| 2. |
- Andersson, Åsa, Professor, 1960-, et al.
(författare)
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Serum Protein Response To A Single High-Intensity Interval Training Bout – Comparison Between Individuals With Spondyloarthritis And Healthy Controls
- 2022
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Ingår i: Annals of the Rheumatic Diseases. - London : BMJ Publishing Group Ltd. - 0003-4967 .- 1468-2060. ; 81:Suppl 1, s. 780-781
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Tidskriftsartikel (refereegranskat)abstract
- Axial spondyloarthritis (axSpA) is a chronic inflammatory disease affecting mainly the axial skeleton. To decrease the risk of cardiovascular comorbidity, aerobic training is recommended as a part of disease management in patients with axSpA. High-intensity interval training (HIIT) interventions are, in addition to other recommended treatments, believed to positively affect the disease activity (1). However, the knowledge about the acute effects of HIIT on the inflammatory process at the molecular level is less studied. Understanding the acute HIIT effects on cytokines and additional serum proteins in axSpA is important for further long-term HIIT interventions and recording of the effect of HIIT on the axSpA disease profile.ObjectivesTo study the acute effects on serum proteins, such as cytokines, myokines, and inflammatory- and bone-related proteins, in response to a single bout of HIIT, and to compare the levels between baseline and post-HIIT in patients with axSpA and healthy controls (HC).MethodsThe pilot study included twenty-one participants (10 female, 11 male), mean (SD) age 40 (7) years, ten with axSpA, and eleven age and sex matched HC, who performed a single HIIT on a cycle ergometer consisting of 4x4 minutes interval (90% heart rate, HR-max) with three minutes active rest in between (70% of HR-max). Disease activity (BASDAI, 0-10) in patients with axSpA was 1.6 (0.8). Health status EuroQol (EQ5D, 0-1) were 0.87 (0.11) for axSpA, and 0.93 (0.10) for HC. The groups were well matched with no difference in baseline data for weight, BMI, EQ5D, blood pressure or aerobic capacity.Blood samples were taken before (baseline) and one hour after the single HIIT. The following serum proteins were analyzed on a Luminex MAGPIX System (Luminex corporation, Austin, TX USA): Interleukin (IL)-6, IL-17, IL-18, TNFαAGPIX System (Luminex corporatiosteoprotegerin, osteocalcin, osteopontin, and FGF-23. A three-way analysis of variance (ANOVA) was used to detect differences between groups, between sexes, and before and after a HIIT bout in a 2(group)*2(sex)*2(time) design. For main effects or interactions significant at p≤0.05, simple effect t-tests were used to determine the specific effects.ResultsA group main effect (p=0.048) showed that the serum level of IL-6 was increased one hour after the HIIT session primarily in the HC, 0.4 pg/ml (SD±0.4) at baseline vs. post-HIIT 1.8 (2.0). The concentration of the cytokines/chemokine IL-17, IL-18, TNFα group main effect (p=0.048) showed that the serum level of IL-6 was increased one hour after the HIIT session primarily in30) in VEGF-A showed that the axSpA group had significantly lower VEGF-A at baseline, 159 pg/ml (138) vs 326 (184) in the control group (which might be due to anti-inflammatory medication). A sex main effect (p=0.029) was observed from baseline to post-HIIT for the bone hormone osteocalcin, with a more pronounced decrease of serum osteocalcin in women with axSpA, 14.0 ng/ml (8.3) vs. post HIIT 13.2 (6.9). Moreover, the level of the multifunctional protein osteopontin was significantly lower (sex main effect, p=0.021) in women, 10.7 ng/ml (7.0) vs. men 20.4 (10.1), post-HIIT.ConclusionThis pilot study shows that one bout of HIIT influences the expression of proteins involved in inflammation and metabolism, and that sex is an important factor in the response to HIIT. The results should be followed up in longer intervention studies including higher numbers of participants.References[1]Sveaas, S. H. et al. (2019). High intensity exercise for 3 months reduces disease activity in axial spondyloarthritis (axSpA): a multicentre randomised trial of 100 patients. British journal of sports medicine, 54(5), 292-297.Disclosure of InterestsÅsa Andersson: None declared, Emma Haglund Consultant of: Novartis, Emma Berthold: None declared, Elisabeth Mogard Consultant of: Novartis, Anna Torell: None declared, M Charlotte Olsson: None declared
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| 4. |
- Middeldorp, Christel M., et al.
(författare)
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The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia : design, results and future prospects
- 2019
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Ingår i: European Journal of Epidemiology. - : Springer Science and Business Media LLC. - 0393-2990 .- 1573-7284. ; 34:3, s. 279-300
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Tidskriftsartikel (refereegranskat)abstract
- The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.
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