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Abstract

Objective

It is well established that a combination of factors, including ethnicity, may influence an individual's response to cold stress. Previous work from our laboratory has demonstrated that when faced with a cold challenge, there is a similar response in heat production between Caucasian (CAU) and African American (AA) individuals that is accompanied by a differential response in core temperature. The objective of this study was to evaluate the influence of ethnicity (CAU vs AA) on the thermoregulatory response after acute cold exposure (ACE-REC, 25°C air).

Methods

Five AA males (20.8 ± 0.5 years) and 10 CAU males (25.6±4.9 years) underwent pre-experimental testing to determine Vo_2max (AA = 37.2 ± 0.1 mL·kg⁻¹·min⁻¹, CAU = 44.3 ± 8.7 mL·kg⁻¹·min⁻¹) and body composition (AA = 14.6 ± 5.4%, CAU = 19.2 ± 5.0%). Participants underwent acute cold exposure that consisted of 120 minutes of exposure to 10°C air (ACE) followed by 120 minutes of recovery in 25°C air (ACE-REC). Rectal temperature (T_re) was measured via a rectal thermistor. Mean skin temperature (T_sk) was assessed with thermistors. Oxygen consumption (Vo₂) was assessed via indirect open circuit spirometry. Rectal temperature and T_sk were measured continuously, and if T_re ≤ 35°C, testing was terminated.

Results

Analysis of variance for ACE-REC revealed a significant main effect for T_sk across time (P < .001), T_re across time (P < .001), and Vo₂ across time (P < .001). In addition, a significant time × ethnicity interaction was revealed for T_re (P = .008), T_sk (P = .042), and Vo₂ (P = .019) during ACE-REC.

Conclusions

Based on these data, there is a differential response between CAU and AA across time for Vo₂, T_re, and T_sk ACE-REC.

Keywords

African American Caucasian ethnicity thermal metabolic cold

Introduction

When an individual is exposed to environmental temperature extremes, the challenge is to maintain thermoregulatory homeostasis. Humans attempt to maintain thermoregulation through the integration of different mechanisms, acting in concert with a variety of contributing factors. The primary physiological responses include an increase in metabolism (shivering thermogenesis), an alteration in the vasomotor response (peripheral vasoconstriction/vasodilation),¹ and a circulatory response (countercurrent heat mechanism). Additionally, such factors as fitness level, body composition, age, gender, and race may also influence the individual's ability to thermoregulate.² ^–7

An understanding of how different individuals thermoregulate is valuable to those who engage in outdoor activities for prolonged periods. The majority of current literature in the field focuses on the cold exposure portion, whereas little research has examined the recovery phase. Acute cold exposure (ACE) has been shown to increase the clotting response during the recovery period, making individuals more susceptible to negative cardiovascular events,⁸^–10 such as heart attacks and strokes. Research in the area of cold exposure has also focused primarily on the Caucasian (CAU) male with very little research available concerning different ethnicities and how they may thermoregulate to the stressor of cold.

It has been well documented that African Americans (AA) suffer a disproportionately higher rate of cardiovascular disease.¹¹ Cardiovascular reactivity has also been shown to be greater among AA after a variety of stressors.¹¹ Further, it is unclear whether morphological or ethnic differences cause potential alterations in cold responsiveness between groups or whether the alterations are due to differences in thermosensitivity. McArdle et al suggests that the differences in thermoregulation at rest during cold stress may be due in part to the sensitivity of the thermogenic response.¹² Previous work from our laboratory has demonstrated that CAU individuals thermoregulate to cold stress by maintaining a higher metabolic rate than their AA counterparts.¹ Although numerous studies have demonstrated that certain physiological changes may ensue with cold stress, research in the area of ethnicity and how the individual may respond to this stressor is limited.^6,13 ^–18 Therefore, the impact of ethnicity (eg, AA vs CAU) on thermoregulation warrants investigation. In an effort to establish possible differences that are involved in thermoregulation, the recovery phase of acute cold exposure (ACE-REC) was explored to discern if individuals who varied on the basis of ethnicity would demonstrate a differential response after ACE. In this differential response, the return of cooled peripheral blood after ACE for 120 minutes may elicit differences between individuals based on ethnicity.

In an effort to establish possible differences involved in thermoregulation between AA and CAU males, we studied ACE-REC to evaluate whether there is a differential thermoregulatory and metabolic response after ACE in individuals of these races.

Methods

Fifteen males (5 AA, 10 CAU) participated in this study. Participant characteristics are presented in Table 1.

Table 1

Study group participant characteristics^*

Each participant experienced 120 minutes of exposure to 10°C air (ACE) and recovery (ACE-REC) wearing only a swimsuit for 120 minutes or until rectal temperature (T_re) was ≤35°C. The complete air exposure trial consisted of 3 periods: a 15-minute baseline (BASE) period followed by a 120-minute ACE, followed by a 120-minute recovery (ACE-REC) in 25°C air. Throughout the ACE and ACE-REC, T_re, skin temperature (T_sk), expired air, and heart rate (HR) were continuously monitored and metabolic rate (Vo₂) was measured at 15-minute increments. The protocol was reviewed and approved by the Kent State University Institutional Review Board. Participants completed a health history questionnaire and signed an informed consent. All trials were completed at the same time of the day and within 12 weeks.

Baseline Period

Upon arrival to the Applied Physiology Laboratory, participants had their body weight measured. They were then instructed to insert a rectal probe (ER400-12, Respiratory Diagnostic Products Inc, Irvine, CA) 13 cm beyond the anal sphincter for the purpose of monitoring T_re. Participants were also outfitted with skin thermistors (Model #409B, Yellow Springs Instruments Inc, Yellow Springs, OH) to measure mean skin temperature. Temperature-sensing thermistors were placed on the tricep, chest, thigh, calf, and forearm and secured with Hy-tape waterproof tape (Hy-tape International, Patterson, NY) for the purpose of collecting T_sk data. Rectal temperature and T_sk thermistors were then interfaced with a data acquisition system (iNet-100HC, Omega Engineering Inc, Stamford, CT), which was interfaced with a desktop computer. Mean skin temperature was calculated using the weighted formula used by Ramanathan.¹⁹ Rectal temperature and T_sk data were monitored continuously and recorded every minute.

After instrumentation, the participant sat quietly, with arms and legs extended and separated, in a semirecumbent position on a plastic lounge chair outside of, and next to, the environmental chamber in a 24–26°C air environment for 15 minutes. During the BASE period, expired air samples, T_re, T_sk, Vo₂, and HR were monitored. Oxygen consumption was assessed via indirect open circuit spirometry with a Parvo metabolic cart (TrueOne 2400, Parvomedics, Sandy, UT) that was calibrated before and after data collection.

Cold Air Exposure/Recovery Period

After completing the BASE period, participants were rolled into the environmental chamber, where they were required to remain seated and quiet in the chair with limbs separated and extended while exposed to 10°C cold air for 120 minutes. Rectal temperature T_sk, Vo₂, and HR were monitored continuously and recorded at predetermined time points (0, 30, 60, 90, and 120 minutes). Upon completion of ACE, the participant sat quietly in the environmental chamber, with arms and legs extended and separated, in a semirecumbent position on a plastic lounge chair in a 25°C air environment for 120 minutes. The chamber required approximately 30 minutes to reach 25°C from 10°C. Throughout the ACE-REC, T_re, T_sk, expired respiratory air samples, and HR were continuously monitored.

Statistical Analysis

Statistical analysis was performed using a 2-way analysis of variance, 2 (group [CAU and AA]) × 6 (time [BASE, 0, 15, 30, 60, 90, and 120 minutes]) with repeated measures for time. An independent t test was used to analyze participant characteristics (anthropometric variables, Vo_2max). SPSS version 13.0 was used to compute all statistical calculations, and the level of significance was set a priori at P ≤ .05. Posthoc analysis was done using pair-wise comparison with Bonferroni adjustments where applicable to determine significant interactions. All values are expressed as mean ± SD.

Results

Fifteen volunteers (5 AA males [20.8 ± 0.5 years], 10 CAU males [25.6 ± 4.9 years]) were recruited to participate in the current study and successfully completed all experimental trials of 120 minutes of ACE followed by 120 minutes of ACE-REC. The groups did not differ statistically with respect to percent body fat (AA = 14.6 ± 5.4%, CAU = 19.2 ± 5.0%). Both groups were similar in height and weight, as well as in lean body mass and body surface area. Likewise, the groups did not differ significantly with respect to maximal oxygen consumption (AA = 37.2 ± 0.1 mL·kg⁻¹·min⁻¹, CAU = 44.3 ± 8.7 mL·kg⁻¹·min⁻¹).

Rectal Temperature

Figure 1 shows a significant difference in T_re (P = .008) between the 2 groups. Posthoc analysis demonstrated significant time × ethnicity interactions (ie, significant difference between groups across time) for T_re at 0 (CAU 36.9 ± 0.3°C, AA 36.5 ± 0.3°C), 30 (CAU 36.7 ± 0.4°C, AA 36.2 ± 0.4°C), 60 (CAU 36.6 ± 0.3°C, AA 36.1 ± 0.4°C), 90 (CAU 36.6 ± 0.4°C, AA 35.4 ± 0.4°C), and 120 (CAU 36.6 ± 0.2°C, AA 36.0 ± 0.4°C) minutes of ACE-REC, during which the AA participants demonstrated a lower T_re. Additionally, a main effect for time (ie, significant difference across time) was demonstrated (P < .001). As ACE-REC time increased, T_re decreased.

Figure 1

Time × ethnicity interaction for rectal temperature during recovery (P = .008). *a, b, c, d, and e denote significant differences between groups at 0, 30, 60, 90, and 120 minutes, respectively, of the recovery phase of acute cold exposure. CAU indicates Caucasian; AA indicates African American.

Mean Skin Temperature

Figure 2 shows a significant difference in T_sk (P = .042) between the 2 groups. Posthoc analysis demonstrated significant time × ethnicity interactions for T_sk at 60 (CAU 27.6 ± 0.4°C, AA 27.0 ± 0.6°C) and 90 minutes (CAU 28.2 ± 0.4°C, AA 27.5 ± 0.3°C) of ACE-REC, during which the AA participants demonstrated a lower T_sk. There was also a significant (P < .001) main effect for time for T_sk. As ACE-REC time increased, T_sk increased.

Figure 2

Time × ethnicity interaction for skin temperature during recovery (P = .042). *a and b denote significant differences between groups at 60 and 90 minutes of the recovery phase of acute cold exposure. CAU indicates Caucasian; AA indicates African American.

Oxygen Consumption

Figure 3 shows a significant difference in Vo₂ (P = .019) between the 2 groups. Posthoc analysis demonstrated significant time × ethnicity interactions for Vo₂ (CAU 7.4 ± 1.8 mL·kg⁻¹·min⁻¹, AA 5.7 ± 0.9 mL·kg⁻¹·min⁻¹) at 0 minutes of ACE-REC, during which the AA participants demonstrated a lower Vo₂. Oxygen consumption was also significant across time (P < .001). It decreased during the first 30 minutes of REC and remained stable for the remainder of REC.

Figure 3

Time × ethnicity interaction for Vo₂ (P = .019). CAU indicates Caucasian; AA indicates African American. *a denotes significant differences between groups at 0 minutes of the recovery phase of acute cold exposure.

Discussion

The present study examined the influence of ethnicity on the thermoregulatory and metabolic responses of AA and CAU males during ACE-REC. When exposed to environmental extremes, the challenge is to maintain thermoregulatory homeostasis. Previous research has suggested that there may be a difference in the intrinsic systems responsible for thermoregulation, which may affect how individuals thermoregulate.^13–14,16^–18 These may include ethnic cardiovascular differences, such as higher resting blood pressure and increased total peripheral resistance among AA.¹¹

The response of T_re demonstrated by the participants is consistent with earlier research conducted in the field of environmental physiology.^1,4,12 As the physiological stress of ACE-REC increased, T_re decreased over time. The primary physiological stress during recovery is due to the return of cold peripheral blood to the core. This phenomenon is commonly referred to as afterdrop. This response differed significantly between the groups and suggests that AA individuals maintained a significantly lower T_re than their CAU counterparts over time (Figure 1). One may speculate that the AA group may be more at risk for hypothermia.

Additional research in the area of ethnicity may focus on thermoregulation to cold exposure employing a more prolonged recovery period or perhaps a greater cold air stressor. Mean skin temperature demonstrated a main effect for time (Figure 2). This response in mean skin temperature demonstrated by the experimental participants is in agreement with the research in the area of environmental physiology, whereby T_sk (over time) is closely linked to ambient temperature.^6,19 ^–22 In addition, there was a significant time × ethnicity interaction (Figure 2), whereby the AA group demonstrated a lower T_sk at 60 and 90 minutes than did the CAU group. This is probably due to the greater heat loss, which was also demonstrated via the lower T_re. In both the T_re and T_sk responses, the initial change and the interaction may be a result of the immediate and initial measurement in the transition from the cold air (10°C) to the warmer ambient air temperature (25°C), which best perhaps represents thermoresponsiveness, or the return of the cold peripheral blood to the core.

Although peripheral vasoconstriction functions to reduce heat loss, an increase in heat production via an increase in oxygen consumption demonstrates an increase in shivering thermogenesis. As recovery from cold exposure time increased, oxygen consumption increased initially with a concomitant decline in T_sk and T_re and then reached a plateau at slightly higher values compared with the baseline.

In a cold environment, the peripheral thermoreceptors are believed to send a signal to the hypothalamus, which then activates the brain centers to increase shivering, among other thermoregulatory responses. These data therefore suggest that external stressors influence homeostasis by altering the involvement of the hypothalamus with both the sympathetic adrenal medulla and the hypothamalmic pituitary axis.¹ The present investigation demonstrated a significant time × ethnicity interaction for T_re and Vo₂, which may suggest a differential response that is centrally mediated between the CAU and AA groups.

The difference in Vo₂ demonstrated by the groups in the present investigation (Figure 3) is in agreement with the experimental literature that ethnicity may influence thermoregulation.^2,23 In the current investigation, the CAU and AA individuals differed over time between groups and over time for T_sk, Vo₂, and T_re. Therefore, the present results demonstrate that the CAU participants expended more energy than their AA counterparts initially during ACE-REC (at 0 minutes) and also maintained a higher T_re. These findings are in agreement with Rennie and Adams,²³ as well as Adams and Covino,² who both found significant differences in metabolic heat production between CAU and AA groups. In contrast to the present investigation, Rennie and Adams observed no difference in core temperature or average skin temperature between groups at any time during the cold exposures.²³

However, there was a difference in metabolism between the groups, whereby the CAU participants exhibited higher values then their AA counterparts. The experimental literature suggests morphological, racial differences between AA and CAU individuals.²⁴ However, the present investigation did not show significance for morphological characteristics. Contrary to the results of the present investigation, Hooton²⁴ demonstrated that AA individuals have a greater surface area in their extremities and have greater subcutaneous fat located more centrally. Both of these factors may elicit greater heat loss through the periphery and, in part, may account for these differences in thermoregulation.

Adams and Covino observed that after 55 minutes of whole body exposure, CAU and Eskimo participants had increased heat production by 22 cal·hr·m² above control levels of 40 and 55 cal·hr·m², respectively, whereas the AA participants, after 85 minutes of exposure, had increased heat production by only 10 cal·hr·m².² Similarly, in the present investigation, the CAU volunteers had an initial increase in energy and a higher T_re compared with their AA counterparts. Further, Adams and Covino observed that after 85 minutes of exposure, the AA participants had not increased heat production to levels equal to that of either of their CAU or Eskimo counterparts.² In the present investigation, after the initial increase in energy expenditure, the CAU group had slightly higher energy expenditure in ACE-REC. This may again suggest that the CAU group was more responsive to the stressor through the return of peripheral cooled blood back to the core than their AA counterparts. This may be due to the central (ie, sympathetic adrenal medulla and hypothamalmic pituitary axis) and/or morphological differences that clearly warrant further investigation in the area of ACE.

The data of the current investigation suggest that although T_re differed between the AA and CAU individuals, the CAU individuals appeared to expend more energy to maintain a higher rectal temperature compared with their AA counterparts at the 0 minute time point of ACE-REC. This “hyper” metabolic heat production exhibited by the CAU group may prove to be beneficial in the maintenance of rectal temperature and ultimately temperature homeostasis over a prolonged period during recovery from cold stress. Further, as a result of the higher metabolic rate, the CAU individuals are at reduced risk for the development of hypothermia compared with AA individuals, as demonstrated by the increase in shivering thermogenesis and energy expenditure, which play a role in the maintenance of temperature homeostasis.

Limitations of the present study include the small sample size and the discrepancy between group sizes. Both of these factors resulted from difficulties in recruiting CAU and AA participants for this study. However, the related literature within this field of research often uses small sample sizes, and this limitation may indicate a possible reduced significance and adequate statistical power.

Conclusions

In conclusion, based on these data there was a differential response between CAU and AA individuals over time for Vo₂ and T_re in the recovery phase after ACE. The results of the current study suggest that this scenario could be extremely detrimental because an increase in resting metabolic rate is needed to maintain core temperature and this response appears to be attenuated in AA individuals during the initial phase of recovery. Further research in this area is necessary to evaluate centrally mediated differences between CAU and AA individuals. Also, further research may evaluate the differences between CAU and AA individuals with respect to the temperature of the cold stressor, exposure time, and recovery from cold while matching individuals based on body composition and morphology.

Footnotes

Funding

This study was funded in part by the Natural Science and Engineering Research Council (Canada).

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The Influence of Ethnicity on Thermoregulation After Acute Cold Exposure

Abstract

Objective

Methods

Results

Conclusions

Keywords

Introduction

Methods

Baseline Period

Cold Air Exposure/Recovery Period

Statistical Analysis

Results

Rectal Temperature

Mean Skin Temperature

Oxygen Consumption

Discussion

Conclusions

Footnotes

Funding

References