Cold-induced Vasodilatation Response Research Articles

Five weeks of intermittent hand exposures to alternating cold and hot stimuli do not modify finger cold-induced vasodilatation response.

We tested the hypothesis that prolonged intermittent hand exposures to transient contrast thermal stimuli would enhance the finger cold-induced vasodilatation (CIVD) response during localized cooling. Eight healthy men participated in a 5-week regimen, during which they immersed, thrice per week, the non-dominant (EXP) hand in 8° and 43°C water, sequentially and at 3-min intervals, for a total period of 60min. The contralateral (i.e., dominant) hand served as the control (CON) hand. Before and after the regimen, subjects conducted two 30-min hand cold (8°C water) provocation trials, one with the EXP hand and the other with the CON hand. In addition, a flow-mediated dilatation test was performed in the brachial artery of the EXP arm. Regardless of the hand tested, the average finger skin temperature [CON hand: pre-trial=10.5 (1.2)°C, post-trial=10.8 (1.3)°C and EXP hand: pre-trial=10.7 (1.1)°C, post-trial 10.9 (1.1)°C; p=0.79], and the incidence of CIVD events [CON hand: pre-trial=1.1 (1.2) events, post-trial=1.2 (1.1) events and EXP hand: pre-trial=1.1 (0.8) events, post-trial=1.1 (0.8) events; p=0.88] were not affected by the 5-week regimen. The sensation of cold-induced pain was transiently alleviated following the regimen (p=0.02). The flow-mediated dilatation response of the EXP brachial artery remained unaltered [pre-trial=5.4 (3.2)%, post-trial=4.7 (3.6)%; p=0.51]. Therefore, five weeks of intermittent hand exposures to alternating cold and hot stimuli do not improve finger temperature responsiveness to sustained localized cold.

Cold-induced vasodilation during sequential immersions of the hand.

A common practice for those operating in cold environments includes repetitive glove doffing and donning to perform specific tasks, which creates a repetitive cycle of hand cooling and rewarming. This study aimed to determine the influence of intraday repeated hand cooling on cold-induced vasodilation (CIVD), sympathetic activation, and finger/hand temperature recovery. Eight males and two females (mean ± SD age: 28 ± 5year; height: 181 ± 9cm; weight: 79.9 ± 10.4kg) performed two 30-min hand immersions in cold (4.3 ± 0.92°C) water in an indoor environment (18°C). Both immersions (Imm1; Imm2) were performed on the same day and both allowed for a 10-min recovery. CIVD components were calculated for each finger (index, middle, ring) during each immersion. CIVD onset time (index, p = 0.546; middle, p = 0.727; ring, p = 0.873), minimum finger temperature (index, p = 0.634; middle, p = 0.493; ring, p = 0.575), and mean finger temperature (index, p = 0.986; middle, p = 0.953; ring, p = 0.637) were all similar between immersions. Recovery rates generally demonstrated similar responses as well. Findings suggest that two sequential CIVD tests analyzing the effect of prior cold exposure of the hand does not impair the CIVD response or recovery. Such findings appear promising for those venturing into cold environments where hands are likely to be repeatedly exposed to cold temperatures.

Thermoregulation of Tuvan pastoralists and Western Europeans during cold exposure.

This study compared the metabolic and vascular responses, to whole-body and finger cold exposure, of a traditional population lifelong exposed to extreme cold winters with Western Europeans. Thirteen cold acclimatized Tuvan pastoralist adults (45 ± 9 years; 24.1 ± 3.2 kg/m2 ) and 13 matched Western European controls (43 ± 15 years; 22.6 ± 1.4 kg/m2 ) completed a whole-body cold (10°C) air exposure test and a cold-induced vasodilation (CIVD) test, which involved the immersion of the middle finger into ice-water for 30 min. During the whole-body cold exposure, the durations until the onset of shivering for three monitored skeletal muscles were similar for both groups. Cold exposure increased the Tuvans' energy expenditure by (mean ± SD) 0.9 ± 0.7 kJ min-1 and the Europeans' by 1.3 ± 1.54 kJ min-1 ; these changes were not significantly different. The forearm-fingertip skin temperature gradient of the Tuvans was lower, indicating less vasoconstriction, than the Europeans during the cold exposure (0 ± 4.5°C vs. 8.8 ± 2.7°C). A CIVD response occurred in 92% of the Tuvans and 36% of the Europeans. In line, finger temperature during the CIVD test was higher in the Tuvans than the Europeans (13.4 ± 3.4°C vs. 3.9 ± 2.3°C). Cold-induced thermogenesis and the onset of shivering were similar in both populations. However, vasoconstriction at the extremities was reduced in the Tuvans compared to the Europeans. The enhanced blood flow to the extremities could be beneficial for living in an extreme cold environment by improving dexterity, comfort, and reducing the risk of cold-injuries.

Central versus peripheral mechanisms of cold-induced vasodilation: a study in the fingers and toes of people with paraplegia

PurposeThis study examined physiological and perceptual parameters related to cold-induced vasodilation (CIVD) in the fingers and toes of people with paraplegia and compared them with responses observed in able-bodied individuals.MethodsSeven participants with paraplegia and seven able-bodied individuals participated in a randomized matched-controlled study involving left-hand and -foot immersion in cold water (8 ± 1 °C) for 40 min during exposure to cool (16 ± 1 °C), thermoneutral (23 ± 1 °C), and hot (34 ± 1 °C) ambient conditions.ResultsSimilar CIVD occurrence was observed in the fingers in the two groups. In toes, three of the seven participants with paraplegia revealed CIVDs: one in cool, two in thermoneutral, and three in hot conditions. No able-bodied participants revealed CIVDs in cool and thermoneutral conditions, while four revealed CIVDs in hot conditions. The toe CIVDs of paraplegic participants were counterintuitive in several respects: they were more frequent in cool and thermoneutral conditions (compared to the able-bodied participants), emerged in these conditions despite lower core and skin temperatures of these participants, and were evident only in cases of thoracic level lesions (instead of lesions at lower spinal levels).ConclusionOur findings demonstrated considerable inter-individual variability in CIVD responses in both the paraplegic and able-bodied groups. While we observed vasodilatory responses in the toes of participants with paraplegia that technically fulfilled the criteria for CIVD, it is unlikely that they reflect the CIVD phenomenon observed in able-bodied individuals. Taken together, our findings favor the contribution of central over peripheral factors in relation to the origin and/or control of CIVD.

Cold-induced vasodilation response in a Japanese cohort: insights from cold-water immersion and genome-wide association studies

BackgroundCold-induced vasodilation (CIVD) occurs after blood vessels in the skin are constricted due to local cold exposure. Although many CIVD studies have been conducted, the underlying molecular mechanisms are yet to be clarified. Therefore, we explored genetic variants associated with CIVD response using the largest-scale dataset reported to date in a CIVD study involving wavelet analysis; thus, the findings improve our understanding of the molecular mechanisms that regulate the CIVD response.MethodsWe performed wavelet analysis of three skin blood flow signals [endothelial nitric oxide (eNO)-independent, eNO-dependent, and neurogenic activities] during finger cold-water immersion at 5 °C in 94 Japanese young adults. Additionally, we conducted genome-wide association studies of CIVD using saliva samples collected from the participants.ResultsWe found that the mean wavelet amplitudes of eNO-independent and neurogenic activities significantly increased and decreased prior to CIVD, respectively. Our results also implied that as many as ~ 10% of the Japanese subjects did not show an apparent CIVD response. Our genome-wide association studies of CIVD using ~ 4,040,000 imputed data found no apparent CIVD-related genetic variants; however, we identified 10 genetic variants, including 2 functional genes (COL4A2 and PRLR) that are associated with notable blunted eNO-independent and neurogenic activity responses in individuals without CIVD response during local cold exposure.ConclusionsOur findings indicate that individuals without CIVD response differentiated by genotypes with COL4A2 and PRLR genetic variants exhibited notable blunted eNO-independent and neurogenic activity responses during local cold exposure.

Influence of acute beetroot juice supplementation on cold-induced vasodilation and fingertip rewarming.

Vasoactive ingredients in beetroot (BR) such as nitrate are known to induce vasodilation in temperate conditions. This study investigated the effect of BR ingestion on cold induced vasodilation (CIVD) and rewarming of finger skin temperature (Tfing) during and after hand immersion in cold water. Twenty healthy males (mean ± SD; age 22.2 ± 0.7 years, height 172.6 ± 6.0cm, body mass 61.3 ± 11.7kg) repeated a hand cold water immersion test twice with prior BR or water beverage ingestion (randomised order). They rested for 2h in thermoneutral conditions (27°C, 40% relative humidity) after consuming the beverage, then immersed their non-dominant hand in 8°C water for 30min. They then rewarmed their hand in the ambient air for 20min. Skin temperature at seven body sites, Tfing, finger skin blood flow (SkBFfing), and blood pressure were measured. During hand immersion parameters of CIVD (Tfing and SkBFfing) were not different between BR and water conditions although skin temperature gradient from proximal to distal body sites was significantly smaller with BR (P < 0.05). During rewarming, SkBFfing and cutaneous vascular conductance were significantly higher with BR than with water (P < 0.05). The rewarming speed in Tfing and SkBFfing was significantly faster with BR at 15- (BR 1.24 ± 0.22 vs water 1.11 ± 0.26°C/min) and 20-min rewarming (P < 0.05). Additionally, individuals with slower rewarming speed with water demonstrated accelerated rewarming with BR supplementation. BR accelerated rewarming in Tfing and SkBFfing after local cold stimulus, whereas, CIVD response during hand cold immersion was not affected by BR ingestion.

Cardiovascular Stress and Characteristics of Cold-Induced Vasodilation in Women and Men during Cold-Water Immersion: A Randomized Control Study.

Simple SummaryCold-induced vasodilation is a phenomenon that refers to a paradoxical increase in finger temperature that sometimes occurs during cold exposure. Differences between sexes in cold-induced vasodilation have been explored in only a handful of studies. These studies investigated finger skin temperature but did not evaluate toe skin temperature, blood flow in the fingers or toes, clothing, as well as potential underlying mechanisms of cutaneous vasomotion. On the whole, our knowledge on the potential impacts of sex differences on CIVD is limited and this may have important implications for workers and how they cope with exposure to cold environments. The aim of the study was to investigate and compare cold-induced vasodilation and other cardiovascular responses between genders, during exposure to different environmental conditions. The present study demonstrated that women experienced elevated cardiovascular strain and higher frequency of CIVD reactions, particularly in the toes, compared to their male counterparts during cold-water immersion.Background: Cold-induced vasodilation (CIVD) is a phenomenon that refers to a paradoxical increase in finger temperature that sometimes occurs during cold exposure. The aim of this study was to compare CIVD responses between women and men, during exposure to different environmental conditions. Methods: Seven men and seven women participated in a matched controlled study consisting of a familiarization protocol followed by three experimental sessions (cool (10.8 °C WBGT), thermoneutral (17.2 °C WBGT), and hot (27.2 °C WBGT)). In each session, participants were asked to immerse their left hand and foot in warm water (35 ± 1 °C) for five minutes. Thereafter, the left hand and foot were immersed in cold water (8 ± 1 °C) for 40 min. After that, the left hand and foot were removed from the water and participants remained seated for five minutes. Results: For a matched thermal stress, women experienced an elevated cardiovascular strain (heart rate and in some cases mean arterial pressure) and higher frequency of CIVD reactions (men: 31 vs. women: 60) in comparison to their male counterparts. Conclusions: The present study demonstrated that women experienced elevated cardiovascular strain and higher frequency of CIVD reactions, particularly in the toes, compared to their male counterparts during cold-water immersion.

Dietary Bioflavanol Supplementation Does Not Improve Cold‐Induced Vasodilation in Healthy Adults

BackgroundCold‐induced vasodilation (CIVD) is a cyclical rise in blood flow to glabrous skin that occurs during cold exposure of the extremities. Nitric oxide (NO) is a proposed mediator of the CIVD response through active vasodilation and/or withdrawal of sympathetic vascular smooth muscle tone. Dietary flavanols augment bioavailable NO by upregulating NO synthase, the main source of NO in the vasculature, and by enhancing removal of reactive oxygen species that are known to breakdown NO. Although acute dietary flavanol intake has been shown to augment skin blood flow, at least in part through increased NO, no studies have examined the impact of flavanol intake on skin perfusion during cold exposure. Improving skin blood flow to the extremities may enhance manual dexterity and reduce the risk of peripheral cold injury, benefits pertinent to warfighters or other populations that spend time in cold environments.PurposeTo examine the effect of high‐dose flavanol supplementation on CIVD. We hypothesized that acute and 8‐day flavanol supplementation would augment CIVD during single‐digit cold water immersion.MethodsEleven healthy adults (24±6 yrs; 10M/1F) ingested cocoa‐based flavanols (FLV; 900 mg/d) or caffeine and theobromine‐matched placebo (PLA) for 8 days in a double‐blind, randomized, crossover design. On Days 1 and 8, CIVD was assessed 2 hours after treatment ingestion. Subjects immersed their middle finger in warm water (42°C) for 15 minutes before cold water immersion (4°C) for 30 min, during which nail bed and finger pad skin temperature were measured continuously.ResultsFlavanol ingestion had no effect (all P &gt; 0.05) on CIVD event frequency (Day 1, FLV: 3±2 vs. PLA: 3±2; Day 8, FLV: 3±2 vs. PLA: 3±1) or amplitude (Day 1, FLV: 4.3±1.7 vs. PLA: 4.9±2.6 °C; Day 8, FLV: 3.9±1.9 vs. PLA: 3.9±2.0 °C) in the finger pad following acute or 8‐day supplementation. Furthermore, average (Day 1, FLV: 9.2±1.5 vs. PLA: 9.2±1.8 °C; Day 8, FLV: 8.3±1.7 vs. PLA: 8.9±1.9 °C), maximum (Day 1, FLV: 11.9±3.0 vs. PLA: 11.2±2.3 °C; Day 8, FLV: 10.1±1.9 vs. PLA: 10.6±2.3 °C), and minimum (Day 1, FLV: 6.2±1.3 vs. PLA: 6.0±1.5 °C; Day 8, FLV: 5.8±1.8 vs. PLA: 6.2±1.7 °C) finger pad temperatures during cold water immersion were not different (all P &gt; 0.05) between treatments on Day 1 or Day 8 of supplementation. Similarly, no differences (all P &gt; 0.05) in CIVD parameters were observed in the nail bed following acute or 8‐day supplementation.ConclusionDietary ingestion of cocoa‐based flavanols does not improve the CIVD response to single‐digit cold water immersion.

Heat acclimation enhances the cold-induced vasodilation response

PurposeIt has been reported that the cold-induced vasodilation (CIVD) response can be trained using either regular local cold stimulation or exercise training. The present study investigated whether repeated exposure to environmental stressors, known to improve aerobic performance (heat and/or hypoxia), could also provide benefit to the CIVD response.MethodsForty male participants undertook three 10-day acclimation protocols including daily exercise training: heat acclimation (HeA; daily exercise training at an ambient temperature, Ta = 35 °C), combined heat and hypoxic acclimation (HeA/HypA; daily exercise training at Ta = 35 °C, while confined to a simulated altitude of ~ 4000 m) and exercise training in normoxic thermoneutral conditions (NorEx; no environmental stressors). To observe potential effects of the local acclimation on the CIVD response, participants additionally immersed their hand in warm water (35 °C) daily during the HeA/HypA and NorEx. Before and after the acclimation protocols, participants completed hand immersions in cold water (8 °C) for 30 min, followed by 15-min recovery phases. The temperature was measured in each finger.ResultsFollowing the HeA protocol, the average temperature of all five fingers was higher during immersion (from 13.9 ± 2.4 to 15.5 ± 2.5 °C; p = 0.04) and recovery (from 22.2 ± 4.0 to 25.9 ± 4.9 °C; p = 0.02). The HeA/HypA and NorEx protocols did not enhance the CIVD response.ConclusionWhole-body heat acclimation increased the finger vasodilatory response during cold-water immersion, and enhanced the rewarming rate of the hand, thus potentially contributing to improved local cold tolerance. Daily hand immersion in warm water for 10 days during HeA/Hyp and NorEx, did not contribute to any changes in the CIVD response.

Cold-induced vasodilation in abstinent smokers with and without a 12-hour nicotine patch.

This study was designed to identify the effects of a 12-h nicotine patch administration on cold induced vasodilation (CIVD) in healthy young chronic smokers following 16 h of abstinence from smoking. Two laser Doppler probes and temperature thermocouples were placed on the dorsal part of the distal phalanx of the middle and ring fingers of 7 smokers (>12 cigarettes/day). Following 16 h of abstinence from smoking, smokers were tested with and without administration of a 21mg transdermal nicotine patch (NicoDerm® ). Each participant's right hand was immersed in cold (~5°C) water for 40 min. Cutaneous vascular conductance (CVC) was calculated from non-invasive arterial finger blood pressure and skin blood flow and expressed as a percentage of peak CVC observed during hand skin heating to 44°C. For comparison purposes, the CIVD response of a non-smoking cohort without nicotine patch (n = 10) was also examined. Baseline CVC was similar in smokers and non-smokers (27.8 ± 12.6 CVC % peak). The initial vasoconstriction during cold-water immersion decreased skin blood flow to 4.0 ± 3.9 CVC % peak in both smokers and non-smokers. The onset of CIVD in smokers (4.5 ± 1.5 min) was delayed compared to non-smoker (3.3 ± 0.8 min, p < .05). The area under the CVC %peak-time curve during cold-water immersion averaged 1250 ± 388 CVC %peak · min in non-smokers which was larger (p < .05) than smokers with or without nicotine (789 ± 542 and 862 ± 517 CVC %peak · min, respectively). Chronic smoking impaired the CIVD response to cold-water immersion of the hand; however, the impaired CIVD response in 16 h of abstinence from smoking was not influenced by application of a 21mg transdermal nicotine patch.

Effects of acute dietary nitrate supplementation on cold-induced vasodilation in healthy males.

Cold-induced vasodilation (CIVD) is a paradoxical rise in blood flow to the digits that occur during prolonged cold exposure. CIVD is thought to occur through active vasodilation and/or sympathetic withdrawal, where nitric oxide (NO) may play a key role in mediating these mechanisms. Beetroot juice (BRJ) is high in dietary nitrate (NO3-) which undergoes sequential reduction to nitrite (NO2-) and subsequently NO. Using a double-blind, randomized, crossover design, we examined the effect of acute BRJ supplementation on the CIVD response in 10 healthy males. Participants had a resting blood pressure measurement taken prior to ingesting 140mL of nitrate-rich BRJ (13mmol NO3-) or a NO3--free placebo (PLA). After 2h, participants immersed their hand in neutral water (~ 35°C) for 10min of baseline before cold water immersion (~ 8°C) for 30min. Laser-Doppler fluxmetry and skin temperature were measured continuously on the digits. Compared to PLA (100 ± 3mmHg), acute BRJ supplementation significantly reduced mean arterial pressure at -30min (96 ± 2mmHg; p = 0.007) and 0min (94 ± 2mmHg; p = 0.008). Acute BRJ supplementation had no effect on Laser-Doppler fluxmetry during CIVD (expressed as cutaneous vascular conductance) measured as area under the curve (BRJ: 843 ± 148 PUmmHg-1s; PLA: 1086 ± 333 PUmmHg-1s), amplitude (BRJ: 0.60 ± 0.12 PUmmHg-1; PLA: 0.69 ± 0.14 PUmmHg-1), and duration (BRJ: 895 ± 60s; PLA: 894 ± 46s). Acute BRJ supplementation does not augment the CIVD response in healthy males.

Effect of Calcium-Channel Blockade on the Cold-Induced Vasodilation Response

Cold-induced vasodilation (CIVD) is seen in the extremities during exposure to cold. A strong vasodilation response has been associated with a decreased risk of cold injury. Increasing CIVD might further decrease this risk. The calcium-channel blocker nifedipine causes vasodilation and is used to treat Raynaud's syndrome and chilblains. Nifedipine is also used for high altitude pulmonary edema and could potentially serve a dual purpose in preventing frostbite. The effects of nifedipine on CIVD have not been studied. A double-blind crossover study comparing nifedipine (30 mg SR (sustained release) orallytwice daily) to placebo was designed using 2 sessions of 4 finger immersion in 5°C water, with 24h of medication pretreatment before each session. Finger temperatures were measured via nailbed thermocouples. The primary outcome was mean finger temperature; secondary outcomes were mean apex and nadir temperatures, first apex and nadir temperatures, subjective pain ranking, and time of vasodilation onset (all presented as mean±SD). Twelve volunteers (age 29±3 [24-34] y) completed the study. No significant difference in finger temperature (9.2±1.1°C nifedipine vs 9.0±0.7°C placebo, P=0.38) or any secondary outcome was found. Pain levels were similar (2.8±1.6 nifedipine vs 3.0±1.5 placebo, P=0.32). The most common adverse event was headache (32% of nifedipine trials vs 8% placebo). Pretreatment with 30 mg of oral nifedipine twice daily does not affect the CIVD response in healthy individuals under cold stress.

Cold-induced vasodilation responses before and after exercise in normobaric normoxia and hypoxia.

Cold-induced vasodilation (CIVD) is known to protect humans against local cold injuries and improve manual dexterity. The current study examined the effects of metabolic heat production on cold-induced vasodilation responses in normobaric hypoxia and normoxia. Ten participants immersed their non-dominant hand into 5°C water for 15min. Minimum finger temperature (Tmin), maximum finger temperature (Tmax), onset time, amplitude, and peak time were measured before and after exercise under normoxia (21% O2) and two levels of normobaric hypoxia (17% O2 and 13% O2). Neither Tmin nor amplitude was affected by hypoxia. However, Tmax was significantly decreased by hypoxia while reduction in onset time and peak time trended towards significance. Tmin, Tmax, and amplitude were significantly higher during post-exercise CIVD than pre-exercise CIVD. The CIVD response may be negatively affected by the introduction of hypoxia whereas metabolic heat production via exercise may counteract adverse effects of hypoxia and improve CIVD responses.

Ski-Everest (8848 m) Expedition: Digit Skin Temperature Responses to Cold Immersion May Reflect Susceptibility to Cold Injury

We tested the hypothesis that individual susceptibility to freezing cold injury might be reflected in an attenuated cold-induced vasodilatation (CIVD) response by comparing the CIVD responses of an elite alpinist with a history of freezing cold injury in the feet (case alpinist) with those of an age- and ability- matched noninjured alpinists control group (controls). According to this hypothesis, the vasomotor responses to a CIVD test of the case alpinist would represent a pathophysiological response when compared with the normal physiological response of a noninjured cohort. The case alpinist and the controls in the cohort group conducted a cold water immersion test comprising sequential immersion of a hand and foot for 5 min in 35°C water, followed by a 30-min immersion in 8°C water and a 10-min recovery period in room air. During this test we monitored the finger and toe skin temperatures. The case alpinist had a significantly attenuated CIVD response and a lower skin temperature in all injured and noninjured digits during immersion (∼2°C lower than in the control group) and an attenuated recovery of finger skin temperatures (∼6°C lower than in the control group). The attenuated CIVD response of the case alpinist may reflect a previously unrecognized enhanced susceptibility to frostbite. In addition to the poor vasomotor response observed in the injured toes, he also exhibited a poor vasomotor response in his noninjured fingers. The results of the present study indicate that a test of vasomotor activity during thermal stress may identify individuals predisposed to cold injury.

Koroška 8000 Himalayan expedition: digit responses to cold stress following ascent to Broadpeak (Pakistan, 8051m).

Cold-induced vasodilatation (CIVD) is a peripheral blood flow response, observed in both the hands and feet. Exercise has been shown to enhance the response, specifically by increasing mean skin temperatures (Tsk), in part due to the increased number of CIVD waves. In contrast, hypobaric hypoxia has been suggested to impair digit skin temperature responses, particularly during subsequent hand rewarming following the cold stimulus. This study examined the combined effect of exercise and hypobaric hypoxia on the CIVD response. We compared the CIVD responses in the digits of both the hands and feet of a team of alpinists (N = 5) before and after a 35-day Himalayan expedition to Broadpeak, Pakistan (8051m). Five elite alpinists participated in hand and foot cold water immersion tests 20 days before and immediately upon return from their expedition. The alpinists summited successfully without supplemental oxygen. Post-expedition, all alpinists demonstrated higher minimum Tsk in their hands (pre: 9.9 ± 1.1, post: 10.1 ± 0.7°C, p = 0.031). Four alpinists had either greater CIVD waves, and, consequently, higher mean Tsk in their hands, or higher recovery temperatures (pre: 26.0 ± 5.5°C post: 31.0 ± 4.1°C, p = 0.052), or faster rewarming rate (pre: 2.6 ± 0.5°Cmin-1 post: 3.1 ± 0.4°Cmin-1,p = 0.052). In the feet, the responses varied: 1/5 had higher wave amplitudes and 1/5 had higher passive recovery temperatures, whereas 3/5 had lower mean toe temperatures during cold exposure. The results of the cold stress test suggest after a 35-day Himalayan expedition, alpinists experienced a slight cold adaptation of the hands, but not the feet.

L-Menthol attenuates the magnitude of cold-induced vasodilation on the extremities of young females

BackgroundMenthol chemically triggers cold-sensitive receptors in the skin without conductive skin cooling. We investigated the effects of menthol-induced activation of cutaneous cold receptors on the cold-induced vasodilation (CIVD) of the finger. We hypothesized that the menthol application would attenuate typical CIVD responses.Methods1.5% l-menthol was fully applied over the left hand and forearm, and then, the middle finger of the left hand was immersed into 4 °C water for 30 min. A trial consisted of 10-min rest followed by 30-min immersion and 20-min recovery in 28 °C air temperature with 20% relative humidity. Another trial without the menthol application was carried out as a control. Seventeen females (24.2 ± 2.6 years in age, 160.5 ± 5.1 cm in height, and 51.2 ± 5.7 kg in body weight) participated in the two trials.ResultsThe results showed that the maximum and average temperatures of the finger during the water immersion were lower in the menthol application when compared to control (P < 0.05), whereas no significant differences appeared in the onset time of CIVD, the frequency of CIVD, and minimum finger temperature. These results imply that stronger stimulation of cold receptors without additional conductive skin cooling did not attenuate the triggering of CIVD responses but intensified vasoconstriction after the first occurrence of CIVD.ConclusionIt is suggested that substantial and conductive heat loss through the skin along with activation of cold receptors may be required to retain rewarming at a certain level.

Effects Of Normobaric Hypoxia And Exercise On Cold-induced Vasodilation, Body Temperature, And Oxygen Saturation

PURPOSE: The purpose of the current study was to investigate the effects of normobaric hypoxia on the thermoregulatory and the cold-induced vasodilation (CIVD) response before and following submaximal exercise. METHODS: Ten apparently healthy men (23±3 years) volunteered for two experimental trials during which they were exposed to differing O2 saturations (13% O2 and 21% O2) in an environmental chamber. Trials were counterbalanced and blinded from the participant. Following a 60-min acclimation the experimental trials consisted of two 15-min exposures to 5°C water of the non-dominant hand. The exposures were separated by a 30-min bout of submaximal exercise producing the equivalent of 400 watts (W) of metabolic heat. Mean body temperature (MBT), oxygen saturation (SaO2), and thermal sensation (TS) were collected during the final 5 min of each stage. CIVD was measured pre- and post-exercise during each of the cold water exposures on the nailbed of the middle finger on the non-dominant hand. RESULTS: ANOVA revealed a significant time (baseline, acclimation, CIVDpre, exercise, and CIVDpost) by condition (13% O2, 21% O2) interaction for SaO2 (F = 38.4, p < 0.001). Significant differences (p < 0.001) between conditions existed at all time-points with the exception of baseline (p = 1.0). A main effect of time was observed for amplitude temperature (F = 20.034, p < 0.001), which was significantly greater (p < 0.001) at CIVDpost compared to CIVDpre (CIVDpost: 1.13 °C; CIVDpre: 0.28 °C). No significant difference across time or condition exists for MBT or TS. In the 13% O2 condition, the reduction in SaO2 during exercise (81.5%) was positively associated (r = 0.656, p = 0.039) with amplitude temperature at CIVDpost (0.69 °C), which was significantly greater (p < 0.05) compared to CIVDpre (0.14 °C). CONCLUSION: It appears that during rest in normobaric hypoxia, a cold stress test has minimal effect on the CIVD response. During exercise, reduced CIVD amplitude is associated with reduced SaO2. It appears that a submaximal bout of cycling exercise is not the proper stimulus to acutely induce a CIVD response to the magnitude at which physiological changes ensue.

Effects of Contralateral Hand Immersion in Hot Water on Physiological Responses and Subjective Perceptions during Finger Cold-induced Vasodilatation Test

This study investigated cold-induced vasodilatation (CIVD) responses in the finger during contralateral hand heating to suggest preventive countermeasures for workers in cold. Thirty three students (23.9 ± 2.4 yr in age, 1.65 ± 0.08 m in height, 55.2 ± 10.5 kg in body mass; 28 females and 5 males) participated in two trials: left middle finger immersion in cold water (4oC) (FC) and right hand immersion in hot water (42oC) combined with FC (FCHH). Both tests consisted of a 10-min rest, 30-min immersion, and 20-min recovery. FCHH had higher mean left middle temperatures compared to FC during immersion and recovery (P<0.05). FCHH had higher Tmin, Tmax, Tmean, amplitude, and resistance index for frostbite when compared to FC (P<0.05). During the immersion and recovery periods, chest and foot temperatures were higher and lower, respectively, in FC than those in FCHH (P<0.05). Heart rate during immersion was higher in FCHH when compared to FC (P<0.05). In summary, the contralateral hand heating during the finger CIVD test resulted in pronounced CIVD responses, and also affected cardiovascular responses. The wearing of at least one glove during cold exposure can be helpful for workers’ comfort and performance.

No association between hand and foot temperature responses during local cold stress and rewarming

PurposeThe purpose was to examine whether associations exist between temperature responses in the fingers vs. toes and hand vs. foot during local cold-water immersion and rewarming phases.MethodsSeventy healthy subjects (58 males, 12 females) immersed their right hand or right foot, respectively, in 8 °C water for 30 min (CWI phase), followed by a 15-min spontaneous rewarming (RW) in 25 °C air temperature.ResultsTemperature was lower in the toes than the fingers during the baseline phase (27.8 ± 3.0 vs. 33.9 ± 2.5 °C, p < 0.001), parts of the CWI phase (min 20–30: 8.8 ± 0.7 vs. 9.7 ± 1.4 °C, p < 0.001), and during the RW phase (peak temperature: 22.5 ± 5.1 vs. 32.7 ± 3.6 °C, p < 0.001). Cold-induced vasodilatation (CIVD) was more common in the fingers than in the toes (p < 0.001). Within the first 10 min of CWI, 61% of the subjects exhibited a CIVD response in the fingers, while only 6% of the subjects had a CIVD response in the toes. There was a large variability of temperature responses both within and between extremities, and there was a weak correlation between finger- and toe temperature both during the CWI (r = 0.21, p = 0.08) and the RW phases (r = 0.26, p = 0.03).ConclusionsResults suggest that there is generally a lower temperature in the toes than the fingers after a short time of local cold exposure and that the thermal responses of the fingers/hands are not readily transferable to the toes/foot.

A New Proposal for Management of Severe Frostbite in the Austere Environment

Despite advances in outdoor clothing and medical management of frostbite, individuals still experience catastrophic amputations. This is a particular risk for those in austere environments, due to resource limitations and delayed definitive treatment. The emerging best therapies for severe frostbite are thrombolytics and iloprost. However, they must be started within 24 hours after rewarming for recombinant tissue plasminogen activator (rt-PA) and within 48 hours for iloprost. Evacuation of individuals experiencing frostbite from remote environments within 24 to 48 hours is often impossible. To date, use of these agents has been confined to hospitals, thus depriving most individuals in the austere environment of the best treatment. We propose that thrombolytics and iloprost be considered for field treatment to maximize chances for recovery and reduce amputations. Given the small but potentially serious risk of complications, rt-PA should only be used for grade 4 frostbite where amputation is inevitable, and within 24 hours of rewarming. Prostacyclin has less risk and can be used for grades 2 to 4 frostbite within 48 hours of rewarming. Until more field experience is reported with these agents, their use should probably be restricted to experienced physicians. Other modalities, such as local nerve blocks and improving oxygenation at high altitude may also be considered. We submit that it remains possible to improve frostbite outcomes despite delayed evacuation using resource-limited treatment strategies. We present 2 cases of frostbite treated with rt-PA at K2 basecamp to illustrate feasibility and important considerations.