Kelly Karen R, Arrington Laura J, Bernards Jake R, Jensen Andrew E
Applied Translational Exercise and Metabolic Physiology Team, Warfighter Performance, Naval Health Research Center, San Diego, CA, United States.
Leidos, Inc., San Diego, CA, United States.
Front Physiol. 2022 Jul 8;13:842612. doi: 10.3389/fphys.2022.842612. eCollection 2022.
Cold water exposure poses a unique physiological challenge to the human body. Normally, water submersion increases activation of parasympathetic tone to induce bradycardia in order to compensate for hemodynamic shifts and reduce oxygen consumption by peripheral tissues. However, elevated stress, such as that which may occur due to prolonged cold exposure, may shift the sympatho-vagal balance towards sympathetic activation which may potentially negate the dive reflex and impact thermoregulation. To quantify the acute stress response during prolonged extreme cold water diving and to determine the influence of acute stress on thermoregulation. Twenty-one ( = 21) subjects tasked with cold water dive training participated. Divers donned standard diving equipment and fully submerged to a depth of ≈20 feet, in a pool chilled to 4°C, for a 9-h training exercise. Pre- and post-training measures included: core and skin temperature; salivary alpha amylase (AA), cortisol (CORT), osteocalcin (OCN), testosterone (TEST) and dehydroepiandosterone (DHEA); body weight; blood glucose, lactate, and ketones. Core, skin, and extremity temperature decreased ( < 0.001) over the 9-h dive; however, core temperature was maintained above the clinical threshold for hypothermia and was not correlated to body size ( = 0.595). There was a significant increase in AA ( < 0.001) and OCN ( = 0.021) and a significant decrease in TEST ( = 0.003) over the duration of the dive. An indirect correlation between changes in cortisol concentrations and changes in foot temperature ( = -0.5, = 0.042) were observed. There was a significant positive correlation between baseline OCN and change in hand temperature ( = 0.66, = 0.044) and significant indirect correlation between changes in OCN concentrations and changes in hand temperature ( = -0.59, = 0.043). These data suggest that long-duration, cold water diving initiates a stress response-as measurable by salivary stress biomarkers-and that peripheral skin temperature decreases over the course of these dives. Cumulatively, these data suggest that there is a relationship between the acute stress response and peripheral thermoregulation.
冷水暴露对人体构成独特的生理挑战。通常,水浸会增加副交感神经张力的激活,从而诱发心动过缓,以补偿血流动力学变化并减少外周组织的耗氧量。然而,压力升高,例如长时间暴露于寒冷中可能出现的压力,可能会使交感-迷走神经平衡向交感神经激活方向转变,这可能会抵消潜水反射并影响体温调节。为了量化长时间极端冷水潜水期间的急性应激反应,并确定急性应激对体温调节的影响。21名接受冷水潜水训练的受试者参与其中。潜水员穿戴标准潜水装备,在冷却至4°C的水池中完全潜入约20英尺的深度,进行为期9小时的训练。训练前和训练后的测量指标包括:核心体温和皮肤温度;唾液α淀粉酶(AA)、皮质醇(CORT)、骨钙素(OCN)、睾酮(TEST)和脱氢表雄酮(DHEA);体重;血糖、乳酸和酮体。在9小时的潜水中,核心体温、皮肤温度和四肢温度均下降(P<0.001);然而,核心体温维持在体温过低的临床阈值以上,且与体型无关(r = 0.595)。在潜水过程中,AA显著增加(P<0.001),OCN增加(P = 0.021),TEST显著降低(P = 0.003)。观察到皮质醇浓度变化与足部温度变化之间存在间接相关性(r = -0.5,P = 0.042)。基线OCN与手部温度变化之间存在显著正相关(r = 0.66,P = 0.044),OCN浓度变化与手部温度变化之间存在显著间接相关性(r = -0.59,P = 0.043)。这些数据表明,长时间冷水潜水会引发应激反应——可通过唾液应激生物标志物测量——并且在这些潜水过程中外周皮肤温度会下降。总体而言,这些数据表明急性应激反应与外周体温调节之间存在关联。