Increase in Muscle Nerve Sympathetic Activity in Humans after Food Intake

1994 ◽  
Vol 86 (2) ◽  
pp. 159-167 ◽  
Author(s):  
JAN Fagius ◽  
Christian Berne

1. The influence of the intake of different nutrients on muscle nerve sympathetic activity was studied by use of microneurography. Muscle nerve sympathetic activity, heart rate, blood pressure and the insulin response were monitored for 90 min in 39 healthy, lean, normotensive subjects (mean age 26 years) who received 100 g of glucose in 300 ml of water (n = 8), 50 g of fat in 250 ml of water (n = 8), 100 g of lean meat corresponding to 40 g of protein with 250 ml of water (n = 8), 300 ml of water only (n = 7) or a mixed meal (1750 kJ) (n = 8). 2. All types of food evoked an increase in muscle nerve sympathetic activity whereas water caused no change. The increase in muscle nerve sympathetic activity was already significant at 15–30 min and was still strongly significant at 90 min. The effect of glucose was significantly greater than that of fat and protein; the mixed meal caused an intermediate response. Blood pressure changes were minor. 3. It is concluded that a sustained increase in muscle nerve sympathetic activity occurs regularly after any type of food intake. A rise in muscle nerve sympathetic activity takes place in the absence of an insulin response, and insulin contributes to only part of the increase after ingestion of glucose or a mixed meal. The muscle nerve sympathetic activity response is thought to be of importance for the redistribution of blood to the splanchnic region after a meal. Lack of this response is likely to explain postprandial hypotension in autonomic failure.

1978 ◽  
Vol 55 (s4) ◽  
pp. 387s-389s ◽  
Author(s):  
G. Sundlöf ◽  
B. G. Wallin

1. Simultaneous recordings of multi-unit muscle nerve sympathetic activity and arterial blood pressure were made in 29 subjects, 17 healthy and 12 hypertensive. The neural activity, quantified by counting the number of pulse-synchronous sympathetic bursts in the mean voltage neurogram (burst incidence), was plotted against blood pressure. The effect of spontaneous temporary blood pressure fluctuations was studied by correlating different pressure parameters of individual heart beats to the occurrence of a sympathetic burst. 2. Between subjects there were marked differences in burst incidence but no correlation was found to interindividual differences in blood pressure level. 3. When for each heart beat the occurrence of a burst was correlated to different pressure parameters there was a close negative correlation to diastolic, a low correlation to systolic, and an intermediate negative correlation to mean blood pressure. 4. In a given subject, when comparing heart beats with the same diastolic pressure, the occurrence and the amplitudes of the sympathetic bursts were higher during falling than during rising pressure. This directional dependence of the muscle—nerve sympathetic activity was slightly more pronounced in the hypertensive group, but this was considered secondary to the hypertension. 5. The findings of an intimate correlation with dynamic variations in blood pressure and the absence of correlation to the static blood pressure suggest that the sympathetic outflow to skeletal muscle is of importance for buffering acute blood pressure changes but has little influence on the long-term blood pressure.


Hypertension ◽  
2003 ◽  
Vol 42 (3) ◽  
pp. 277-282 ◽  
Author(s):  
Giuseppe Mancia ◽  
Gianfranco Parati ◽  
Paolo Castiglioni ◽  
Roberto Tordi ◽  
Elena Tortorici ◽  
...  

1981 ◽  
Vol 60 (5) ◽  
pp. 483-489 ◽  
Author(s):  
W. Kiowski ◽  
F. R. Bühler ◽  
P. Vanbrummelen ◽  
F. W. Amann

1. Plasma noradrenaline concentrations and blood pressure were measured in 45 patients with essential hypertension and 34 matched normotensive subjects. Plasma noradrenaline was similar in both groups, but in the hypertensive patients plasma noradrenaline correlated with blood pressure. 2. The increase in forearm flow in response to an intra-arterial infusion of phentolamine was determined in 12 of the hypertensive and 14 of the normotensive subjects to assess the α-adrenoceptor-mediated component of vascular resistance. Although the dilator response to phentolamine was similar in both groups, in the hypertensive patients it was correlated with the control plasma noradrenaline (r = 0.83, P<0.01) as well as the height of mean blood pressure (r = 0.73, P<0.01). 3. These results suggest that in hypertensive patients plasma noradrenaline can be a marker for both sympathetic activity and the α-adrenoceptor-mediated component of vascular resistance.


2010 ◽  
Vol 108 (4) ◽  
pp. 882-890 ◽  
Author(s):  
Colin N. Young ◽  
Shekhar H. Deo ◽  
Areum Kim ◽  
Masahiro Horiuchi ◽  
Catherine R. Mikus ◽  
...  

Nutrient intake is accompanied by increases in central sympathetic outflow, a response that has been mainly attributed to insulin. Insulin-mediated sympathoexcitation appears to be blunted in insulin-resistant conditions, suggesting that aside from peripheral insulin insensitivity, such conditions may also impair the central action of insulin in mediating sympathetic activation. What remains unclear is whether an insulin-sensitive state, such as that induced by chronic endurance training, alters the central sympathetic effects of insulin during postprandial conditions. To examine this question plasma insulin and glucose, muscle sympathetic nerve activity (MSNA), heart rate, and arterial blood pressure were measured in 11 high-fit [HF; peak oxygen uptake (V̇o2peak) 65.9 ± 1.4 ml·kg−1·min−1] and 9 average-fit (AF; V̇o2peak 43.6 ± 1.3 ml·kg−1·min−1) male subjects before and for 120 min after ingestion of a mixed meal drink. As expected, the insulin response to meal ingestion was lower in HF than AF participants (insulin area under the curve0–120: 2,314 ± 171 vs. 4,028 ± 460 μIU·ml−1·120−1, HF vs. AF, P < 0.05), with similar plasma glucose responses between groups. Importantly, following consumption of the meal, the HF subjects demonstrated a greater rise in MSNA compared with the AF subjects (e.g., 120 min: Δ21 ± 1 vs. 8 ± 3 bursts/100 heart beats, HF vs. AF, P < 0.05). Furthermore, when expressed relative to plasma insulin, HF subjects exhibited a greater change in MSNA for any given change in insulin. Arterial blood pressure responses following meal intake were similar between groups. Collectively, these data suggest that, in addition to improved peripheral insulin sensitivity, endurance training may enhance the central sympathetic effect of insulin to increase MSNA following consumption of a mixed meal.


2011 ◽  
Vol 33 (6) ◽  
pp. 373-380 ◽  
Author(s):  
Oreste Marrone ◽  
Adriana Salvaggio ◽  
Anna Lo Bue ◽  
Anna Bonanno ◽  
Loredana Riccobono ◽  
...  

1998 ◽  
Vol 274 (6) ◽  
pp. H2110-H2115 ◽  
Author(s):  
David L. Jardine ◽  
Hamid Ikram ◽  
Christopher M. Frampton ◽  
Rachell Frethey ◽  
Sinclair I. Bennett ◽  
...  

In the pathophysiological study of vasovagal syncope, the nature of the interaction between baroreceptor sensitivity (BS), sympathetic withdrawal, and parasympathetic activity has yet to be ascertained. Altered BS may predispose toward abnormal sympathetic and parasympathetic responses to orthostasis, causing hypotension that may progress to syncope if there is sympathetic withdrawal. To examine this hypothesis, we monitored blood pressure (BP), heart rate (HR), BS, forearm blood flow, and muscle nerve sympathetic activity (MNSA) continuously in 18 vasovagal patients during 60° head-up tilt, syncope, and recovery. Results were compared with those of 17 patients who were able to tolerate tilt for 45 min. During early tilt, BP was maintained in both groups by an increase in HR and MNSA from baseline ( P < 0.01), but BS decreased more in the syncopal group ( P < 0.05). At the start of presyncope (mean 2.7 ± 0.2 min before syncope and 15.2 ± 12 min after tilt), when BP fell, HR and sympathetic activity remained increased from baseline ( P< 0.01). Thereafter, BP and HR correlated directly with sympathetic activity and regressed in linear fashion until syncope ( P < 0.001), whereas BS increased to baseline. At syncope, BP, HR, and sympathetic activity fell below baseline ( P < 0.01, P < 0.05, and P < 0.01, respectively), but BS did not increase. During recovery, sympathetic activity increased to baseline and BS increased ( P < 0.05), whereas HR and BP remained low ( P < 0.01 and P < 0.05, respectively). The mechanism for the initiation of hypotension during presyncope remains unknown, but BS may contribute. Vasodilatation and bradycardia during presyncope appear to be more closely related to withdrawal of sympathetic activity than to increased parasympathetic cardiac activity.


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