Recent studies suggest that transitory blood flow restriction (BFR) may improve the outcomes of training from anatomical (hypertrophy) and neural control perspectives. Whilst the chronic consequences of BFR on local metabolism and tissue adaptation have been extensively investigated, its acute effects on motor control are not yet fully understood. In this study, we compared the neuromechanical effects of continuous BFR against non-restricted circulation (atmospheric pressure—AP), during isometric elbow flexions. BFR was achieved applying external pressure either between systolic and diastolic (lower pressure—LP) or 1.3 times the systolic pressure (higher pressure—HP). Three levels of torque (15, 30, and 50% of the maximal voluntary contraction—MVC) were combined with the three levels of pressure for a total of 9 (randomized) test cases. Each condition was repeated 3 times. The protocol was administered to 12 healthy young adults. Neuromechanical measurements (torque and high-density electromyography—HDEMG) and reported discomfort were used to investigate the response of the central nervous system to BFR. The investigated variables were: root mean square (RMS), and area under the curve in the frequency domain—for the torque, and average RMS, median frequency and average muscle fibres conduction velocity—for the EMG. The discomfort caused by BFR was exacerbated by the level of torque and accumulated over time. The torque RMS value did not change across conditions and repetitions. Its spectral content, however, revealed a decrease in power at the tremor band (alpha-band, 5–15 Hz) which was enhanced by the level of pressure and the repetition number. The EMG amplitude showed no differences whilst the median frequency and the conduction velocity decreased over time and across trials, but only for the highest levels of torque and pressure. Taken together, our results show strong yet transitory effects of BFR that are compatible with a motor neuron pool inhibition caused by increased activity of type III and IV afferences, and a decreased activity of spindle afferents. We speculate that a compensation of the central drive may be necessary to maintain the mechanical output unchanged, despite disturbances in the afferent volley to the motor neuron pool.