Volume 11 Supplement 1

Proceedings of the Eleventh International Society of Sports Nutrition (ISSN) Conference and Expo

Open Access

A comparison of the effects of ursolic acid and l-leucine supplementation on IGF-1 receptor and AKT-mTOR signaling in response to resistance exercise in trained men

  • David Church1,
  • Neil Schwarz1,
  • Mike Spillane1,
  • Sarah McKinley1,
  • Tom Andre1 and
  • Darryn S Willoughby1Email author
Journal of the International Society of Sports Nutrition201411(Suppl 1):P19

https://doi.org/10.1186/1550-2783-11-S1-P19

Published: 1 December 2014

Background

Resistance exercise stimulates skeletal muscle protein synthesis (MPS) during post-exercise recovery due to up-regulation of the mammalian target of rapamycin (mTOR) signaling pathway. L-leucine supplementation is also known to stimulate MPS by activating mTOR signaling. However, recent research has discovered a natural compound called ursolic acid which also appears to stimulate MPS by activating the mTOR signaling pathway, and has been presumed to occur due to IGF-1 receptor (IGF-1R) up-regulation. Ursolic acid is a natural pentacyclic triterpenoid carboxylic acid that is widely found in apple skin and other fruits such as cranberries. The main purpose of this study was to compare the effects of a single dose of ursolic acid or L-leucine supplementation given immediately after resistance exercise on IGF-1 (a serum regulator of MPS) and the subsequent effects of IGF-1 on phosphorylating/activating its receptor (IGF-1RTyr1131). Furthermore, the purpose was to also determine the effects on signaling intermediates of MPS contained within the Akt/mTOR pathway (phosphorylated levels of AktThr308, mTORSer2448, p70S6KThr389).

Methods

In a randomized, cross-over design, 9 apparently healthy, resistance-trained [regular, consistent resistance training (i.e. thrice weekly) for at least 1 year prior to the onset of the study], men between the ages of 18-30 volunteered to participate in this study and performed three separate testing sessions of lower-body resistance exercise involving 4 sets of 8-10 repetitions at 75-80% 1-RM on the angled leg press and knee extension exercises. Immediately after each resistance exercise session, participants orally ingested 3 grams (0.043 g/kg equivalent) of cellulose placebo (PLC), L-leucine (LEU), or ursolic acid (UA). A venous blood sample was obtained before, and 0.5, 2, and 6 hr post-exercise, whereas a vastus lateralis muscle biopsy was obtained before and 2 and 6 hr post-exercise. Each testing session was separated by 7 days to allow full recovery between sessions. Statistical analyses were performed utilizing separate two-way ANOVA for each criterion variable employing a probability level of ≤ 0.05. Consent to publish the results was obtained from all participants.

Results

Using ELISA, no significant differences were observed among the three supplements for serum IGF-1 (p > 0.05). Also using ELISA, for skeletal muscle phosphoproteins, no significant differences existed among the three supplements for phosphorylated IGF-1R, Akt, and p70S6K (p > 0.05). However, the LEU supplement significantly increased phosphorylated mTOR compared to UA and PLC (p = 0.001).

Conclusion

At the 3 g dose provided, ursolic acid was unable to increase IGF-1R signaling and, unlike L-leucine, ursolic acid had no positive effect on mTOR signaling activity. Therefore, ursolic acid appears to have no effect on mTOR activity when ingested immediately following resistance exercise.

Authors’ Affiliations

(1)
Baylor University

Copyright

© Church et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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