Description: Known as dilutional anemia or pseudoanemia
Epidemiology: The most common cause of anemia found in the athletic population. Dilutional pseudoanemia is not pathologic but rather an adaptation to endurance training and normalizes after training cessation. It is postulated to occur as a result of plasma volume expansion. It is hypothesized that dilutional anemia enhances the efficiency of oxygen delivery by decreasing blood viscosity and increasing cardiac output.
Etiology: Dilutional anemia occurs when the plasma expansion is greater than the red blood cell (RBC) mass increase. Typically, there is no change or an actual increase in RBC mass and total RBCs. Within 3–5 hours after exercise, plasma volume levels equilibrate, and subsequently, volume expansion occurs secondary to an increase in renin, aldosterone, and vasopressin levels, along with an increase in albumin production.
Laboratory tests: Laboratory test results reveal mild anemia (hemoglobin levels: 13 g/dL in men and 11.5 g/dL in women), which resolves within 3–5 days of discontinuing exercise.
Treatment: Dilutional anemia should not negatively affect athletic performance, and no treatment is required.
Epidemiology: Iron-deficiency anemia is the most common true anemia in athletes and the most common nutritional deficiency in the United States, affecting 3%–5% of women and <1% of men.
Presentation: It may be asymptomatic but often presents with weakness, lassitude, palpitations, shortness of breath, and pica (craving for starch, ice, or clay). Paleness, glossitis, angular cheilitis, and koilonychias (spoon-shaped nails) may be found in severe cases ( Fig. 31.1 ).
Etiology: It is primarily caused by insufficient iron uptake from the gut or increased loss of iron; it is important to differentiate the cause. Most commonly, the blood loss results from menstruation or the gastrointestinal tract, but other causes include sweating and iron sequestration in response to inflammation. Hepcidin, a peptide hormone that inhibits iron absorption, may increase in response to exercise. In addition, nonsteroidal antiinflammatory (NSAID)-induced gastritis may frequently occur in athletes.
Laboratory testing: A low hemoglobin level in adults (<12 g/dL in women and <14 g/dL in men), mean corpuscular volume <75 fL, a hypochromic and microcytic blood smear, low serum iron with high total iron-binding capacity, and serum ferritin levels <12 µg/L
Treatment: Oral iron therapy in the form of elemental iron, 50 mg three times a day.
Absorption is best between meals, and orange juice or ascorbic acid increases absorption. Treatment should be continued for 6–12 months to completely replenish iron stores. Empiric treatment in borderline cases is warranted for 8 weeks, with the aim of a 1-g increase in hemoglobin. Women with documented cases of recurrent iron deficiency should be administered prophylactic doses of iron.
Iron Deficiency Without Anemia
Overview: Iron deficiency without anemia affects 12%–16% of premenopausal women and 2% of adult men. Importance in athletic performance is unclear and controversial with certain studies demonstrating an effect on V̇O 2 max and several others reporting a decline in physical and cognitive function in deficient athletes, specifically in endurance athletes such as marathoners.
Laboratory testing: Laboratory test results will show decreased serum ferritin levels with normal hemoglobin.
Treatment: There are conflicting studies on the effects of iron deficiency without anemia on athletic performance. If an athlete presents with iron deficiency and borderline or low hemoglobin, a trial of oral iron therapy may be considered. Several studies have advocated supplementation if basal ferritin is <35 mg/L. Unnecessary treatment with iron can lead to gastrointestinal disturbances and occasionally more serious issues such as hemosiderosis.
Foot-Strike Hemolysis/Exercise-Induced Hemolysis/Hemoglobinuria
Overview: Rarely severe enough to cause clinically significant anemia or iron deficiency
Typically, healthy individuals can counteract the degree of hemolysis with reticulocytosis.
Etiology: Mechanical forces from muscle contractions and heel-strike have been shown to be a reproducible cause of RBC hemolysis leading to hemoglobinuria. Studies have suggested that hemolysis in the plantar vessels is caused by a combination of poorly cushioned shoes, running style, and hard running surfaces. In addition, elevated body temperature aids in increased RBC fragility, leading to “runner’s macrocytosis” secondary to the loss of the older microcytes. Hemolysis has been documented in swimmers, dancers, rowers, and triathletes. Once hemolysis occurs, hemoglobin is released into the intravascular space. Haptoglobin, an intravascular protein, binds to the free hemoglobin; once haptoglobin becomes saturated, the free hemoglobin spills into the urine, producing hemoglobinuria.
Laboratory studies: Urinalysis reveals hemoglobinuria, which resolves within 3–5 days with exercise cessation. Laboratory test results typically reveal a macrocytic anemia with an increased reticulocyte count. Haptoglobin levels may be low or immeasurable, leading to urinary loss of iron.
Treatment: Treatment is not necessary but includes changes in gait, shoes, running surfaces, and intensity of the training regimen.