Cold-induced Vasodilatation Response Research Articles

Relationships of self-identified cold tolerance and cold-induced vasodilatation in the finger

Thermal environments in daily life, such as occupational cold exposure and the use of heating facilities and warm clothing, affect acclimatization to both cold and heat. Also, cold tolerance can be cognized by self-identified evaluation. Thermal life-style during daily life might be one of the factors which affect cold-induced vasodilatation (CIVD) when different degrees of thermal stimuli are considered. Therefore, this study investigated whether or not CIVD response is related to self-identified cold and heat tolerances which is attributable to thermal life-style.

Cold-induced vasodilation during single digit immersion in 0°C and 8°C water in men and women.

The present study compared the thermal responses of the finger to 0 and 8°C water immersion, two commonly used temperatures for cold-induced vasodilation (CIVD) research. On two separate and counterbalanced occasions 15 male and 15 female participants immersed their index finger in 20°C water for 5 min followed by either 0 or 8°C water for 30 min. Skin temperature, cardiovascular and perceptual data were recorded. Secondary analyses were performed between sexes and comparing 0.5, 1 and 4°C CIVD amplitude thresholds. With a 0.5°C threshold, CIVD waves were more prevalent in 8°C (2 (1 – 3) than in 0°C (1.5 (0 – 3)), but the amplitude was lower (4.0 ± 2.3 v 9.2 ± 4.0°C). Mean, minimum and maximum finger temperatures were lower in 0°C during the 30 min immersion, and CIVD onset and peak time occurred later in 0°C. Thermal sensation was lower and pain sensation was higher in 0°C. There were no differences between males and females in any of the physiological or CIVD data with the exception of SBP, which was higher in males. Females reported feeling higher thermal sensations in 8°C and lower pain sensations in 0°C and 8°C compared to males. Fewer CIVD responses were observed when using a 4°C (1 (0 – 3)) threshold to quantify a CIVD wave compared to using a 1°C (2 (0 – 3)) or 0.5°C (2 (0 – 3)) amplitude. In conclusion, both 0 and 8 °C can elicit CIVD but 8°C may be more suitable when looking to optimise the number of CIVD waves while minimising participant discomfort. The CIVD response to water immersion does not appear to be influenced by sex. Researchers should consider the amplitude threshold that was used to determine a CIVD wave when interpreting previous data.

Effect of Caffeine Intake on Finger Cold-Induced Vasodilation

The purpose of the study was to investigate the effect of caffeine intake on finger cold-induced vasodilation (CIVD). Ten healthy men underwent 6 experimental trials characterized by control (NCAFF) or caffeine intake (CAFF) via chewing gum (300 mg of caffeine) while resting on a chair or performing submaximal (70% maximal oxygen consumption) or maximal (100% maximal oxygen consumption) treadmill exercise (Bruce protocol) followed by immersion of the middle finger in a water bath (5°C) for 20 minutes. Finger temperature (Tf ) and time parameters of the first CIVD cycle and post-test norepinephrine were measured. Exercise duration for submaximal and maximal exercise was 8.9 ± 0.9 and 12.4 ± 0.8 minutes, respectively. CAFF had no effect on Tf, but exercise increased minimal Tf in NCAFF (9.08 ± 1.27°C, 13.02 ± 2.13°C, and 13.25 ± 1.63°C in rest, submaximal, and maximal exercise, respectively) and CAFF (8.76 ± 1.39°C, 12.50 ± 1.91°C, and 12.79 ± 1.20°C). Maximal Tf was significantly higher in NCAFF (15.98 ± 1.04°C, 16.18 ± 1.56°C, and 15.14 ± 1.52°C) than in CAFF (13.56 ± 1.19°C, 15.52 ± 1.31°C, and 14.39 ± 1.43°C), resulting in a significant difference between minimal and maximal Tf in rest (NCAFF, 6.89 ± 1.56°C and CAFF, 4.79 ± 1.23°C), but not in exercise conditions. CAFF had no effect on CIVD time responses, but exercise significantly shortened CIVD onset and peak time compared with rest in both NCAFF and CAFF. Norepinephrine concentration was significantly greater in CAFF (290.6 ± 113.0 pg/mL, 278.1 ± 91.4 pg/mL, and 399.8 ± 125.5 pg/mL) than NCAFF (105.6 ± 29.5 pg/mL, 199.6 ± 89.6 pg/mL, and 361.5 ± 171.3 pg/mL). Caffeine intake before finger immersion in cold water does not result in a thermogenic effect and adversely affects CIVD responses, whereas exercise modifies CIVD temperature and time responses.

Cold-induced vasodilatation in cold-intolerant rats after nerve injury

Cold-induced vasodilatation (CIVD) is a cyclic regulation of blood flow during prolonged cooling of protruding body parts. It is generally considered to be a protective mechanism against local cold injuries and cold intolerance after peripheral nerve injury. The aim of this study was to determine the role of the sympathetic system in initiating a CIVD response. Eight rats were operated according to the spared nerve injury (SNI) model, eight underwent a complete sciatic lesion (CSL) and six underwent a sham operation. Prior to operation, 3, 6 and 9 weeks postoperatively, both hind limbs were cooled and the skin temperature was recorded to evaluate the presence of CIVD reactions. Cold intolerance was determined using the cold plate test and mechanical hypersensitivity measured using the Von Frey test. No significant difference in CIVD was found comparing the lateral operated hind limb for time (preoperatively and 3, 6 and 9 weeks postoperatively; p=0.397) and for group (SNI, CSL and Sham; p=0.695). SNI and CSL rats developed cold intolerance and mechanical hypersensitivity. Our data show that the underlying mechanisms that initiate a CIVD reaction are not affected by damage to a peripheral nerve that includes the sympathetic fibres. We conclude that the sympathetic system does not play a major role in the initiation of CIVD in the hind limb of a rat. No substantial changes in the CIVD reaction after peripheral nerve injury imply that the origin of cold intolerance after a traumatic nerve injury is initiated by local factors and has a more neurological cause. This is an important finding for future developing treatments for this common problem, as treatment focussing on vaso-regulation may not help diminish symptoms of cold-intolerant patients.

Cold-induced vasodilation and vasoconstriction in the finger of tropical and temperate indigenes

While heat acclimatization reflects the development of heat tolerance, it may weaken an ability to tolerate cold. The purpose of this study was to explore cold-induced vasodilation (CIVD) responses in the finger of tropical indigenes during finger cold immersion, along with temperate indigenes. Thirteen tropical male indigenes (subjects born and raised in the tropics) and 11 temperate male indigenes (subjects born and raised in Japan and China) participated. Subjects immersed their middle finger at 4.3±0.8°C water for 30min. Rectal temperature, skin temperatures, finger skin blood flow, blood pressure and subjective sensations were recorded during the test. The results showed that: (1) the tropical group demonstrated a lower minimum (Tmin), maximum (Tmax) and mean finger temperature (Tmean) compared to those of the temperate group (P<0.05); (2) seven tropical indigenes demonstrated a late-plateau type of CIVD pattern, which is characterized by a pronounced 1st vasoconstriction and a single CIVD with a faint and weak 2nd vasoconstriction, whereas no temperate indigene demonstrated the late-plateau type; and (3) the hand temperature at the end of finger immersion was 3°C lower in the tropical than the temperate group (P<0.05). These results indicate that tropical indigenes have less active responses of arterio-venous anastomoses in the finger and weaker vasoconstrictions after the first CIVD response during finger cold immersion, which can be considered as being more vulnerable to cold injury of the periphery in severe cold.

Cold-induced vasodilatation response in the fingers at 4 different water temperatures

We evaluated the cold-induced vasodilatation (CIVD) response at 4 different water temperatures. Nine healthy young male subjects immersed their right hands in 35 °C water for 5 min, and immediately thereafter for 30 min in a bath maintained at either 5, 8, 10, or 15 °C. The responses of finger skin temperatures, subjective ratings of thermal comfort and temperature sensation scores were compared between the 4 immersion trials. The number of subjects who exhibited a CIVD response was higher during immersion of the hand in 5 and 8 °C (100%) compared with 10 and 15 °C water (87.5% and 37.5%, respectively). The CIVD temperature amplitude was 4.2 ± 2.6, 3.4 ± 2.0, 2.1 ± 1.6, and 2.8 ± 2.0 °C at 5, 8, 10, and 15 °C trials, respectively; higher in 5 and 8 °C compared with 10 and 15 °C water (p = 0.003). No differences in CIVD were found between the 5 and 8 °C immersions. However, during immersion in 5 °C, subjects felt "uncomfortable" while in the other trials felt "slightly uncomfortable" (p = 0.005). The temperature sensation score was "cold" for 5 °C and "cool" for the other trials, but no statistical differences were observed. Immersion of the hand in 8 °C elicits a CIVD response of similar magnitude as immersion in 5 °C, but with less thermal discomfort.

The Effect of a Sleep High–Train Low Regimen on the Finger Cold-Induced Vasodilation Response

The present study evaluated the effect of a sleep high-train low regimen on the finger cold-induced vasodilation (CIVD) response. Seventeen healthy males were assigned to either a control (CON; n=9) or experimental (EXP; n=8) group. Each group participated in a 28-day aerobic training program of daily 1-h exercise (50% of peak power output). During the training period, the EXP group slept at a simulated altitude of 2800 meters (week 1) to 3400 m (week 4) above sea level. Normoxic (CIVD(NOR); CON and EXP groups) and hypoxic (CIVD(HYPO); F(I)O(2)=0.12; EXP group only) CIVD characteristics were assessed before and after the training period during a 30-min immersion of the hand in 8°C water. After the intervention, the EXP group had increased average finger skin temperature (CIVD(NOR): +0.5°C; CIVD(HYPO): +0.5°C), number of waves (CIVD(NOR): +0.5; CIVD(HYPO): +0.6), and CIVD amplitude (CIVD(NOR): +1.5°C; CIVD(HYPO): +3°C) in both CIVD tests (p<0.05). In contrast, the CON group had an increase in only the CIVD amplitude (+0.5°C; p<0.05). Thus, the enhancement of aerobic performance combined with altitude acclimatization achieved with the sleep high-train low regimen contributed to an improved finger CIVD response during cold-water hand immersion in both normoxic and hypoxic conditions.

Dynamic Adaptation of the Peripheral Circulation to Cold Exposure

Humans residing or working in cold environments exhibit a stronger cold-induced vasodilation (CIVD) reaction in the peripheral microvasculature than those living in warm regions of the world, leading to a general assumption that thermal responses to local cold exposure can be systematically improved by natural acclimatization or specific acclimation. However, it remains unclear whether this improved tolerance is actually due to systematic acclimatization, or alternately due to the genetic pre-disposition or self-selection for such occupations. Longitudinal studies of repeated extremity exposure to cold demonstrate only ambiguous adaptive responses. In field studies, general cold acclimation may lead to increased sympathetic activity that results in reduced finger blood flow. Laboratory studies offer more control over confounding parameters, but in most studies, no consistent changes in peripheral blood flow occur even after repeated exposure for several weeks. Most studies are performed on a limited amount of subjects only, and the variability of the CIVD response demands more subjects to obtain significant results. This review systematically surveys the trainability of CIVD, concluding that repeated local cold exposure does not alter circulatory dynamics in the peripheries, and that humans remain at risk of cold injuries even after extended stays in cold environments.

Trainability of cold induced vasodilatation in fingers and toes

Subjects that repeatedly have to expose the extremities to cold may benefit from a high peripheral temperature to maintain dexterity and tissue integrity. Therefore, we investigated if repeated immersions of a hand and a foot in cold water resulted in increased skin temperatures. Nine male and seven female subjects (mean 20.4; SD 2.2 years) immersed their right (trained) hand and foot simultaneously in 8°C water, 30 min daily for 15 days. During the pre and post-test (days 1 and 15, respectively) the left (untrained) hand and foot were immersed as well. Pain, tactile sensitivity and skin temperatures were measured every day. Mean (SD) toe temperature of the trained foot increased from 9.49°C (0.89) to 10.03°C (1.38) (p < 0.05). The trained hand, however, showed a drop in mean finger temperature from 9.28°C (0.54) to 8.91°C (0.44) (p < 0.001) and the number of cold induced vasodilation (CIVD) reactions decreased from 52% during the first test to 24% during the last test. No significant differences occurred in the untrained extremities. Pain diminished over time and tactile sensitivity decreased with skin temperature. The combination of less CIVD responses in the fingers after training, reduced finger skin temperatures in subjects that did show CIVD and the reduced pain and tactile sensitivity over time may lead to an increased risk for finger cold injuries. It is concluded that repeated cold exposure of the fingers does not lead to favorable adaptations, but may instead increase the injury risk.

The effect of repeated mild cold water immersions on the adaptation of the vasomotor responses

There are several types of cold adaptation based on the alteration of thermoregulatory response. It has been thought that the temperature of repeated cold exposures during the adaptation period is one of the factors affecting the type of cold adaptation developed. This study tested the hypothesis that repeated mild cold immersions would induce an insulative cold adaptation but would not alter the metabolic response. Seven healthy male participants were immersed to their xiphoid process level repeatedly in 26°C water for 60 min, 3 days every week, for 4 weeks. During the first and last exposure of this cold acclimation period, the participants underwent body immersion tests measuring their thermoregulatory responses to cold. Separately, they conducted finger immersion into 5°C water for 30 min to assess their cold-induced vasodilation (CIVD) response before and after cold acclimation. During the immersion to xiphoid process, participants showed significantly lower mean skin temperature and skin blood flow in the forearm post-acclimation, while no adaptation was observed in the metabolic response. Additionally, blunted CIVD responses were observed after cold acclimation. From these results, it was considered that the participants showed an insulative-type of cold acclimation after the repeated mild cold immersions. The major finding of this study was the acceptance of the hypothesis that repeated mild cold immersion was sufficient to induce insulative cold adaptation but did not alter the metabolic response. It is suggested that the adaptation in the thermoregulatory response is specific to the response which is repeatedly stimulated during the adaptation process.

Cold-Induced Vasodilatation Following Traumatic Median or Ulnar Nerve Injury

Peripheral nerve injury of the upper extremity frequently causes changes in the thermoregulatory system of the hands and fingers and leads to reports of cold intolerance. In this study, we aimed to measure the influence of median or ulnar nerve injury on cold-induced vasodilatation (CIVD) during prolonged cooling at low temperatures. We tested 12 patients with a median (n = 6) or ulnar (n = 6) injury 4 to 76 months after nerve repair. The palmar sides of both hands were cooled continuously using a cold plate at 5°C. We measured the skin temperature of the fingers using videothermography and plotted graphs of the temperature changes of the nailbed. The presence of a CIVD reaction was defined as a minimum increase in temperature of 2.5°C starting at the distal phalanx. Furthermore, we measured self-reported symptoms of cold intolerance using the Cold Intolerance Severity Scale questionnaire. A CIVD reaction was absent in the affected digits of 4 patients (follow-up, 6-37 mo), whereas the CIVD reaction in the uninjured hand was present. The CIVD was present in 6 patients after 50 months' follow-up (range, 24-76 mo). Two patients had no CIVD reaction in the injured or uninjured fingers. All patients with a CIVD response had at least diminished protective sensation. Presence of the CIVD reaction did not exclude self-reported symptoms of cold intolerance. After peripheral nerve injury, it is possible to recover the CIVD reaction. This might be an indication of nerve recovery. However, a positive CIVD reaction does not exclude subjective symptoms of posttraumatic cold intolerance. Diagnostic III.

Enhancement of the finger cold-induced vasodilation response with exercise training

Cold-induced vasodilatation (CIVD) is a cyclical increase in finger temperature that has been suggested to provide cryoprotective function during cold exposures. Physical fitness has been suggested as a potential factor that could affect CIVD response, possibly via central (increased cardiac output, decreased sympathetic nerve activity) and/or peripheral (increased microcirculation) cardiovascular and neural adaptations to exercise training. Therefore, the purpose of this study was to investigate the effect of endurance exercise training on the CIVD response. Eighteen healthy males trained 1 h d(-1) on a cycle ergometer at 50% of peak power output, 5 days week(-1) for 4-weeks. Pre, Mid, Post, and 10 days after the cessation of training and on separate days, subjects performed an incremental exercise test to exhaustion (.VO(2peak)) and a 30-min hand immersion in 8 degrees C water to examine their CIVD response. The exercise-training regimen significantly increased .VO(2peak) (Pre: 46.0 +/- 5.9, Mid: 52.5 +/- 5.7, Post: 52.1 +/- 6.2, After: 52.6 +/- 7.6 ml kg(-1) min(-1); P < 0.001). There was a significant increase in average finger skin temperature (Pre: 11.9 +/- 2.4, After: 13.5 +/- 2.5 degrees C; P < 0.05), the number of waves (Pre: 1.1 +/- 1.0, After: 1.7 +/- 1.1; P < 0.001) and the thermal sensation (Pre: 1.7 +/- 0.9, After: 2.5 +/- 1.4; P < 0.001), after training. In conclusion, the aforementioned endurance exercise training significantly improved the finger CIVD response during cold-water hand immersion.

Can inter-population variation in the extent of cold-induced vasodilation response serve as a window into adaptations to seasonal cold and subsequent population movements?

Can inter-population variation in the extent of cold-induced vasodilation response serve as a window into adaptations to seasonal cold and subsequent population movements?

The effect of exercise-induced elevation in core temperature on cold-induced vasodilatation response in toes

Cold-induced vasodilatation (CIVD) has been proposed as a potential protective mechanism against cold injuries during exposure of extremities to a cold environment. The purpose of this study was to evaluate the effect of exercise and the associated elevation in core temperature on toe skin temperatures during immersion of the foot in cold (8 degrees C) water. Subjects (N = 8) participated in two trials. In one, they conducted an incremental exercise to exhaustion (exercise) on a cycle ergometer, which was followed by immersion of the right foot in 8 degrees C water. In the second trial (control), immersion of the foot in cold water was not preceded by exercise. Upon completion of the exercise in the exercise trial, and at the onset of the immersion of the foot in cold water, tympanic temperature was 0.6 degrees C (P < 0.01) higher than pre-exercise levels. There was a significant increase (P < 0.05) in the number of CIVD waves, but not their amplitudes, in the exercise trial compared to the control trial. A CIVD response occurred in 57.5% of all toes in the exercise trial, and in only 27.5% in the control trial. Additionally, 50% of subjects exhibited CIVD in at least one toe in the control trial, and 87.5% during the exercise trial. It is concluded that exercise, and particularly the associated elevation in core temperature, enhances the frequency of the toe CIVD responses, and can therefore potentially act as a protective mechanism against cold injury.

Finger and Toe Temperatures on Exposure to Cold Water and Cold Air

Subjects with a weak cold-induced vasodilatation response (CIVD) to experimental cold-water immersion of the fingers in a laboratory setting have been shown to have a higher risk for local cold injuries when exposed to cold in real life. Most of the cold injuries in real life, however, occur in the foot in cold air rather than in the hand in cold water. Therefore, an experiment was conducted to investigate the within-subject relation between CIVD in the fingers and toes exposed to cold water and cold air. In 4 experimental sessions, 11 healthy male subjects immersed their toes and fingers in 5 degrees C water and exposed the fingers and toes to -18 degrees C cold air for 30 min. The pad temperature of the middle three digits was measured. CIVD in water was more pronounced in the fingers (onset time 5.1 +/- 1.8 min; amplitude 5.0 +/- 2.1 degrees C) than in the toes (onset time 10.6 +/- 6.0 min; amplitude 3.0 +/- 1.0 degrees C). Out of 22 skin temperature responses to cold air, 13 were not identifiable as CIVD. The mean skin temperatures for fingers and toes during the last 20 min of cold exposure were 25.6 +/- 7.1 degrees C and 20.9 +/- 6.8 degrees C, respectively, for air and 9.3 +/- 1.9 degrees C and 7.1 +/- 1.3 degrees C for water immersion. There was a strong relation between the mean temperature of the fingers during cold-water immersion and toes during cold air exposure (r = 0.83, P < 0.01), showing that a weak CIVD response in the hand is related to a weak response in the foot. We conclude that the cold-water finger immersion test is related to the temperature response in the toes and may thus continue to serve as a valid indicator for the risk of local cold injuries.

The Influence of an Acute Dose of Aspirin on Cold-Induced Vasodilation

When the fingers are exposed to the cold there is a cyclic response between vasoconstriction and cold-induced vasodilation (CIVD) which serves to decrease and increase finger skin temperature (TSK). The exact mechanisms responsible for CIVD are not completely understood but the release of vasodilatory substances may contribute to CIVD. Aspirin (ASP) may decrease the release of nitric oxide and prostaglandins. PURPOSE: To examine the effects of an acute dose of ASP on the CIVD response during submersion of the hand in cold water. METHODS: Six subjects (5 males, 1 female; mean age: 23.0 ± 3.3 yrs) performed two experimental trials for the assessment of CIVD. During one experimental trial, subjects ingested 650 mg of ASP dissolved in 125 mL of orange juice 30 minutes prior to the trial. During the other experimental trial, subjects ingested a placebo (PL) (125 mL of orange juice). The order of the experimental trials was counter-balanced and a double-blind placebo controlled design was utilized. Each experimental trial consisted of a 30 minute baseline period (27°C air), 40 minute cold exposure (hand submersed in 5°C water), and a 15 minute recovery period (27°C air). TSK of the second and third fingers was measured continuously using thermocouples. The following variables were used to assess the CIVD response during the cold exposure: onset time (time from onset of cold exposure to increase in finger TSK), TMIN (minimum finger TSK), TMAX (maximum finger TSK), peak time (time from onset of cold exposure to TMAX), TMEAN (average finger TSK from onset time to end of cold exposure), and amplitude (TMAX - TMEAN). RESULTS: There were no differences between PL and ASP for onset time (PL = 710 ± 440, ASP = 728 ± 422 sec), TMIN (PL = 5.29 ± 0.52, ASP = 5.39 ± 0.37°C), TMAX (PL = 6.36 ± 1.13, ASP = 6.22 ± 0.88°C), peak time (PL = 1222 ± 579, ASP = 1350 ± 468 sec), TMEAN (PL = 5.79 ± 0.64, ASP = 5.80 ± 0.61°C), and amplitude (PL = 0.57 ± 0.61, ASP = 0.42 ± 0.31°C) (all P > 0.05). CONCLUSIONS: The ingestion of 650 mg of ASP had no effect on the finger TSK when the hand is submersed in 5°C cold water. These results indicate that 650 mg of ASP may not have been sufficient to inhibit the release of vasodilatory substances or, if ASP was effective in inhibiting the release of vasodilatory substances, these substances may not be involved in CIVD.

Comparison of the Patterns of Cold-induced Vasodilation Response Between Runners and Swimmers

Comparison of the Patterns of Cold-induced Vasodilation Response Between Runners and Swimmers

Enhancement of cold-induced vasodilatation following acclimatization to altitude

The present study evaluated the effect of high-altitude acclimatisation on the cold-induced vasodilatation (CIVD) response. A group of highly trained mountaineers (N = 9; Alpinists) were tested before and after a 3 week high-altitude Himalayan expedition (altitude ranging from 3,985 to 6,828 m). A control group (N = 7) with no mountaineering experience was tested at the same time points. During each test, subjects first immersed their hand to the styloid process in 37 degrees C water for 5 min and then in 10 degrees C water for 30 min. Upon completion of the hand immersion, the same procedure was repeated for the foot. Skin temperature of the pads of all immersed digits was measured throughout the immersion and for 10 min following the immersion. In the Alpinists, a significant increase in amplitude of CIVD and absolute maximum finger skin temperature during immersion was observed in the hand post-expedition. For the foot, peak time of CIVD was significantly shorter in the Alpinist group, and there were significant increases in minimum and maximum toe skin temperature during CIVD, mean toe skin temperature during immersion, absolute minimum and maximum toe skin temperature during immersion, and absolute amplitude during immersion. The results demonstrate a significant enhancement of the CIVD response as a consequence of a brief high altitude acclimatisation, and that these changes were especially prominent in the toes.

The trainability and contralateral response of cold-induced vasodilatation in the fingers following repeated cold exposure

Cold-induced vasodilatation (CIVD) is proposed to be a protective response to prevent cold injuries in the extremities during cold exposure, but the laboratory-based trainability of CIVD responses in the hand remains equivocal. Therefore, we investigated the thermal response across the fingers with repeated local cold exposure of the whole hand, along with the transferability of acclimation to the fingers of the contralateral hand. Nine healthy subjects immersed their right hand up to the styloid process in 8 degrees C water for 30 min daily for 13 days. The left hand was immersed on days 1 and 13. Skin temperature was recorded on the pads of the five fingertips and the dorsal surface of the hand. The presence of CIVD, defined as an increase in finger skin temperature of 0.5 degrees C at any time during cooling, occurred in 98.5% of the 585 (9 subjects x 5 sites x 13 trials) measurements. Seven distinct patterns of thermal responses were evident, including plateaus in finger temperature and superimposed waves. The number (N) of CIVD waves decreased in all digits of the right hand over the acclimation period (P = 0.02), from average (SD) values ranging from 2.7 (1.7) to 3 (1.4) in different digits on day 1, to 1.9 (0.9) and 2.2 (0.7) on day 13. Average (SD) finger skin temperature (T (avg)) ranged from 11.8 (1.4) degrees C in finger 5 to 12.7 (2.8) degrees C in finger 3 on day 1, and then decreased significantly (P < 0.001) over the course of the training immersions, attaining values ranging from 10.8 (0.9) degrees C in finger 4 to 10.9 (0.9) degrees C in finger 2 on day 13. In the contralateral hand, N was reduced from 2.5 to 1.5 (P < 0.01) and T (avg) by approximately 2 degrees C (P < 0.01). No changes were observed in thermal sensation or comfort of the hand over the acclimation. We conclude that, under conditions of whole-hand immersion in cold water, CIVD is not trainable and may lead to systemic attenuation of thermal responses to local cooling.

Cold-induced vasodilatation in the foot is not homogenous or trainable over repeated cold exposure

Cold-induced vasodilatation (CIVD) is proposed to be a protective response to preserve tissue integrity in the extremities during cold exposure, but little research exists on either the trainability or the spatial pattern of CIVD response in the foot. We investigated the thermal response across the foot with repeated cold exposure. Ten healthy subjects immersed their left foot to the ankle in 8 degrees C water for 30 min 5 days/week for 3 weeks. Skin temperature was recorded on the medial side of the nail bed of the 5 toes and the dorsum of the foot. The presence of CIVD, defined as an increase of 1 degrees C at any time during cooling, was rare with our protocol. While a CIVD response was observed at least once in 8 of the 10 subjects, only 122 instances of CIVD were observed out of a total of 900 possible observations (10 subjects x 6 sites x 15 trials). Furthermore, thermal habituation was not evident, with toe temperatures at the end of each immersion (8-11 degrees C) remaining near water temperature throughout the 15 sessions. Even within the two subjects exhibiting the most incidence of CIVD, high variability existed in the occurrence, magnitude, and/or onset times. Synchronicity was often observed where more than one toe exhibited CIVD, though the magnitude varied greatly (range 1-9 degrees C). We conclude that, under realistic conditions of whole-foot immersion in cold water, CIVD is not a common or trainable response.