Abstract
It has been hypothesized that force can be transmitted between adjacent muscles. Intermuscle force transmission violates the assumption that muscles act in mechanical isolation, and implies that predictions from biomechanical models are in error due to mechanical interactions between muscles, but the functional relevance of intermuscle force transmission is unclear. To investigate intermuscle force transmission between human flexor pollicis longus and the index finger part of flexor digitorum profundus, we compared finger flexion force produced by passive thumb flexion after one of three conditioning protocols: passive thumb flexion-extension cycling, thumb flexion maximal voluntary contraction (MVC), and thumb extension stretch. Finger flexion force increased after all three conditions. Compared to passive thumb flexion-extension cycling, change in finger flexion force was less after thumb extension stretch (mean difference 0.028 N, 95% CI 0.005 to 0.051 N), but not after thumb flexion MVC (0.007 N, 95% CI -0.020 to 0.033 N). As muscle conditioning changed finger flexion force produced by passive thumb flexion, the change in force is likely due to intermuscle force transmission. Thus, intermuscle force transmission resulting from passive stretch of an adjacent muscle is probably small enough to be ignored.
Highlights
When muscles produce force, it is thought that force is only transmitted in series from muscles to tendon and bone
Intermuscle force transmission violates the assumption that muscles act in mechanical isolation, and implies that predictions from many biomechanical models could be in error because of mechanical interactions between muscles
Thumb angle signals were sampled at 50 Hz, index finger force signals were sampled at 500 Hz, and EMG signals were bandpass filtered at 10-500 Hz and sampled at 2000 Hz using Spike2 software with a 16-bit Cambridge Electronic Design 1401plus data acquisition board (CED, Cambridge, UK)
Summary
When muscles produce force, it is thought that force is only transmitted in series from muscles to tendon and bone. This idea implies that muscles act in mechanical isolation and forms the basis for many animal and human biomechanical models [1]. It has been speculated that abnormal intermuscle force transmission may underlie pathological conditions such as spasticity and contracture [7]. Intermuscle force transmission violates the assumption that muscles act in mechanical isolation, and implies that predictions from many biomechanical models could be in error because of mechanical interactions between muscles.
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