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We investigated the effects of ambient temperature on the sudomotor and vasoconstrictor components of skin sympathetic nerve activity (SSNA). The sympathetic traffic was measured by simultaneous microneurographic recording from post-ganglionic nerve fibres in the tibial and the peroneal nerves. When the ambient temperature was raised from 25 degrees C to 34 degrees C, both sudomotor and vasoconstrictor components of SSNA were enhanced in the peroneal nerve but were suppressed in the tibial nerve. The sudomotor and vasoconstrictor sympathetic outflows were elevated in both nerves when the temperature was lowered from 34 degrees C to 18 degrees C. Our results suggested that the sudomotor and the vasoconstrictor components of SSNA are differently modulated by ambient temperature. The difference in sudomotor and vasoconstrictor components of SSNA in the tibial and the peroneal nerves at different ambient temperature may have been responsible for the differences observed in sweating and vasoconstriction in glabrous and hairy skin.

We examined the relative contributions of hormones and nervous system to the total 2-deoxy-D-glucose (2-DG)-induced central nervous system-mediated hyperglycemia. 2-DG was injected into the third cerebral ventricle in the following four groups of rats, and hepatic venous plasma glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine were measured: 1) intact rats; 2) intact rats receiving somatostatin with insulin infusion through the femoral vein to inhibit glucagon secretion and maintain the basal insulin level; 3) bilateral adrenalectomized (ADX) rats to prevent epinephrine secretion; and 4) ADX rats receiving somatostatin with insulin infusion. Comparing areas under glucose curves among the intact rats, those receiving somatostatin with insulin infusion, ADX rats, and ADX rats receiving somatostatin with insulin infusion, the area under the glucose curve was intact rats greater than intact rats receiving somatostatin with insulin infusion greater than ADX rats receiving somatostatin with insulin infusion greater than ADX rats. These results suggest that there are three distinct sympathetic nervous system responses to 2-DG-induced central nervous system-mediated hyperglycemia. 2-DG-induced hyperglycemia is not dependent on only one of those three systems, it is dependent on all of them. The relative potency of the factors to 2-DG-induced hyperglycemia increases in the following order: direct neural innervation of liver (including suppressive epinephrine action on insulin secretion), glucagon, and direct epinephrine action on liver.

Muscle sympathetic nerve activity (MSA) was recorded by microneurographic technique from the human tibial nerve before and during voluntary sustained and rhythmic handgrip exercises. The MSA increased significantly during sustained contractions but not during rhythmic contractions, whereas no differences in resting activity before the two modes of handgrip were seen at rest. The results demonstrate that MSA responses to sustained and rhythmic exercises are distinctly different, showing less sympathetic outflow during rhythmic than during sustained contraction.

The effects of periodic, restricted feeding (RF) for two hours at a fixed time of day on the circadian rhythms of locomotor activity were examined in CS and C57BL/6J mice, kept under continuous dim, red lights (LLdim). In C57BL/6J mice, free-running rhythms were not affected by an RF schedule, although anticipatory behavior prior to the food access period was observed. On the other hand, the free-running rhythms of CS mice did entrain to an RF schedule, exhibiting anticipatory behavior. The free-running rhythms of none of the control animals in either strain exhibited any effects resulting from the periodic disturbances occurring concurrently with the performance of RF. These results indicate that the circadian pacemaker couples with the food entrainable oscillator (FEO) in CS mice, but that such coupling may not exist, or may be very weak, in C57BL/6J mice.

The experiments were designed to determine the contribution of the leg muscle relaxation to the sensitization of the vestibular function under weightlessness. The neuromuscular unit (NMU) discharges were continuously recorded with microelectrodes from the anti-gravitational soleus muscle and its antagonist, the tibialis anterior, of a man standing first upright on the level floor of a dry water tank, and then gradually being immersed in water till it reached his neck; while he was buoyed with an airtube placed under his armpit. In each of the successive states, the caloric nystagmus was evoked, analyzed and compared with the NMU discharge as well as with subjective symptoms associated with the nystagmus. The results indicate that the nystagmogenic activity had a significant correlation with the appearance of the active NMU in the soleus, and they also suggest that the reduction of ascending signals from the antigravity muscles might be one of the causes of atypical vestibular responses occuring in weightlessness.

Responses in muscle sympathetic activity (MSA) to acute hypoxia were studied in 13 healthy male subjects under hypobaric hypoxic conditions at a simulated altitude of 4,000, 5,000, and 6,000 m. Efferent postganglionic MSA was recorded directly with a tungsten microelectrode inserted percutaneously into the tibial nerve. Heart rate (HR) and respiratory rate (RR) were counted respectively from the R wave of an electrocardiogram and from the respiratory tracing recorded by the strain-gauge method. The average values of the MSA burst rate and total activity of MSA (burst rate x mean burst amplitude) at 4,000, 5,000, and 6,000 m were 36.4 +/- 2.6, 39.1 +/- 3.1, and 40.2 +/- 4.2 (SE) bursts/min and 616 +/- 138, 794 +/- 190, and 764 +/- 227 arbitrary units, respectively. These values were significantly higher than the values of 27.1 +/- 2.9 bursts/min and 446 +/- 28 at sea level. HR increased significantly at altitudes, but RR did not show significant change. Under severe hypoxic conditions beyond 5,000 m, there were large interindividual differences in the MSA responsiveness to hypoxia. The results indicate that MSA is activated under hypoxia by stimulating the chemoreceptors. However, the central controlling mechanisms that would be affected by hypoxia may also influence the MSA responsiveness under severe hypoxia.

To clarify whether sympathetic nerve activity increases in relation to the tension of a sustained muscle contraction, muscle sympathetic nerve activity (MSA) was recorded directly from the peroneal nerve fascicle at the popliteal fossa by means of tungsten microelectrodes in five healthy male subjects. A sustained muscle contraction was performed by handgrip for two minutes in a supine position at tensions of 10, 30 and 45% of maximal grip strength (MGS). MSA, electrocardiogram (ECG) using bipolar electrodes from the chest and surface electromyogram (EMG) from the extensor pollicis longus were recorded simultaneously before and during the sustained handgrip. Arterial blood pressure was measured at the resting upper arm by auscultation. During handgrip with tensions of 10, 30 and 45% MGS, average MSA burst rate (bursts · min−1) increased to 122, 152 and 230% of the resting value, respectively. During the same experimental procedures with tensions of 10, 30 and 45% MGS, average heart rate increased to 105, 110 and 111% of the resting value. These results confirm that sympathetic outflow to a resting muscle is increased with elevation of tension in an active muscle. This process would promote perfusion pressure in the active muscle.

In order to clarify the human sympathetic response to thyrotropin-releasing hormone (TRH), microneurographic analysis was performed in 12 healthy subjects. Multi-unit vasoconstrictive impulses of muscle nerve sympathetic activity (MSA) were directly recorded from tibial nerve fascicles together with ECG and blood pressure. Subcutaneous injection of saline (1 ml) had no effect on blood pressure and neurograms of MSA. Following s.c. injection of TRH (0.5 mg, 1 ml), however, a significant increase in heart rate and blood pressure occurred 2 min after injection; the change was statistically correlated with increased MSA, and disappeared after about 10 min. The observation suggests that TRH-activated vasoconstrictive impulses of MSA increase the peripheral vascular resistance and elevate blood pressure. We speculate that TRH directly activates vasomotor centers or higher autonomic centers rather than peripheral organs, because the parallel increase of blood pressure and MSA after TRH injection counteracts the effect of baroreflex mechanism.

The relationships between neuromuscular performance and biomechanical variables were studied in maximum vertical jumps to examine the factors influencing the performance of a noncountermovement jump. Keeping their knee and hip joint fully extended, five healthy subjects performed four kinds of noncountermovement jumps and one countermovement jump, during which ankle joint angle, platform force, and surface electromyograms of a triceps surae muscle were recorded. In the four noncountermovement jumps, the magnitude of activation and force at the onset of a shortening contraction of the triceps surae muscle were controlled at four different levels. Performance parameters of the noncountermovement jumps, maximum angular velocity of the ankle angle and flight time, correlated with the platform force at the onset of the plantar flexion. Furthermore the integrated electromyograms of the triceps surae muscle before the plantar flexion were correlated with the maximum angular velocity of the ankle angle and the force at the plantar flexion onset. The findings suggest that the efficient utilization of the muscle characteristic contributes to an enhancement of the noncountermovement jump.