# Role of Electrically Evoked Muscle Hypertrophy on Spasticity in Persons with Spinal Cord Injury

## TL;DR

This study found that electrically induced muscle growth in people with spinal cord injury did not worsen spasticity, suggesting it could be a safe way to build muscle without increasing stiffness.

## Contribution

The study is the first to investigate whether electrically evoked muscle hypertrophy affects spasticity indices in individuals with chronic spinal cord injury.

## Key findings

- Electrically induced muscle hypertrophy did not increase spasticity indices at different angular velocities.
- Muscle hypertrophy was significantly greater in the NMES-RT+TT group compared to TT-only in leg lean mass and thigh CSA.
- Extensor passive torque increased at higher angular velocities but did not significantly change spasticity indices.

## Abstract

Study Design: Pilot randomized clinical trial. Objective: To examine the effect of electrically evoked muscle hypertrophy on indices of spasticity, as measured by Biodex after spinal cord injury (SCI). Setting: Medical research center. Methods: Thirteen males with chronic SCI were randomized into sixteen weeks of either surface neuromuscular resistance training (NMES-RT) + testosterone treatment (TT) (n = 7) or a TT-only group (n = 6). A Biodex isokinetic dynamometer was used to measure knee extensor and flexor muscle spasticity at the beginning (baseline; BL) and at the end (post-intervention; PI) of 16 weeks. The passive tension of the right knee extensor and flexor muscle groups were evaluated at angles of 5°, 30°, 60°, 90°, 180°, and 270° per second (sec). Dual energy X-ray absorptiometry and magnetic resonance imaging were used to measure leg lean mass and thigh muscle cross-sectional areas (CSAs). Results: Robust muscle hypertrophy was noted in leg lean mass [11%, p = 0.023] as well as whole thigh [17%, p = 0.001] and knee extensor muscle [28%, p = 0.001] CSAs in the NMES-RT+TT compared to the TT-only group. There was no difference in extensor or flexor spasticity between the NMES-RT+TT or TT-only groups at different angular velocities following 16 weeks of intervention. Collapsing the extensor passive torques indicated an (24–28%) increase (p < 0.004) in response to angular velocities at BL and following PI measurements [180 deg/sec (23%; p = 0.03) and 270 deg/sec (32%; p = 0.009)] compared to 5 deg/sec. The extensor slope showed a non-significant (p > 0.05) decrease of 15–28% across all angular velocities. The catch-AB slopes were non-significantly lower in the TT-only group compared to the NMES-RT+TT at higher speeds [90 deg/sec and 270 deg/sec] and attained a trend towards lower passive torque at 180 deg/sec [180 deg/sec: 15.5%, p = 0.05]. Conclusions: Evoking skeletal muscle hypertrophy did not increase spasticity indices at different angular velocities following sixteen weeks of NMES-RT+TT or TT in persons with chronic SCI. Augmenting muscle hypertrophy is likely to attenuate the hyper reflexive slope of the extensor spasticity. The findings may suggest that evoking muscle hypertrophy following NMES-RT does not increase indices of spasticity after SCI. The clinical implications are highly important in managing spasticity after SCI.