Jacob L Barber1, William E Kraus2, Timothy S Church3, James M Hagberg4, Paul D Thompson5, David B Bartlett2, Michael W Beets1, Conrad P Earnest6, Kim M Huffman2, Rian Q Landers-Ramos4, Arthur S Leon7, D C Rao8, Richard L Seip5, James S Skinner9, Cris A Slentz2, Kenneth R Wilund10, Claude Bouchard3, Mark A Sarzynski11. 1. Department of Exercise Science, University of South Carolina, Columbia, SC, USA. 2. Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC, USA. 3. Pennington Biomedical Research Center, Baton Rouge, LA, USA. 4. Department of Kinesiology, University of Maryland, College Park, MD, USA. 5. Cardiology Division, Hartford Hospital, Hartford, CT, USA. 6. Department of Health & Kinesiology, Texas A&M University, College Station, TX, USA. 7. School of Kinesiology, University of Minnesota, Minneapolis, MN, USA. 8. Division of Biostatistics, Washington University School of Medicine, St. Louis, MO, USA. 9. Professor Emeritus of Kinesiology, Indiana University, Bloomington, IN, USA. 10. Department of Kinesiology and Community Health, University of Illinois, Urbana-Champaign, IL, USA. 11. Department of Exercise Science, University of South Carolina, Columbia, SC, USA. Electronic address: sarz@mailbox.sc.edu.
Abstract
BACKGROUND AND AIMS: GlycA is a relatively new biomarker for inflammation as well as cardiometabolic disease risk. However, the effect of exercise on GlycA is largely unknown. Therefore, the purpose of this study was to examine the effects of regular exercise on the inflammatory marker GlycA across seven studies and 14 exercise interventions. METHODS: Nuclear magnetic resonance spectroscopy, specifically signal amplitudes originating from the N-acetyl methyl group protons of the N-acetylglucosamine residues on the glycan branches of glycoproteins, was used to quantify GlycA concentrations. GlycA was measured before and after completion of an exercise intervention in 1568 individuals across seven studies and 14 exercise interventions. Random effects inverse variance weighting models were used to pool effects across interventions. RESULTS: Combined analysis of unadjusted data showed that regular exercise significantly (p = 2 × 10-6) reduced plasma GlycA (-8.26 ± 1.8 μmol/L). This reduction remained significant (-9.12 ± 1.9 μmol/L, p = 1.22 × 10-6) following adjustment for age, sex, race, baseline BMI, and baseline GlycA. Changes in GlycA were correlated with changes in traditional inflammatory markers, C-reactive protein, interleukin-6, and fibrinogen, however, these correlations were relatively weak (range r: 0.21-0.38, p < 0.0001). CONCLUSIONS: Regular exercise significantly reduced plasma GlycA across 14 different exercise interventions despite differences in exercise programs and study populations. The current study provides a greater understanding of the use of exercise as a potential therapy for the reduction of systemic inflammation. Further research is needed to understand the mechanisms behind the exercise-related reductions in GlycA.
BACKGROUND AND AIMS: GlycA is a relatively new biomarker for inflammation as well as cardiometabolic disease risk. However, the effect of exercise on GlycA is largely unknown. Therefore, the purpose of this study was to examine the effects of regular exercise on the inflammatory marker GlycA across seven studies and 14 exercise interventions. METHODS: Nuclear magnetic resonance spectroscopy, specifically signal amplitudes originating from the N-acetyl methyl group protons of the N-acetylglucosamine residues on the glycan branches of glycoproteins, was used to quantify GlycA concentrations. GlycA was measured before and after completion of an exercise intervention in 1568 individuals across seven studies and 14 exercise interventions. Random effects inverse variance weighting models were used to pool effects across interventions. RESULTS: Combined analysis of unadjusted data showed that regular exercise significantly (p = 2 × 10-6) reduced plasma GlycA (-8.26 ± 1.8 μmol/L). This reduction remained significant (-9.12 ± 1.9 μmol/L, p = 1.22 × 10-6) following adjustment for age, sex, race, baseline BMI, and baseline GlycA. Changes in GlycA were correlated with changes in traditional inflammatory markers, C-reactive protein, interleukin-6, and fibrinogen, however, these correlations were relatively weak (range r: 0.21-0.38, p < 0.0001). CONCLUSIONS: Regular exercise significantly reduced plasma GlycA across 14 different exercise interventions despite differences in exercise programs and study populations. The current study provides a greater understanding of the use of exercise as a potential therapy for the reduction of systemic inflammation. Further research is needed to understand the mechanisms behind the exercise-related reductions in GlycA.
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