BackgroundThe efficacy of exercise therapy for ankylosing spondylitis (AS) is well-documented, but dearth of information is for non-radiographic axial spondyloarthritis (nr-axSpA).Biomarkers like serum calprotectin, interleukins IL-6, IL-17 and tumour necrosis factor (TNF)-α may reflect the disease activity of axial spondyloarthritis (axSpA). In this study, we investigated clinical and laboratory parameters of both axSpA subgroups in response to intensive physical exercise.MethodsAltogether, 46 patients with axSpA, characterised according to the Assessment of SpondyloArthritis International Society criteria as having nr-axSpA or AS underwent 6-month exercise programme. Clinical outcomes of disease activity, Bath AS Disease Activity Index (BASDAI), AS Disease Activity Index (ASDAS-CRP), mobility, Bath AS Metrology Index (BASMI) and function, Bath AS Functional Index (BASFI) were evaluated at baseline and at the end of the exercise programme. Serum IL-6 and IL-17, TNF-α and calprotectin were measured via ELISA. The clinical and laboratory data of 29 control axSpA patients were used for the evaluation of the results.ResultsIn all axSpA patients, the ASDAS-CRP (2.10 ± 0.12 to 1.84 ± 0.11, p <0.01) and BASMI (1.28 ± 0.14 to 0.66 ± 0.84, p <0.0001) improved after 6 months of exercise therapy. There was a significant improvement in the ASDAS-CRP in the nr-axSpA subgroup (2.01 ± 0.19 to 1.73 ± 0.16, p <0.05) and in the BASMI in both, the nr-axSpA and the AS subgroups (1.09 ± 0.12 to 0.47 ± 0.08, p <0.0001 and 1.43 ± 0.24 to 0.82 ± 0.23, p <0.0001, respectively). Both, ASDAS-CRP and BASDAI, were significantly improved in the exercise axSpA group compared to the control axSpA group (mean -0.26 vs. -0.13 and -0.49 vs. 0.12, respectively, all p <0.05). Only calprotectin was significantly reduced after the exercise programme in nr-axSpA and AS patients (from 2379.0 ± 243.20 to 1779.0 ± 138.30 μg/mL and from 2430.0 ± 269.70 to 1816.0 ± 148.20 μg/mL, respectively, all p <0.01). The change in calprotectin was more profound in the axSpA intervention group (mean -604.56) than in the control axSpA (mean -149.28, p <0.05).ConclusionThis study demonstrated similar efficacy for an intensive exercise programme in both nr-axSpA and AS patients. A significant decrease in serum calprotectin levels in both subgroups of axSpA patients after the exercise programme reflected an improvement in the disease activity and spinal mobility.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-016-1180-1) contains supplementary material, which is available to authorized users.
Achieving the maximum possible impact force of the front kick can be related to the isokinetic lower limb muscle strength. Therefore, we aimed to determine the regression model between kicking performance and the isokinetic peak net moment of hip rotators, flexors, and hip extensors and flexors at various speeds of contraction. Twenty-five male soldiers (27.7 ± 7.2 yrs, 83.8 ± 6.1 kg, 180.5 ± 6.5 cm) performed six barefoot front kicks, where impact forces (N) and kick velocity (m∙s-1) were measured. The 3D kinematics and isokinetic dynamometry were used to estimate the kick velocity, isokinetic moment of kicking lower limb hip flexors and extensors (60, 120, 240, 300°∙s-1), and stance lower limb hip internal and external rotators (30, 90°∙s-1). Multiple regression showed that a separate component of the peak moment concentric hip flexion and extension of the kicking lower limb at 90°∙s-1 can explain 54% of the peak kicking impact force variance (R2 = 0.54; p < 0.001). When adding the other 3 components of eccentric and concentric hip internal and external rotations at 30°∙s-1, the internal and external hip rotation ratios at 30°∙s-1 on the stance limb and the concentric ratio of kicking limb flexion and extension at 300°∙s-1 that explained the variance of impact force were 75% (p = 0.003). The explosive strength of kicking limb hip flexors and extensors is the main condition constraint for kicking performance. The maximum strength of stance limb internal and external rotators and speed strength of kicking limb hip flexors and extensors are important constraints of kicking performance that should be considered to improve the front kick efficiency.
The objective of this study was to investigate the patient-reported outcomes (PROs) and matrix metalloproteinase (MMP) derived extracellular matrix (ECM) biomarkers in non-radiographic (nr)-axial spondyloarthritis (axSpA) and radiographic (r)-axSpA after exercise intervention. Forty-six axSpA patients with stable disease and treatment underwent 24 weeks long exercise intervention. The clinical and laboratory assessments were performed at baseline and at follow-up. The PROs included evaluation of patient's global disease activity (PGDA), disease activity (DA7), pain (PAIN7) and fatigue during last week and quality of life questionnaires. ELISAs for MMP-degraded collagen type II, C-reactive protein (CRPM) and citrullinated vimentin were used. The data of 23 r-axSpA and 19 nr-axSpA were analysed. The PDGA was similar for nr-axSpA (35.2 ± 18.9) and r-axSpA (33.4 ± 22.3) at baseline, improved significantly after intervention (p < 0.01) and the change of PDGA was almost identical for nr-axSpA (- 10.0 ± 15.4) and r-axSpA (- 9.8 ± 11.9). Evaluations of DA7 and PAIN7 were significantly improved only in nr-axSpA (3.5 ± 2.3 and 34.7 ± 25.6 at baseline vs. 2.1 ± 1.9 and 21.0 ± 20.5, respectively, p < 0.01). The decline of DA7 and PAIN7 was more profound, but not significantly in nr-axSpA than in r-axSpA (- 1.4 ± 1.6 and - 13.7 ± 17.4 vs. - 0.5 ± 3.1 and - 3.7 ± 3.3, respectively). The quality of life was not changed. At baseline, increased levels of CRPM were found in r-axSpA (14.85 ± 4.10) compared to nr-axSpA (11.83 ± 3.20), p < 0.05, but all three biomarkers were not influenced by exercise therapy. We found that exercise therapy mainly in the nr-axSpA improves PROs, but not ECM turnover biomarkers. This indicates that exercise therapy is important for patients' health but does not affect ECM turnover.
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