This information was compiled from various sources (class notes, text books, previous board review study guides) in preparation for the National Boards of 1996.  I expect that human physiology hasn't changed much since then and this information should still be accurate.    This posting is intended as a nuts and bolts physiology review.   Please report any errors or submit any additions by e-mail. 

Misc. Notes:

Signs of Possible Nutritional Imbalances:  

Laboratory Tests that may be indicated:     

Hemoglobin, hematocrit, MCV, WBC's (with diff), serum glucose, serum cholesterol, serum albumin, serum transferrin, BUN, prothrombin time, alkaline phosphatase

Excess Leanness:

                   

Management: 

Fuel Source:

Restricted to glucose from dietary carbohydrates or certain amino acids (aa's) through gluconeogenesis.  Krebs's cycle is fueled by carbohydrates (glucose), fatty acids and amino acids (valine, isoleucine and methionine). 

Glycogen:  "animal starch".  Storage form of carbohydrates.  Glycogen is usually formed from sugar (glucose).  Related disease(s):  Glycogen storage disease.   Stored in the liver and in muscle.  Deplete glycogen stores by working out hard on a low carbohydrate diet.  Saturate glycogen stores by light workouts and high carbohydrate diets (1 week before event, deplete for the first 3 days and saturate for the second 3 days.  Depletion of glycogen in athletes:  "hitting the wall", weakness, depression, irritability. 

Glycogen formation from carbohydrates:       glycogenesis

Glycogen from non-carbohydrates:                glyconeogenesis

Glucose from glycogen:                                  glycogenolysis

       

Choice of fuel: 

Carbohydrates are limited to blood sugar and glycogen stores in the liver and muscle. This fuel is used in high intensity/short duration events.  Glycogen stores are usually at about 350 gm,  which is only enough energy to supply needs for ½ day.   After about three hours of continuous exercise at 70-80% VO2 max., athletes tire due to hypoglycemia ("hitting the wall").  To replace glycogen, consume 50-70% of diet as carbohydrates.    Marathon runners  are known to "Glycogen Load".  With training and diet, the amount of glycogen able to be stored in muscle can be increased, thereby increasing the aerobic capacity of the athlete. 

Fats are the best fuel for low to moderate activity.  RDA is 30% of total caloric intake. 

Vitamins and minerals in athletes should be adequate due to the increased caloric consumption. 

Iron: 

Fe++(ferrous), Fe+++(ferric).  Functions in hemoglobin (Hgb), myoglobin (Mgb), and the cytochromes (oxidative phosphorylation). Iron deficiency anemia limits aerobic endurance and capacity for work (pt. feels tired and fatigued).  Supplement with vitamin C and ferrous sulfate 50- 200 mg (vitamin C will keep iron in the ferrous state)

Test:    

With infection serum iron will test low.  Bacteria need it to grow, so the body takes it out of circulation.  Iron is always bound in the blood (for the same reason, to keep away from

unauthorized users?) via transferrin (a globulin that binds and transports iron) and is stored as hemosiderin (an iron containing pigment from the hemoglobin of lysed RBC's) until needed for making new hemoglobin and as ferritin, which is stored in the tissues, especially the reticuloendothelial cells of the liver spleen and bone marrow.   Related diseases:  Iron deficiency anemia, hemosiderosis. 

Sports Anemia:

Heavy training can cause a transient anemia with a decreased RBC count, Hgb, Hct. (hematocrit).   RBC morphology and color is normal (normocytic/normochromic) and athletic performance does not deteriorate.  Possibly due to hemodilution (expanded blood volume) and increased RBC destruction due to intra vascular hemolysis.  Supplementation is not necessary unless low serum ferritin is found.

Ca++.  Female athletes that must maintain low body fat weights, become amenorrheic which can lead to a reduction in bone mineral content.  Encourage the RDA for Ca++ in the diet.  Reduction in training and a gain in body fat does increase bone density.  (fats related to estrogen synthesis balance  estradiol??)

Examples: 

100 meter dash:  Anaerobic.  High intensity at 85-90% of VO2 max.  Carbohydrates from     glycogen is the primary energy source.

Treadmill at 4-5 mph:   Low to moderate intensity.  < 60% of VO2 max.  Energy comes mainly from fats (fatty acids, beta oxidation to acetyl CoA which enters the Krebs's cycle)

[refine the relationship between glucose and oxaloacetate, beta oxidation, ketone bodies, pyruvate and acetyl CoA.  Increase in beta oxidation with diabetes mellitus (DM) because glucose is unavailable or  not utilized as energy (also occurs in starvation,  high fat diet, pregnancy).  Increase in ketone bodies (acetone, beta-hydroxybutyric acid, and acetoacetic acid), can lead to diabetic ketoacidosis.  Large quantities of ketones can be released and detected in the urine.  Patients have a "fruity" smell (?).

Causes of magnesium Deficiency:

       

1. Decreased Intake (take more)

       

2. Impaired Absorption  (taking more does nothing)

3. Renal Loss (taking more does nothing)

4. Endocrine

Neuromuscular:  muscle weakness, twitching, cramps, tetany, convulsions, paresthesias, mental status changes (confusion, agitation, delirium, coma, depression). 

Cardiac:  arrhythmias (PVC, atrial fibrillation), ST and T wave changes, prolongation of P-R, QRS and Q-T intervals, coronary artery spasm, increased size of myocardial infarcts.

Metabolic:  refractory hypokalemia, insulin resistance, hypertension, hypocalcemia

Neonates:  weakness, apnea, high pitched cry, convulsions, jitteriness

 

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