee
  • Samuel L. Buckner
  • J. Grant Mouser
  • Jeremy P. LoennekeEmail author
Invited Review

Abstract

Many reviews conclude that metabolites play an important role with respect to muscle hypertrophy during resistance exercise, but their actual physiologic contribution remains unknown. Some have suggested that metabolites may work independently of muscle contraction, while others have suggested that metabolites may play a secondary role in their ability to augment muscle activation via inducing fatigue. Interestingly, the studies used as support for an anabolic role of metabolites use protocols that are not actually designed to test the importance of metabolites independent of muscle contraction. While there is some evidence in vitro that metabolites may induce muscle hypertrophy, the only study attempting to answer this question in humans found no added benefit of pooling metabolites within the muscle post-exercise. As load-induced muscle hypertrophy is thought to work via mechanotransduction (as opposed to being metabolically driven), it seems likely that metabolites simply augment muscle activation and cause the mechanotransduction cascade in a larger proportion of muscle fibers, thereby producing greater muscle growth. A sufficient time under tension also appears necessary, as measurable muscle growth is not observed after repeated maximal testing. Based on current evidence, it is our opinion that metabolites produced during resistance exercise do not have anabolic properties per se, but may be anabolic in their ability to augment muscle activation. Future studies are needed to compare protocols which produce similar levels of muscle activation, but differ in the magnitude of metabolites produced, or duration in which the exercised muscles are exposed to metabolites.

Keywords

Blood flow restriction Fatigue Lactate Metabolic stress Motor unit recruitment Resistance training 

Abbreviations

1RM

One-repetition maximum

AMPK

AMP-activated protein kinase

CAMKII

Calcium–calmodulin protein kinase II

EMG

Electromyography

FAK

Focal adhesion kinase

MAPK

Mitogen-activated protein kinase

mTORC1

Mechanistic target of rapamycin complex 1

TSC2

Tuberous sclerosis complex 2

Notes

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

Funding

None.

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Copyright information

© Springer-Verlag GmbH Germany 2017

Authors and Affiliations

  • Scott J. Dankel
    • 1
  • Kevin T. Mattocks
    • 1
  • Matthew B. Jessee
    • 1
  • Samuel L. Buckner
    • 1
  • J. Grant Mouser
    • 1
  • Jeremy P. Loenneke
    • 1
    Email author
  1. 1.Kevser Ermin Applied Physiology Laboratory, Department of Health, Exercise Science, and Recreation ManagementThe University of MississippiUniversityUSA

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