Isometric hip and knee torque measurements as an outcome measure in robot assisted gait training

Strength changes in lower limb muscles following robot assisted gait training (RAGT) in subjects with incomplete spinal cord injury (ISCI) has not been quantified using objective outcome measures. To record changes in the force generating capacity of lower limb muscles (recorded as peak voluntary isometric torque at the knee and hip), before, during and after RAGT in both acute and subacute/chronic ISCI subjects using a repeated measures study design. Eighteen subjects with ISCI participated in this study (Age range: 26–63 years mean age = 49.3 ± 11 years). Each subject participated in the study for a total period of eight weeks, including 6 weeks of RAGT using the Lokomat system (Hocoma AG, Switzerland). Peak torques were recorded in hip flexors, extensors, knee flexors and extensors using torque sensors that are incorporated within the Lokomat. All the tested lower limb muscle groups showed statistically significant (p < 0.001) increases in peak torques in the acute subjects. Comparison between the change in peak torque generated by a muscle and its motor score over time showed a non-linear relationship. The peak torque recorded during isometric contractions provided an objective outcome measure to record changes in muscle strength following RAGT

Development and validation of a low-cost, portable and wireless gait assessment tool

Background: Performing gait analysis in a clinical setting can often be challenging due to time, cost and the availability of sophisticated three-dimensional (3D) gait analysis systems. This study has developed and tested a portable wireless gait assessment tool (wi-GAT) to address these challenges. Aim: To investigate the concurrent validity of the wi-GAT in measuring spatio-temporal gait parameters such as stride length, stride duration, cadence, double support time (DST), stance and swing time compared to a 3D Vicon motion analysis system. Methods: Ten healthy volunteers participated in the study (age range 23–30 years). Spatio-temporal gait parameters were recorded simultaneously by the Vicon and the wi-GAT systems as each subject walked at their self-selected speed. Results: The stride length and duration, cadence, stance duration and walking speed recorded using the wi-GAT showed strong agreement with those same parameters recorded by the Vicon (ICC of 0.94–0.996). A difference between the systems in registering “toe off” resulted in less agreement (ICC of 0.299–0.847) in gait parameters such as %stance and %swing and DST. Discussion and conclusion: The study demonstrated good concurrent validity for the wi-GAT system. The wi-GAT has the potential to be a useful assessment tool for clinicians

Diltiazem improves contractile properties of skeletal muscle in dysferlin-deficient BLAJ mice, but does not reduce contraction-induced muscle damage

B6.A-Dysf prmd /GeneJ (BLAJ) mice model human limb-girdle muscular dystrophy 2B (LGMD2B), which is linked to mutations in the dysferlin (DYSF) gene. We tested the hypothesis that, the calcium ion (Ca 2+ ) channel blocker diltiazem (DTZ), reduces contraction-induced skeletal muscle damage, in BLAJ mice. We randomly assigned mice (N = 12; 3–4 month old males) to one of two groups – DTZ (N = 6) or vehicle (VEH, distilled water, N = 6). We conditioned mice with either DTZ or VEH for 1 week, after which, their tibialis anterior (TA) muscles were tested for contractile torque and susceptibility to injury from forced eccentric contractions. We continued dosing with DTZ or VEH for 3 days following eccentric contractions, and then studied torque recovery and muscle damage. We analyzed contractile torque before eccentric contractions, immediately after eccentric contractions, and at 3 days after eccentric contractions; and counted damaged fibers in the injured and uninjured TA muscles. We found that DTZ improved contractile torque before and immediately after forced eccentric contractions, but did not reduce delayed-onset muscle damage that was observed at 3 days after eccentric contractions

The effects of concentric and eccentric training in murine models of dysferlin‐associated muscular dystrophy

© 2020 Wiley Periodicals, Inc. Introduction: Dysferlin-deficient murine muscle sustains severe damage after repeated eccentric contractions. Methods: With a robotic dynamometer, we studied the response of dysferlin-sufficient and dysferlin-deficient mice to 12 weeks of concentrically or eccentrically biased contractions. We also studied whether concentric contractions before or after eccentric contractions reduced muscle damage in dysferlin-deficient mice. Results: After 12 weeks of concentric training, there was no net gain in contractile force in dysferlin-sufficient or dysferlin-deficient mice, whereas eccentric training produced a net gain in force in both mouse strains. However, eccentric training induced more muscle damage in dysferlin-deficient vs dysferlin-sufficient mice. Although concentric training produced minimal muscle damage in dysferlin-deficient mice, it still led to a prominent increase in centrally nucleated fibers. Previous exposure to concentric contractions conferred slight protection on dysferlin-deficient muscle against damage from subsequent injurious eccentric contractions. Discussion: Concentric contractions may help dysferlin-deficient muscle derive the benefits of exercise without inducing damage

The effects of concentric and eccentric training in murine models of dysferlin-associated muscular dystrophy

© 2020 Wiley Periodicals, Inc. Introduction: Dysferlin-deficient murine muscle sustains severe damage after repeated eccentric contractions. Methods: With a robotic dynamometer, we studied the response of dysferlin-sufficient and dysferlin-deficient mice to 12 weeks of concentrically or eccentrically biased contractions. We also studied whether concentric contractions before or after eccentric contractions reduced muscle damage in dysferlin-deficient mice. Results: After 12 weeks of concentric training, there was no net gain in contractile force in dysferlin-sufficient or dysferlin-deficient mice, whereas eccentric training produced a net gain in force in both mouse strains. However, eccentric training induced more muscle damage in dysferlin-deficient vs dysferlin-sufficient mice. Although concentric training produced minimal muscle damage in dysferlin-deficient mice, it still led to a prominent increase in centrally nucleated fibers. Previous exposure to concentric contractions conferred slight protection on dysferlin-deficient muscle against damage from subsequent injurious eccentric contractions. Discussion: Concentric contractions may help dysferlin-deficient muscle derive the benefits of exercise without inducing damage