The Hexoskin physiological monitoring shirt does not impair whole-body heat loss during exercise in hot-dry conditions

2019 ◽  
Vol 44 (3) ◽  
pp. 332-335 ◽  
Author(s):  
Andrew W. D’Souza ◽  
Sean R. Notley ◽  
Erin K. Brown ◽  
Martin P. Poirier ◽  
Glen P. Kenny

Using direct calorimetry, we determined if the Hexoskin shirt (Carré Technologies Inc., Que., Canada), a wearable device for monitoring physiological strain, would compromise whole-body heat loss and exacerbate body heat storage during moderate-intensity activity in hot-dry conditions. The shirt did not impair heat dissipation and resulted in similar body heat storage when worn alone relative to a semi-nude condition (214 vs. 211 kJ) or when worn underneath a work uniform compared with a cotton undershirt (307 vs. 318 kJ).

2020 ◽  
Vol 319 (2) ◽  
pp. E438-E446
Author(s):  
Vojtěch Škop ◽  
Naili Liu ◽  
Juen Guo ◽  
Oksana Gavrilova ◽  
Marc L. Reitman

Understanding mouse thermal physiology informs the usefulness of mice as models of human disease. It is widely assumed that the mouse tail contributes greatly to heat loss (as it does in rat), but this has not been quantitated. We studied C57BL/6J mice after tail amputation. Tailless mice housed at 22°C did not differ from littermate controls in body weight, lean or fat content, or energy expenditure. With acute changes in ambient temperature from 19 to 39°C, tailless and control mice demonstrated similar body temperatures (Tb), metabolic rates, and heat conductances and no difference in thermoneutral point. Treatment with prazosin, an α1-adrenergic antagonist and vasodilator, increased tail temperature in control mice by up to 4.8 ± 0.8°C. Comparing prazosin treatment in tailless and control mice suggested that the tail’s contribution to total heat loss was a nonsignificant 3.4%. Major heat stress produced by treatment at 30°C with CL316243, a β3-adrenergic agonist, increased metabolic rate and Tb and, at a matched increase in metabolic rate, the tailless mice showed a 0.72 ± 0.14°C greater Tb increase and 7.6% lower whole body heat conductance. Thus, the mouse tail is a useful biomarker of vasodilation and thermoregulation, but in our experiments contributes only 5–8% of whole body heat dissipation, less than the 17% reported for rat. Heat dissipation through the tail is important under extreme scenarios such as pharmacological activation of brown adipose tissue; however, non-tail contributions to heat loss may have been underestimated in the mouse.


1999 ◽  
Vol 276 (2) ◽  
pp. R298-R307 ◽  
Author(s):  
Edward L. Robinson ◽  
Charles A. Fuller

Whole body heat production (HP) and heat loss (HL) were examined to determine their relative contributions to light masking of the circadian rhythm in body temperature (Tb). Squirrel monkey metabolism ( n = 6) was monitored by both indirect and direct calorimetry, with telemetered measurement of body temperature and activity. Feeding was also measured. Responses to an entraining light-dark (LD) cycle (LD 12:12) and a masking LD cycle (LD 2:2) were compared. HP and HL contributed to both the daily rhythm and the masking changes in Tb. All variables showed phase-dependent masking responses. Masking transients at L or D transitions were generally greater during subjective day; however, L masking resulted in sustained elevation of Tb, HP, and HL during subjective night. Parallel, apparently compensatory, changes of HL and HP suggest action by both the circadian timing system and light masking on Tb set point. Furthermore, transient HL increases during subjective night suggest that gain change may supplement set point regulation of Tb.


1982 ◽  
Vol 53 (2) ◽  
pp. 316-323 ◽  
Author(s):  
C. J. Gordon

Male CBA/J mice were administered heat loads of 0–28 J X g-1 at specific absorption rates (SARs) of either 47 or 93 W X kg-1 by exposure to 2,450-MHz microwave radiation at an ambient temperature of 30 degrees C while evaporative heat loss (EHL) was continuously monitored with dew-point hygrometry. At an SAR of 47 W X kg-1 a threshold heat load of 10.5 J X g-1 had to be exceeded before EHL increased. An approximate doubling of SAR to 93 W X kg-1 reduced the threshold to 5.2 J X g-1. Above threshold the slopes of the regression lines were 1.15 and 0.929 for the low- and high-SAR groups, respectively. Thus the difference in threshold and not slope attributes to the significant increase in EHL when mice are exposed at a high SAR (P less than 0.02). In separate experiments a SAR of 47 W X kg-1 raised the deep body temperature of anesthetized mice at a rate of 0.026 degrees C X s-1, whereas 93 W X kg-1 raised temperature at 0.049 degrees C X s-1. Hence the sensitivity of the EHL mode of heat dissipation is directly proportional to the rate of heat absorption and to the rate of rise in body temperature. These data contradict the notion that mammals have control over whole-body heat exchange only (i.e., thermoregulation) but instead indicate that the EHL system is highly responsive to the rate of heat absorption (i.e., temperature regulation).


2013 ◽  
Vol 305 (6) ◽  
pp. R619-R629 ◽  
Author(s):  
Joanie Larose ◽  
Heather E. Wright ◽  
Jill Stapleton ◽  
Ronald J. Sigal ◽  
Pierre Boulay ◽  
...  

Studies in young adults show that a greater proportion of heat is gained shortly following the start of exercise and that temporal changes in whole body heat loss during intermittent exercise have a pronounced effect on body heat storage. The consequences of short-duration intermittent exercise on heat storage with aging are unclear. We compared evaporative heat loss (H E) and changes in body heat content (ΔHb) between young (20–30 yr), middle-aged (40–45 yr), and older males (60–70 yr) of similar body mass and surface area, during successive exercise (4 × 15 min) and recovery periods (4 × 15 min) at a fixed rate of heat production (400 W) and under fixed environmental conditions (35°C/20% relative humidity). H E was lower in older males vs. young males during each exercise (Ex1: 283 ± 10 vs. 332 ± 11 kJ, Ex2: 334 ± 10 vs. 379 ± 5 kJ, Ex3: 347 ± 11 vs. 392 ± 5 kJ, and Ex4: 347 ± 10 vs. 387 ± 5 kJ, all P < 0.02), whereas H E in middle-aged males was intermediate to that measured in young and older adults (Ex1: 314 ± 13, Ex2: 355 ± 13, Ex3: 371 ± 13, and Ex4: 365 ± 8 kJ). H E was not significantly different between groups during the recovery periods. The net effect over 2 h was a greater ΔHb in older (267 ± 33 kJ; P = 0.016) and middle-aged adults (245 ± 16 kJ; P = 0.073) relative to younger counterparts (164 ± 20 kJ). As a result of a reduced capacity to dissipate heat during exercise, which was not compensated by a sufficiently greater rate of heat loss during recovery, both older and middle-aged males had a progressively greater rate of heat storage compared with young males over 2 h of intermittent exercise.


2011 ◽  
Vol 300 (4) ◽  
pp. R958-R968 ◽  
Author(s):  
Daniel Gagnon ◽  
Glen P. Kenny

Previous studies have suggested that greater core temperatures during intermittent exercise (Ex) are due to attenuated sweating [upper back sweat rate (SR)] and skin blood flow (SkBF) responses. We evaluated the hypothesis that heat loss is not altered during exercise-rest cycles (ER). Ten male participants randomly performed four 120-min trials: 1) 60-min Ex and 60-min recovery (60ER); 2) 3 × 20-min Ex separated by 20-min recoveries (20ER); 3) 6 × 10-min Ex separated by 10-min recoveries (10ER), or 4) 12 × 5-min Ex separated by 5-min recoveries (5ER). Exercise was performed at a workload of 130 W at 35°C. Whole body heat exchange was determined by direct calorimetry. Core temperature, SR (by ventilated capsule), and SkBF (by laser-doppler) were measured continuously. Evaporative heat loss (EHL) progressively increased with each ER, such that it was significantly greater ( P ≤ 0.05) at the end of the last compared with the first Ex for 5ER (299 ± 39 vs. 440 ± 41 W), 10ER (425 ± 51 vs. 519 ± 45 W), and 20ER (515 ± 63 vs. 575 ± 74 W). The slope of the EHL response against esophageal temperature significantly increased from the first to the last Ex within the 10ER (376 ± 56 vs. 445 ± 89 W/°C, P ≤ 0.05) and 20ER (535 ± 85 vs. 588 ± 28 W/°C, P ≤ 0.05) conditions, but not during 5ER (296 ± 96 W/°C vs. 278 ± 95 W/°C, P = 0.237). In contrast, the slope of the SkBF response against esophageal temperature did not significantly change from the first to the last Ex (5ER: 51 ± 23 vs. 54 ± 19%/°C, P = 0.848; 10ER: 53 ± 8 vs. 56 ± 21%/°C, P = 0.786; 20ER: 44 ± 20 vs. 50 ± 27%/°C, P = 0.432). Overall, no differences in body heat content and core temperature were observed. These results suggest that altered local and whole body heat loss responses do not explain the previously observed greater core temperatures during intermittent exercise.


2019 ◽  
Vol 126 (2) ◽  
pp. 286-293 ◽  
Author(s):  
Sean R. Notley ◽  
Sheila Dervis ◽  
Martin P. Poirier ◽  
Glen P. Kenny

Menstrual cycle phase has long been thought to modulate thermoregulatory function. However, information pertaining to the effects of menstrual phase on time-dependent changes in whole body dry and evaporative heat exchange during exercise-induced heat stress and the specific heat load at which menstrual phase modulates whole body heat loss remained unavailable. We therefore used direct calorimetry to continuously assess whole body dry and evaporative exchange in 12 habitually active, non-endurance-trained, eumenorrheic women [21 ± 3 (SD) yr] within the early-follicular, late-follicular, and midluteal menstrual phases during three 30-min bouts of cycling at increasing fixed exercise intensities of 40% (Low), 55% (Moderate), and 70% (High) peak oxygen uptake, each followed by a 15-min recovery, in hot, dry conditions (40°C, 15% relative humidity). This model elicited equivalent rates of metabolic heat production among menstrual phases ( P = 0.80) of ~250 (Low), ~340 (Moderate), and ~430 W (High). However, dry and evaporative heat exchange and the resulting changes in net heat loss (dry ± evaporative heat exchange) were similar among phases (all P > 0.05), with net heat loss averaging 216 ± 43 (Low), 287 ± 63 (Moderate), and 331 ± 75 W (High) across phases. Accordingly, cumulative body heat storage (summation of heat production and loss) across all exercise bouts was similar among phases ( P = 0.55), averaging 464 ± 122 kJ. For some time, menstrual cycle phase has been thought to modulate heat dissipation; however, we show that menstrual cycle phase does not influence the contribution of whole body dry and evaporative heat exchange or the resulting changes in net heat loss or body heat storage, irrespective of the heat load. NEW & NOTEWORTHY Menstrual phase has long been thought to modulate thermoregulatory function in eumenorrheic women during exercise-induced heat stress. Contrary to that perception, we show that when assessed in young, non-endurance-trained women within the early-follicular, late-follicular, and midluteal phases during three incremental exercise-induced heat loads in hot, dry conditions, menstrual phase does not modify whole body dry and evaporative heat exchange or the resulting changes in body heat storage, regardless of the heat load employed.


Diabetologia ◽  
2019 ◽  
Vol 62 (6) ◽  
pp. 1087-1089 ◽  
Author(s):  
Sean R. Notley ◽  
Martin P. Poirier ◽  
Jane E. Yardley ◽  
Ronald J. Sigal ◽  
Glen P. Kenny

2019 ◽  
Vol 44 (12) ◽  
pp. 1383-1386
Author(s):  
Andrew W. D’Souza ◽  
Sean R. Notley ◽  
Robert D. Meade ◽  
Glen P. Kenny

Lower-limb intermittent sequential pneumatic compression (ISPC) improves circulation and vascular function in elderly adults. We evaluated the hypothesis that ISPC would also augment whole-body heat loss (WBHL) in elderly adults (aged 69 ± 4 years) resting in extreme heat (40 °C). While ISPC increased mean arterial pressure (91 ± 9 mm Hg) relative to no-ISPC (83 ± 5 mm Hg; P = 0.013) at the end of the exposure, no influence on WBHL was observed (81 ± 7 and 86 ± 11 W for ISPC and no-ISPC, respectively, P = 0.310). Novelty When assessed in elderly adults during an extreme heat exposure, intermittent sequential pneumatic compression augmented mean arterial pressure but did not enhance whole-body heat loss.


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