Micronutrients, including vitamins and minerals, are integral in supporting energy creation through various metabolic pathways (1). Under strenuous exercise, there is an increased demand on metabolic pathways, leading to free-radical production and cellular DNA damage. Despite the increased need for energy production during exercise, gut absorption of micronutrients is decreased, and loss of micronutrients from sweat, urine, and stool is increased (2). Micronutrients are largely, adequately obtained via diet alone, with the greatest concern for micronutrient deficiencies in those athletes with suboptimal or restrictive diets. Supplementation of micronutrients is reserved for those who have clinical pathology, secondary to micronutrient deficiency (1). In this article, we will discuss micronutrients in terms of their daily recommended intake (DRI), physiologic role, and symptoms of deficiency, with an emphasis on those micronutrients (vitamin D, iron, calcium, and antioxidants) that most commonly benefit from supplementation (1).
Water-soluble vitamins, B vitamins and vitamin C, have little storage within the body and are lost in the urine. Water-soluble vitamins are replenished daily through diet alone (1) (see Table 1). Research does not support a recommendation for daily supplementation of water-soluble vitamins outside of an adequate diet to enhance exercise capacity (3).
Table 1 -
Water-soluble vitamins (2,3
|Vitamin/DRI/Foods Containing Vitamin
||Metabolic Pathway Involvement
Men: 1.2 mg·d−1;
Women: 1.1 mg·d−1
Foods: yeast, pork, fortified grains, legumes
|– Cofactor for synthesis of acetyl-CoA to enter the tricarboxylic acid cycle
– Cofactor for synthesis of NADPH, deoxyribose, and ribose sugars in the pentose phosphate pathway
– Component of branch-chain amino acid metabolism
|Weakness, decreased endurance, weight loss, cardiac failure, neuropathy, gastrointestinal disturbances (Beriberi and Wernicke Korsakoff)
Men: 1.3 mg·d−1;
Women: 1.1 mg·d−1
Foods: milk, almonds, liver, eggs, bread, fortified cereals
|– Oxidative metabolism and electron transport system
– Cofactor for synthesis of FMN and FAD, which contribute to glucose, fatty acid, glycerol and amino acid metabolism
– Used in conversion of B6, niacin, and folate to their active forms
|Sore throat, cracked/red lips, bloodshot eyes, dermatitis, altered nervous system function
Men: 16 mgNE·d−1;
Women: 14 mgNE·d−1
Foods: meats/fish, legumes, cereals
|– Oxidative metabolism and electron transport system as precursor for NAD and NADP
– Plays role in beta-oxidation and amino acid synthesis
|Pellagra (dermatitis, diarrhea, dementia/death)
|Pantothenic acid (B5)
Men and women: 5 mg·d−1
Foods: liver, egg yolk, mushrooms, peanuts, yogurt, broccoli
|– Facilitates metabolism of fatty acids, amino acids, and carbohydrates
– Role in synthesis of cholesterol, steroid hormones, vitamins A and D
|Muscle cramps, fatigue, apathy, nausea/vomiting
Men and women: 1.3 mg·d−1
Foods: meats, whole grains, vegetables, nuts
|– Gluconeogenesis, niacin formation, lipid metabolism, erythrocyte function and metabolism, and hormone modulation
||Anemia, dermatitis, convulsions
Men and women: 30 μg·d−1
Foods: liver, egg yolk, soybeans, yeast, cereals, legumes, nuts
|- Cofactor in synthesis of fatty acids, gluconeogenesis, and metabolism of leucine
||Dermatitis/eczema, alopecia, conjunctivitis, fatigue
Men and women: 400 μg·d−1
Foods: yeast, liver, green vegetables, strawberries
|– Hemoglobin and nucleic acid formation
||Megaloblastic anemia, fatigue, birth defects in newborns (spina bifida)
Men and women: 2.4 μg·d−1
Foods: organ meats, shellfish, dairy
|– Hemoglobin formation, fat, carbohydrate, and protein metabolism
||Pernicious/megaloblastic anemia, neurologic symptoms, poor vision
|Ascorbic acid (C)
Men: 90 mg·d−1;
Women: 75 mg·d−1
Foods: citrus fruits, green vegetables, peppers, tomatoes, berries, potatoes
|– Antioxidant, involved in collagen formation, carnitine biosynthesis, neurotransmitter synthesis, and iron absorption
– Maintains the immune system under high stress (i.e., excessive training)
|Fatigue, loss of appetite, bleeding gums, loose teeth, easy bruising, poor wound healing (Scurvy)
NADPH, nicotinamide adenine dinucleotide phosphate reduced; FMN, flavin mononucleotide; FAD, flavin adenine dinucleotide; NAD, nicotinamide adenine dinucleotide; NADP, nicotinamide adenine dinucleotide phosphate.
Fat-soluble vitamins include vitamins A, D, E, and K, which dissolve in fat and are readily stored in the body (2) (see Table 2). Because of prolonged periods of storage, toxicity from fat-soluble vitamins can occur when consumed in excess. Additionally, research has not shown an increase in exercise performance or capacity with supplementation of fat-soluble vitamins (3).
Table 2 -
Fat-soluble vitamins (2,3
||Metabolic Pathway Involvement
Men: 900 μg·d−1;
Women: 700 μg·d−1
Foods: broccoli, squash, sweet potatoes, pumpkin, cantaloupe, liver, milk, eggs
|– Vision, immune response, epithelial cell growth, and repair
|Dry skin and hair, broken fingernails, susceptibility to infections, vision loss/night blindness, poor growth
Men and women: 15 mg·d−1
Foods: vegetable oils, unprocessed cereal grains, green leafy vegetables, nuts
||Retinopathy, neuropathy, myopathy, hemolysis
Men: 120 μg·d−1;
Women: 90 μg·d−1
Foods: green leafy vegetables, cereal, organ meats, dairy products, eggs
|– Blood clotting
– Bone mineralization
|Excessive bleeding, decrease bone mineral density
Vitamin D's primary functions are in regulating calcium and phosphorus absorption and metabolism for bone maintenance and stimulating skeletal muscle contraction (1,3). Sunlight triggers the production of previtamin D from cholesterol in the skin which serves as the primary source for vitamin D with only small amounts being provided through the diet (fatty fish, egg yolks, fortified milks, and cereals). The DRI of vitamin D is 600 international units (IU) daily with an increased recommendation for active individuals up to 2000 IU (3). Vitamin D insufficiency is defined as 31 to 39 ng·mL−1 and deficiency is less than 30 ng·mL−1; hypertension, heart disease, osteomalacia, and osteoporosis are byproducts of vitamin D deficiency (1,3). Athletes who compete indoors, live at high altitudes, have a dark complexion, have high body fat, train in the early morning or late evening, or wear clothing, equipment, or sunscreen are at the greatest risk for vitamin D deficiency (1,3). As athletes age, their risk for vitamin D deficiency also increases. Athletes experiencing stress fractures, bone or joint injury, muscle pain or weakness associated with any of the previously mentioned risk factors may benefit from supplementation and additional UV light exposure (1). In addition to a healthy diet, vitamin D 1000 to 2000 IU should be considered to supplement the symptomatic athlete. Additional exposure to sunlight is more controversial and has been refuted by the American Academy of Dermatology, because of the concern for skin cancer and the inconsistency of sunlight absorption; increased sunlight exposure should be reserved for those with minimal-to-no daily exposure (2,4).
Exercise induces an oxidative stress with a 10- to 15-fold increase in oxygen consumption and the creation of lipid peroxide by-products, which cause damage to cell membranes. Antioxidants, including vitamins A and E, help protect against oxidative damage by reducing free radical production, decreasing inflammation, and supporting immune function (1). Antioxidant deficiencies are seen with restrictive diets with limited fats, fruits, and vegetables and result in muscle soreness or stiffness with long-term effects of premature skin aging, cancer, and cardiovascular disease (2). With an adequate diet, research does not support antioxidant supplements, and the evidence for enhanced athletic performance is weak (1,2).
Iron is a component of hemoglobin and myoglobin and functions to transport oxygen in red blood cells (1,3). Iron deficiency, with or without a microcytic anemia, results in decreased muscle function and work capacity. Deficiency can lead to fatigue, lack of stamina, breathlessness, headaches, and insomnia (1,3). Iron is depleted via intravascular hemolysis, sweat (0.3 to 0.4 mg·d−1), stool (0.86 mg·d−1), urine (0.1 to 0.15 mg·d−1), and, in women, menstrual blood loss (0.3 to 0.4 mg·d−1) (2). Deficiencies of iron can be associated with limited iron intake from heme food sources (need 6 mg iron per 1000 kcal consumed), rapid growth, training at high altitudes, foot-strike hemolysis, blood donation, or injury (1). Heme-containing food sources include red meats, seafood, beans, leafy green vegetables, and molasses (3). Because of their high risk for iron deficiency, the DRI for female athletes is higher at 18 mg·d−1 of iron for premenopausal women, compared with 8 mg·d−1 for all other groups, including men, postmenopausal women, and sedentary individuals (1). Athletes may take up to 1000 mg·d−1 of iron, though, at excessive amounts, iron can accumulate to toxic levels and will not increase the rate of hemoglobin synthesis (2). It takes 3 to 6 months of appropriate daily iron intake to reverse iron deficiency anemia (1).
Calcium plays a role in the growth, maintenance, and repair of bone tissue along with the management of muscle contractions, nerve conduction, and blood clotting (1–3). Calcium deficiency is often secondary to restrictive diets, disordered eating, or the avoidance of dairy and other calcium-rich foods, such as pinto and black beans, spinach, fortified cereal, and orange juice. Calcium deficiency leads to osteopenia and osteoporosis, tetany, muscle pain, and spasms (3). Female athletes with low body weight, restrictive diets, and menstrual dysfunction are at the highest risk for calcium deficiency, because they often will have lower levels of estrogen, which has a protective effect on bone (2). The DRI for calcium in both men and women is 1000 mg·d−1, which is obtained largely via diet alone. Supplementation with 1500 mg·d−1 of calcium and 1500 to 2000 IU·d−1 of vitamin D can be utilized for diets deficient in calcium and for optimizing bone health in athletes with evidence of calcium deficiency (1). Research does not support the supplementation of calcium above the DRI without calcium deficiency, and supplementation does not enhance athletic performance (3).
The authors declare no conflict of interest and do not have any financial disclosures.
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2. Beavers KM, Serra MC. Essential and nonessential micronutrients and sport. In: Nutritional Supplements in Sports and Exercise
. Cham (NJ): Springer International Publishing; 2015. pp. 121–65.
3. Daries H. Nutrition for Sport and Exercise: A Practical Guide
. John Wiley & Sons, Incorporated; 2012.
4. American Academy of Dermatology. Position statement on Vitamin D. 2009. [cited 2020 August 27]. Available from: https://server.aad.org/forms/policies/Uploads/PS/AAD_PS_Vitamin_D.pdf