Alteration in dopamine metabolism in the thermoregulatory center of exercising rats

Hasegawa, Hiroshi; Yazawa, Tetsuo; Yasumatsu, Mikinobu; Otokawa, Minoru; Aihara, Yasutsugu

doi:10.1016/s0304-3940(00)01276-3

Cited by 57 publications

(35 citation statements)

References 17 publications

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“…It is not completely clear why a difference in core temperature was apparent between drug and placebo trials under temperate conditions, as power output was similar in these trials. Bupropion has been reported to possess thermogenic properties (Liu et al 2002), possibility relating to its amphetamine-like structure (Nestler et al 2001), and catecholaminergic neurotransmission may influence thermoregulation during exercise (Hasegawa et al 2000). This may account for the different core temperature response during the TT in temperate conditions, but does not explain why no change in core temperature was measured during the fixed-intensity exercise and in the warm trials.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, dopamine has also been implicated in the control of body temperature (Hasegawa et al 2000) and tolerance to exercise in the heat (Bridge et al 2003). The aim of the present study was to investigate the influence of an acute dose of bupropion, a dual dopaminergic and noradrenergic reuptake inhibitor, on performance, thermoregulation and the hormonal responses to exercise in temperate and warm environmental conditions.…”

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Acute dopamine/noradrenaline reuptake inhibition enhances human exercise performance in warm, but not temperate conditions

Watson

Hasegawa

Roelands

et al. 2005

The Journal of Physiology

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191

228

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Nine healthy endurance-trained males were recruited to examine the effect of a dual dopamine/noradrenaline reuptake inhibitor on performance, thermoregulation and the hormonal responses to exercise. Subjects performed four trials, ingesting either a placebo (pla) or 2 × 300 mg bupropion (bup), prior to exercise in temperate (18• C) or warm (30 • C) conditions. Trials consisted of 60 min cycle exercise at 55% W max immediately followed by a time trial (TT). TT performance in the heat was significantly improved by bupropion (pla: 39.8 ± 3.9 min, bup: 36.4 ± 5.7 min; P = 0.046), but no difference between treatments was apparent in temperate conditions (pla: 30.6 ± 2.2 min, bup: 30.6 ± 1.9 min; P = 0.954). While TT power output was consistently lower in the heat when compared to temperate conditions, this decrement was attenuated by bupropion. At the end of the TT in the heat, both core temperature (pla 39.7 ± 0.3• C, bup 40.0 ± 0.3 • C; P = 0.017) and HR (pla 178 ± 7 beats min −1 , bup 183 ± 12 beats min −1 ; P = 0.039), were higher in the bupropion trial than in the placebo. Circulating pituitary and adrenal hormone concentrations increased throughout exercise in all trials. Circulating serum prolactin was elevated above temperate levels during exercise in a warm environment (P < 0.001). These data indicate that performance in warm conditions is enhanced by acute administration of a dual dopamine/noradrenaline reuptake inhibitor. No such effect was apparent under temperate conditions. It appears that bupropion enabled subjects to maintain a greater TT power output in the heat with the same perception of effort and thermal stress reported during the placebo trial, despite the attainment of a higher core temperature.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Acute dopamine/noradrenaline reuptake inhibition enhances human exercise performance in warm, but not temperate conditions

Watson

Hasegawa

Roelands

et al. 2005

The Journal of Physiology

Self Cite

191

228

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“…Recently, it has been shown that cholinergic synapses within the preoptic area and the paraventricular nucleus of the rat are important in temperature regulation (48,50). However, these may be linked to serotonergic (18,25,49) or dopaminergic (21) pathways to exert the final thermoregulatory effects.…”

Section: Discussionmentioning

confidence: 99%

Intracerebroventricular physostigmine facilitates heat loss mechanisms in running rats

Rodrigues

Lima²,

Coimbra³

et al. 2004

Journal of Applied Physiology

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Rodrigues, Alex G., Nilo R. V. Lima, Cândido C. Coimbra, and Umeko Marubayashi. Intracerebroventricular physostigmine facilitates heat loss mechanisms in running rats. J Appl Physiol 97: 333-338, 2004. First published March 19, 2004 10.1152/japplphysiol. 00742.2003.-The aim of this study was to evaluate the participation of central cholinergic transmission in the regulation of metabolic rate, core temperature, and heat storage in untrained rats submitted to exercise on a treadmill (20 m/min, 5% inclination) until fatigue. The animals were separated into eight experimental groups, and core temperature or metabolic rate was measured in the rats while they were exercising or while they were at rest after injection of 2 l of 5 ϫ 10 Ϫ3 M physostigmine (Phy) or 0.15 M NaCl solution (Sal) into the lateral cerebral ventricle. Metabolic rate was determined by the indirect calorimetry system, and colonic temperature was recorded as an index of core temperature. In resting animals, Phy induced only a small increase in metabolic rate compared with Sal injection, without having any effect on core temperature. During exercise, the Phytreated animals showed a lower core heating rate (0.022 Ϯ 0.003°C/ min Phy vs. 0.033 Ϯ 0.003°C/min Sal; P Ͻ 0.02), lower heat storage (285 Ϯ 37 cal Phy vs. 436 Ϯ 34 cal Sal; P Ͻ 0.02) and lower core temperature at fatigue point than the Sal-treated group (38.5 Ϯ 0.1°C Phy vs. 39.0 Ϯ 0.1°C Sal; P Ͻ 0.05). However, despite the lower core heating rate, heat storage, and core temperature at fatigue, the Phytreated rats showed a similar running time compared with the Saltreated group. We conclude that the activation of the central cholinergic system during exercise increases heat dissipation and attenuates the exercise-induced increase in core temperature without affecting running performance. body temperature; oxygen consumption; central cholinergic system; fatigue ACCORDING TO THE HEAT REGULATION hypothesis (52), high body temperature is the result rather than the cause of control, whereas metabolic heat production is an independent variable that is constantly adjusted to meet the changing need for energy and heat loss adjusted to match heat production. Heat loss has known physiological effectors that may be influenced and limited by other nonthermoregulatory restraints such as cardiovascular and respiratory control. Therefore, delay in its adjustment during exercise may limit heat loss, increase both heat storage and body core temperature, and induce fatigue.Internal body temperature is considered to be a limiting factor during prolonged physical exercise (14,16,39). However, the mechanisms responsible for exercise fatigue related to increasing body temperature are still not well understood, including whether exercise temperature increase is due to a rise in set point levels or occurs passively through an unwanted accumulation of heat (2). Controversy also exists as to whether there is a critical absolute value of BT, heat storage rate, or both that determines the point of fatigue. Fuller et al. (...

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“…Increased concentrations of MHPG have been found in most brain regions [35], 147 while increased concentrations of DOPAC and HVA have been shown, particularly in the 148 brainstem and hypothalamus [42,43]. 149…”

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confidence: 99%

Developing the catecholamines hypothesis for the acute exercise-cognition interaction in humans: Lessons from animal studies

McMorris

2016

Physiology & Behavior

145

129

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Alteration in dopamine metabolism in the thermoregulatory center of exercising rats

Cited by 57 publications

References 17 publications

Acute dopamine/noradrenaline reuptake inhibition enhances human exercise performance in warm, but not temperate conditions

Acute dopamine/noradrenaline reuptake inhibition enhances human exercise performance in warm, but not temperate conditions

Intracerebroventricular physostigmine facilitates heat loss mechanisms in running rats

Developing the catecholamines hypothesis for the acute exercise-cognition interaction in humans: Lessons from animal studies

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