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NUTR 380 > Module 5 Vitamins, Minerals and Sport Performance > Flashcards

Module 5 Vitamins, Minerals and Sport Performance Flashcards

1
Q

Role of vitamins

A

Organic compounds/ catalysts involved in metabolic reactions
* Do not provide energy

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2
Q

How are vitamins obtained?

A

Must be obtained from the diet, except:
* Vitamin D: synthesized from sunlight
* Vitamin K: synthesized by bacteria in the intestine

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3
Q

When can vitamin deficiency develop

A

develop in 3-4 weeks

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4
Q

Excess of vitamins

A

can lead to toxicity (acute or chronic) depending on vitamin

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5
Q

Vitamins: Functions and Requirements - Athletes

A
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6
Q

Macrominerals

A

major

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7
Q

microminerals

A

Trace Elements

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8
Q

Minerals: Functions and Requirements – Athletes

A
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9
Q

Adequacy of Current Recommendations for Athletes

A

the current recommendations for micronutrient intakes for the general population are also adequate for athletes.
* micronutrient supplements are unnecessary for athletes who consume a diet providing high energy availability (EA) from a variety of nutrient-dense foods.

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10
Q

Low EA link to micronutrients

A

linked to micronutrient deficiencies in athletes when they do occur.
* Micronutrient supplementation is only considered to be necessary for athletes who are consume suboptimal amounts of micronutrients.

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11
Q

What often leads to micronutrient deficiency in athletes?

A
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12
Q

What is the exception to adequate diet = adequate micronutrient intake in athletes?

A

female iron status

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13
Q

Benefit of vitamins in excess through supplementation

A

There is no evidence to show that exceeding the AI for any of the micronutrients results in performance gains unless the athlete is in a deficient state.
* micronutrient supplements are unnecessary for athletes who consume a diet providing high energy availability (EA) from a variety of nutrient-dense foods.

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14
Q

Association between oxygen and ATP

A

Without oxygen, metabolic production of energy (ATP) is compromised.

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15
Q

Role of RBCs

A
  • Deliver oxygen to working muscles
  • Carry CO2 back to the lungs
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16
Q

What is oxygen carrying capacity proportional to?

A

proportional to the [Hb] in RBC.
* Athletes need to have adequate numbers of RBC AND adequate Hb within each RBC

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17
Q

Micronutrients necessary for Hb and RBC synthesis

A

co-factors for the enzymes responsible for Hb synthesis or RBC formation
* Iron
* Copper
* Folate
* Vitamin B12

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18
Q

Iron role Hb

A

Heme ➔ iron containing molecule at the centre of each Hb unit
which Binds O2 and CO2 reversibly

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19
Q

Iron role in myoglobin

A

An Fe and O2-binding protein found in the muscle tissue
* Acts as a storage “vessel,” for oxygen, as it holds oxygen inside cardia and skeletal muscles.
* Only found in the bloodstream when it is released following muscle injury (abnormal finding)

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20
Q

Dietary forms of iron

A
  • heme
  • non-heme
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21
Q

dietary sources of heme and non-heme iron

A
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22
Q

Factors that enhance iron absorption

A
  • heme iron
  • increased demand for iron
  • Vitamin C in the meal
  • high gastric acid production
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23
Q

Factors that inhibit iron absorption

A
  • decreased iron demand
  • factors in meal that complex with iron and decrease absorption
  • mineral-mineral interactions, causing minerals to compete for transport
  • high antacid use
24
Q

RDA for Iron

A
  • Adult men (all age groups) = 8 mg/day.
  • Pre-menopausal women = 18 mg/day.
  • Post-menopausal women = 8 mg /day.
25
Q

Athlete RDA for iron

A

unknown but believed to be higher than in the general population.
* People being treated for iron deficiency may require intakes far above the RDA to replete their iron stores.

26
Q

A hormone that regulates iron metabolism in the gut and macrophages.

A

hepcidin

27
Q

How does hepcidin regulation metabolism?

A

Influences iron metabolism by degrading the iron transporter known as ferroportin (Fpn), located on the brush border membrane of duodenal enterocytes.
* A degradation of the Fpn transporters can result in decreased dietary iron absorption from the small intestine.

28
Q

major regulator of iron metabolism

A

hepcidin

29
Q

How does PA effect hepcidin?

A

Intense physical activity upregulates Hepcidin.
* It is thought that this activity-driven upregulation of Hepcidin decreases iron absorption, increases iron needs, and presents an additional risk for anemia.

30
Q

Key measures of iron status

A
  • ferritin
  • transferrin saturation
  • total iron binding capacity
  • hemoglobin
  • hematocrit
31
Q

Ferritin

A

Serum ferritin levels reflects tissue iron stores
* 1 ug ferritin/L = 8 mg stored iron
* Decreases when iron status is low

32
Q

Transferrin Saturation

A

Transferrin saturation is a measure of how much iron is bound and being actively carried by Transferrin
* Normally 30% of Transferrin is saturated with iron, with normal saturation ranges from 16-50%
* Decreases when iron availability in blood is low and is a measure of iron status

33
Q

TIBC

A

Total Iron Binding Capacity - Measures the total capacity for transferrin to bind and carry iron
* Increases if iron status is low

34
Q

hemoglobin

A

If HB is low, iron shortages have been occurring for some time

35
Q

hematocrit

A

Measure of actual volume of RBC in whole blood to total blood volume.
* Low hematocrit = fewer RBC
* Indicative of anemia (multiple causes)

36
Q

generic term for any condition in which Hb levels are low.

A

anemia

37
Q

Causes of Iron Deficiency Anemia

A
  • physiological state
  • blood loss
  • poor intake
  • poor absorption
38
Q

Clinical Symptoms of Iron Deficiency Anemia

A
  • pallor
  • fatigue: loss of endurance capacity & reduction in strength
  • lowered immunity
  • itchiness
  • “spoon” nails (Koilonychia)
  • cognitive function
  • inability to regulate temp.
  • pica (odd cravings - i.e. Clay)
  • low hemoglobin, hematocrit and serum ferritin levels.
39
Q

Stages of iron deficiency

A
  1. iron deficiency: iron stores are low
  2. iron deficiency erythropoesis: ability to synthesize new RBCs is decreased
  3. iron deficiency anemia: number of RBCs is decreased because iron is not available
40
Q

Prevalence of Iron Deficiency Anemia in general public

A

In the general population, the prevalence of iron-deficiency anemia among youth and adults is estimated at 2% to 5% in females and 1% to 2% in males.

41
Q

Prevalence of Iron Deficiency Anemia in athletes

A
  • Up to 52% of female adolescent athletes.
  • 30–50% of athletes participating in endurance sports
  • Iron Deficiency anemia is most common in female athletes (15–35%), but it is not an exclusively female health concern.
  • 5–15% of the male athletes are also iron-deficient.
42
Q

What enhances iron needs in athletes?

A
  • high physiological demands
  • inadequate consumption of dietary iron
  • high iron loss, mostly from blood loss
43
Q

Exercise induced hemolysis

A

has been reported for more than 50 years. In particular, distance running has been associated with significant destruction of red blood cells (RBC) with RBC turnover being substantially higher in runners compared with untrained controls. Several groups have suggested that mechanical damage to RBC occurs as they pass through the capillaries of the foot during the footstrike phase

44
Q

Possible Mechanisms for Exercise-Induced Iron Deficiency

A
45
Q

Treatment of Anemia

A

Determining the cause is critical!
* The cause determines the treatment modality - need to know if bleeding, disease or malnutrition is the primary cause.

46
Q

Iron Deficiency Treatment

A
  • Iron Supplementation: 100-200 mg elemental iron per day
  • Check iron stores 2-4 weeks post therapy for repletion.
  • Check iron stores after 2-4 months to ensure ID doesn’t recur.
  • Continue with iron therapy for additional 4-6 months if Hb normal.
  • Maintenance with a low dose of iron therapy may be required for patients with ongoing needs e.g., menses, dietary, growth spurts.
47
Q

Reccomendations for iron supplementation

A
  • Ferrous form of iron
  • Taken on an empty stomach with full glass of water or fruit juice
  • Taken in the morning or earlier in the day.
  • Taken with a source of Vitamin C (e.g. fruit juice, oranges, tomatoes).
  • Should not be taken with Calcium products (e.g. supplements, certain antacids, milk or milk products)
  • Avoid high-oxalate foods (e.g., coffee, tea, spinach, kale, broccoli).
48
Q

Blood volume (amount of blood in total) expands in response to training.

A

sports anemia

49
Q

Another name for sports anemia

A

Dilutional Pseudoanemia
* not a true form of anemia, no response to Fe-therapy and no markers of blood loss

50
Q

Why is sport anemia nothing to worry about?

A

Expansion of blood volume is an expected benefit of training.
* Blood volume expansion is a temporary effect of training.
* [Hb] may not be parallel to increase in BV
* Random blood draws, if taken at a time of BV expansion can mimic anemia BUT THIS IS NOT THE CASE
* E.g. low Hb relative to blood volume

51
Q

Treatment of sport anemia

A

diagnosis of exclusion
* Given time the situation will normalize provided dietary iron intake is adequate.
* Need to rule out dietary or medical causes of anemia

52
Q

Sport Factors Related to Sport Anemia

A
  • type of sport - Endurance sports change iron status assessment parameters more than other sports
  • intensity or duration of training - Greater intensity or longer duration = greater chance for finding of sport anemia
  • adaptations to training - Sport anemia is more likely to be found in early stages of a new training regime rather than after a long period of adaptation
53
Q

prevalance of Hemochromatosis

A

most prevalent genetic disorder in North Americans:
* 1 in 300 Canadians

54
Q

hemochromatosis

A

Results in heightened iron absorption and excessive storage of iron in the skin, heart, liver, pancreas, pituitary glad and joints.

55
Q

What is excess storage of iron related to?

A
  • CHD
  • Cirrhosis of the liver and/or liver cancer

NUTR 380 (23 decks)

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