Indices of adrenal cortical activity in men exposed to cold

Thesis (M.A.)--Boston UniversityEvidence of physiological acclimatization of man to cold is scanty and not clear-cut. Certainly no adaptations have been described comparable to the dramatic changes which occur when men are acclimatized to heat. This study is an attempt to demonstrate acclimatization to cold in man, not in terms of indices specific for cold stress, but rather by measurement of the systemic strain placed on the body. Experiments were designed to answer two questions: (a) Does cold exposure result in a systemic strain on the body? and (b) Does continued cold exposure give rise to (unknown) specific physiologic a aptations with a consequent reduced strain? Since stimulation of tne pituitary-adrenal cortical axis seems to be a common denominator in all known stress situations, adrenal cortical activity was used as a measure of the degree of distortion to the homeostasis. The following experimental design was used: Twelve young soldiers previously brought into good physical condition by mild exercise were exposed to the following successive sets of conditions: four weeks of no cold exposure (baseline period) during which control measurements were made; twelve consecutive days of continuous cold exposure at 60°F.; nine days of no cold exposure; five days of re-exposure to cold (60°F.); five days of no cold exposure. Adrenal cortical activity was assessed by means of circulating eosinophil counts and urinary uric acid: creatinine ratios. During cold exposure periods the men remained continuously in the cold room, leaving it only for meals, bathing and control procedures (a total of 4 1/4 hours daily). They reclined nude except for cotton shorts on army beds from 8:00 A.M. till noon and from 1:15 P.M. till 4:30 P.M. In order to obtain comparable conditions throughout all experimental periods for the assessment of basal levels of adrenal cortical activity, the men lay quietly from 7:00- 8:00A.M. in a constant temperature room maintained at 85°F. +/- 1°F.; at the end of this hour, urine was collected and blood drawn. These samples also served as controls for the measurement of acute responses after four hours in the cold. Sixty degrees Fahrenheit was selected as the cold temperature because it eliminated the danger of cold injury, making it unnecessary to rewarm the men periodically or to clothe them. It was deemed an adequate stimulus because men exhibit the usual cold responses at this temperature - shivering, diuresis, hemoconcentration and peripheral vasoconstriction - within 45 minutes to two hours after the start of exposure. Furthermore preliminary experiments showed this temperature to produce marked discomfort which, however, was tolerable for prolonged periods. The following results were obtained: 1. There was a significant depression of basal eosinophil counts on the fourth and eighth days of the first cold period, with a return to approximately control levels on the eleventh day. 2. A "rebound" of basal eosinophil counts to levels significantly above controls was observed in the nine-day period between cold exposures. 3. Eosinophil counts taken on the fourth day of re-exposure were not significantly different from controls, but were significantly below "rebound" values. 4. No marked differences from normal diurnal variation were observed in the eosinophil counts after four hours of cold exposure at 60°F. 5. No trends were observed in basal uric acid: creatinine ratios. 6. During acute four-hour exposure, uric acid: creatinine ratios were significantly higher than controls. Although no correlation existed between eosinophil and (U-A)/C changes, there was a significant correlation between rate of urine flow and (U-A)/C. Although both eosinophil counts and uric acid: creatinine ratios are preserved to measure activity related to 11-oxygenated corticosteroids, the results show a qualitative difference between the two indices. The eosinophil data indicate changes in basal activity but no marked response to acute exposure, whereas the (U-A)/C data suggest acute responses but no change in basal levels. This confirms the findings of previous workers of a lack of parallelism between these indices in conditions of mild stress. The changes in basal eosinophil counts suggest positive findings of acclimatization to cold. The significant decreases on the fourth and eighth days of exposure indicate increased adrenal cortical activity; the return toward pre-exposure levels on the eleventh day suggest a return of activity toward normal. These results are consistent with, but do not prove, the thesis that cold exposure under the conditions described results in a systemic strain on the body, and that the strain is lessened on extended exposure. This suggests that physiological acclimatization to cold occurs. These conclusions are based on assumptions that (a) changes in circulating eosinophil counts reflect changes in adrenal cortical activity and (b) changes in such activity are a measure of the severity of strain placed on the body

Thermoregulation in rats: Effects of varying duration of hypergravic fields

The effects of hypergravitational fields on the thermoregulatory system of the rat are examined. The question underlying the investigation was whether the response of the rat to the one hour cold exposure depends only upon the amplitude of the hypergravic field during the period of cold exposure or whether the response is also dependent on the amplitude and duration of the hypergravic field prior to cold exposure. One hour of cold exposure applied over the last hour of either a 1, 4, 7, 13, 19, 25, or 37 hr period of 3G evoked a decrease in core temperature (T sub c) of about 3 C. However, when rats were subjected concurrently to cold and acceleration following 8 days at 3G, they exhibited a smaller fall in T sub c, suggesting partial recovery of the acceleration induced impairment of temperature regulation. In another series of experiments, the gravitational field profile was changed in amplitude in 3 different ways. Despite the different gravitational field profiles used prior to cold, the magnitude of the fall in T sub c over the 1 hr period of cold exposure was the same in all cases. These results suggest that the thermoregulatory impairment has a rapid onset, is a manifestation of an ongoing effect of hypergravity, and is not dependent upon the prior G profile

Photoplethysmography for Quantitative Assessment of Sympathetic Nerve Activity (SNA) During Cold Stress

The differences in the degree of sympathetic nerve activity (SNA) over cutaneous blood vessels, although known to be more prominent in the periphery than the core vasculature, has not been thoroughly investigated quantitatively. Hence, two studies were carried out to investigate the differences in SNA between the periphery and the core during the cold pressor test (CPT) (right-hand immersion in ice water) and cold exposure (whole body exposed to cold air) using photoplethysmography (PPG). Two methods utilizing PPG, namely differential multi-site PTT measurements and low-frequency spectral analysis were explored for quantitative determination of SNA. Each study involved 12 healthy volunteers, and PPG signals were acquired from the right index finger (RIF), left index finger (LIF) (periphery) and the ear canal (core). During CPT, Pulse Transit Time (PTT) was measured to the respective locations and the mean percentage change in PTT during ice immersion at each location was used as an indicator for the extent of SNA. During cold exposure, the low-frequency spectral analysis was performed on the acquired raw PPGs to extract the power of the sympathetic [low-frequency (LF): 0.04–0.15 Hz] and parasympathetic components [high-frequency (HF): 0.15–0.4 Hz]. The ratio of LF/HF components was then used to quantify the differences in the influence of SNA on the peripheral and core circulation. PTT measured from the EC, and the LIF has dropped by 5 and 7%, respectively during ice immersion. The RIF PTT, on the other hand, has dropped significantly (P < 0.05) by 12%. During the cold exposure, the LF/HF power ratio at the finger has increased to 86.4 during the cold exposure from 19.2 at the baseline (statistically significant P = 0.002). While the ear canal LF/HF ratio has decreased to 1.38 during the cold exposure from 1.62 at baseline (P = 0.781). From these observations, it is evident that differential PTT measurements or low-frequency analysis can be used to quantify SNA. The results also demonstrate the effectiveness of the central auto-regulation during both short and long-term stress stimulus as compared to the periphery

Effects of Acute Cold Exposure on Plasma Biomarkers Associated with Cardiovascular Disease Risk

Background and Aims: The underlying cause of the majority of the cases of CVD is atherosclerosis, which is a condition initiated and progressed by chronic inflammation and hyperlipidemia. We are interested in evaluating the efficacy of cold-exposure to increase shivering- and non-shivering thermogenesis energy expenditure (RMR) as a non-pharmaceutical weight loss tool analogous to low intensity exercise. Naturally, we are concurrently evaluating the possible effects of cold exposure on risk factors associated with CVD risk. Inflammatory cytokines and lipid mediators are used as biomarkers for CVD risk. This proposed study aims to measure cardiovascular inflammatory and lipid biomarkers to expand our knowledge of cold exposure and CVD risk. The two biomarkers collected during this study were Interleukin-1 Beta (IL-β) and Chemokine Ligand 2 (CCL2). The hypothesis was that there would be no change in biomarker values before and after cold exposure. Methods: Twenty subjects were recruited and subjected to a 30-min cold exposure test while a metabolic cart collected metabolic data via indirect calorimetry. Venous plasma collected at: pre cold exposure, immediately after cold exposure, and 2 hours post cold exposure was centrifuged for subsequent biomarkers analysis. Results: RMR increases dramatically during acute cold exposure during shivering and remains increased 5 minutes after the cessation of shivering. Five minutes post-cold exposure, RMR rapidly decreases to pre-cold exposure RMR and is maintained for up to 120 minutes. There was no change in CCL2 values when comparing the three stages. IL-β values increased between blood draws immediately after cold exposure and 2 hours post cold exposure, however this increase was not statistically significant. Conclusions: With these pilot results, we conclude that cold exposure has no effect on biomarkers for CVD risk. However, this study was limited by 1) accuracy of analysis techniques, 2) cold exposure protocol, 3) analysis of only two representative biomarkers. Further biomarker analysis is underway for a more comprehensive picture of the purported cold exposure effects

"Cold training" affects rat liver responses to continuous cold exposure.

Continuous exposure of homeothermic animals to low environmental temperatures elicits physiological adaptations necessary for animal survival, which are associated to higher generation of pro-oxidants in thermogenic tissues. It is not known whether intermittent cold exposure (cold training) is able to affect tissue responses to continuous cold exposure. Therefore, we investigated whether rat liver responses to continuous cold exposure of 2 days are modified by cold training (1h daily for 5 days per week for 3 consecutive weeks). Continuous cold increased liver oxidative metabolism by increasing tissue content of mitochondrial proteins and mitochondrial aerobic capacity. Cold training did not affect such parameters, but attenuated or prevented the changes elicited by continuous cold exposure. Two-day cold exposure increased lipid hydroperoxide and protein-bound carbonyl levels in homogenates and mitochondria, whereas cold training decreased such effects although it decreased only homogenate protein damage in control rats. The activities of the antioxidant enzymes GPX and GR and H2O2 production were increased by continuous cold exposure. Despite the increase in GPX and GR activities, livers from cold-exposed rats showed increased susceptibility to in vitro oxidative challenge. Such cold effects were decreased by cold training, which in control rats reduced only H2O2 production and susceptibility to stress. The changes of PGC-1, NRF-1, and NRF-2 expression levels were consistent with those induced by cold exposure and cold training in mitochondrial protein content and antioxidant enzyme activities. However, the mechanisms by which cold training attenuates the effects of the continuous cold exposure remain to be elucidated

Energy Expenditure following Acute Cold Exposure

TACSM Abstract - Energy Expenditure following Acute Cold Exposure Stelly S, Bravo D, Hines N, Koehler L, Levi M and Fogt D Exercise Biochemistry & Metabolism Laboratory; Department of Kinesiology, Health & Nutrition; The University of Texas at San Antonio; San Antonio, TX Category: Masters Advisor / Mentor: Fogt, Donovan ([email protected]) ABSTRACT Whole body energy expenditure (i.e., RMR) increases during acute cold exposure. Whether this increase in energy expenditure persists in the post-cold term in humans due to non-shivering thermogenesis has not yet been evaluated. Therefore we tested the hypothesis that RMR would be different directly following acute cold exposure. RMR (kcal•min-1) was assessed via indirect calorimetry on eight (8) males and seven (7) females at six time points: prior to cold exposure (T1), at the end of 30 minutes of cold exposure (T2), immediately post-cold-post-shivering (T3), at 35 minutes post-cold (T4), at 75 minutes post-cold (T5), and at 115 minutes post-cold (T6). This RMR data for the aforementioned time points was analyzed using paired, dependent t-tests and one way ANOVA; the significance level was placed at p \u3c 0.05. The RMR data for each time point was as follows: T1 (1.19±0.21), T2 (2.30±0.94), T3 (1.37±0.25), T4 (1.12±0.19), T5 (1.14±0.22), and T6 (1.14±0.22). The analysis of the RMR data showed a significant difference between the cold (T2) data and all other time points (T1, T3, T4, T5, and T6). Additionally there was a significant difference between the pre-cold (T1) and the immediately post-cold (T3) data. However there was no significant difference between the pre-cold (T1) data when compared with the remaining post-cold data (T4 – T6). These results suggest that the human body is capable of returning RMR to baseline levels relatively immediately following the cessation of acute cold exposure

Pathogenesis of sudden death following water immersion (immersion syndrome)

Sympathetic activity under cold stress is investigated. Predominantly vagal cardio-depressive reflexes are discussed besides currently known mechanisms of sudden death after water immersion. Pronounced circulatory centralization in diving animals as well as following exposure in cold water indicates additional sympathetic activity. In cold water baths of 15 C, measurements indicate an increase in plasma catecholamine levels by more than 300 percent. This may lead to cardiac arrhythmias by the following mechanisms: cold water essentially induces sinus bradycardia; brady-and tachycardiarrhythmias may supervene as secondary complications; sinusbradycardia may be enhanced by sympathetic hypertonus. Furthermore, ectopic dysrhythmias are liable to be induced by the strictly sympathetic innervation of the ventricle. Myocardial ischemia following a rise in peripheral blood pressure constitutes another arrhythmogenic factor. Some of these reactions are enhanced by alcohol intoxication

Pulmonary vasospasm in systemic sclerosis: noninvasive techniques for detection

In a subgroup of patients with systemic sclerosis (SSc), vasospasm affecting the pulmonary circulation may contribute to worsening respiratory symptoms, including dyspnea. Noninvasive assessment of pulmonary blood flow (PBF), utilizing inert-gas rebreathing (IGR) and dual-energy computed-tomography pulmonary angiography (DE-CTPA), may be useful for identifying pulmonary vasospasm. Thirty-one participants (22 SSc patients and 9 healthy volunteers) underwent PBF assessment with IGR and DE-CTPA at baseline and after provocation with a cold-air inhalation challenge (CACh). Before the study investigations, participants were assigned to subgroups: group A included SSc patients who reported increased breathlessness after exposure to cold air (n = 11), group B included SSc patients without cold-air sensitivity (n = 11), and group C patients included the healthy volunteers. Median change in PBF from baseline was compared between groups A, B, and C after CACh. Compared with groups B and C, in group A there was a significant decline in median PBF from baseline at 10 minutes (−10%; range: −52.2% to 4.0%; P < 0.01), 20 minutes (−17.4%; −27.9% to 0.0%; P < 0.01), and 30 minutes (−8.5%; −34.4% to 2.0%; P < 0.01) after CACh. There was no significant difference in median PBF change between groups B or C at any time point and no change in pulmonary perfusion on DE-CTPA. Reduction in pulmonary blood flow following CACh suggests that pulmonary vasospasm may be present in a subgroup of patients with SSc and may contribute to worsening dyspnea on exposure to cold

Renal neuroendocrine control of desiccation and cold tolerance by Drosophila suzukii

Background: Neuropeptides are central to the regulation of physiological, and behavioural processes in insects, directly impacting cold and desiccation survival. However, little is known about the control mechanisms governing these responses in D. suzukii. The close phylogenetic relationship of D. suzukii with D. melanogaster allows, through genomic and functional studies, an insight into the mechanisms directing stress tolerance in D. suzukii. Results: Capa, Leucokinin, DH44 and DH31 neuropeptides demonstrate a high level of conservation between D. suzukii and D. melanogaster with respect to peptide sequences, neuronal expression, receptor localisation, and diuretic function in the Malpighian tubules. Despite D. suzukii’s ability to populate cold environments, they proved sensitive to both cold and desiccation. Furthermore, in D. suzukii, Capa acts as a desiccation-and cold stress-responsive gene, while DH44 gene expression is increased only after desiccation exposure, and the LK gene after nonlethal cold stress recovery. Conclusion: This study provides a comparative investigation into stress tolerance mediation by neuroendocrine signalling in two Drosophila species, providing evidence that similar signalling pathways control fluid secretion in the Malpighian tubules. Identifying processes governing specific environmental stresses affecting D. suzukii could lead to the development of targeted integrated management strategies to control insect pest populations