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Review
. 2016 Jan 4;3(1):119-45.
doi: 10.1080/23328940.2015.1131506. eCollection 2016 Jan-Mar.

Body temperature regulation in diabetes

Glen P Kenny  1 , Ronald J Sigal  2 , Ryan McGinn  3
Affiliations
Review

Body temperature regulation in diabetes

Glen P Kenny et al. Temperature (Austin). .

Abstract

The effects of type 1 and type 2 diabetes on the body's physiological response to thermal stress is a relatively new topic in research. Diabetes tends to place individuals at greater risk for heat-related illness during heat waves and physical activity due to an impaired capacity to dissipate heat. Specifically, individuals with diabetes have been reported to have lower skin blood flow and sweating responses during heat exposure and this can have important consequences on cardiovascular regulation and glycemic control. Those who are particularly vulnerable include individuals with poor glycemic control and who are affected by diabetes-related complications. On the other hand, good glycemic control and maintenance of aerobic fitness can often delay the diabetes-related complications and possibly the impairments in heat loss. Despite this, it is alarming to note the lack of information regarding diabetes and heat stress given the vulnerability of this population. In contrast, few studies have examined the effects of cold exposure on individuals with diabetes with the exception of its therapeutic potential, particularly for type 2 diabetes. This review summarizes the current state of knowledge regarding the impact of diabetes on heat and cold exposure with respect to the core temperature regulation, cardiovascular adjustments and glycemic control while also considering the beneficial effects of maintaining aerobic fitness.

Keywords: cardiovascular; cold stress; fitness; glycemia; heat stress; type 1 diabetes; type 2 diabetes.

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Figures

Figure 1.
Figure 1.
A schematic diagram demonstrating the rate of heat production (red circles, metabolic rate minus rate of external work) and rate of net loss (blue diamonds, dry + evaporative) during prolonged exercise in the heat. The amount of heat stored in the body - represented by the red shaded area - is the cumulative difference between the rates of heat production and whole-body heat loss by combined evaporative (from sweat and respiration) and dry (conduction/convection and radiation) heat exchange. The metabolic heat production during exercise results in elevated body heat storage and a corresponding increase in core and muscle tissue temperatures, the magnitude of which is determined by the relative intensity of the exercise performed. As long as the rate of heat gain does not exceed the body's physiological capacity to dissipate heat, heat balance will be achieved such as during low (A) and moderate intensity exercise (B). However, as exercise intensity (and therefore the rate of heat production) increases a concomitant increase in rate of heat loss is required to offset this higher rate of heat production and achieve heat balance (such as occurs during transition from A to B). However, there occurs a threshold past which the rate of metabolic heat production exceeds the body's physiological ability to dissipate heat (C). As a consequence, the body will continue to store heat for the duration of the exercise period. Noteworthy, exercise that is performed in the heat will present an added heat load for the body and consequently even moderate intensity exercise performed in the heat may become uncompensable (shift from B to C).
Figure 2.
Figure 2.
The measurement of the onset threshold, the thermosensitivity, and the maximal or plateau level of local and whole-body heat loss during exposure to heat stress (i.e., with environmental and/or metabolic heat loads). The heat loss response (i.e., skin blood flow and sweating) are activated at a given onset mean body temperature threshold (A and D). The heat loss responses then increase proportionally to the increase in mean body temperature, the linear portion of which represents the thermosensitivity of the response (B and E). Once the heat loss responses reach maximal values, a plateau is observed, whereby no further increase in heat loss occurs despite increasing mean body temperature (C and F). There are number of factors (hydration, acclimation, sex, age, chronic health conditions such as diabetes and others) that can affect the activation of heat loss responses which can result in a decrease (Panels A-C, blue shaded area) or increase (Panels D-F, red shaded area) in the amount of heat stored during heat stress. In the latter situation (i.e., greater heat storage) this can occur when: 1) the onset threshold is shifted to the right, such that a greater change in mean body temperature is required to initiate the activation of the heat loss response (D), 2) the thermosensitivity of the response is decreased, such that a lower change in heat loss occurs for a given change in mean body temperature (E), and; 3) the maximal heat loss response is reduced, such that lower maximal values are attained for a given change in mean body temperature (F).
Figure 3.
Figure 3.
Type 1 and Type 2 Diabetes Mellitus are associated with impairments in vasodilation which explain in part the reduction in the capacity to dissipate heat. This is primarily related to a reduction in the thermosensitivity of the response as the onset threshold and the maximal or plateau level of skin blood flow is similar during heat stress. While the mechanisms remain to be fully elucidated, some studies have found a role for endothelium-dependent and –independent vasodilation as well as other factors (e.g., an absence of C-peptide).
Figure 4.
Figure 4.
Type 1 and Type 2 Diabetes Mellitus are associated with impairments in eccrine sweating which leads to a marked reduction in the capacity to dissipate heat. This is primarily explained by a reduced thermosensivity and a lower maximal or plateau level of sweating with no changes in the onset threshold. The mechanisms have yet to be completely understood; however, there is evidence for both centrally- and peripherally-mediated changes in the functioning of the sweat glands.
Figure 5.
Figure 5.
Schematic depicting the change in the rate of heat loss (bars) and the increase in core temperature (arrows) during exercise in those with type 1 diabetes (T1D) and their healthy controls (CON). Studies show that active individuals with type 1 diabetes with good-to-moderate glycemic control (HbA1c< 8.5%) demonstrate a similar capacity to dissipate heat at heat loads ≤ 400 W as compared to their healthy counterparts matched for age, fitness and body composition (see ref 57 and 58). However, diabetes-related impairments in heat loss are observed at progressively greater heat loads leading to significantly greater increases in core temperature (see ref 58). Despite a higher state of hyperthermia measured at end exercise, individuals with Type 1 diabetes demonstrate a similar rate of heat loss relative to their healthy counterparts during the recovery period with core temperature remaining elevated above baseline resting for a minimum of 60 minutes (see ref 59). Future studies are required to determine the extent to which type 1 diabetes reduces the body's maximal ability to dissipate heat such that no further increase in heat loss will occur despite increases in the rate of heat produced/gained (as defined by the dashed contoured bar at a heat load >600W.
Figure 6.
Figure 6.
The factors of age, fitness level, hydration status and acclimation status as well as hemoglobin A1c (HbA1c) in individuals with diabetes which are well known to impact the capacity to dissipate heat in humans during heat stress associated with a passive heat exposure (e.g., hot ambient conditions), exercise, or a combination of both. While there is a substantial amount of research examining such factors in healthy young adults, there is little known with regards to individuals with Type 1 or Type 2 Diabetes Mellitus.
Figure 7.
Figure 7.
Schematic depicting the predicted level of thermal strain, and therefore the amount of heat stored, for a given level of heat stress induced by a passive exposure (top panel) or exercise (bottom panel). During a passive heat exposure, young adults store less heat than their inactive older counterparts. However, recent evidence shows no difference in the level of heat storage between older adults and their counterparts with Type 2 diabetes (see ref. 118). It remains unclear how factors such as level of physical activity/fitness, acclimation, hydration status, blood glucose control (for individuals with diabetes) may influence this pattern of response (orange square). In contrast, the age-related decrement in heat loss during exercise is further exacerbated in older adults with Type 2 Diabetes and the level of fitness appears to be an important component (see ref. 119).
Figure 8.
Figure 8.
This represents a summary of the consequences of diabetes mellitus with respect to glycemic control, fitness, and cardiovascular function as well as during exposure to cold and heat stress. Each of these concepts is discussed in detail in this review. While the most commonly tracked and reported diabetes-related complications include neuropathy, retinopathy, and nephropathy, individuals with diabetes can be at particular risk during exposure to heat and cold stress. More research is required to further characterize these disturbances in temperature regulation and cardiovascular control as well as the potential role for fitness and glycemic control. HbA1c, hemoglobin A1c; ST, shivering thermogenesis; NST, non-shivering thermogenesis; BAT, brown adipose tissue.
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