Animal and in vitro studies have shown that the sympathetic nervous system modulates the contractility of skeletal muscle fibres, which may require adjustments in the motor drive to the muscle in voluntary contractions. In this study, these mechanisms were investigated in the tibialis anterior muscle of humans during sympathetic activation induced by the cold pressor test (CPT; left hand immersed in water at 4°C). In the first experiment, 11 healthy men performed 20 s isometric contractions at 10% of the maximal torque, before, during and after the CPT. In the second experiment, 12 healthy men activated a target motor unit at the minimum stable discharge rate for 5 min in the same conditions as in experiment 1. Intramuscular electromyographic (EMG) signals and torque were recorded and used to assess the motor unit discharge characteristics (experiment 1) and spike-triggered average twitch torque (experiment 2). CPT increased the diastolic blood pressure and heart rate by (mean ±s.d.) 18 ± 9 mmHg and 4.7 ± 6.5 beats min−1 (P < 0.01), respectively. In experiment 1, motor unit discharge rate increased from 10.4 ± 1.0 pulses s−1 before to 11.1 ± 1.4 pulses s−1 (P < 0.05) during the CPT. In experiment 2, the twitch half-relaxation time decreased by 15.8 ± 9.3% (P < 0.05) during the CPT with respect to baseline. These results provide the first evidence of an adrenergic modulation of contractility of muscle fibres in individual motor units in humans, under physiological sympathetic activation
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