Exploring the human thermoneutral zone - A dynamic approach.

To date, the position and shape of the human thermoneutral zone (TNZ) remain uncertain. Indications exist that the individual TNZ might be influenced by age, body composition and level of acclimatisation. The objective of the present study was to explore the individual metabolic TNZ, using dynamic thermal conditions to assess both metabolic lower and upper critical temperatures (LCT and UCT) and, secondly, to test the effect of passive mild heat acclimation on the human metabolic TNZ. A dynamic protocol consisting of two experimental conditions was designed: starting from a thermoneutral condition (28.8 ±â€¯0.3 °C), temperature gradually increased to 37.5 ±â€¯0.6 °C during warming (UP) or decreased to 17.8 ±â€¯0.6 °C during cooling (DOWN). For six participants, temperature increased further to 41.6 ±â€¯1.0 °C during UP. Eleven healthy men (19-31 y) underwent UP and DOWN twice, i.e. before and after passive mild heat acclimation (PMHA, 7 days at ~33 °C for 6 h/day). Energy expenditure, body temperatures and heart rate were measured during UP and DOWN. We show that the generally assumed LCT of approximately 28 °C for an average male person does not match the dynamically assessed LCTs in this study, as those were considerably lower in most cases (23.3 ±â€¯3.2 °C pre-acclimation; 23.4 ±â€¯2.0 °C post-acclimation). Distinct inter-individual variation of the dynamic LCT was evident (range pre-PMHA:9.7 °C; post-PMHA:5.4 °C). Regarding the metabolic response to increasing temperatures, only minor or no increases in energy metabolism occurred. PMHA did not significantly change the positioning of the LCTs, but lowered Tcore (pre-PMHA: -0.13 ±â€¯0.13 °C, P = 0.011; post-PMHA: -0.14 ±â€¯0.15 °C, P = 0.026) and affected skin temperature distribution. The applied method allowed for the determination of individual dynamic LCTs, however, distinct metabolic UCTs were not evident in humans. For a better understanding of the human UCT, future studies should incorporate individualised temperature ranges and also a measurement of evaporative heat loss, to allow for a two-factor analysis of both metabolic and evaporative human UCT.

Modulation of thermogenesis and metabolic health: a built environment perspective.

Lifestyle interventions, obviating the increasing prevalence of the metabolic syndrome, generally focus on nutrition and physical activity. Environmental factors are hardly covered. Because we spend on average more that 90% of our time indoors, it is, however, relevant to address these factors. In the built environment, the attention has been limited to the (assessment and optimization of) building performance and occupant thermal comfort for a long time. Only recently well-being and health of building occupants are also considered to some extent, but actual metabolic health aspects are not generally covered. In this review, we draw attention to the potential of the commonly neglected lifestyle factor 'indoor environment'. More specifically, we review current knowledge and the developments of new insights into the effects of ambient temperature, light and the interaction of the two on metabolic health. The literature shows that the effects of indoor environmental factors are important additional factors for a healthy lifestyle and have an impact on metabolic health.

Thermophysiological adaptations to passive mild heat acclimation.

Passive mild heat acclimation (PMHA) reflects realistic temperature challenges encountered in everyday life. Active heat acclimation, combining heat exposure and exercise, influences several important thermophysiological parameters; for example, it decreases core temperature and enhances heat exchange via the skin. However, it is unclear whether PMHA elicits comparable adaptations. Therefore, this study investigated the effect of PMHA on thermophysiological parameters. Participants were exposed to slightly increased temperatures (∼33°C/22% RH) for 6 h/d over 7 consecutive days. To study physiologic responses before and after PMHA, participants underwent a temperature ramp (UP), where ambient temperature increased from a thermoneutral value (28.8 ± 0.3°C) to 37.5 ± 0.6°C. During UP, core and skin temperature, water loss, cardiovascular parameters, skin blood flow and energy expenditure were measured. Three intervals were selected to compare data before and after PMHA: baseline (minutes 30-55: 28.44 ± 0.21°C), T1 (minutes 105-115: 33.29 ± 0.4°C) and T2 (minutes 130-140: 35.68 ± 0.61°C). After 7 d of PMHA, core (T1: -0.13 ± 0.13°C, P = 0.011; T2: -0.14 ± 0.15°C, P = 0.026) and proximal skin temperature (T1: -0.22 ± 0.29°C, P = 0.029) were lower during UP, whereas distal skin temperature was higher in a thermoneutral state (baseline: +0.74 ± 0.77°C, P = 0.009) and during UP (T1: +0.49 ± 0.76°C, P = .057 (not significant), T2:+0.51 ± 0.63°C, P = .022). Moreover, water loss was reduced (-30.5 ± 33.3 ml, P = 0.012) and both systolic (-7.7 ± 7.7 mmHg, P = 0.015) and diastolic (-4.4 ± 4.8 mmHg, P = 0.001) blood pressures were lowered in a thermoneutral state. During UP, only systolic blood pressure was decreased (T2: -6.1 ± 4.4 mmHg, P = 0.003). Skin blood flow was significantly decreased at T1 (-28.35 ± 38.96%, P = 0.037), yet energy expenditure remained unchanged. In conclusion, despite the mild heat stimulus, we show that PMHA induces distinct thermophysiological adaptations leading to increased resilience to heat.

Low brown adipose tissue activity in endurance-trained compared with lean sedentary men.

BACKGROUND/OBJECTIVES: It has now been unequivocally demonstrated that humans possess functional brown adipose tissue (BAT) and that human BAT can be recruited upon chronic cold stimulation. Recruitment of BAT has been postulated as a potential strategy to counteract the current global obesity epidemic. Recently, it was shown in rodents that endurance exercise training could stimulate the recruitment of brown-like adipocytes within white adipose tissue (WAT) via exercise-induced myokines such as irisin (the cleaved circulating product of the type 1 membrane protein FNDC5) and interleukin-6 (IL-6). Our objective was to test whether endurance-trained athletes had increased cold-stimulated BAT activity and browning of subcutaneous WAT compared with lean sedentary males. SUBJECTS/METHODS: Twelve endurance-trained athletes and 12 lean sedentary males were measured during 2 h of mild cold exposure to determine cold-induced BAT activity via [(18)F]fluorodeoxyglucose-positron emission tomography-computed tomography ([(18)F]FDG-PET-CT) scanning. Skeletal muscle FNDC5 expression, as well as plasma irisin and IL-6 levels were determined. In addition, a subcutaneous abdominal WAT biopsy was taken to measure gene expression of several markers for browning of WAT. RESULTS: Cold-induced BAT activity was significantly lower in athletes, and no differences in gene expression of classical brown and beige adipocyte markers were detected in subcutaneous WAT between the groups. As expected, mRNA expression of FNDC5 in skeletal muscle was significantly higher in endurance athletes but plasma irisin and Il-6 levels were similar in both groups. CONCLUSIONS: These results indicate that chronic endurance exercise is not associated with brown and beige adipocyte recruitment; in fact endurance training appears to be linked to lower the metabolic activity of BAT in humans.