title: Forced-exercise attenuates experimental autoimmune neuritis.
abstract: Physical inactivity in combination with a sedentary lifestyle is strongly associated with an increased risk of development of inflammatory-mediated diseases, including autoimmune disorders. Recent studies suggest that anti-inflammatory effects of physical exercise may be of therapeutic value in some affected individuals. In this study, we determined the effects of forced-exercise (treadmill running) on the development and progression of experimental autoimmune neuritis (EAN), an established animal model of Guillain-Barré syndrome. Adult male Lewis rats were subjected to sedentary (control) or forced-exercise (1.2 km per day, 5 days a week) for three weeks prior to induction of EAN. P2 (53-78)-immunized sedentary control rats developed a monophasic course of EAN beginning on post-injection day 12.33 ± 0.59 (n = 18) and reaching peak severity on day 15.83 ± 0.35 (n = 18). At near peak of disease, ankle- and sciatic notch-evoked compound muscle action potential (CMAP) amplitudes in sedentary control rats were reduced (~50%) while motor nerve conduction velocity (MNCV) was slowed (~30%) compared with pre-induction evoked responses. In marked contrast, rats undergoing forced-exercise exhibited a significantly less severe clinical course of EAN beginning on post-injection day 12.63 ± 0.53 (n = 16) and reaching peaking severity on day 14.69 ± 0.73 (n = 16). At near peak of disease, ankle- and sciatic-notch-evoked CMAP amplitudes in forced-exercised rats were preserved while EAN-associated slowing of MNCV was modestly attenuated by exercise. Three weeks of forced-exercise reduced by 46% total plasma corticosterone content while elevating the levels of corticosteroid binding globulin. We conclude from this study that forced-exercise administered prior to and during development of EAN affords a novel measure of protection against autoimmune-associated deficits in peripheral nerve evoked responses independent of steroid-induced immune suppression.
authors.affiliation: Research Service, Department of Veterans Affairs, Edward Hines Jr. VA Hospital, Hines, IL 60141, USA.
authors.forename: Michael W
authors.initials: MW
authors.lastname: Calik
authors.forename: Sahadev A
authors.initials: SA
authors.lastname: Shankarappa
authors.forename: Evan B
authors.initials: EB
authors.lastname: Stubbs
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D003345:Corticosterone / Q000097:blood; D003711:Demyelinating Diseases / Q000276:immunology / Q000473:pathology; D019054:Evoked Potentials, Motor / Q000502:physiology; D005081:Exercise Therapy / Q000379:methods*; D007165:Immunosuppression Therapy; D008297:Male; D009431:Neural Conduction / Q000502:physiology; D009444:Neuritis, Autoimmune, Experimental / Q000276:immunology / Q000628:therapy*; D010523:Peripheral Nervous System Diseases / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D010805:Physical Conditioning, Animal; D051381:Rats; D011917:Rats, Inbred Lew; D012584:Sciatic Nerve / Q000503:physiopathology; D014156:Transcortin / Q000032:analysis
chemical_list: D014156:Transcortin; D003345:Corticosterone