Michael J Buono1,2, Taylor Krippes2, Fred W Kolkhorst2, Alexander T Williams3, Pedro Cabrales3. 1. Department of Biology, San Diego State University, San Diego, CA, 92182, USA. 2. School of Exercise and Nutritional Sciences, San Diego State University, San Diego, CA, 92182, USA. 3. Department of Bioengineering, University of California, San Diego, San Diego, CA, 92093, USA.
Abstract
NEW FINDINGS: 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.
NEW FINDINGS: 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.
Authors: Vivek P Jani; Ozlem Yalcin; Alexander T Williams; Mark A Popovsky; Pedro Cabrales Journal: Clin Hemorheol Microcirc Date: 2017 Impact factor: 2.375
Authors: Elie Nader; Sarah Skinner; Marc Romana; Romain Fort; Nathalie Lemonne; Nicolas Guillot; Alexandra Gauthier; Sophie Antoine-Jonville; Céline Renoux; Marie-Dominique Hardy-Dessources; Emeric Stauffer; Philippe Joly; Yves Bertrand; Philippe Connes Journal: Front Physiol Date: 2019-10-17 Impact factor: 4.566