Metabolic regulation of sympathetic nervous system activity: lessons from intraneural nerve recordings

Intraneural recordings of sympathetic nerve discharge give access to two subdivisions of the sympathetic nervous system: muscle nerve sympathetic activity and skin nerve sympathetic activity. Muscle nerve sympathetic activity (MSA) involves baroreceptor-controlled vasoconstrictor impulses to the resistance vessels in skeletal muscles. MSA is time-locked to the heart rhythm, correlates at rest to plasma noradrenaline concentrations and increases with age, but displays large inter-individual variations, the causes of which are poorly understood. Skin nerve sympathetic activity (SSA) is irregular with no relation to the pulse, is composed of sudomotor and cutaneous vasoconstrictor impulses and is practically absent in relaxed subjects in a thermoneutral environment. MSA and the sudomotor component of SSA are stimulated by acute insulin-induced hypoglycaemia, whereas the vasoconstrictor component of SSA is inhibited. MSA is stimulated by oral D-glucose but not by intravenous D-glucose or water. Under euglycaemia, insulin stimulates MSA in a dose-dependent fashion. Neither oral glucose nor insulin stimulate SSA. Exposure to carbohydrate intake and insulin have variable influences on the sympathetic nerve discharge. Various mechanisms are likely to operate in these interactions, including stimulation of central sympathetic motoneurons, baroreceptor control, and input from peripheral receptors in the vasculature or the gastrointestinal tract.