title: Gradually increased training intensity benefits rehabilitation outcome after stroke by BDNF upregulation and stress suppression.
abstract: Physical training is necessary for effective rehabilitation in the early poststroke period. Animal studies commonly use fixed training intensity throughout rehabilitation and without adapting it to the animals' recovered motor ability. This study investigated the correlation between training intensity and rehabilitation efficacy by using a focal ischemic stroke rat model. Eighty male Sprague-Dawley rats were induced with middle cerebral artery occlusion/reperfusion surgery. Sixty rats with successful stroke were then randomly assigned into four groups: control (CG, n = 15), low intensity (LG, n = 15), gradually increased intensity (GIG, n = 15), and high intensity (HG, n = 15). Behavioral tests were conducted daily to evaluate motor function recovery. Stress level and neural recovery were evaluated via plasma corticosterone and brain-derived neurotrophic factor (BDNF) concentration, respectively. GIG rats significantly (P < 0.05) recovered motor function and produced higher hippocampal BDNF (112.87 ± 25.18 ng/g). GIG and LG rats exhibited similar stress levels (540.63 ± 117.40 nM/L and 508.07 ± 161.30 nM/L, resp.), which were significantly lower (P < 0.05) than that (716.90 ± 156.48 nM/L) of HG rats. Training with gradually increased intensity achieved better recovery with lower stress. Our observations indicate that a training protocol that includes gradually increasing training intensity should be considered in both animal and clinical studies for better stroke recovery.
authors.affiliation: Interdisciplinary Division of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong.
authors.forename: Jing
authors.identifier: 0000-0001-9847-3372
authors.initials: J
authors.lastname: Sun
authors.affiliation: Interdisciplinary Division of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong.
authors.forename: Zheng
authors.initials: Z
authors.lastname: Ke
authors.affiliation: Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong.
authors.forename: Shea Ping
authors.identifier: 0000-0002-2170-8185
authors.initials: SP
authors.lastname: Yip
authors.affiliation: Interdisciplinary Division of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong.
authors.forename: Xiao-ling
authors.identifier: 0000-0003-3188-3005
authors.initials: XL
authors.lastname: Hu
authors.affiliation: College of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou 310027, China.
authors.forename: Xiao-xiang
authors.initials: XX
authors.lastname: Zheng
authors.affiliation: Interdisciplinary Division of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong.
authors.forename: Kai-yu
authors.identifier: 0000-0003-4375-653X
authors.initials: KY
authors.lastname: Tong
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology / Q000534:rehabilitation*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D004195:Disease Models, Animal; D006801:Humans; D020244:Infarction, Middle Cerebral Artery / Q000473:pathology; D008297:Male; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D013312:Stress, Physiological; D020521:Stroke / Q000378:metabolism / Q000473:pathology; D000071939:Stroke Rehabilitation; D016896:Treatment Outcome
chemical_list: D019208:Brain-Derived Neurotrophic Factor; C579455:BDNF protein, human