Buono Michael J, Krippes Taylor, Kolkhorst Fred W, Williams Alexander T, Cabrales Pedro
Department of Biology, San Diego State University, San Diego, CA, 92182, USA.
School of Exercise and Nutritional Sciences, San Diego State University, San Diego, CA, 92182, USA.
Exp Physiol. 2016 Feb;101(2):332-42. doi: 10.1113/EP085504.
What is the central question of this study? The purpose of the present study was to determine the effects of exercise-induced haemoconcentration and hyperthermia on blood viscosity. What is the main finding and its importance? Exercise-induced haemoconcentration, increased plasma viscosity and increased blood aggregation, all of which increased blood viscosity, were counterbalanced by increased red blood cell (RBC) deformability (e.g. RBC membrane shear elastic modulus and elongation index) caused by the hyperthermia. Thus, blood viscosity remained unchanged following prolonged moderate-intensity exercise in the heat. Previous studies have reported that blood viscosity is significantly increased following exercise. However, these studies measured both pre- and postexercise blood viscosity at 37 °C even though core and blood temperatures would be expected to have increased during the exercise. Consequently, the effect of exercise-induced hyperthermia on mitigating change in blood viscosity may have been missed. The purpose of this study was to isolate the effects of exercise-induced haemoconcentration and hyperthermia and to determine their combined effects on blood viscosity. Nine subjects performed 2 h of moderate-intensity exercise in the heat (37 °C, 40% relative humidity), which resulted in significant increases from pre-exercise values for rectal temperature (from 37.11 ± 0.35 to 38.76 ± 0.13 °C), haemoconcentration (haematocrit increased from 43.6 ± 3.6 to 45.6 ± 3.5%) and dehydration (change in body weight = -3.6 ± 0.7%). Exercise-induced haemoconcentration significantly (P < 0.05) increased blood viscosity by 9% (from 3.97 to 4.33 cP at 300 s(-1)), whereas exercise-induced hyperthermia significantly decreased blood viscosity by 7% (from 3.97 to 3.69 cP at 300 s(-1)). When both factors were considered together, there was no overall change in blood viscosity (from 3.97 to 4.03 cP at 300 s(-1)). The effects of exercise-induced haemoconcentration, increased plasma viscosity and increased red blood cell aggregation, all of which increased blood viscosity, were counterbalanced by increased red blood cell deformability (e.g. red blood cell membrane shear elastic modulus and elongation index) caused by the hyperthermia. Thus, blood viscosity remained unchanged following prolonged moderate-intensity exercise in the heat.
本研究的核心问题是什么?本研究的目的是确定运动诱导的血液浓缩和体温过高对血液粘度的影响。主要发现及其重要性是什么?运动诱导的血液浓缩、血浆粘度增加和血液聚集增加,所有这些都会增加血液粘度,但由体温过高引起的红细胞(RBC)变形性增加(例如RBC膜剪切弹性模量和伸长指数)起到了平衡作用。因此,在高温环境下进行长时间中等强度运动后血液粘度保持不变。先前的研究报告称运动后血液粘度会显著增加。然而,这些研究在37°C下测量运动前后的血液粘度,即便预计运动期间核心体温和血液温度会升高。因此,运动诱导的体温过高对减轻血液粘度变化的影响可能被忽视了。本研究的目的是分离运动诱导的血液浓缩和体温过高的影响,并确定它们对血液粘度的综合影响。九名受试者在高温环境(37°C,相对湿度40%)下进行了2小时的中等强度运动,这导致直肠温度(从37.11±0.35升高至38.76±0.13°C)、血液浓缩(血细胞比容从43.6±3.6升高至45.6±3.5%)和脱水(体重变化=-3.6±0.7%)相较于运动前显著增加。运动诱导的血液浓缩使血液粘度显著(P<0.05)增加9%(在300 s-1时从3.97升高至4.33 cP),而运动诱导的体温过高使血液粘度显著降低7%(在300 s-1时从3.97降低至3.69 cP)。当同时考虑这两个因素时,血液粘度没有总体变化(在300 s-1时从3.97变为4.03 cP)。运动诱导的血液浓缩、血浆粘度增加和红细胞聚集增加,所有这些都会增加血液粘度,但由体温过高引起的红细胞变形性增加(例如红细胞膜剪切弹性模量和伸长指数)起到了平衡作用。因此,在高温环境下进行长时间中等强度运动后血液粘度保持不变。