Thermal energy is transferred within and between bodies via several avenues, but for most unprotected human cold exposures, particularly during immersion, convective heat loss dominates. Lower tissue temperatures stimulate thermoreceptors, and the resultant afferent flow elicits autonomic homoeostatic responses (thermogenesis and vasoconstriction) that regulate body temperature within a narrow range. The most powerful effector responses occur when both superficial and deep thermoreceptors are cooled simultaneously, but thermoeffector activation can also occur as a result of peripheral cooling alone. The responses to cold, and the hazards associated with cold exposure, are moderated by factors which influence heat production and heat loss, including the severity and duration of cold stimuli, accompanying exercise, the magnitude of the metabolic response, and individual characteristics such as body composition, age, and gender. Cold stress can quickly overwhelm human thermoregulation with consequences ranging from impaired performance to death. This review provides a comprehensive overview of the human physiological responses to acute cold exposure.

Human physiological responses to cold exposure.

Background A variety of studies have noted seasonal variation in blood lipid levels. Although the mechanism for this phenomenon is not clear, such variation could result in larger numbers of people being diagnosed as having hypercholesterolemia during the winter. Methods We conducted a longitudinal study of seasonal variation in lipid levels in 517 healthy volunteers from a health maintenance organization serving central Massachusetts. Data collected during a 12-month period for each individual included baseline demographics and quarterly anthropometric, blood lipid, dietary, physical activity, light exposure, and behavioral information. Data were analyzed using sinusoidal regression modeling techniques. Results The average total cholesterol level was 222 mg/dL (5.75 mmol/L) in men and 213 mg/dL (5.52 mmol/L) in women. Amplitude of seasonal variation was 3.9 mg/dL (0.10 mmol/L) in men, with a peak in December, and 5.4 mg/dL (0.14 mmol/L) in women, with a peak in January. Seasonal amplitude was greater in hypercholesterolemic participants. Seasonal changes in plasma volume explained a substantial proportion of the observed variation. Overall, 22% more participants had total cholesterol levels of 240 mg/dL or greater (≥6.22 mmol/L) in the winter than in the summer. Conclusions This study confirms seasonal variation in blood lipid levels and suggests greater amplitude in seasonal variability in women and hypercholesterolemic individuals, with changes in plasma volume accounting for much of the variation. A relative plasma hypervolemia during the summer seems to be linked to increases in temperature and/or physical activity. These findings have implications for lipid screening guidelines. Further research is needed to better understand the effects of a relative winter hemoconcentration.

https://jamanetwork.com/journals/jamainternalmedicine/articlepdf/216973/ioi30014.pdf

Seasonal variation in serum cholesterol levels: treatment implications and possible mechanisms.

Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Thermoregulatory physiology sustains health by keeping body core temperature within a degree or two of 37°C, which enables normal cellular function. Heat production and dissipation are dependent on a coordinated set of autonomic responses. The clinical detection of thermoregulatory impairment provides important diagnostic and localizing information in the evaluation of disorders that impair thermoregulatory pathways, including autonomic neuropathies and ganglionopathies. Failure of neural thermoregulatory mechanisms or exposure to extreme or sustained temperatures that overwhelm the body's thermoregulatory capacity can also result in potentially life-threatening departures from normothermia. Hypothermia, defined as a core temperature of 40.5°C, may present with sweating, flushing, tachycardia, fatigue, lightheadedness, headache, and paresthesia, progressing to weakness, muscle cramps, oliguria, nausea, agitation, hypotension, syncope, confusion, delirium, seizures, and coma. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion. Management requires the immediate reduction of core temperature. Ice water immersion has been shown to be superior to alternative cooling measures. Avoidance of thermal risk and early recognition of cold or heat stress are the cornerstones of preventive therapy.

Thermoregulatory disorders and illness related to heat and cold stress.

In meat-type chickens, an inadequacy of vascular capacity for blood flow through the lung to provide the tissues with the oxygen needed for rapid growth is the primary cause of pulmonary hypertensioninduced ascites. There are a variety of other factors that can trigger the ascites syndrome. These factors may cause increased blood flow because of a higher metabolic rate (cold, heat, certain nutrients, chemicals, etc.) or they may cause pulmonary hypertension-induced ascites in rapidly growing chickens because of greater resistance to blood flow in the lung by: (i) increased blood viscosity or red blood cell rigidity; or (ii) reduced vascular capacity in the lung. Some secondary factors, such as high sodium from salt in feed or water, may cause both increased flow and increased resistance to flow. Measures to reduce the ascites syndrome must address the primary genetic cause of insufficient vascular flow capacity in the lung and oxygen delivery to tissues, and the secondary factors that increase oxygen requ...

https://www.tandfonline.com/doi/pdf/10.1080/03079450020016751

Physiological, management and environmental triggers of the ascites syndrome: a review

Hormonal and Metabolic Adaptation to Exercise

Classically, cold induced plasma volume reduction is explained by an increased diuresis which is generated by an inhibition of antidiuretic hormone release. However, most of the haemoconcentration appears to be reversible during rewarming. This observation weakens the former statement. The aim of this study was to clarify the mechanisms involved in the reversal of the cold induced haemoconcentration. Six young males, resting in a dorsal reclining position, were exposed successively to a thermoneutral environment (30 min), a cold environment (1 degrees C; cold) or thermoneutrality (control) for 120 min, and during a 60-min recovery period in thermoneutral conditions. During cold stress, a reduction of 15% (i.e. 510 ml) of the plasma volume was observed, and osmolality was unchanged. After the 60-min recovery under thermoneutral conditions, plasma volume variation between the Cold and the Control experiments was reduced and reached 3% (i.e. 100 ml). This volume equalled the increased amount of urine production observed during the cold stress experiment. Haemoconcentration cannot be explained by increased urinary water loss (+/- 100 ml) alone. Therefore a transient shift of plasma water from vascular to interstitial spaces, due to an increase of blood pressure, could be involved in the reduction of plasma volume.

Reversal of cold induced haemoconcentration.

The affect of negative thermal stress on hematological variables at rest, and during submaximal (sub ex) and maximal exercise (max ex) were observed for young males who volunteered in two experimental sessions, performed in cold (0 degree C) and in normal room temperature (20 degrees C). At rest, hematological variables such as RBC and derivates Hb and Hct were significantly increased (P less than 0.05) during cold stress exposure, while plasma volume decreased. The findings of this study suggest that the major factor inducing hypovolemia during low thermal stress can be imputed to local plasma water-shift mechanisms and especially to a transient shift of plasma water from intra- to extravascular compartments. Rest values for WBC and platelets (Pla) were also slightly increased during cold stress exposure. However this increase can partly be related to hemoconcentration but also to the cold induced hyperventilation activating the lung circulation. Maximal exhaustive exercise induced, in both experimental temperatures, significant (P less than 0.05) increments of RBC, Hb, Hct, and WBC while plasma volume decreased. However, Pla increase was less marked. On the other hand, cold stress raised slightly the observed variations of the different hematological variables. Submaximal exercise induced a similar, though non-significant, pattern for the different hematological variables in both experimental conditions. Observed plasma volume (delta PV%) reduction appears during exercise. However cold stress induced resting plasma volume variations that are transferred at every exercise level. Neither exercise nor cold inducement significantly modified the hematological indices (MCH, MCV, MCHC). In conclusion hematological variables are affected by cold stress exposure, even when subjects perform a physical activity.

Hematological variations at rest and during maximal and submaximal exercise in a cold (0°C) environment

The purpose of this study was to determine the effects of cold stress on routine hematologic parameters when subjects are submitted on long-lasting exercise. Eight male subjects, aged 22.7 +/- 1.3 years with a peak oxygen consumption of 54.3 +/- 5.2 mL/kg/min performed, respectively at 20 degrees C and 0 degrees C, a two-hour submaximal cyclergometry at an intensity of 40% of that performed during a previous exhaustive test. A 21-gauge catheter was inserted into an ante cubital vein for collection of the blood samples. Platelets and WBC count was significantly (p less than 0.05) increased during exercise in both 20 degrees C and 0 degrees C environmental temperatures. A slight but not statistically significant increase of RBC, Hb and Hct and a plasma concentration during cold exposure was observed. Indices are unchanged in both experiments. The findings of this study suggest that physical exercise is a major factor inducing hypervolemia and that low thermal environment does not appear to be an effective factor influencing hematologic variables during exercise.

[Hematological variations with submaximal long-term physical exercise].

Variations hematologiques à l'exercice physique sous maximal de longue durée.

Cette etude a pour but d'etudier les variations physiologiques et metaboliques tant au repos, qu'au cours d'efforts physiques de longue duree (2h) a 40% de la puissance maximale et d'efforts exhaustifs dans des conditions d'hypothermie ambiante (0‡C) en comparaison de valeurs recueillies en conditions thermiques neutres (20‡C). L'ensemble des epreuves furent executees en chambre climatique par: d'une part 11 sujets mâles pour l'effort exhaustif et d'autre part 8 sujets mâles pour l'exercice sous-maximal. Nous avons observe une legere bradycardie a 0‡C pour nos deux groupes a la fin de l'effort. La VO2 et la ventilation pulmonaire sont plus elevees a 0‡C lors de l'effort maximal, nous observons toutefois le phenomene inverse lors de l'exercice sousmaximal. Les concentrations plasmatiques en acide lactique sons moins elevees et les bicarbonates plus eleves en ambiance thermique froide pour les deux conditions experimentales. Le pH et la temperature rectale demeurent stables. Le RQ ne presente pas de differences significatives a la fin de chacun des deux efforts a 20‡C et 0‡C.

Variations cardio-respiratoires et metaboliques à l'effort sous-maximal (P=40% Pmax) et maximal (Vita Max) en conditions thermiques froide (0‡C) et neutre (20‡C)

M Brasseur

Papers

Reversal of cold induced haemoconcentration.

Hematological variations at rest and during maximal and submaximal exercise in a cold (0°C) environment

[Hematological variations with submaximal long-term physical exercise].

Variations hematologiques à l'exercice physique sous maximal de longue durée.

Variations cardio-respiratoires et metaboliques à l'effort sous-maximal (P=40% Pmax) et maximal (Vita Max) en conditions thermiques froide (0‡C) et neutre (20‡C)