Metabolic heat production and cold tolerance during cold stress of different intensity of adult and aged male C57BL/6J mice

Adult and aged male C57BL/6J mice were subjected to a 3-h cold stress test at either 24°C, 18°C, 12°C, or 6°C. Body mass was measured before the test, and colonic temperature, O₂ consumption, and CO₂ production were measured during the test. The slopes of colonic temperature over time of test and the mean metabolic heat production were calculated for each animal. While adult mice had a relatively small reduction in colonic temperature during the test at all four ambient temperatures, in the aged mice ambient temperatures resulted in steeper reductions of colonic temperature. In adult mice, an increase in metabolic heat production was proportional to ambient cold. The thermogenic response of aged mice at 24°C and at 18°C was similar to adult mice, suggesting that the ability of aged mice to respond to cold by increasing heat production does not diminish with age. However, in aged mice metabolic heat production at 12°C and 6°C was significantly below that of adult mice, which indicated a reduced capacity for thermogenesis.     

Nonshivering thermogenesis during acute cold exposure in adult and aged C57BL/6J mice

In C57BL/6J adult and aged mice, housed at room temperature (22.5 ± 1°C), we measured O₂ consumption and CO₂ production and calculated metabolic heat production under conditions of anesthesia and myorelaxation during acute cold stimulation when body temperature was lowered 7.5°C below control level. An independent group of mice was subjected to a three hour partial physical restraint at 6°C and concentration of uncoupling protein (thermogenin) was measured in interscapular brown adipose tissue mitochondria at different times after cold exposure. Heat production under anesthesia and myorelaxation was about 57–66% lower than in nonanesthetized conditions, but increased significantly during cold stimulation in both age groups. Under anesthesia and myorelaxation before and during cold stimulation aged mice produced about 20% more heat than adult mice. Because in these experiments all sources of facultative thermogenesis, except nonshivering, were suppressed by anesthesia and myorelaxation, and because brown adipose tissue is the major source of nonshivering thermoproduction, we concluded that aged mice housed at room temperature have an increased thermogenesis in brown adipose tissue. This conclusion was also supported by the finding that the concentration of uncoupling protein measured in the mitochondria of brown adipose tissue after single cold exposure was significantly higher in aged than in adult mice. Therefore, we propose that the lower, cold-induced, heat production typically observed in nonanesthetized aged mice may reflect reduced thermogenic capacity of skeletal muscles. While aged mice have less brown adipose tissue than adult animals, the remaining brown adipose tissue may compensate by increasing the concentration of uncoupling protein.     

The effect of exercise training in a cold environment on thermoregulation in adult and aged C57BL/6J mice

We studied the effect of exercise training in cold environment (six weeks of daily, one-hour runs on a treadmill at ambient temperature of 6 ± I°C at 60±65% of VO_2max) on cold-induced metabolic heat production, heat loss, and cold tolerance in adult and aged C57BL/6J male mice. In adult mice, exercise training in cold environment resulted in greater cold-induced heat production and cold tolerance without changes in heat loss, similar to the effects of daily cold exposure without exercise. In aged mice, daily cold exposures did not affect cold tolerance and cold-induced heat production, but exercise training in the cold resulted in greater cold-induced heat production and cold tolerance. Heat loss in aged mice increased similarly after both repeated cold exposures and exercise training in the cold. Therefore, mechanisms of effect of exercise training on cold tolerance are different in adult and aged animals. Exercise training in cold environment does not affect cold-induced heat production and cold tolerance in adult mice, but improves them in aged animals.     

Effect of intermittent feeding on thermoregulatory abilities of young and aged C57BL/6J mice

At 6 mth of age, male C57BL/6J mice were subjected to an intermittent schedule of feeding (every-other-day) or continued to be maintained on an ad libitum diet (24% protein). This regimen of dietary restriction resulted in increased mean and maximum lifespan (11%) compared to the survival of ad libitum-fed mice. At 8 and 26 mth of age, different groups of mice were tested for cold tolerance during 3 h exposure to 10 degrees C. Aged mice (26 mth) fed ad libitum compared to young mice (8 mth) on the same diet had significantly lower baseline colonic temperatures prior to cold exposure, and impaired cold tolerance, as measured by the rate of decline in colonic temperature during cold exposure. Dietary restriction by intermittent feeding had no significant effect on cold tolerance in young mice or baseline colonic temperature in young or aged mice. However, the cold tolerance of aged mice subjected to 20 mth of intermittent feeding was markedly improved over that of aged cohorts maintained on an ad libitum diet and in fact was indistinguishable from that of young counterparts. Thus, it appeared that this regimen of dietary restriction when implemented in young adults prevented the age-related decline in cold tolerance observed among ad libitum fed mice of this strain.     

A longitudinal study of tolerance to cold stress among C57BL/6J mice

C57BL/6J male mice of different ages were movement-restricted and exposed to 10 degrees C for 3-hr periods every other week while colonic temperature was measured. A longitudinal trend in cold tolerance related to age and to initial colonic temperature was demonstrated. Adaptative thermoregulatory changes during cold exposure occurred during the first two tests. These were similar for all age groups except 30-month-old mice. There was no adaptation of colonic temperature during cold exposure among aged mice with repeated testing; however, their baseline colonic temperatures prior to testing increased after the first two tests. This finding suggests that old animals adjust to repeated cold stress differently than do younger mice. Specifically, younger animals are capable of adjusting their thermoregulatory response during cold stress with no change in baseline (pre-stress) temperature. Old animals do not modify the responses emitted during the stress; however, they do adapt by raising their baseline temperatures. Repeated cold exposure started later in life increased mortality among old animals but did not affect maximum lifespan.     

The effect of exercise training in cold on shivering and nonshivering thermogenesis in adult and aged C57BL/6J mice

To understand the mechanisms of improvement of cold-induced heat production in aged mice following exercise training, the relative contributions of shivering and nonshivering thermogenesis to cold-induced metabolic responses were assessed in adult and aged C57BL/6J male mice, which inhabited sedentarily at room temperature, or were subjected either to a regimen of moderate intensity exercise training at 6°C, or to sedentary repeated exposures to the same temperature. The main findings were that (1) aged mice had greater cold-induced nonshivering thermogenesis, but lower shivering than adult mice; (2) exercise training in a cold environment enhanced cold-induced nonshivering thermogenesis in adult mice, but suppressed it in aged animals; (3) exercise training in a cold environment increased shivering thermogenesis in both age groups, but this increase was much greater in aged mice; (4) the increase of cold-induced shivering thermogenesis was mainly responsible for increased cold tolerance in aged mice after exercise training in a cold environment.     

Age-related differences in response to acute cold challenge (-10 degrees C) in male F344 rats

Male F344 rats, 3, 12, and 24 months of age, were acclimated to either 5 degrees C (CA) or 23 degrees C (non-CA). At the end of acclimation, all CA rats exhibited higher basal oxygen uptake than the non-CA when measured at 28 degrees C. When challenged by a 3-hour exposure to -10 degrees C, significant difference in tolerance to cold was observed not only between the CA and non-CA rats but among the different age groups. The 3-month-olds tolerated cold better than 12-month-olds, and the 12-month-olds did better than the 24-month-olds. The ranking order for cold tolerance in -10 degrees C was: 3-month CA greater than 12-month CA greater than 3-month non-CA = 12-month non-CA = 24-month CA greater than 24-month non-CA. Total 3-hour O2 uptake decreased progressively with advancing age. Heat productions were doubled in -10 degrees C in all age groups, and all CA rats had higher heat production than non-CAs. The increase of heat production in -10 degrees C was insufficient to maintain body temperature in all animals. All animals had loss of body heat content, the loss becoming greater with advancing age. Non-CA rats had greater loss of heat content or faster decline of colonic temperature than the CAs. Significant strain-related difference in cold tolerance was noted between the F344 and Sprague-Dawley (S-D) rats, because 24-month-old non-CA male F344 rats still exhibited a better tolerance to -10 degrees C than 3-month-old CA S-D rats.     

Nonshivering thermogenesis in adult and aged C57BL/6J mice housed at 22°C and at 29°C

Twelve- and 28-month-old C57BL/6J male mice were housed either at room temperature of 22°C or at thermoneutrality (29°C) during the two months prior to experiments. Acute experiments were conducted under anesthesia, myorelaxation, and artificial ventilation. We recorded efferent electrical impulse activity in one of the sympathetic nerves innervating the interscapular brown adipose tissue in response to acute cold stimulation, when body temperature was lowered 7.5°C below control level. In separate experiments we measured O₂ consumption and CO₂ production and calculated the nonshivering thermogenesis. We also measured the concentration of uncoupling protein in interscapular brown adipose tissue before and after three-hour cold stress. In aged mice, both sympathetic nervous activity and nonshivering thermogenesis were lower in animals housed at thermoneutrality (29°C) than in mice housed at 22°. Among mice maintained at 22°C, but not at thermoneutrality, aged animals had greater nonshivering thermogenesis and greater cold induced concentration of uncoupling protein in the brown adipose tissue than adults. Sympathetic nervous outflow to brown adipose tissue was always greater in aged mice, regardless of the temperature of acclimation. We concluded that aged mice, housed at 22°C, showed the changes in nonshivering thermogenesis associated with cold acclimation. However, an increased sympathetic outflow to brown adipose tissue in aged animals reflects an age-related elevation of the tone and responsiveness of the sympathetic nervous system.     

The effect of cold acclimation and exercise training on cold tolerance in aged C57BL/6J mice

We investigated whether intermittent cold acclimation and low intensity exercise training, two interventions known to improve thermoregulatory function in young rodents, enhanced cold tolerance in aged C57BL/6J mice. Mice, aged 18 to 20 months, were randomly assigned to four treatment conditions: (a) intermittent cold acclimation (CA) (50 min per day, 5 times per week for 3 weeks at 5 degrees C), (b) submaximal treadmill exercise (EX) (15 m min-1 for 30 min, 5 times per week for 8 weeks, (c) sequential treatment of CA + EX, and (d) control group. Mice were exposed to a 3-hr cold stress test (15 degrees C) prior to and following treatment. CA aged mice maintained normothermia and demonstrated significant increases in oxygen consumption and brown adipose tissue protein concentration compared with controls; enhanced cold tolerance was probably due to increased utilization of nonshivering thermogenesis. EX aged mice had elevated O2 consumption and increased skeletal muscle enzyme activity compared with controls; however, cold tolerance was not enhanced compared with CA mice. The data suggest that intermittent CA effectively reduces hypothermia during cold challenge in aged mice.     

Effect of chronic restraint on open field activity of aging C57BL/6N mice

Fight, 20, and 31 month old male C57BL/6N mice were exposed to three 24-hour restraint sessions per week, or to a nontreatment condition. All mice received five 2-minute open field tests after 5 and after 6 weeks of treatment. The activity of restrained mice tended to be greater than that of nonrestrained animals. In general 8 month old mice were more active than older subjects. Age related activity decrements were prominent in the first series of open field tests, while restraint effects were most pronounced in the second series.     

Heat loss during cold exposure in ADULT and AGED C57BL/6J mice

Metabolic heat production (MHP), colonic temperature (Tco), and nonevaporative (dry) heat loss were measured in ADULT and AGED C57BL/6J male mice during cold exposure. Dry heat loss was assessed as a differential temperature (Td) between incoming and outgoing air through the chamber for indirect calorimetry. The average Td during cold exposure normalized to surface area for ADULT mice was significantly higher than that for the AGED animals (0.0618 ± 0.0003°C/cm² and 0.0553 ± 0.0005°C/cm², respectively). Linear regression analysis showed that at the same Tco AGED mice showed lower values of Td normalized to surface area, indicating that at the same body temperature they were losing less heat than ADULT animals. It was concluded that age-related decline in cold tolerance in mice is not due to a lack of ability to reduce heat loss during cold exposure. On the contrary, AGED animals had lower heat loss in comparison with ADULT. We suggest that augmentation of heat conservation mechanisms is an adaptive response to diminishing cold-induced heat production.     

Continuous antegrade blood cardioplegia: cold vs. tepid

BACKGROUND: Continuous antegrade blood cardioplegia (CABCP) is used at different temperatures. We investigated the consequences of CABCP at 6 degrees C (COLD) vs. 28 degrees C (TEPID). METHODS: Anesthetized open-chest pigs (25 +/- 2 kg) were placed on cardiopulmonary bypass (CPB). The hearts were arrested for 30 min by 6 degrees C cold or 28 degrees C tepid CABCP (n = 8 each). After an initial 3 min antegrade application of high potassium (20 mEq) cold (6 degrees C) blood cardioplegia, the hearts were arrested for a subsequent 27 min by normokalemic blood delivered antegrade at either 6 degrees C or 28 degrees C. After this, the hearts underwent perfusion with warm systemic blood for an additional 30 min on CPB. Biochemical cardiac data (MVO2 [ml/min/100 g], release of creatine kinase [CK U/min/100 g] and lactate [mg/min/100 g]) were measured during CPB. Total tissue water content (%) and left ventricular stroke work index (SWI g x m/kg) were determined 30 min after discontinuation of CPB and compared to pre-CPB controls. RESULTS: Cold CABCP kept all hearts continuously arrested. The COLD hearts showed no biochemical or functional disturbance. The TEPID hearts intermittently fibrillated and required additional high potassium BCP shots. The TEPID hearts showed a marked CK leakage (2.6 +/- 0.4 vs. 0.7 +/- 0.4), lactate production (4.0 +/- 1.6 vs. extraction from the COLD group) despite the non-ischemic protocol, an impaired initial oxygen consumption (4.2 +/- 1.3 vs. 7.1 +/- 1.6) at the end of cardiac arrest, the formation of myocardial edema (79.5 +/- 1.0 vs. 77.0 +/- 0.8), and a depressed recovery of SWI (0.69 +/- 0.15 degrees vs. 1.41 +/- 0.13). *p < 0.05 for comparison of TEPID vs. COLD hearts using Student's t-test for unpaired data; degrees p < 0.05 for intergroup-comparison of TEPID vs. COLD vs. controls using ANOVA adjusted for repeated measures. CONCLUSIONS: Uninterrupted cardioplegia can be safely performed with cold normokalemic CABCP. In contrast, tepid normokalemic CABCP leads to fibrillation, jeopardizes the heart, and should be avoided.UND     

Ethanol Tolerance in a Genetically Insensitive Selected Mouse Line

Mouse lines genetically susceptible (COLD) or resistant (HOT) to the acute hypothermic effects of ethanol were previously shown to differ in tolerance development: HOT mice did not develop tolerance, while COLD mice did. The present experiment increased the thermal load on HOT and COLD mice by administering ethanol chronically at an ambient temperature of 4 degrees C. Under these conditions, initial hypothermic responses were as large as 10 degrees C. Both HOT and COLD mouse lines developed significant tolerance by the third daily injection. Tolerance was dose-dependent: significant tolerance was seen only at the higher doses. HOT and COLD mouse lines developed approximately equal degrees of tolerance. Results support the hypothesis of a role for functional demand in the development of tolerance.     

Filtered platelet concentrates from pooled buffy coats show comparable storage lesions when stored for 9 d at 20-24 degrees C or when supplemented with thromboSol at 2-6 degrees C

The present study investigated the quality of platelet concentrates from pooled buffy coat (PCBC) along different production steps and during storage to characterize storage lesions reflected by platelet activation, changing metabolic and cell turnover status (pH, LDH activity). These criteria were compared in conventionally stored PCBCs (20-24 degrees C, n = 8, Group I) to cold stored PCBCs (2-6 degrees C, n = 8, Group II) when supplemented with ThromboSol. Platelet activation was measured on days 1, 3, 7 and 9 by flow cytometry using fluoresceinisothiocyanate-labeled monoclonal antibodies (mAbs) against glycoprotein IIb/IIIa (CD41a, PAC-1 and LIBS-1), P-selectin (CD62P) or CD40 ligand receptor (CD40L) in combination with a phycoerythrin-labeled panspecific platelet marker against GPIb (CD42b). The platelet activation assessed with mAbs PAC-1, CD41a, LIBS-1 and CD40L showed an overall activation of 98 +/- 4% (mean value +/- 1 SD) at day 7 in both groups, except for CD62P, which was significantly lower in Group II. A storage-dependent greater platelet loss occurred in Group II compared to Group I, 42% vs. 19% (p < 0.05 on day 9). We could demonstrate that platelets stored in ThromboSol show about the same in-vitro activation as conventionally stored PCBCs, but their clinical usefulness needs to be investigated.     

Effects of a warm environment on energy balance in obese (ob/ob) mice

Low rates of thermoregulatory heat production associated with low metabolic activity of brown adipose tissue, the primary site of thermoregulatory heat production, contribute substantially to the high efficiency of energy retention in obese (ob/ob) mice housed at 20 degrees C to 28 degrees C. To eliminate the need for thermoregulatory heat production lean and ob/ob mice were housed at 34.5 degrees C. At this temperature ob/ob mice still retained energy with a greater efficiency than lean littermates. Next, we investigated the possibility that the high efficiency of energy retention in ob/ob mice housed at 34.5 degrees C was related to depressed dietary-induced thermogenesis associated with low metabolic activity of brown adipose tissue. The sympathetic nervous system is a primary regulator of brown adipose tissue metabolism. Therefore, rates of norepinephrine (NE) turnover in brown adipose tissue, as an indicator of sympathetic nervous system stimulation of the tissue, were measured. Lean and ob/ob mice housed at 34.5 degrees C had equally low rates of NE turnover in their brown adipose tissue. Thus, the high efficiency of energy retention in ob/ob mice maintained at 34.5 degrees C is caused by factors other than low sympathetic stimulation of brown adipose tissue.     

Thermoregulatory and cardiac responses of infant spontaneously hypertensive and Wistar-Kyoto rats to cold exposure.

Cardiovascular function during cold exposure is dependent on effective thermoregulation. This dependence is particularly apparent in infants. For example, we have previously demonstrated that in infant rats during cold exposure, cardiac rate is directly related to their ability to produce heat endogenously. The primary source of endogenous heat production for infant rats is brown adipose tissue (BAT). Because of the dependence of cardiac rate on effective thermoregulation in the cold and because hypertension in spontaneously hypertensive rats (SHR) is influenced by the preweanling environment, in this study we examined the thermoregulatory and cardiac rate responses of infant SHR and Wistar-Kyoto rats (WKY) to varying levels of cold exposure. In experiment 1, 7- to 8-day-old SHR and WKY were acclimated at a thermoneutral air temperature (35 degrees C) and then exposed to successive decreases in ambient temperature (30.5 degrees C, 26.5 degrees C, 23 degrees C, and 17 degrees C) while thermal and metabolic measures were recorded. Although both strains increased BAT thermogenesis and oxygen consumption in response to cold exposure, SHR cooled more than WKY and exhibited lower levels of oxygen consumption at the lowest air temperatures. Experiment 2 was identical to experiment 1 except that cardiac rate was also measured. Again, SHR exhibited substantial thermoregulatory deficits compared with WKY; in addition, they were less able than WKY to maintain cardiac rate at the 2 lowest air temperatures tested. Finally, in experiment 3, infant SHR exhibited diminished BAT thermogenesis in response to a range of doses of a selective beta3-adrenoceptor agonist. We hypothesize that long-term thermoregulatory deficits during the early postnatal period influence cardiovascular function and contribute to the development of hypertension in SHR.     

The Relationship Between Ethanol-induced Hyperglycemia and Hypothermia: Evidence of Genetic Correlation

The hyperglycemic and hypothermic responses to acute ethanol exposure (0, 2, 4, 6 g/kg, intraperitoneally) were examined in non-fasted mice selectively bred for sensitivity (COLD line) or insensitivity (HOT line) to ethanol-induced hypothermia. Blood samples and rectal temperatures were obtained immediately before injection and hourly for 4 hr after injection. As expected, COLD mice demonstrated greater and more prolonged reductions in body temperature than HOT mice, especially at the 4 g/kg dose (HOT: -2.58 degrees C, COLD: -5.08 degrees C). Ethanol produced significant dose-dependent elevations in blood glucose levels over the 4-hr sampling period in both lines. The greatest elevations in blood glucose levels were seen at 4 g/kg, with COLD mice (mean = 225.1 mg/dl) showing significantly greater elevations in blood glucose levels compared to HOT mice (mean = 177.0 mg/dl). These results support the hypothesis that the thermic and glycemic effects produced by ethanol are due to related neural processes that share a common genetic component.     

Cold acclimation of obese (ob/ob) mice: effects of energy balance

Obese (ob/ob) and lean mice at 4 weeks of age were housed at 23 degrees C or 14 degrees C for 4 to 8 weeks to examine effects of acclimation to mild cold on energy balance. Energy intake of young lean mice increased by about 50% when housed at 14 degrees C, but energy intake of cold-acclimated obese mice increased by only 8%. Efficiency of energy retention (ratio of energy gain to energy intake) in obese mice declined from 22% +/- 1.2% at 23 degrees C to 10% +/- 1.8% after 4 weeks at 14 degrees C. Lean mice exhibited a less pronounced response to temperature; their efficiency of energy retention declined from 7% +/- 1.3% at 23 degrees C to 4% +/- 2.2% after 4 weeks at 14 degrees C. After 8 weeks of cold exposure, body weights and efficiency of energy retention became equal in obese and lean mice. Calculated heat production of cold-acclimated obese and lean mice was 40% higher than that of respective controls. Obese mice reacclimated to 23 degrees C after being kept for 4 weeks at 14 degrees C consumed the same amount of energy and were 16% more efficient than obese maintained at 23 degrees C; reacclimated lean mice consumed 12% more energy but were 53% less efficient than lean mice maintained at 23 degrees C. The results indicate that obese mice are able to increase heat production and markedly reduce their efficiency of energy retention when acclimated to mild cold but that they, unlike lean mice, rapidly revert to a high efficiency of energy retention after 4 weeks of reacclimation to 23 degrees C.     

Energy turnover and heat exchange in mature lean and obese Zucker rats acutely exposed to three environmental temperatures for 24 hours

Differences between lean (FA/?, n = 6) and obese (fa/fa, n = 6) mature male Zucker rats' energy turnover and heat storage were compared during a 24-h period when the animals were exposed to ambient temperatures of 30, 15 or 5 degrees C. Energy turnover was examined through measurements of heat production rates via indirect calorimetry and heat loss rates via direct calorimetry. Heat storage rates were calculated as the difference between heat production and heat loss rates. Predicted heat storage rates were also calculated as the product of the change in core temperature and the calculated specific heat of the animal based on body composition (carcass) analysis. A minimal heat loss rate was determined for each animal representing a period of least activity. Various comparisons were made: between groups (lean/obese), temperature (30, 15, 5 degrees C), calorimetry method (indirect/direct), period (light/dark), heat storage (experimental/predicted), and minimal heat loss. Immediately before a test, pretest weight and colonic temperature were obtained. Then, the animal was placed into the calorimeter chamber and remained there unrestrained for 24 h. Normal light/dark periods were maintained. On removal from the calorimeter, core temperature and body weight measurements were again obtained. Upon completion of all tests, body composition was analyzed and surface area determined. Energy turnover, i.e. both heat production and heat loss in the lean and obese animals differed among the 30, 15 and 5 degrees C exposures. The obese animals had relatively greater heat production rate and heat loss rate (kcal/day or kcal/kg (FFM)/day than the lean animals at 30, 15 and 5 degrees C. But, on a relative basis, the increments in heat production in the cold environments were greater for the lean animals. Both the lean and obese animals tended to be more active during the dark period when at 30 degrees C, but the difference was less at 15 degrees C and even less at 5 degrees C. Experimental heat storage rates did not differ significantly from predicted values at any of the temperatures with the possible exception of the animals at 5 degrees C. It was concluded that the mature obese Zucker rats had no major discernible defect in thermoregulation as revealed by rates of heat production and loss, although three of the obese rats did elicit a drop in colonic temperature during exposure to 5 degrees C, i.e. their excessive subcutaneous adiposity and thermal insulation did not prevent a fall in colonic temperature.(ABSTRACT TRUNCATED AT 400 WORDS)     

Fat oxidation after acipimox-induced reduction in plasma nonesterified fatty acids during exercise at 0 degrees C and 20 degrees C

The main aim of this study was to investigate if whole body fat oxidation, after acipimox administration, during submaximal exercise in the cold, is different from that at temperate environments. Seven healthy recreationally active male subjects cycled at 70% Vo(2peak) for 60 minutes; once at 0 degrees C and once at 20 degrees C. To exclude availability, and therefore oxidation of plasma-derived nonesterified fatty acids (NEFA), 90 minutes before each cycling bout, subjects ingested 250 mg of the antilipolytic drug, acipimox. Blood and expired gas measurements were obtained at rest, immediately before exercise, and at 15, 30, 45, and 60 minutes of exercise. In both trials, after the ingestion of acipimox, plasma NEFA concentrations fell dramatically and immediately before and during exercise were lower than 0.05 mmol. L(-1) in both trials. Pre-exercise and exercise values of glycerol, glucose, triacylglycerol (TG), and rectal temperature (T(re)) were not different between the 0 degrees C and 20 degrees C trials. During exercise at 0 degrees C, skin temperature (T(sk)) was significantly reduced from pre-exercise values (P <.05) and at all time points was significantly lower than during exercise at 20 degrees C. Muscle temperature did not differ between trials but in both trials was lower (P <.05) at 1 cm depth than at 3 cm and 2 cm. Gross energy expenditure of cycling (0 degrees C trial, 3.6 +/- 0.1 MJ; 20 degrees C trial, 3.6 +/- 0.1 MJ), the oxidation rates of carbohydrate (0 degrees C, 32.4 +/- 0.5 KJ. min(-1); 20 degrees C, 32.6 +/- 0.7 KJ. min(-1)) and fat (0 degrees C, 24.6 +/- 1.2 KJ. min(-1); 20 degrees C, 23.0 +/- 1.8 KJ. min(-1)), and the proportion of energy derived from fat (0 degrees C, 45 +/- 1 %; 20 degrees C, 40 +/- 4%) and carbohydrate (0 degrees C, 55 +/- 1%; 20 degrees C, 58 +/- 3%) were not different between the 2 trials. In conclusion, after acipimox administration, whole body fat oxidation during exercise, designed to avoid adjustment of core temperature or thermogenesis, is not different at 0 degrees C compared with 20 degrees C. This allows the inference that during submaximal exercise, cold has no effect on the utilization of intramuscular TG (IMTG).