Experimental autoimmune encephalomyelitis (EAE) induces significant reduction of the body mass concomitant to sickness behavior and anorexia. We investigated whether regular physical exercise prevents metabolic alterations associated with body mass loss occurring during EAE inflammatory peak. Female C57BL/6 mice were assigned to the unexercised and exercised (trained) groups. In four weeks, EAE was induced in half of the animals in each group, and the exercise protocol was maintained until 10 days post-induction (dpi 10) completing 6 weeks of regular exercise (forced swimming). At dpi 14, the relative mass of metabolic tissues, serum levels of triglycerides, cholesterol, and glucose, glycogen contents in the muscle and liver, and muscle levels of cytokines were measured. A significantly decreased clinical score associated with attenuation of the body mass loss in exercised EAE animals, as compared to the non-exercised ones, was observed. The associated metabolic parameters were not modified by this approach, although negative correlations between some parameters and clinical score at dpi 14 were observed. Although the prior program of aerobic exercise is capable of decreasing clinical score and body mass loss, it is not sufficient to modify metabolic outcomes associated with inflammation at the EAE peak.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
A. Kutzelnigg and H. Lassmann, “Pathology of multiple sclerosis and related inflammatory demyelinating diseases,” Handb. Clin. Neurol., 122, 15-58 (2014).
M. S. Recks, K. Addicks, and S. Kuerten, “Spinal cord histopathology of MOG peptide 35-55-induced experimental autoimmune encephalomyelitis is timeand score-dependent,” Neurosci. Lett., 494, No. 3, 227-231 (2011).
Y. Pollak, H. Ovadia, E. Orion, et al., “The EAEassociated behavioral syndrome: I. Temporal correlation with inflammatory mediators,” J. Neuroimmunol., 137, Nos. 1-2, 94-99 (2013).
D. W. Gould, I. Lahart, A. R. Carmichael, et al., “Cancer cachexia prevention via physical exercise: molecular mechanisms”, J. Cachexia Sarcopenia Muscle, 4, No. 2, 111-124 (2013).
D. Bernardes, O. C. Oliveira-Lima, T. Vitarelli-Silva, et al., “Differential brain and spinal cord cytokine and BDNF levels in experimental autoimmune encephalomyelitis are modulated by prior and regular exercise, “ J Neuroimmunol., 264, Nos. 1-2, 24-34 (2013).
D. Bernardes, M. S. J. Manzoni, C. Souza, et al., “Efeitos da dieta hiperlipídica e do treinamento de natação somre o metabolismo de recuperação ao exercício em ratos,” Rev.Paul. Educ. Fís. (ISSN 0102-7549. Cessou em 2003. Continuação ISSN 1807-5509, Revista Brasileira de Educação Física e Esporte)., 18, No. 2, 191-200 (2004).
R. K. Dishman, H. R. Berthoud, F. W. Booth, et al., “Neurobiology of exercise,” Obesity (Silver Spring), 14, No. 3, 345-356 (2006).
J. M. Argiles, S. Busquets, F. J. Lopez-Soriano, et al., “Are there any benefits of exercise training in cancer cachexia?” J. Cachexia Sarcopenia Muscle, 3, No. 2, 73-76 (2012). 9. W. Cendrowski, W. Szajbel, E. Waszkiewicz, and K. Niedzielska, “Serum lipid studies in multiple sclerosis,” Z. Klin. Chem. Klin. Biochem., 6, 423-425 (1968).
W. Cendrowski, W. Szajbel, E. Waszkiewicz, and K. Niedzielska, “Serum lipid studies in multiple sclerosis,” Z. Klin. Chem. Klin. Biochem., 6, 423-425 (1968).
J. N. Cumings, R. C. Shortman, and T. Skrbic, “Lipid studies in the blood and brain in multiple sclerosis and motor neurone disease,” J. Clin. Pathol., 18, No. 5, 641-644 (1965).
A. Montfoort, R. W. R. Baker, R. H. S. Thompson, and K. J. Zilkha, “Plasma phospholipids and their fatty acid composition in multiple sclerosis,” J. Neurol. Neurosurg. Psychiat., 29, No. 2, 99-102 (1966).
A. de Haan, M. R. van der Vliet, J. J. Hendriks, et al., “Changes in characteristics of rat skeletal muscle after experimental allergic encephalomyelitis,” Muscle Nerve, 29, No. 3, 369-375 (2004).
V. Polacow and A. H. Lancha Jr., “Dietas hiperglicídicas: efeitos da substituição isoenergética de gordura por carboidratos sobre o metabolismo de lipídios, adiposidade corporal e sua associação com atividade física e com o risco de doença cardiovascular,” Arq. Bras. Endocrinol. Metab., 51, No. 3, 389-400 (2007).
M. Buffelli, E. Pasino, and A. Cangiano, “Paralysis of rat skeletal muscle equally affects contractile properties as does permanent denervation,” J. Muscle Res. Cell Motil., 18, No. 6, 683-695 (1997).
J. Vogt, F. Paul. O. Aktas, et al., “Lower motor neuron loss in multiple sclerosis and experimental autoimmune encephalomyelitis,” Ann. Neurol., 66, No. 3, 310-322 (2009).
S. Deforges, J. Branchu, O. Biondi, et al., “Motoneuron survival is promoted by specific exercise in a mouse model of amyotrophic lateral sclerosis,” J. Physiol., 587, Pt. 14, 3561-3572 (2009).
D. Bernardes, R. Brambilla, V. Bracchi-Ricard, et al. “Prior regular exercise improves clinical outcome and reduces demyelination and axonal injury in experimental autoimmune encephalomyelitis,” J. Neurochem., 136 (Suppl. 1), 63–73, (2015).
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Bernardes, D., Oliveira-Lima, O.C., da Silva, T.V. et al. Metabolic Alterations in Experimental Autoimmune Encephalomyelitis in Mice: Effects of Prior Physical Exercise. Neurophysiology 48, 117–121 (2016). https://doi.org/10.1007/s11062-016-9577-7
Received:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s11062-016-9577-7