scholarly journals Low-intensity exercise delays the shivering response to core cooling

2019 ◽  
Vol 316 (5) ◽  
pp. R535-R542 ◽  
Author(s):  
Tomomi Fujimoto ◽  
Bun Tsuji ◽  
Yosuke Sasaki ◽  
Kohei Dobashi ◽  
Yasuo Sengoku ◽  
...  

Hypothermia can occur during aquatic exercise despite production of significant amounts of heat by the active muscles. Because the characteristics of human thermoregulatory responses to cold during exercise have not been fully elucidated, we investigated the effect of low-intensity exercise on the shivering response to core cooling in cool water. Eight healthy young men (24 ± 3 yr) were cooled through cool water immersion while resting (rest trial) and during loadless pedaling on a water cycle ergometer (exercise trial). Before the cooling, body temperature was elevated by hot water immersion to clearly detect a core temperature at which shivering initiates. Throughout the cooling period, mean skin temperature remained around the water temperature (25°C) in both trials, whereas esophageal temperature (Tes) did not differ between the trials ( P > 0.05). The Tes at which oxygen uptake (V̇o2) rapidly increased, an index of the core temperature threshold for shivering, was lower during exercise than rest (36.2 ± 0.4°C vs. 36.5 ± 0.4°C, P < 0.05). The sensitivity of the shivering response, as indicated by the slope of the Tes-V̇o2 relation, did not differ between the trials (−441.3 ±177.4 ml·min−1·°C−1 vs. −411.8 ± 268.1 ml·min−1·°C−1, P > 0.05). The thermal sensation response to core cooling, assessed from the slope and intercept of the regression line relating Tes and thermal sensation, did not differ between the trials ( P > 0.05). These results suggest that the core temperature threshold for shivering is delayed during low-intensity exercise in cool water compared with rest although shivering sensitivity is unaffected.

2012 ◽  
Vol 113 (9) ◽  
pp. 1388-1397 ◽  
Author(s):  
Bun Tsuji ◽  
Yasushi Honda ◽  
Naoto Fujii ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu

Elevation of core temperature leads to increases in ventilation in both resting subjects and those engaged in prolonged exercise. We compared the characteristics of the hyperthermic hyperventilation elicited during passive heating at rest and during prolonged moderate and light exercise. Twelve healthy men performed three trials: a rest trial in which subjects were passively heated using hot-water immersion (41°C) and a water-perfused suit and two exercise trials in which subjects exercised at 25% (light) or 50% (moderate) of peak oxygen uptake in the heat (37°C and 50% relative humidity) after first using water immersion (18°C) to reduce resting esophageal temperature ( Tes). This protocol enabled detection of a Tes threshold for hyperventilation during the exercise. When minute ventilation (V̇e) was expressed as a function of Tes, 9 of the 12 subjects showed Tes thresholds for hyperventilation in all trials. The Tes thresholds for increases in V̇e during light and moderate exercise (37.1 ± 0.4 and 36.9 ± 0.4°C) were both significantly lower than during rest (38.3 ± 0.6°C), but the Tes thresholds did not differ between the two exercise intensities. The sensitivity of V̇e to increasing Tes (slope of the Tes-V̇e relation) above the threshold was significantly lower during moderate exercise (8.7 ± 3.5 l·min−1·°C−1) than during rest (32.5 ± 24.2 l·min−1·°C−1), but the sensitivity did not differ between light (10.4 ± 13.0 l·min−1·°C−1) and moderate exercise. These results suggest the core temperature threshold for hyperthermic hyperventilation and the hyperventilatory response to increasing core temperature in passively heated subjects differs from that in exercising subjects, irrespective of whether the exercise is moderate or light.


2018 ◽  
Vol 124 (1) ◽  
pp. 225-233 ◽  
Author(s):  
Bun Tsuji ◽  
Davide Filingeri ◽  
Yasushi Honda ◽  
Tsubasa Eguchi ◽  
Naoto Fujii ◽  
...  

Elevating core temperature at rest causes increases in minute ventilation (V̇e), which lead to reductions in both arterial CO2 partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (Tes) to reach 39°C. During heating in two separate trials, end-tidal CO2 partial pressure decreased from the level before heating (39.4 ± 2.0 mmHg) to the end of heating (30.5 ± 6.3 mmHg) ( P = 0.005) in the Control trial. This decrease was prevented by breathing CO2-enriched air throughout the heating such that end-tidal CO2 partial pressure did not differ between the beginning (39.8 ± 1.5 mmHg) and end (40.9 ± 2.7 mmHg) of heating ( P = 1.00). The sensitivity to rising Tes (i.e., slope of the Tes − V̇E relation) did not differ between the Control and CO2-breathing trials (37.1 ± 43.1 vs. 16.5 ± 11.1 l·min−1·°C−1, P = 0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P < 0.01), despite the absence of hyperventilation-induced hypocapnia. CO2 breathing increased MCAV relative to Control at the end of heating ( P = 0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia and that most of the decrease in cerebral blood flow occurs independently of hypocapnia. NEW & NOTEWORTHY Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The last may underlie central fatigue. We are the first to demonstrate that hyperthermia-induced hyperventilation is not suppressed by the resultant hypocapnia and that hypocapnia explains only 36% of cerebral hypoperfusion elicited by hyperthermia. These new findings advance our understanding of the mechanisms controlling ventilation and cerebral blood flow during heat stress, which may be useful for developing interventions aimed at preventing central fatigue during hyperthermia.


Author(s):  
Nicole T. Vargas ◽  
Christopher L. Chapman ◽  
Blair D. Johnson ◽  
Rob Gathercole ◽  
Matthew N. Cramer ◽  
...  

We tested the hypothesis that thermal behavior alleviates thermal discomfort and accelerates core temperature recovery following low intensity exercise. Methods: In a 27 ± 0 °C, 48 ± 6% relative humidity environment, 12 healthy subjects (six females) completed 60 min of exercise followed by 90 min of seated recovery on two occasions. Subjects wore a suit top perfusing 34 ± 0 °C water during exercise. In the control trial, this water continually perfused throughout recovery. In the behavior trial, the upper body was maintained thermally comfortable by pressing a button to receive cool water (3 ± 2 °C) perfusing through the top for 2 min per button press. Results: Physiological variables (core temperature, p ≥ 0.18; mean skin temperature, p = 0.99; skin wettedness, p ≥ 0.09; forearm skin blood flow, p = 0.29 and local axilla sweat rate, p = 0.99) did not differ between trials during exercise. Following exercise, mean skin temperature decreased in the behavior trial in the first 10 min (by −0.5 ± 0.7 °C, p < 0.01) and upper body skin temperature was reduced until 70 min into recovery (by 1.8 ± 1.4 °C, p < 0.05). Core temperature recovered to pre-exercise levels 17 ± 31 min faster (p = 0.02) in the behavior trial. There were no differences in skin blood flow or local sweat rate between conditions during recovery (p ≥ 0.05). Whole-body thermal discomfort was reduced (by −0.4 ± 0.5 a.u.) in the behavior trial compared to the control trial within the first 20 min of recovery (p ≤ 0.02). Thermal behavior via upper body cooling resulted in augmented cumulative heat loss within the first 30 min of recovery (Behavior: 288 ± 92 kJ; Control: 160 ± 44 kJ, p = 0.02). Conclusions: Engaging in thermal behavior that results in large reductions in mean skin temperature following exercise accelerates the recovery of core temperature and alleviates thermal discomfort by promoting heat loss.


2020 ◽  
Vol 32 (7) ◽  
pp. 444-448
Author(s):  
Mami Yamashiro ◽  
Yukihide Nishimura ◽  
Yukio Mikami ◽  
Ken Kouda ◽  
Yuta Sakurai ◽  
...  

2018 ◽  
Vol 13 (7) ◽  
pp. 917-925 ◽  
Author(s):  
Jessica M. Stephens ◽  
Ken Sharpe ◽  
Christopher Gore ◽  
Joanna Miller ◽  
Gary J. Slater ◽  
...  

Purpose: To examine the effect of postexercise cold-water immersion (CWI) protocols, compared with control (CON), on the magnitude and time course of core temperature (Tc) responses. Methods: Pooled-data analyses were used to examine the Tc responses of 157 subjects from previous postexercise CWI trials in the authors’ laboratories. CWI protocols varied with different combinations of temperature, duration, immersion depth, and mode (continuous vs intermittent). Tc was examined as a double difference (ΔΔTc), calculated as the change in Tc in CWI condition minus the corresponding change in CON. The effect of CWI on ΔΔTc was assessed using separate linear mixed models across 2 time components (component 1, immersion; component 2, postintervention). Results: Intermittent CWI resulted in a mean decrease in ΔΔTc that was 0.25°C (0.10°C) (estimate [SE]) greater than continuous CWI during the immersion component (P = .02). There was a significant effect of CWI temperature during the immersion component (P = .05), where reductions in water temperature of 1°C resulted in decreases in ΔΔTc of 0.03°C (0.01°C). Similarly, the effect of CWI duration was significant during the immersion component (P = .01), where every 1 min of immersion resulted in a decrease in ΔΔTc of 0.02°C (0.01°C). The peak difference in Tc between the CWI and CON interventions during the postimmersion component occurred at 60 min postintervention. Conclusions: Variations in CWI mode, duration, and temperature may have a significant effect on the extent of change in Tc. Careful consideration should be given to determine the optimal amount of core cooling before deciding which combination of protocol factors to prescribe.


2006 ◽  
Vol 28 (4) ◽  
pp. 265-268 ◽  
Author(s):  
Stéphane Auvin ◽  
Marie-Dominique Lamblin ◽  
Florence Pandit ◽  
Maria Bastos ◽  
Philippe Derambure ◽  
...  
Keyword(s):  

2000 ◽  
Vol 88 (5) ◽  
pp. 1643-1649 ◽  
Author(s):  
Nina S. Stachenfeld ◽  
Celso Silva ◽  
David L. Keefe

To test the hypothesis that progestin-mediated increases in resting core temperature and the core temperature threshold for sweating onset are counteracted by estrogen, we studied eight women (24 ± 2 yr) at 27°C rest, during 20 min of passive heating (35°C), and during 40 min of exercise at 35°C. Subjects were tested four times, during the early follicular and midluteal menstrual phases, after 4 wk of combined estradiol-norethindrone (progestin) oral contraceptive administration (OC E+P), and after 4 wk of progestin-only oral contraceptive administration (OC P). The order of the OC P and OC E+P were randomized. Baseline esophageal temperature (Tes) at 27°C was higher ( P < 0.05) in the luteal phase (37.08 ± 0.21°C) and in OC P (37.60 ± 0.31°C) but not during OC E+P (37.04 ± 0.23°C) compared with the follicular phase (36.66 ± 0.21°C). Tes remained above follicular phase levels throughout passive heating and exercise during OC P, whereas Tes in the luteal phase was greater than in the follicular phase throughout exercise ( P < 0.05). The Testhreshold for sweating was also greater in the luteal phase (38.02 ± 0.28°C) and OC P (38.07 ± 0.17°C) compared with the follicular phase (37.32 ± 0.11°C) and OC E+P (37.46 ± 0.18°C). Progestin administration raised the Testhreshold for sweating during OC P, but this effect was not present when estrogen was administered with progestin, suggesting that estrogen modifies progestin-related changes in temperature regulation. These data are also consistent with previous findings that estrogen lowers the thermoregulatory operating point.


2012 ◽  
Vol 302 (1) ◽  
pp. R94-R102 ◽  
Author(s):  
Bun Tsuji ◽  
Yasushi Honda ◽  
Naoto Fujii ◽  
Narihiko Kondo ◽  
Takeshi Nishiyasu

We investigated whether a core temperature threshold for hyperthermic hyperventilation is seen during prolonged submaximal exercise in the heat when core temperature before the exercise is reduced and whether the evoked hyperventilatory response is affected by altering the initial core temperature. Ten male subjects performed three exercise trials at 50% of peak oxygen uptake in the heat (37°C and 50% relative humidity) after altering their initial esophageal temperature (Tes). Initial Tes was manipulated by immersion for 25 min in water at 18°C (Precooling), 35°C (Control), or 40°C (Preheating). Tes after the water immersion was significantly higher in the Preheating trial (37.5 ± 0.3°C) and lower in the Precooling trial (36.1 ± 0.3°C) than in the Control trial (36.9 ± 0.3°C). In the Precooling trial, minute ventilation (V̇e) showed little change until Tes reached 37.1 ± 0.4°C. Above this core temperature threshold, V̇e increased linearly in proportion to increasing Tes. In the Control trial, V̇e increased as Tes increased from 37.0°C to 38.6°C after the onset of exercise. In the Preheating trial, V̇e increased from the initially elevated levels of Tes (from 37.6 to 38.6°C) and V̇e. The sensitivity of V̇e to increasing Tes above the threshold for hyperventilation (the slope of the Tes-V̇e relation) did not significantly vary across trials (Precooling trial = 10.6 ± 5.9, Control trial = 8.7 ± 5.1, and Preheating trial = 9.2 ± 6.9 L·min−1·°C−1). These results suggest that during prolonged submaximal exercise at a constant workload in humans, there is a clear core temperature threshold for hyperthermic hyperventilation and that the evoked hyperventilatory response is unaffected by altering initial core temperature.


1979 ◽  
Vol 56 (6) ◽  
pp. 601-606 ◽  
Author(s):  
C. D. Auld ◽  
I. M. Light ◽  
J. N. Norman

1. Twenty lightly anaesthetized dogs were cooled to 29°C by cold-water immersion. Ventilation was spontaneous and the animals were allowed to shiver freely. Metabolic heat production and respiratory heat exchange were measured during rewarming. 2. The animals were divided into four groups each of five dogs and each group was rewarmed by a different technique. The control group was allowed to rewarm spontaneously; a second group was given warm (45–50°C) fully humidified air to breathe in addition; a third group was rewarmed in a hot-water bath (42–44°C) and the remaining group was given a muscle relaxant to abolish shivering and rewarmed by warm inspired air only. 3. The group rewarmed in hot water achieved normal core temperature most rapidly but there was no difference in the rewarming rates of the group rewarmed spontaneously and of the group given warm air to breathe in addition. 4. The group given a muscle relaxant and rewarmed with warm inspired air required 12 h to achieve the same core temperature as the shivering groups achieved in 2 h. Compared with the heat produced by shivering the amount of heat which it was possible to transfer across the respiratory tract was so small that it did not materially influence the rate of rewarming.


2021 ◽  
pp. 113531
Author(s):  
Tomomi Fujimoto ◽  
Naoto Fujii ◽  
Kohei Dobashi ◽  
Yinhang Cao ◽  
Ryoko Matsutake ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document