Disuse atrophy occurs during periods of immobilisation or unloading and is typically characterised by loss of muscle mass and strength. Commonly observed in clinical settings such as bone or joint injury, nerve trauma and bed rest, deleterious effects manifest within as little as 5 days (1). Different muscles express diverging atrophy profiles, with striking differences even within agonist-antagonist muscle pairs such as the atrophy-resistant tibialis anterior (TA) and atrophy-susceptible medial gastrocnemius (MG) (2). While differing reductions in mass across different muscles in response to disuse is relatively well studied, the functional adaptations of motor units (MU) between such muscles are not well understood. The aim of this investigation was to study the adaptation of MU characteristics of the TA and MG as an agonist-antagonist muscle group with respect to their diverging atrophy profiles.
8 young healthy males underwent 15-day unilateral lower limb immobilisation preceded and followed by measurements of muscle cross-sectional area (CSA) using ultrasound and maximal voluntary isometric contractions (MVC) in the immobilised limb. Intramuscular electromyography (iEMG) was used to sample individual MU potentials (MUPs) during isometric contractions at 25% MVC. MUP characteristics were calculated from decomposed iEMG recordings using decomposition-based quantitative electromyography software (DQEMG). CSA and MVC were analysed using repeated-measures 2-way ANOVA. MUP characteristics were analysed using multi-level mixed-effects linear regression. Significance was accepted at p<0.05.
Following immobilisation, MG CSA was reduced (15.60 ± 3.20 cm2 to 13.82 ± 3.10 cm2, -11%, p<0.001) while TA MVC remained unchanged (6.43 ± 0.93 cm2 to 6.31 ± 0.97 cm2, p=0.84). MVC reduced in both plantar flexion (2262.50 ± 86.78 N to 202.50 ± 83.58 N, -23%, p<0.01) and dorsiflexion (202.93 ± 49.63 N to 157.58 ± 34.22 N, -22%, p<0.05). MU firing rate (FR) was significantly reduced in the MG (β = -0.691 Hz, 95% CI: -1.311 to -0.0715, p<0.05) yet remained unchanged in the TA (β = 0.233, 95% CI: -0.363 to 0.829, p=0.44). MU FR variability significantly increased in the MG (β = 0.0178, 95% CI: 0.00510 to 0.0305, p<0.01) but was unchanged in the TA (β = -0.00338, 95% CI: -0.0154 to -0.00866 p=0.58).
As previously reported, the MG reduced in size with immobilisation, while the TA resisted atrophy (3). Despite this divergence in atrophy profiles, reductions in strength were observed in both muscles. Suppression of FR and increased FR variability appear to contribute to functional reductions in the MG only. MU FR is modulated via net synaptic input to spinal motoneurons (4) which may be dysregulated following immobilisation. Impaired neural input to muscle may explain strength reductions in the absence of size reduction as seen in the TA. Consequently, central neural adaptations as a result of short-term immobilisation warrant further investigation to uncover specific impairments targeting muscle function.