Human physiological tremor consists of mechanical-reflex and neurogenic components. The origin of the neurogenic component, classically detected in the frequency range 7-12 Hz, has been much debated. We have studied six subjects with X-linked Kallmann's syndrome (XKS) and mirror movements. In these subjects unilateral magnetic brain stimulation results in abnormal bilateral EMG responses. Furthermore, abnormal sharing of central nervous inputs between the left and right motoneurone pools results in both abnormal motor unit synchronisation between left and right EMGs and abnormal sharing of long but not short-latency cutaneomuscular reflexes. XKS subjects with mirror movements thus provide a model for studying the central origin of physiological tremor. During sustained co-extension of the left and right index fingers, simultaneous finger tremor and extensor indicis (EI) EMGs were recorded and cross-correlated. The tremor and EMG signals were also subjected to time and frequency domain analysis.Results of frequency domain analysis between ipsilateral finger tremor and EI EMG were similar for both control and XKS subjects. However, in contrast to the controls, short-term synchronisation of left and right EI motor unit activity and significant coherence between left and right EMG, left and right tremor, left EMG and right tremor and right EMG and left tremor were found in XKS subjects. The frequency range (6-40 Hz) and coherence values between left and right were similar to ipsilateral coherence values of rectified EMG and tremor. These data provide strong evidence to support the hypothesis that the neurogenic component of physiological tremor is supraspinal in origin and ranges from 6 to 40 Hz.

The increase in blood pressure observed during physical activities is exaggerated in patients with hypertension, exposing them to a higher cardiovascular risk. Neural signals from the skeletal muscles appear to be overactive, resulting in this abnormal response in hypertensive patients. In the present study, we tested whether the attenuation of these neural signals in hypertensive patients could normalize their abnormal increase in blood pressure during physical activity. Attenuation of the neural signals from the leg muscles with intrathecal fentanyl injection reduced the blood pressure of hypertensive men during cycling exercise to a level comparable to that of normotensive men. Skeletal muscle afferent overactivity causes the abnormal cardiovascular response to exercise and was reverted in this experimental model, appearing as potential target for treatment. Hypertensive patients present an exaggerated increase in blood pressure and an elevated cardiovascular risk during exercise. Although controversial, human studies suggest that group III and IV skeletal muscle afferents might contribute to this abnormal response. In the present study, we investigated whether attenuation of the group III and IV muscle afferent signal of hypertensive men eliminates the exaggerated increase in blood pressure occurring during exercise. Eight hypertensive men performed two sessions of 5 min of cycling exercise at 40 W. Between sessions, the subjects were provided with a lumbar intrathecal injection of fentanyl, a μ-opioid receptor agonist, aiming to attenuate the central projection of opioid-sensitive group III and IV muscle afferent nerves. The cardiovascular response to exercise of these subjects was compared with that of six normotensive men. During cycling, the hypertensive group demonstrated an exaggerated increase in blood pressure compared to the normotensive group (mean ± SEM: +17 ± 3 vs. +8 ± 1 mmHg, respectively; P < 0.05), whereas the increase in heart rate, stroke volume, cardiac output and vascular conductance was similar (P > 0.05). Fentanyl inhibited the blood pressure response to exercise in the hypertensive group (+11 ± 2 mmHg) to a level comparable to that of the normotensive group (P > 0.05). Moreover, fentanyl increased the responses of vascular conductance and stroke volume to exercise (P < 0.05), whereas the heart rate response was attenuated (P < 0.05) and the cardiac output response was maintained (P > 0.05). The results of the present study show that attenuation of the exercise pressor reflex normalizes the blood pressure response to cycling exercise in hypertensive individuals.