Endocrinological and Metabolic Responses to Acute and Chronic Heat Exposures

Francesconi, Ralph P.

doi:10.1002/cphy.cp040112

Cited by 12 publications

(18 citation statements)

References 171 publications

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“…The actual mechanism of the post-exercise thermal response remains unclear. However, it is equally plausible that the cardiovascular (either central or peripheral: Kellogg et al 1990Kellogg et al , 1991; metabolic (Cannon and Kluger 1983); endocrine (Cannon and Kluger 1983;Francesconi 1996), or neurochemical (i.e., interleukin-1, a-interferon, dopamine, and thyroid releasing hormone : Francesconi 1996) changes that occur during exercise have residual thermal eects that may have the potential to alter hypothalamic temperature regulation.…”

Section: Possible Explanations For the Resultsmentioning

confidence: 99%

“…These results are consistent with an increase in the threshold for active vasodilation during recovery. This residual eect is not a result of the exercise-induced elevation of whole-body heat content (Kenny et al 1996), but is most likely due to residual exercise-related factors [i.e., endocrine changes (Francesconi 1996), endogenous and metabolic byproducts (Cannon and Kluger 1983;Francesconi 1996), or barore¯ex activity (Kellogg et al 1990(Kellogg et al , 1991 may exert the residual thermoregulatory eects]. When subjects were immersed in water at 42°C until es increased to levels comparable to those induced by 15 min of moderate exercise, es rapidly returned to control values within 10 min of recovery.…”

Section: Introductionmentioning

confidence: 99%

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The effect of dynamic exercise on resting cold thermoregulatory responses measured during water immersion

Kenny

Denis

Proulx

et al. 1999

European Journal of Applied Physiology

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The purpose of this study was to evaluate the effect of exercise on the subsequent post-exercise thresholds for vasoconstriction and shivering measured during water immersion. On 2 separate days, seven subjects (six males and one female) were immersed in water (37.5 degrees C) that was subsequently cooled at a constant rate of approximately 6.5 degrees C x h(-1) until the thresholds for vasoconstriction and shivering were clearly established. Water temperature was then increased to 37.5 degrees C. Subjects remained immersed for approximately 20 min, after which they exited the water, were towel-dried and sat in room air (22 degrees C) until both esophageal temperature and mean skin temperature (Tsk) returned to near-baseline values. Subjects then either performed 15 min of cycle ergometry (at 65% maximal oxygen consumption) followed by 30 min of recovery (Exercise), or remained seated with no exercise for 45 min (Control). Subjects were then cooled again. The core temperature thresholds for both vasoconstriction and shivering increased significantly by 0.2 degrees C Post-Exercise (P < 0.05). Because the Tsk at the onset of vasoconstriction and shivering was different during Pre- and Post-Exercise Cooling, we compensated mathematically for changes in skin temperatures using the established linear cutaneous contribution of skin to the control of vasoconstriction and shivering (20%). The calculated core temperature threshold (at a designated skin temperature of 32.0 degrees C) for vasoconstriction increased significantly from 37.1 (0.3) degrees C to 37.5 ( 0.3) degrees C post-exercise (P < 0.05). Likewise, the shivering threshold increased from 36.2 (0.3) degrees C to 36.5 (0.3) degrees C post-exercise (P < 0.05). In contrast to the post-exercise increase in cold thermal response thresholds, sequential measurements demonstrated a time-dependent similarity in the Pre- and Post-Control thresholds for vasoconstriction and shivering. These data indicate that exercise has a prolonged effect on the post-exercise thresholds for both cold thermoregulatory responses.

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Section: Possible Explanations For the Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effect of dynamic exercise on resting cold thermoregulatory responses measured during water immersion

Kenny

Denis

Proulx

et al. 1999

European Journal of Applied Physiology

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“…The post-exercise elevation in T es could be a function of either: (1) some exercise-related response which has thermal eects, such as an endocrine response and metabolic by-products (Francesconi 1996), changes in compartmental osmolarity (Mack and Nadel 1996), and barore¯ex activity (Johnson and Proppe 1996); or (2) the eect of a signi®cant elevation in heat load and wholebody heat content (Webb 1995). In an eort to investigate the latter mechanism, we previously immersed subjects in warm water (42°C) to a T es level similar to that induced by 15 min of exercise.…”

Section: Introductionmentioning

confidence: 99%

The effect of ambient temperature and exercise intensity on post-exercise thermal homeostasis

Kenny

Reardon

Giesbrecht

et al. 1997

European Journal of Applied Physiology

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We have previously demonstrated a prolonged (65 min or longer) elevated plateau of esophageal temperature (T(es)) (0.5-0.6 degrees C above pre-exercise values) in humans following heavy dynamic exercise (70% maximal oxygen consumption, VO2max) at a thermoneutral temperature (T(a)) of 29 degrees C. The elevated T(es) value was equal to the threshold T(es) at which active skin vasodilation was initiated during exercise (Th(dil)). A subsequent observation. i.e., that successive exercise/recovery cycles (performed at progressively increasing pre-exercise T(es) levels) produced parallel increases of Th(dil) and the post-exercise T(es), further supports a physiological relationship between these two variables. However, since all of these tests have been conducted at the same T(a) (29 degrees C) and exercise intensity (70% VO2max) it is possible that the relationship is limited to a narrow range of T(a)/exercise intensity conditions. Therefore, five male subjects completed 18 min of treadmill exercise followed by 20 min of recovery in the following T(a)/exercise intensity conditions: (1) cool with light exercise, T(a) = 20 degrees C, 45% VO2max (CL); (2) temperature with heavy exercise, T(a) = 24 degrees C, 75% VO2max (TH); (3) warm with heavy exercise, T(a) = 29 degrees C, 75% VO2max (WH); and (4) hot with light exercise, T(a) = 40 degrees C, 45% VO2max (HL). An abrupt decrease in the forearm-to-finger temperature gradient (T(fa) - T(fi)) was used to identify the Th(dil) during exercise. Mean pre-exercise T(es) values were 36.80, 36.60, 36.72, and 37.20 degrees C for CL, TH, WH, and HL conditions respectively. T(es) increased during exercise, and end post-exercise fell to stable values of 37.13, 37.19, 37.29, and 37.55 degrees C for CL, TH, WH, and HL trials respectively. Each plateau value was significantly higher than pre-exercise values (P < 0.05). Correspondingly, Th(dil) values (i.e., 37.20, 37.23, 37.37, and 37.48 degrees C for CL, TH, WH, and HL) were comparable to the post-exercise T(es) values for each condition. The relationship between Th(dil) and post-exercise T(es) remained intact in all T(a)/exercise intensity conditions, providing further evidence that the relationship between these two variables is physiological and not coincidental.

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“…Leppaluoto et al [4] showed no change in plasma ACTH or 17-hydroxycorticosteroid (17-0HCS) levels after sauna exposure (100°C,22% RH, 15min) when the Tre rose as much as 3°C. Apparently, when thermal stress induces marked discomfort or physiological strain, the HPA axis is significantly stimulated [1]. Obminski and Stupnicki [91] reported that in vitro the free fraction of cortisol increased by 30% when temperature was increased from 36°C to 39°C; and they suggested that in vivo the free, biologically active fraction of cortisol may increase owing to hyperthermia at a constant concentration of total cortisol.…”

Section: Corticotropin-releasing Factor Acth Cortisol (3-endorphinmentioning

confidence: 99%

“…On these occasions, the endocrine responses induced by the changes in Teare should be considered. Hormonal responses and their relation to the immune system during exercise in the heat and passive hyperthermia have been reviewed [1][2][3], but little attention has been paid to the relation of endocrine responses to the change in Teare. Body heating and cooling paradigms may include concurrent psychological stress.…”

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confidence: 99%

Endocrine Responses to Heat and Cold Stress

Matsumoto

Nishiyama

Nishimura

et al. 2001

Thermotherapy for Neoplasia, Inflammation, and Pain

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Summary. This review focuses on the endocrine responses to thermal stimuli during passive heat or cold exposure, with particular reference to the relation of these responses to the changes in the body core temperature (Teare). Mild to moderate hyperthermia (<1°C rise in Teare) induces the release of growth hormone and prolactin (PRL). Moderate hypothermia (la_2°C fall in Teore) suppresses PRL release. A positive correlation between plasma PRL and Teare suggests some role for PRL in thermoregulation. Hypothermia activates the hypothalamo-pituitary-thyroid (HPT) axis and releases thyrotropin-releasing hormone, thyroid-stimulating hormone (TSH), and thyroid hormones and increases the metabolic rate. Enhancement of extrathyroidal production of triiodothyronine (T3) from thyroxine (T4) may precede the TSH response to cold. Both severe hyperthermia and hypothermia (1°_3°C changes in Teare) activate the hypothalamo-pituitary-adrenal (HPA) axis and the sympathetic nervous system, resulting in release of corticotropin-releasing factor, adrenocorticotropic hormone, cortisol, and norepinephrine. The responses in the HPT axis and the HPA axis are not apparent in humans, as they are in rats, probably owing to the larger body mass of humans. Hyperthermia stimulates the renin-angiotensin-aldosterone system and the release of arginine vasopressin (AVP) and atrial natriuretic peptide, but this might be due to nonthermal factors. Diuresis due to suppression of AVP release is induced by cold. Gonadal response to thermal stimuli is possibly suppressive. The hormonal responses induced by thermal stress are mostly dependent on the change in Teare in humans; in small animals they are also dependent on the change in skin temperature. I ntrod uctionBody core temperature (Teare) may increase during physical exercise and passive heating (while sauna bathing, with head-out water immersion, and exposure to hot environments); it decreases during cold exposure. Changes in Teare induce various endocrine responses to maintain homeostasis of the body. Recently, local and whole-body hyperthermia therapy for cancer and some benign diseases and induced hypothermia treatment to protect the important organs from hypoxic damage have been developed and widely utilized. On these occasions, the endocrine responses induced by the changes in Teare should be considered. Hormonal responses and their relation to the immune system during exercise in the heat and passive hyperthermia have been reviewed [1][2][3], but little attention has been paid to the relation of endocrine responses to the change in Teare. Body heating and cooling paradigms may include concurrent psychological stress. This review focuses on the endocrine responses to thermal stimuli during passive heating and cooling, with particular reference to their relation to changes in Teare. The study was undertaken to elucidate the thermal influence alone, excluding the influence of non thermal stress. Growth HormoneThere have been many consistent findings that hyperthermia induces a rapid rise in ci...

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Endocrinological and Metabolic Responses to Acute and Chronic Heat Exposures

Cited by 12 publications

References 171 publications

The effect of dynamic exercise on resting cold thermoregulatory responses measured during water immersion

The effect of dynamic exercise on resting cold thermoregulatory responses measured during water immersion

The effect of ambient temperature and exercise intensity on post-exercise thermal homeostasis

Endocrine Responses to Heat and Cold Stress

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