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A positive inotropic action by the sympathetic nervous system on skeletal muscles has been observed and investigated in animal and in vitro studies. This action provided a theoretical basis for the putative ergogenic action of catecholamines and adrenergic agonists, although there is no clear evidence of this effect in humans. The aim of this study was to investigate the occurrence of inotropic effects associated to physiological sympathetic activation in healthy subjects. The muscle force capacity was investigated in the tibialis anterior (n = 9 subjects) and in the soleus (n = 9) muscles electrically stimulated with single pulses and double pulses with variable interspike interval (4-1,000 ms) and short pulse trains (frequency: 5-14 Hz) before, during, and after sympathetic activation by the cold pressor test (CPT). CPT significantly decreased by 10.4 ± 7.2 and 10.6 ± 4.4% the force produced by single and double pulse stimulation, respectively, and produced smaller decreases in the force obtained by train stimulation in the tibialis anterior, while no significant changes were observed in either type of contraction in the soleus muscle. CPT failed to induce any increase in the force capacity of the investigated muscles. The prevalent decrease in force evidenced in this study supports the concept that the weakening sympathetic action on type I fiber, already shown to occur in humans, prevails over the putative potentiating action.

The sympathetic nervous system (SNS) modulates several functions in skeletal muscle fibers, including metabolism, ionic transport across the membrane, and contractility. These actions, together with the sympathetic control of other organ systems, support intense motor activity. However, some SNS actions on skeletal muscles may not always be functionally advantageous. Implications for motor control and sport performance are discussed.

In the complex neurovascular control of the orofacial area, the only vasoconstrictor action is mediated by the sympathetic nervous system; however, its functional role is still unclear as little evidence exists of vasoconstrictor responses to physiological stimuli in both animal and human models. Aim of the present study was to investigate, orofacial vascular responses to acute stress in conscious rabbits. Twenty rabbits, implanted with chronic perivascular flow probes on the facial artery and with a telemetric probe for arterial blood pressure, were subjected to different alerting/stress stimuli, i.e., noise, taps on the rabbit's box, air jet, noxious cutaneous stimuli. Smaller groups of animal also underwent electromyographic (EMG) activity recording from the masseter muscle, unilateral section of the cervical sympathetic nerve (n=8), and alpha-adrenergic blockade with phentolamine (n=6). On average, all stressors evoked a pressor response accompanied by variable changes in heart rate and induced a marked, short-latency reduction in facial artery blood flow, corresponding to a decrease of 37-50% in vascular conductance of the facial artery. Local sympathetic denervation abolished the short-latency (<15s) vasoconstrictor response to all stressors and attenuated the late (>15s) phase of the long-lasting response to the air jet. All vasoconstrictor effects were blocked by phentolamine. Increases in blood flow were observed only in concomitance with masseter EMG activity either during masticatory activity or in the form of brief occasional spontaneous contractions. This study provides evidence of an effective vasoconstrictor control by the sympathetic system in the orofacial area under stress conditions.

The sympathetic nervous system (SNS), that is activated under condition of physical, psychological and psychosocial stress, affects force production and fatigability of muscles by controlling both muscle blood flow and the intracellular contractile mechanism. In addition SNS may affect motor function by modulating afferent activity from muscle spindles that are highly concentrated in jaw-closing muscles. Possible implications of these actions on masticatory function and myofascial pain are discussed.

There is increasing interest about the possible involvement of the sympathetic nervous system (SNS) in initiation and maintenance of chronic muscle pain syndromes of different aetiology. Epidemiological data show that stresses of different nature, e.g. work-related, psychosocial, etc., typically characterised by SNS activation, may be a co-factor in the development of the pain syndrome and/or negatively affect its time course. In spite of their clear traumatic origin, whiplash associated disorders (WAD) appear to share many common features with other chronic pain syndromes affecting the musculo-skeletal system. These features do not only include symptoms, like type of pain or sensory and motor dysfunctions, but possibly also some of the pathophysiological mechanisms that may concur to establish the chronic pain syndrome. This review focuses on WAD, particular emphasis being devoted to sensorimotor symptoms, and on the actions exerted by the sympathetic system at muscle level. Besides its well-known action on muscle blood flow, the SNS is able to affect the contractility of muscle fibres, to modulate the proprioceptive information arising from the muscle spindle receptors and, under certain conditions, to modulate nociceptive information. Furthermore, the activity of the SNS itself is in turn affected by muscle conditions, such as its current state of activity, fatigue and pain signals originating in the muscle. The possible involvement of the SNS in the development of WAD is discussed in light of the several positive feedback loops in which it is implicated.

The aim of this study was to evaluate, in a context of general inhibition of the sympathetic nervous system, the cerebral haemodynamic response to -30 degrees head-down tilt (HDT), a manoeuvre that produces an increase in intracranial arterial pressure. Nineteen healthy subjects were studied according to the following protocol: 10 min lying in supine position, 10 min HDT, 10 min recovery. Inhibition of the sympathetic system was confirmed by the decrease in heart rate (-3.6 bpm) and arterial blood pressure (-5.9 mmHg, p<0.05) in the late phase of the test. Blood velocity and blood pusatility index initially increased (+3.2 cm s(-1) and +9% respectively, p<0.01) then returned towards baseline before the end of HDT, while the cerebrovascular resistance index (=arterial blood pressure/blood velocity) dropped significantly and remained below control level (-7%, p<0.01) throughout the test. The changes in both these indices were opposite to those reported in several sympathetic activation tests, such as the handgrip and cold pressor tests. Conversely, arterial pressure at cranial level increased during HDT (as it also does during sympathetic activation tests), due to the development of a hydrostatic pressure gradient between heart and brain levels. Therefore, the effects observed on the pulsatility and resistance indices are not secondary to the increase in intracranial arterial pressure. It is suggested that the changes in these cerebrovascular indices are mediated by a reduction of sympathetic tone that presumably involves the cerebral as well as the peripheral vascular bed.

Abstract: This study is the first to report on vascular effect of the chromogranin A derived Vasostatin-I (CgA1-76) in vivo. Cardiovascular parameters were recorded in 29 rabbits with sympathetically decentralized right carotid vascular bed. The recombinant human STA CgA1-78 (VS-1) was infused at 480μg/kg over 25min. Group I was kept awake while groups II-V were anesthetized with Ketamine-xylazine. VS-1 was given alone in groups I-II while in presence of either phentolamine, phentolamine plus propranolol or hexamethonium in groups III-V. Serum VS-1 peaked at 2μg/ml (200nM) before onset of vascular effects and declined rapidly to ~200ng/ml within 30min. In all groups but III and IV VS-1 induced a brief vasoconstriction, being larger in intact than in sympathetically decentralized beds. The VS-1 induced vasoconstriction was not altered by hexamethonium but was abolished by phentolamine. In presence of the α-adrenergic blocker a long lasting vasodilatation, unaffected by propranolol, was apparent on both innervated and decentralized sides. In conclusion, VS-1 induced an α-adrenoceptor-mediated vasoconstriction presumably brought about by noradrenaline release from sympathetic nerves when infused at a dose giving an initial serum concentration of ~200nM. This initial vasoconstriction masked a persistent adrenoceptor-independent vasodilatation, consistent with previous reports from in vitro models. [Copyright &y& Elsevier]