scholarly journals Effect of Preinduction Amino Acid Infusion on Body Core Temperature

1999 ◽  
Vol 36 (2) ◽  
pp. 197
Author(s):  
Kyu Taek Choi ◽  
Jong Hyun Lee ◽  
Eun Ju Lee ◽  
Dong Myung Lee
2004 ◽  
Vol 100 (3) ◽  
pp. 634-639 ◽  
Author(s):  
Yasufumi Nakajima ◽  
Akira Takamata ◽  
Takashi Matsukawa ◽  
Daniel I. Sessler ◽  
Yoshihiro Kitamura ◽  
...  

Background Administration of protein or amino acids enhances thermogenesis, presumably by stimulating oxidative metabolism. However, hyperthermia results even when thermoregulatory responses are intact, suggesting that amino acids also alter central thermoregulatory control. Therefore, the authors tested the hypothesis that amino acid infusion increases the thermoregulatory set point. Methods Nine male volunteers each participated on 4 study days in randomized order: (1) intravenous amino acids infused at 4 kJ x kg(-1) x h(-1) for 2.5 h combined with skin-surface warming, (2) amino acid infusion combined with cutaneous cooling, (3) saline infusion combined with skin-surface warming, and (4) saline infusion combined with cutaneous cooling. Results Amino acid infusion increased resting core temperature by 0.3 +/- 0.1 degrees C (mean +/- SD) and oxygen consumption by 18 +/- 12%. Furthermore, amino acid infusion increased the calculated core temperature threshold (triggering core temperature at a designated mean skin temperature of 34 degrees C) for active cutaneous vasodilation by 0.3 +/- 0.3 degrees C, for sweating by 0.2 +/- 0.2 degrees C, for thermoregulatory vasoconstriction by 0.3 +/- 0.3 degrees C, and for thermogenesis by 0.4 +/- 0.5 degrees C. Amino acid infusion did not alter the incremental response intensity (i.e., gain) of thermoregulatory defenses. Conclusions Amino acid infusion increased the metabolic rate and the resting core temperature. However, amino acids also produced a synchronous increase in all major autonomic thermoregulatory defense thresholds; the increase in core temperature was identical to the set point increase, even in a cold environment with amble potential to dissipate heat. In subjects with intact thermoregulatory defenses, amino acid-induced hyperthermia seems to result from an increased set point rather than increased metabolic rate per se.


Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 867
Author(s):  
Yasuyuki Sakata ◽  
Chikako Yoshida ◽  
Yuka Fujiki ◽  
Yutaka Matsunaga ◽  
Hirohiko Nakamura ◽  
...  

Food ingestion has been shown to affect thermoregulation during exercise, while the impact of protein degradant consumption remains unclear. We investigated the effects of casein hydrolysate ingestion on thermoregulatory responses during exercise in the heat. In a randomized, placebo-controlled, double-blind, crossover trial, five men and five women consumed either 5 g of casein hydrolysate or placebo. Thirty minutes after ingestion, participants cycled at 60% VO2max until voluntary exhaustion wearing a hot-water (43 °C) circulation suit. Exercise time to exhaustion, body core temperature, forearm sweat rate, and forearm cutaneous vascular conductance did not differ different between the conditions. However, chest sweat rate and mean skin temperature increased upon casein hydrolysate ingestion compared with placebo during exercise. Increased chest sweat rate upon casein hydrolysate ingestion was associated with elevated sudomotor sensitivity to increasing body core temperature, but not the temperature threshold for initiating sweating. A positive correlation was found between chest sweat rate and plasma total amino acid concentration during exercise. These results suggest that casein hydrolysate ingestion enhances sweating heterogeneously by increasing peripheral sensitivity of the chest’s sweating mechanism and elevating skin temperature during exercise in the heat. However, the physiological link between plasma amino acid concentration and sweat rate remains unclear.


Diabetes ◽  
1989 ◽  
Vol 38 (1) ◽  
pp. 75-83 ◽  
Author(s):  
R. Nosadini ◽  
R. Trevisan ◽  
P. Fioretto ◽  
A. Semplicini ◽  
B. Sama ◽  
...  

2017 ◽  
Vol 14 (9) ◽  
pp. 703-711 ◽  
Author(s):  
Dallon T. Lamarche ◽  
Robert D. Meade ◽  
Andrew W. D'Souza ◽  
Andreas D. Flouris ◽  
Stephen G. Hardcastle ◽  
...  

2005 ◽  
Vol 58 (2) ◽  
pp. 229-234 ◽  
Author(s):  
Mushtaq A Godil ◽  
Thomas A Wilson ◽  
Peter J Garlick ◽  
Margaret A McNurlan

2008 ◽  
Vol 294 (2) ◽  
pp. F309-F315 ◽  
Author(s):  
Joo Lee Cham ◽  
Emilio Badoer

Redistribution of blood from the viscera to the peripheral vasculature is the major cardiovascular response designed to restore thermoregulatory homeostasis after an elevation in body core temperature. In this study, we investigated the role of the hypothalamic paraventricular nucleus (PVN) in the reflex decrease in renal blood flow that is induced by hyperthermia, as this brain region is known to play a key role in renal function and may contribute to the central pathways underlying thermoregulatory responses. In anesthetized rats, blood pressure, heart rate, renal blood flow, and tail skin temperature were recorded in response to elevating body core temperature. In the control group, saline was microinjected bilaterally into the PVN; in the second group, muscimol (1 nmol in 100 nl per side) was microinjected to inhibit neuronal activity in the PVN; and in a third group, muscimol was microinjected outside the PVN. Compared with control, microinjection of muscimol into the PVN did not significantly affect the blood pressure or heart rate responses. However, the normal reflex reduction in renal blood flow observed in response to hyperthermia in the control group (∼70% from a resting level of 11.5 ml/min) was abolished by the microinjection of muscimol into the PVN (maximum reduction of 8% from a resting of 9.1 ml/min). This effect was specific to the PVN since microinjection of muscimol outside the PVN did not prevent the normal renal blood flow response. The data suggest that the PVN plays an essential role in the reflex decrease in renal blood flow elicited by hyperthermia.


2002 ◽  
Vol 80 (3) ◽  
pp. 226-232 ◽  
Author(s):  
Frédéric Canini ◽  
Nadine Simler ◽  
Lionel Bourdon

The effects of MK801 (dizocilpine), a glutamate NMDA receptor antagonist, on thermoregulation in the heat were studied in awake rats exposed to 40°C ambient temperature until their body core temperature reached 43°C. Under these conditions, MK801-treated rats exhibited enhanced locomotor activity and a steady rise in body core temperature, which reduced the heat exposure duration required to reach 43°C. Since MK801-treated rats also showed increased striatal dopaminergic metabolism at thermoneutrality, the role of dopamine in the MK801-induced impairment of thermoregulation in the heat was determined using co-treatment with SCH23390, a dopamine D1 receptor antagonist. SCH23390 normalized the locomotor activity in the heat without any effect on the heat exposure duration. These results suggest that the MK801-induced impairment of thermoregulation in the heat is related to neither a dopamine metabolism alteration nor a locomotor activity enhancement.Key words: heatstroke, NMDA receptor, thermoregulation, dopamine, locomotion.


2013 ◽  
Vol 84 (11) ◽  
pp. 1153-1158 ◽  
Author(s):  
Jayme D. Limbaugh ◽  
Gregory S. Wimer ◽  
Lynn H. Long ◽  
William H. Baird

Sign in / Sign up

Export Citation Format

Share Document