The Thermostatic Control of Human Metabolic Heat Production

Benzinger, T. H.; Pratt, Arnold W.; Kitzinger, C.

doi:10.1073/pnas.47.5.730

Cited by 87 publications

(33 citation statements)

References 17 publications

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“…As a tentative and oversimplified explanation of the present data in terms of Benzinger's model (Benzinger et al, 1961), it is postulated that the thermosensitive heat loss center is comprised of serotonergic neurons, whereas noradrenergic neurons make up the sympathetic center which controls both heat production and the circulatory responses to thermal stress. In order to prevent a fall in body temperature during cold exposure, the heal production center is stimulated, and an increased turnover of NE is observed.…”

Section: A Model For Temperature Regulation By the Brainmentioning

confidence: 83%

Brain Amines and Temperature Regulation

et al. 1968

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Section: A Model For Temperature Regulation By the Brainmentioning

confidence: 83%

Brain Amines and Temperature Regulation

et al. 1968

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“…Other studies have demonstrated a reduction in the sweating threshold during exercise in dogs (Jackson and Hammel 1963) and humans (Jequier 1970;Tam et al 1978;Lopez et al 1995); the eect being greater as exercise intensity increases from 40 to 70% of maximum O 2 (Tam et al 1978). However, some studies have demonstrated no decrease in the sweating threshold during exercise in humans (Benzinger et al 1961;Kellogg et al 1991), while others report an increase (Johnson and Park 1981;Mekjavic and Bligh 1989). Lopez et al (1995) conducted the only other study of post-exercise sweating thresholds.…”

Section: Discussionmentioning

confidence: 99%

Intense exercise increases the post-exercise threshold for sweating

Kenny

Chen

Johnston

et al. 1997

European Journal of Applied Physiology

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We demonstrated previously that esophageal temperature (T(es)) remains elevated by approximately 0.5 degrees C for at least 65 min after intense exercise. Following exercise, average skin temperature (T(avg)) and skin blood flow returned rapidly to pre-exercise values even though T(es) remained elevated, indicating that the T(es) threshold for vasodilation is elevated during this period. The present study evaluates the hypothesis that the threshold for sweating is also increased following intense exercise. Four males and three females were immersed in water (water temperature, T(w) = 42 degrees C) until onset of sweating (Immersion 1), followed by recovery in air (air temperature, T(a) = 24 degrees C). At a T(a) of 24 degrees C, 15 min of cycle ergometry (70% VO2max) (Exercise) was then followed by 30 min of recovery. Subjects were then immersed again (T(w) = 42 degrees C) until onset of sweating (Immersion 2). Baseline T(es) and T(skavg) were 37.0 (0.1) degrees C and 32.3 (0.3) degrees C, respectively. Because the T(skavg) at the onset of sweating was different during Exercise [30.9 (0.3) degrees C] than during Immersion 1 and Immersion 2 [36.8 (0.2) degrees C and 36.4 (0.2) degrees C, respectively] a corrected core temperature, T((es) (calculated)), was calculated at a single designated skin temperature, T((sk)(designated)), as follows: T((es)(calculated)) = T(es) + [beta/(1-beta)][T(skavg)-T((sk)(designated))]. The T((sk)(designated)) was set at 36.5 degrees C (mean of Immersion 1 and Immersion 2 conditions) and beta represents the fractional contribution of T(skavg) to the sweating response (beta for sweating = 0.1). While T((es)(calculated)) at the onset of sweating was significantly lower during exercise [36.7 (0.2) degrees C] than during Immersion 1 [37.1 (0.1) degrees C], the threshold of sweating during Immersion 2 [37.3 (0.1) degrees C] was greater than during both Exercise and Immersion 1 (P < 0.05). We conclude that intense exercise decreases the sweating threshold during exercise itself, but elicits a subsequent short-term increase in the resting sweating threshold.

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“…This suggests but, in the absence of sufficient microelectrode experimentation, not altogether proves that brain temperature is "sensed" in this discrete prosencephalic region and that shivering can be evoked by its thermal activation without the support of a peripheral input from cudtaneous "cold" fibers. Similarly, it seems equally as evident that shivering can be evoked by lowering skin temperature with little or no change in brain temperature (Benzinger et al, 1961;Chatonnet, 1961). In one cat from the present results (S13) vigorous shivering was present after destruction of pre-optic anterior hypothalamic tissue including the allegedly thermally sensitive area.…”

Section: Hypothalamic Activation Of Shiveringmentioning

confidence: 98%