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Red blood cells in sports: effects of exercise and training on oxygen supply by red blood cells.

Mairbäurl H - Front Physiol (2013)

Bottom Line: Trained athletes, particularly in endurance sports, have a decreased hematocrit, which is sometimes called "sports anemia." This is not anemia in a clinical sense, because athletes have in fact an increased total mass of red blood cells and hemoglobin in circulation relative to sedentary individuals.The slight decrease in hematocrit by training is brought about by an increased plasma volume (PV).Together, these adjustments cause a decrease in the average age of the population of circulating red blood cells in trained athletes.

View Article: PubMed Central - PubMed

Affiliation: Medical Clinic VII, Sports Medicine, University of Heidelberg Heidelberg, Germany.

ABSTRACT
During exercise the cardiovascular system has to warrant substrate supply to working muscle. The main function of red blood cells in exercise is the transport of O2 from the lungs to the tissues and the delivery of metabolically produced CO2 to the lungs for expiration. Hemoglobin also contributes to the blood's buffering capacity, and ATP and NO release from red blood cells contributes to vasodilation and improved blood flow to working muscle. These functions require adequate amounts of red blood cells in circulation. Trained athletes, particularly in endurance sports, have a decreased hematocrit, which is sometimes called "sports anemia." This is not anemia in a clinical sense, because athletes have in fact an increased total mass of red blood cells and hemoglobin in circulation relative to sedentary individuals. The slight decrease in hematocrit by training is brought about by an increased plasma volume (PV). The mechanisms that increase total red blood cell mass by training are not understood fully. Despite stimulated erythropoiesis, exercise can decrease the red blood cell mass by intravascular hemolysis mainly of senescent red blood cells, which is caused by mechanical rupture when red blood cells pass through capillaries in contracting muscles, and by compression of red cells e.g., in foot soles during running or in hand palms in weightlifters. Together, these adjustments cause a decrease in the average age of the population of circulating red blood cells in trained athletes. These younger red cells are characterized by improved oxygen release and deformability, both of which also improve tissue oxygen supply during exercise.

No MeSH data available.


Related in: MedlinePlus

Schematic presentation of mechanisms increasing muscle oxygen supply acutely during exercise and by training discussed in this review. During exercise local blood flow is increased by mediators causing local vasodilation, which is supported by red blood cell-mediated NO production. Acidosis, CO2 and hyperthermia decrease Hb-O2-affinity and enhance O2 release from its bond to hemoglobin. These improvements may in part be blunted by increased blood viscosity (not shown in scheme). Training stimulates erythropoiesis to increase the O2-transport capacity. The newly formed cells also have an improved deformability which facilitates muscle blood flow. Training also increases red blood cell 2,3-DPG (not shown), which further enhances O2 release from Hb.
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Figure 3: Schematic presentation of mechanisms increasing muscle oxygen supply acutely during exercise and by training discussed in this review. During exercise local blood flow is increased by mediators causing local vasodilation, which is supported by red blood cell-mediated NO production. Acidosis, CO2 and hyperthermia decrease Hb-O2-affinity and enhance O2 release from its bond to hemoglobin. These improvements may in part be blunted by increased blood viscosity (not shown in scheme). Training stimulates erythropoiesis to increase the O2-transport capacity. The newly formed cells also have an improved deformability which facilitates muscle blood flow. Training also increases red blood cell 2,3-DPG (not shown), which further enhances O2 release from Hb.

Mentions: There are many mechanisms that contribute to an increased tissue oxygen supply during exercise. Figure 3 summarizes those, where red blood cell are involved. They involve adjustments during exercise and to training. During exercise the increased O2 demand of skeletal muscle is mainly matched by increasing muscle blood flow by increasing cardiac output, by modulating blood flow distribution among active and inactive organs, and by optimizing microcirculation (Laughlin et al., 2012). Red blood cells support local blood flow by providing the vasodilator NO by direct conversion from nitrate and by release of ATP causing endothelial NO release. At any given capillary blood flow the amount of O2 unloaded from Hb to the cells of working muscle can be increased greatly by decreasing Hb-O2 affinity. This happens as the cells enter the capillaries supplying the muscle cells, where they are exposed to increased temperature, H+ and CO2. Training further enhances O2 flux to the working muscle at all levels of regulation: It increases maximal cardiac output, improves blood flow to the muscles by stimulating vascularization, and improves the rheological properties of red blood cells. Training increases total hemoglobin mass by stimulating erythropoiesis, which increases the amount of O2 that can be carried by blood. It also increases red blood cell 2,3-DPG, which increases the sensitivity of Hb-O2 affinity to acidification dependent O2-release. The system appears to be optimized for exercise at low altitude, because in an hypoxic environment the decreased arterial PO2, which is the major determinant for O2 diffusion, cannot be compensated adequately by the above mentioned O2 transport mechanisms resulting in a decrease in performance with increasing degree of hypoxia (Cerretelli and DiPrampero, 1985).


Red blood cells in sports: effects of exercise and training on oxygen supply by red blood cells.

Mairbäurl H - Front Physiol (2013)

Schematic presentation of mechanisms increasing muscle oxygen supply acutely during exercise and by training discussed in this review. During exercise local blood flow is increased by mediators causing local vasodilation, which is supported by red blood cell-mediated NO production. Acidosis, CO2 and hyperthermia decrease Hb-O2-affinity and enhance O2 release from its bond to hemoglobin. These improvements may in part be blunted by increased blood viscosity (not shown in scheme). Training stimulates erythropoiesis to increase the O2-transport capacity. The newly formed cells also have an improved deformability which facilitates muscle blood flow. Training also increases red blood cell 2,3-DPG (not shown), which further enhances O2 release from Hb.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3824146&req=5

Figure 3: Schematic presentation of mechanisms increasing muscle oxygen supply acutely during exercise and by training discussed in this review. During exercise local blood flow is increased by mediators causing local vasodilation, which is supported by red blood cell-mediated NO production. Acidosis, CO2 and hyperthermia decrease Hb-O2-affinity and enhance O2 release from its bond to hemoglobin. These improvements may in part be blunted by increased blood viscosity (not shown in scheme). Training stimulates erythropoiesis to increase the O2-transport capacity. The newly formed cells also have an improved deformability which facilitates muscle blood flow. Training also increases red blood cell 2,3-DPG (not shown), which further enhances O2 release from Hb.
Mentions: There are many mechanisms that contribute to an increased tissue oxygen supply during exercise. Figure 3 summarizes those, where red blood cell are involved. They involve adjustments during exercise and to training. During exercise the increased O2 demand of skeletal muscle is mainly matched by increasing muscle blood flow by increasing cardiac output, by modulating blood flow distribution among active and inactive organs, and by optimizing microcirculation (Laughlin et al., 2012). Red blood cells support local blood flow by providing the vasodilator NO by direct conversion from nitrate and by release of ATP causing endothelial NO release. At any given capillary blood flow the amount of O2 unloaded from Hb to the cells of working muscle can be increased greatly by decreasing Hb-O2 affinity. This happens as the cells enter the capillaries supplying the muscle cells, where they are exposed to increased temperature, H+ and CO2. Training further enhances O2 flux to the working muscle at all levels of regulation: It increases maximal cardiac output, improves blood flow to the muscles by stimulating vascularization, and improves the rheological properties of red blood cells. Training increases total hemoglobin mass by stimulating erythropoiesis, which increases the amount of O2 that can be carried by blood. It also increases red blood cell 2,3-DPG, which increases the sensitivity of Hb-O2 affinity to acidification dependent O2-release. The system appears to be optimized for exercise at low altitude, because in an hypoxic environment the decreased arterial PO2, which is the major determinant for O2 diffusion, cannot be compensated adequately by the above mentioned O2 transport mechanisms resulting in a decrease in performance with increasing degree of hypoxia (Cerretelli and DiPrampero, 1985).

Bottom Line: Trained athletes, particularly in endurance sports, have a decreased hematocrit, which is sometimes called "sports anemia." This is not anemia in a clinical sense, because athletes have in fact an increased total mass of red blood cells and hemoglobin in circulation relative to sedentary individuals.The slight decrease in hematocrit by training is brought about by an increased plasma volume (PV).Together, these adjustments cause a decrease in the average age of the population of circulating red blood cells in trained athletes.

View Article: PubMed Central - PubMed

Affiliation: Medical Clinic VII, Sports Medicine, University of Heidelberg Heidelberg, Germany.

ABSTRACT
During exercise the cardiovascular system has to warrant substrate supply to working muscle. The main function of red blood cells in exercise is the transport of O2 from the lungs to the tissues and the delivery of metabolically produced CO2 to the lungs for expiration. Hemoglobin also contributes to the blood's buffering capacity, and ATP and NO release from red blood cells contributes to vasodilation and improved blood flow to working muscle. These functions require adequate amounts of red blood cells in circulation. Trained athletes, particularly in endurance sports, have a decreased hematocrit, which is sometimes called "sports anemia." This is not anemia in a clinical sense, because athletes have in fact an increased total mass of red blood cells and hemoglobin in circulation relative to sedentary individuals. The slight decrease in hematocrit by training is brought about by an increased plasma volume (PV). The mechanisms that increase total red blood cell mass by training are not understood fully. Despite stimulated erythropoiesis, exercise can decrease the red blood cell mass by intravascular hemolysis mainly of senescent red blood cells, which is caused by mechanical rupture when red blood cells pass through capillaries in contracting muscles, and by compression of red cells e.g., in foot soles during running or in hand palms in weightlifters. Together, these adjustments cause a decrease in the average age of the population of circulating red blood cells in trained athletes. These younger red cells are characterized by improved oxygen release and deformability, both of which also improve tissue oxygen supply during exercise.

No MeSH data available.


Related in: MedlinePlus