Metabolomics of Aerobic Exercise in Chronic Stroke Survivors: A Pilot Study

• Authors: Monica Serra, Emory University; Carolyn Accardi, Emory University; Carolyn Ma, Emory University; Younja Park, Emory University; ViLinh Tran, Emory University; Dean Jones, Emory University; Charlene E. Hafer-Macko, University of Maryland; Alice S. Ryan, University of Maryland
• Journal Title: Journal of Stroke and Cerebrovascular Diseases
• Volume: Volume 28, Number 12
• Publisher: Elsevier Inc. | 2019-12-01, Pages 104453-104453
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1016/j.jstrokecerebrovasdis.2019.104453
• Subjects: Biology, Neuroscience
• Keywords: Science & Technology; Life Sciences & Biomedicine; Neurosciences; Peripheral Vascular Disease; Neurosciences & Neurology; Cardiovascular System & Cardiology; Stroke; metabolomics; exercise; aerobic fitness; PENTOSE-PHOSPHATE PATHWAY; CONJUGATED LINOLEIC-ACID; HEPARAN-SULFATE; MASS-SPECTROMETRY; CAPACITY; DISEASE; RISK; INTENSITY; MARKERS

Abstract

Background: Understanding the metabolic response to exercise may aid in optimizing stroke management. Therefore, the purpose of this pilot study was to evaluate plasma metabolomic profiles in chronic stroke survivors following aerobic exercise training. Methods: Participants (age: 62 ± 1 years, body mass index: 31 ± 1 kg/m2, mean ± standard error of the mean) were randomized to 6 months of treadmill exercise (N = 17) or whole-body stretching (N = 8) with preintervention and postintervention measurement of aerobic capacity (VO2peak). Linear models for microarray data expression analysis was performed to determine metabolic changes over time, and Mummichog was used for pathway enrichment analysis following analysis of plasma samples by high-performance liquid chromatography coupled to ultrahigh resolution mass spectrometry. Results: VO2peak change was greater following exercise than stretching (18.9% versus −.2%; P <. 01). Pathway enrichment analysis of differentially expressed metabolites results showed significant enrichment in 4 pathways following treadmill exercise, 3 of which (heparan-, chondroitin-, keratan-sulfate degradation) involved connective tissue metabolism and the fourth involve lipid signaling (linoleate metabolism). More pathways were altered in pre and post comparisons of stretching, including branched-chain amino acid, tryptophan, tyrosine, and urea cycle, which could indicate loss of lean body mass. Conclusions: These preliminary data show different metabolic changes due to treadmill training and stretching in chronic stroke survivors and suggest that in addition to improved aerobic capacity, weight-bearing activity, like walking, could protect against loss of lean body mass. Future studies are needed to examine the relationship between changes in metabolomic profiles to reductions in cardiometabolic risk after treadmill rehabilitation.