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Acute ankle sprain leads in 40% of all cases to chronic ankle instability (CAI). CAI is related to a variety of motor adaptations at the lower extremities. Previous investigations identified increased muscle activities while landing in CAI compared to healthy control participants. However, it remains unclear whether muscular alterations at the knee muscles are limited to the involved (unstable) ankle or are also present at the uninvolved leg. The latter might potentially indicate a risk of ankle sprain or future injury on the uninvolved leg. Purpose: To assess if there is a difference of knee muscle activities between the involved and uninvolved leg in participants with CAI during perturbed walking. Method: 10 participants (6 females; 4 males; 26±4 years; 169±9 cm; 65±7 kg) with unilateral CAI walked on a split-belt treadmill (1m/s) for 5 minutes of baseline walking and 6 minutes of perturbed walking (left and right side, each 10 perturbations). Electromyography (EMG) measurements were performed at biceps femoris (BF) and rectus femoris (RF). EMG amplitude (RMS; normalized to MVIC) were analyzed for 200ms pre-heel contact (Pre200), 100ms post heel contact (Post100) and 200ms after perturbation (Pert200). Data was analyzed by paired t-test/Wilcoxon test based on presence or absence of normal distribution (Bonferroni adjusted α level p≤ 0.0125). Results: No statistical difference was found between involved and uninvolved leg for RF (Pre200: 4±2% and 11± 22%, respectively, p= 0.878; Post100: 10± 5 and 18±31%, p=0.959; Pert200: 6±3% and 13±24%, p=0.721) as well as for BF (Pre200: 12±7% and 11±6, p=0.576; Post100: 10±7% and 9±7%, p=0.732; Pert200: 7±4 and 7±7%, p=0.386). Discussion: No side differences in muscle activity could be revealed for assessed feedforward and feedback responses (perturbed and unperturbed) in unilateral CAI. Reduced inter-individual variability of muscular activities at the involved leg might indicate a rather stereotypical response pattern. It remains to be investigated, whether muscular control at the knee is not affected by CAI, or whether both sides adapted in a similar style to the chronic condition at the ankle.
Chronic ankle instability (CAI) is not only an ankle issue, but also affects sensorimotor system. People with CAI show altered muscle activation in proximal joints such as hip and knee. However, evidence is limited as controversial results have been presented regarding changes in activation of hip muscles in CAI population. PURPOSE: To investigate the effect of CAI on activity of hip muscles during normal walking and walking with perturbations. METHODS: 8 subjects with CAI (23 ± 2 years, 171 ± 7 cm and 65 ± 4 kg) and 8 controls (CON) matched by age, height, weight and dominant leg (25 ± 3 years, 172 ± 7 cm and 65 ± 6 kg) walked shoed on a split-belt treadmill (1 m/s). Subjects performed 5 minutes of baseline walking and 6 minutes walking with 10 perturbations (at 200 ms after heel contact with 42 m/s2 deceleration impulse) on each side. Electromyography signals from gluteus medius (Gmed) and gluteus maximus (Gmax) were recorded while walking. Muscle amplitudes (Root Mean Square normalized to maximum voluntary isometric contraction) were calculated at 200 ms before heel contact (Pre200), 100 ms after heel contact (Post100) during normal walking and 200 ms after perturbations (Pert200). Differences between groups were examined using Mann Whitney U test and Bonferroni correction to account for multiple testing (adjust α level p≤ 0.0125). RESULT: In Gmed, CAI group showed lower muscle amplitude than CON group after heel contact (Post100: 18±7 % and 47±21 %, p< .01) and after walking perturbations ( 31±13 % and 62±26 %, p< .01), but not before heel contact (Pre200: 5±2 % and 11±10 %, p= 0.195). In Gmax, no difference was found between CAI and CON groups in all three time points (Pre200: 12±5 % and 17±12 %, p= 0.574; Post100: 41±21 % and 41±13 %, p= 1.00; Pert200: 79±46 % and 62±35 %, p= 0.505). CONCLUSION: People with CAI activated Gmed less than healthy control in feedback mechanism (after heel contact and walking with perturbations), but not in feedforward mechanism (before heel contact). Less activation on Gmed may affect the balance in frontal plane and increase the risk of recurrent ankle sprain, giving way or feeling ankle instability in patients with CAI during walking. Future studies should investigate the effect of Gmed strengthening or neuromuscular training on CAI rehabilitation.
Eccentric (ECC) exercises might cause muscle damage, characterized by delayed-onset muscle soreness, elevated creatine kinase (CK) levels and local muscle oedema, shown by elevated T2 times in magnet resonance imaging (MRI) scans. Previous research suggests a high inter-individual difference regarding these systemic and local responses to eccentric workload. PURPOSE: To analyze ECC exercise-induced muscle damage in lumbar paraspinal muscles assessed via MRI. METHODS: Ten participants (3f/7m; 33±6y; 174±8cm; 71±12kg) were included in the study. Quantitative paraspinal muscle constitution of M. erector spinae and M. multifidius were assessed in supine position before and 72h after an intense eccentric trunk exercise bout in a mobile 1.5 tesla MRI device. MRI scans were recorded on spinal level L3 (T2-weighted TSE echo sequences, 11 slices, 2mm slice thickness, 3mm gap, echo times: 20, 40, 60, 80, 100ms, TR time: 2500ms). Muscle T2 times were calculated for manually traced regions of interest of the respective muscles with an imaging software. The exercise protocol was performed in an isokinetic device and consisted of 120sec alternating ECC trunk flexion-extension with maximal effort. Venous blood samples were taken before and 72h after the ECC exercise. Descriptive statistics (mean±SD) and t-testing for pre-post ECC exercises were performed. RESULTS: T2 times increased from pre- to post-ECC MRI measurements from 55±3ms to 79±28ms in M. erector spinae and from 62±5ms to 78±24ms in M. multifidius (p<0.001). CK increased from 126±97 U/L to 1447±20579 U/L. High SDs of T2 time and CK in post-ECC measures could be due to inter-individual reactions to ECC exercises. 3 participants showed high local and systemic reactions (HR) with T2 time increases of 120±24% (M. erector spinae) and 73±50% (M. multifidius). In comparison, the remaining 7 participants showed increases of 11±12% (M. erector spinae) and 7±9% (M. multifidius) in T2 time. Mean CK increased 9.5-fold in the 3 HR subjects compared with the remaining 7 subjects. CONCLUSIONS: The 120sec maximal ECC trunk flexion-extension protocol induced high amounts of muscle damage in 3 participants. Moderate to low responses were found in the remaining 7 subjects, assuming that inter-individual predictors play a role regarding physiological responses to ECC workload.
Eccentric exercises (ECC) induce reversible muscle damage, delayed-onset muscle soreness and an inflammatory reaction that is often followed by a systemic anti-inflammatory response. Thus, ECC might be beneficial for treatment of metabolic disorders which are frequently accompanied by a low-grade systemic inflammation. However, extent and time course of a systemic immune response after repeated ECC bouts are poorly characterized.
PURPOSE: To analyze the (anti-)inflammatory response after repeated ECC loading of the trunk.
METHODS: Ten healthy participants (33 ± 6 y; 173 ± 14 cm; 74 ± 16 kg) performed three isokinetic strength measurements of the trunk (concentric (CON), ECC1, ECC2, each 2 wks apart; flexion/extension, velocity 60°/s, 120s MVC). Pre- and 4, 24, 48, 72, 168h post-exercise, muscle soreness (numeric rating scale, NRS) was assessed and blood samples were taken and analyzed [Creatine kinase (CK), C-reactive protein (CRP), Interleukin-6 (IL-6), IL-10, Tumor necrosis factor-α (TNF-α)]. Statistics were done by Friedman‘s test with Dunn‘s post hoc test (α=.05).
RESULTS: Mean peak torque was higher during ECC1 (319 ± 142 Nm) than during CON (268 ± 108 Nm; p<.05) and not different between ECC1 and ECC2 (297 ± 126 Nm; p>.05). Markers of muscle damage (peaks post-ECC1: NRS 48h, 4.4±2.9; CK 72h, 14407 ± 19991 U/l) were higher after ECC1 than after CON and ECC2 (p<.05). The responses over 72h (stated as Area under the Curve, AUC) were abolished after ECC2 compared to ECC1 (p<.05) indicating the presence of the repeated bout effect. CRP levels were not changed. IL-6 levels increased 2-fold post-ECC1 (pre: 0.5 ± 0.4 vs. 72h: 1.0 ± 0.8 pg/ml). The IL-6 response was enhanced after ECC1 (AUC 61 ± 37 pg/ml*72h) compared to CON (AUC 33 ± 31 pg/ml*72h; p<.05). After ECC2, the IL-6 response (AUC 43 ± 25 pg/ml*72h) remained lower than post-ECC1, but the difference was not statistically significant. Serum levels of TNF-α and of the anti-inflammatory cytokine IL-10 were below detection limits. Overall, markers of muscle damage and immune response showed high inter-individual variability.
CONCLUSION: Despite maximal ECC loading of a large muscle group, no anti-inflammatory and just weak inflammatory responses were detected in healthy adults. Whether ECC elicits a different reaction in inflammatory clinical conditions is unclear.
History without borders
(2020)
The Research Data Policy of the University of Potsdam has been ratified by Senate on September 25, 2019 and published in Amtliche Bekanntmachungen “Official Notices” September 30, 2019. It applies to all researchers and research support staff.
The Recommendations for the Handling of Research Data at the University of Potsdam specify and complement the Research Data Policy of the University of Potsdam. They are aimed at all researchers and research support staff have been adopted by Senate’s Commission for Research and Junior Academics (FNK) on on October 9, 2019.
This record provides a non-official translation of both documents from the German original.