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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/25968

Title: Twelve Weeks of Medium-Intensity Exercise Therapy Affects the Lipoprotein Profile of Multiple Sclerosis Patients.
Authors: Jorissen, Winde
Vanmierlo, Tim
Wens, Inez
Somers, Veerle
Van Wijmeersch, Bart
Bogie, Jeroen F. J.
Remaley, Alan
Op 't Eijnde, Bert O.
Hendriks, Jerome J. A.
Issue Date: 2018
Citation: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 19(1), p. 1-11 (Art N° 139)
Abstract: Multiple sclerosis (MS) is an inflammatory auto-immune disease of the central nervous system (CNS). Serum glucose alterations and impaired glucose tolerance (IGT) are reported in MS patients, and are commonly associated with the development of cardio-metabolic co-morbidities. We previously found that a subgroup of MS patients shows alterations in their lipoprotein profile that are similar to a pre-cardiovascular risk profile. In addition, we showed that a high-intensity exercise training has a positive effect on IGT in MS patients. In this study, we hypothesize that exercise training positively influences the lipoprotein profile of MS patients. To this end, we performed a pilot study and determined the lipoprotein profile before (controls, n = 40; MS patients, n = 41) and after (n = 41 MS only) 12 weeks of medium-intensity continuous training (MIT, n = 21, ~60% of VO2max) or high-intensity interval training (HIT, n = 20, ~100–200% of VO2max) using nuclear magnetic resonance spectroscopy (NMR). Twelve weeks of MIT reduced intermediate-density lipoprotein particle count ((nmol/L); −43.4%; p < 0.01), low-density lipoprotein cholesterol (LDL-c (mg/dL); −7.6%; p < 0.05) and VLDL size ((nm); −6.6%; p < 0.05), whereas HIT did not influence the lipoprotein profile. These results show that MIT partially normalizes lipoprotein alterations in MS patients. Future studies including larger patient and control groups should determine whether MIT can reverse other lipoprotein levels and function and if these alterations are related to MS disease progression and the development of co-morbidities.
Notes: Hendriks, JJA (reprint author), Hasselt Univ, Sch Life Sci, BIOMED, B-3590 Diepenbeek, Belgium, winde.jorissen@uhasselt.be; tim.vanmierlo@uhasselt.be; inez.wens@uhasselt.be; veerle.somers@uhasselt.be; bart.vanwijmeersch@uhasselt.be; jeroen.bogie@uhasselt.be; Alan.Remaley@nih.gov; bert.opteijnde@uhasselt.be; jerome.hendriks@uhasselt.be
URI: http://hdl.handle.net/1942/25968
DOI: 10.3390/ijms19010193
ISI #: 000424407200190
ISSN: 1422-0067
Category: A1
Type: Journal Contribution
Appears in Collections: Research publications

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