Effects of Exercise Intensity in Experimental Autoimmune EncephalomyelitisWens I1*, Broekmans T1, Hendriks JJA1, Savelberg HH2, Hesselink MK2, Eijnde BO1
- Corresponding Author:
- Inez Wens
REVAL – Rehabilitation Research Center
Biomedical Research Institute (BIOMED) Hasselt University
Martelarenlaan 42, B-3500 Hasselt, Belgium
Tel: +32 (0)11 26 93 70
E-mail: [email protected]
Received date: November 11, 2014; Accepted date: January 19, 2015; Published date: January 23, 2015
Citation: Wens I, Broekmans T, Hendriks JJA, Savelberg HH, Hesselink MK et al. (2015) Effects of Exercise Intensity in Experimental Autoimmune Encephalomyelitis. J Mult Scler 2:133. doi:10.4172/2376-0389.1000133
Copyright: ©2014 Wens I, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Background: Research on muscle contractile properties and disease progression following experimental autoimmune encephalomyelitis (EAE) and physical exercise remains conflicting. Objective: To investigate the effect of different exercise intensities on muscle contractile properties and hindquarter paralysis during EAE in Lewis rats.
Methods: A control and EAE group were divided in sedentary, light, moderate and high intensity running subgroups. During EAE course, hind limb paralysis, body weight and food intake were registered. Following EAE recovery isokinetic foot extensor strength was measured during 115 maximal contractions and fiber characteristics of m. tibialis anterior (TA) and m. extensor digitorum longus (EDL) were analysed.
Results: EAE reduced CSA of type IIb+x fibers of TA and EDL, while type I and IIa fibers CSA were not affected by EAE. Exercise did not change CSA of type I, IIa and IIb+x fibers of EDL nor TA, except for TA type IIa fibers CSA, which increased in EAE moderate and EAE high intensity groups. Muscle work peak was absent in all EAE animals during isokinetic muscle contractions. Intense exercise delayed onset of hindquarter paralysis in EAE, while disease peak and remission were not affected by exercise.
Conclusion: This study suggests that EAE reduces CSA of type IIb+x fibers of TA and EDL. This possibly explains the absence of peak muscle work during the first of a series of isokinetic muscle contractions. Furthermore, exercise was not able to reduce muscle fiber atrophy, whereas high intensity exercise delayed onset of hindquarter paralysis.