Activin A suppression during acute exercise

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 389-405-Signaling Originating from Membrane Receptors
Basic/Translational
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-398
Jakob Hansen*1, Anders Rinnov1, Claus Brandt2 and Peter Plomgaard3
1Centre of Inflammation and Metabolism, Department of Infectious Diseases and CMRC, Rigshospitalet, Faculty of Health Science, University of Copenhagen, Denmark, 2Centre of Inflammation and Metabolism, Department of Infectious Diseases and CMRC, Rigshospitalet, Faculty of Health Science, University of Copenhagen, Denmark, Copenhagen, Denmark, 3Rigshospitalet, Copenhagen, Denmark
Background

Activin A plays an important role in the inflammatory response but it has recently been demonstrated to correlate with markers of insulin resistance in patients with type 2 diabetes. The endogenous antagonist of activin A, follistatin, is elevated after an acute exercise bout. In the present study, we evaluated plasma activin A in relation to an acute exercise bout. Furthermore, we evaluated the interaction between plasma activin A and follistatin during exercise.

Methods

Study 1. Ten subjects went through three hours of bicycle exercise at an intensity of 50% of individual VO2 max followed by a six hours recovery period of supine rest. During the three hour exercise bout, blood samples were obtained every hour, while blood samples were obtained at time points 5h, 6h and 9h during recovery (and again 24h post-exercise).

Study 2. Twenty-four female NMRI (Taconic, Bomholtgaard, Denmark) mice (age 8-10 weeks) went through one hour of swimming exercise. Eight mice were sacrificed at time points 1h, 3h and 6h after the exercise bout. Eight mice served as controls (0h). The following tissues were collected from all mice: gastrocnemius and soleus muscle, subcutaneous (inguinal) and visceral (gonadal) adipose tissue, heart, liver kidney and spleen.

Results

Study 1.During the three hour exercise bout, plasma activin A is unaffected at a concentration of 223.9-242.5 (pg/ml). Two hours after the cessation of the exercise bout plasma activin A decreases by ~ 40% to 138.3 (pg/ml)(p<0.05) and remains decreased by  ~ 40% at time points 6h and 9h (both p<0.05) during recovery. After 24h, plasma activin A is back to baseline at a concentration of 206.8 (pg/ml).

Whereas plasma activin A decreases during recovery from exercise, plasma follistatin increases during the recovery period. During the exercise bout plasma follistatin is unaffected, but two hours into recovery plasma follistatin is increased by ~ 5-fold (p<0.05) and remains elevated at time points 6h (6-fold) and 9h (3.5-fold) (both p<0.05) during recovery. After 24h, plasma follistatin is back to baseline.

When analysed in a regression model, a correlation between individually lowest plasma activin A level and highest plasma follistatin level exist (p<0.004). 

Study 2. Tissue-specific activin A mRNA expression was detected in all tissues at all time points. No significant change in activin A mRNA is detectable in skeletal muscle, adipose tissue, heart, kidney or spleen. However, in the liver activin A mRNA content is decreased by 50% at time point 3h (p<0.05).

Conclusions

We demonstrate that plasma activin A is suppressed and activin A mRNA is down-regulated in the murine liver during the recovery from acute exercise. These data indicate that the activin A-follistatin axis is highly regulated during recovery from exercise, which could have implications for both glucose metabolism and skeletal muscle regeneration in relation to exercise.

Nothing to Disclose: JH, AR, CB, PP

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm