Sympathetic nerve activity in metabolic control – some basic concepts

Abstract

A role for the sympathetic nervous system in hypertension has been looked for in relation to the 'metabolic syndrome' with associations between body weight, insulin sensitivity and hypertension. By use of microneurography human sympathetic responses to hypoglycaemia, normoglycaemic hyperinsulinaemia and food intake have been studied. A strong but differentiated influence of insulin-induced hypoglycaemia comprises increase in muscle sympathetic nerve activity (MSNA) and the sudomotor part of skin sympathetic nerve activity (SSNA), whereas vasoconstrictor SSNA is inhibited. Responses to infusion of 2-deoxy-D-glucose are identical, suggesting central nervous system glucopenia and not insulin to be the causative factor. Insulin infusion during normoglycaemia evokes a moderate increase in MSNA; SSNA and blood pressure does not change. After glucose ingestion MSNA displays a sustained increase, which is only partly elicited by insulin. A significant albeit weaker increase occurs after pure protein or fat meals, and after glucose ingestion in C-peptide-negative diabetic patients, with no insulin secretion. In healthy elderly people the MSNA response to food intake is weak, because of a high outflow already at rest; this is suggested to explain postprandial hypotension in the elderly, a paradoxical mechanism behind clinical autonomic failure. A pathophysiological role of MSNA in the metabolic syndrome with hypertension has been speculated. An association between obesity and elevated level of MSNA at rest is established; observed relationships to chronic insulin levels and hypertension are less unanimous. The adipose tissue regulating hormone leptin has become one focus of interest in ongoing attempts to elucidate a possible role of the human sympathetic nervous system in the 'metabolic syndrome' and hypertension.

Aging is associated with myocardial insulin resistance and mitochondrial dysfunction

“…We observed modest but significant increases in resting heart rates and blood pressures and modest increases in LV mass, but not LV/body weight ratios, seen in association with increased plasma norepinephrine and cardiac norepinephrine spillover. There is an extensive literature linking chronic hyperinsulinemia associated with whole body insulin resistance to increased sympathetic nervous system activation (5,7,30), leading to hypertension. In this regard, there was significant impairment in isovolumic relaxation time, LV stroke work, and external mechanical efficiency.…”

The effects of Ramadan fasting on heart rate variability in healthy individuals: A prospective study

“…Sympathetic (SNS) and parasympathetic nervous system (PNS) support the distinct and opposite functions in the alertness and physiology. In humans, within the relation to a hunger-satiety shift, changes of the SNS and PNS activity can occur before nutritional hormone levels are secreted, as demonstrated by the instant changes in the states of alertness (16-18), muscle sympathetic nerve activity (19), and cardiac output (20), which may be part of cephalic phase responses (21) after food intake. An inverse relationship of SNS activity and body fat, which suggests a role of β-adrenergic receptors in peripheral and central control of eating, emphasizes the importance of the SNS in food intake (22).…”

Low-frequency electroacupuncture and physical exercise decrease high muscle sympathetic nerve activity in polycystic ovary syndrome

“…Despite few studies in healthy humans showing a possible increase (55) or decrease (23) in MSNA, there is no convincing evidence that exercise alters resting MSNA. Heart failure and type 2 diabetes are associated with high sympathetic nerve activity (13). Conversely, exercise has been shown to reduce MSNA in heart failure (16) and to improve HRV in type 2 diabetes (83).…”