Motor skill acquisition in the lower limb may induce modifications of spinal network excitability. We hypothesized that short-term motor adaptation in precision grip tasks would also induce modifications of cervical spinal network excitability. In a first series of experiments, we studied the impact of two different precision grip force control tasks (a visuomotor force-tracking task and a control force task without visual feedback) on cervical spinal network excitability in healthy subjects. We separately tested the efficacy of two key components of the spinal circuitry: (i) presynaptic inhibition on flexor carpi radialis (FCR) Ia terminals, and (ii) disynaptic inhibition directed from extensor carpi radialis (ECR) to FCR. We found that disynaptic inhibition decreased temporarily after both force control tasks, independently of the presence of visual feedback. In contrast, the amount of presynaptic inhibition on FCR Ia terminals decreased only after the visuomotor force tracking task. This temporary decrease was correlated with improved tracking accuracy during the task (i.e. short-term motor adaptation). A second series of experiments confirmed these results and showed that the visuomotor force-tracking task resulted also in an increase of the Hmax/Mmax ratio and the slope of the ascending part of the H-reflex recruitment curve. In order to address the role of presynaptic inhibition in the motor adaptation process, we conducted a third series of experiments during which presynaptic inhibition was recorded before and after two consecutive sessions of visuomotor force tracking. The results showed that (i) improved tracking accuracy occurred during both sessions, and (ii) presynaptic inhibition decreased only after the first session of visuomotor force tracking. Taken together, these results suggest thus that the nature of the motor task performed has a specific impact on the excitability of these cervical spinal circuits. These findings also suggest that early motor adaptation is associated with a modulation of presynaptic Ia inhibition in the upper limb.