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 ± 5 year; height: 181 ± 9 cm; weight: 79.9 ± 10.4 kg) 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.

Cold-Induced Vasodilation, Rewarming, and Dexterity Impairment Following Second-Degree Frostbite.

Frostbite, a severe cold injury resulting from exposure to subfreezing temperatures, damages the skin and underlying tissues of the affected area and ranges in severity from first to fourth degree. This case report investigates the impact of second-degree frostbite suffered by a marine during winter training on cold-induced vasodilation (CIVD). Comparisons of CIVD before and after the injury revealed significant alterations in CIVD responses. CIVD, a physiological mechanism characterized by blood vessel dilation in response to cold exposure, plays a crucial role in operating in cold-weather environments and enhancing dexterity. The marine exhibited prolonged CIVD onset time, lower finger temperatures, increased pain sensations, and diminished dexterity after the frostbite injury during follow-up CIVD testing. The findings suggest that the frostbite-induced damage possibly compromised the microvascular function, contributing to the observed changes in CIVD. The marine reported persistent cold sensitivity and difficulty in maintaining hand warmth when assessed postinjury. This case underscores the potential long-term consequences of frostbite on CIVD and manual dexterity, emphasizing the importance of understanding these physiological changes for individuals engaged in cold-weather activities, particularly for military and occupational personnel.

The effect of heat acclimation on the sweat lactate concentration vs. sweat rate relationship.

It is well known that there is a high concentration of lactate in sweat. Interest in measuring sweat lactate has arisen from its potential role in several clinical and sport performance applications. However, the effect of heat acclimation on sweat lactate concentration is still under debate. This is partly because sweat lactate concentration is greatly affected by sweat rate, which is known to increase during heat acclimation. Thus, to better understand this issue it is necessary to account for sweat rate - which has not been done previously in the literature. Therefore, the purpose of the current study was to determine the effect of heat acclimation on the relationship between sweat rate vs. sweat lactate concentration. Six subjects completed a 7-day heat acclimation protocol. The daily 2-h exercise bout was split into three 40-min intervals with exercise intensity increasing with each successive interval. This was done to induce three different sweat rates to determine the sweat rate vs. sweat lactate concentration relationship before and after heat acclimation for each participant. A 2 (heat acclimation) x 3 (sweat rate) repeated measures ANOVA was conducted to determine statistical significance. There was a significant (p < 0.05) decrease in the grand mean sweat lactate concentration over the course of seven days of heat acclimation from 17.0 ± 5.0 to 11.3 ± 1.1 mmol/L (p < 0.05). A significant (p < 0.05) heat acclimation x sweat rate ordinal interaction was also found. The results of the current study show that heat acclimation significantly decreases the sweat lactate concentration. In addition, there was a significant ordinal interaction which suggests that the impact of sweat rate on sweat lactate concentration is decreased following heat acclimation.

Pathogenic troponin T mutants with opposing effects on myofilament Ca2+ sensitivity attenuate cardiomyopathy phenotypes in mice.

Mutations in cardiac troponin T (TnT) associated with hypertrophic cardiomyopathy generally lead to an increase in the Ca2+ sensitivity of contraction and susceptibility to arrhythmias. In contrast, TnT mutations linked to dilated cardiomyopathy decrease the Ca2+ sensitivity of contraction. Here we tested the hypothesis that two TnT disease mutations with opposite effects on myofilament Ca2+ sensitivity can attenuate each other's phenotype. We crossed transgenic mice expressing the HCM TnT-I79N mutation (I79N) with a DCM knock-in mouse model carrying the heterozygous TnT-R141W mutation (HET). The results of the Ca2+ sensitivity in skinned cardiac muscle preparations ranked from highest to lowest were as follow: I79N > I79N/HET > NTg > HET. Echocardiographic measurements revealed an improvement in hemodynamic parameters in I79N/HET compared to I79N and normalization of left ventricular dimensions and volumes compared to both I79N and HET. Ex vivo testing showed that the I79N/HET mouse hearts had reduced arrhythmia susceptibility compared to I79N mice. These results suggest that two disease mutations in TnT that have opposite effects on the myofilament Ca2+ sensitivity can paradoxically ameliorate each other's disease phenotype. Normalizing myofilament Ca2+ sensitivity may be a promising new treatment approach for a variety of diseases.

Prevalence of hypothermia and critical hand temperatures during military cold water immersion training.

Cold-weather military operations can quickly undermine warfighter readiness and performance. Specifically, accidental cold-water immersion (CWI) contributes to rapid body heat loss and impaired motor function. This study evaluated the prevalence of hypothermia and critical hand temperatures during CWI. One-hundred seventeen (N = 117) military personnel (mean ± SD age: 27 ± 6 yr, height: 176 ± 8 cm, weight: 81.5 ± 11.6 kg) completed CWI and rewarming during cold-weather training, which included a 10-min outdoor CWI (1.3 ± 1.4°C) combined with cold air (-4.2 ± 8.5°C) exposure. Following CWI, students removed wet clothing, donned dry clothing, and entered sleeping systems. Core (Tc) and hand (Thand) temperatures were recorded continuously during the training exercise. Tc for 96 students (mean ± SD lowest Tc = 35.6 ± 0.9°C) revealed that 24 students (25%) experienced Tc below 35.0°C. All of 110 students (100%) experienced Thand below 15.0°C, with 71 students (65%) experiencing Thand at or below 8.0°C. Loss of hand function and hypothermia should be anticipated in warfighters who experience CWI in field settings. Given the high prevalence of low Thand, focus should be directed on quickly rewarming hands to recover function.