Need Help? Customer Support 1-866-236-8417

Dietary Intervention For Athletes: Part 2.

Although proteins have become the center of attention in the nutritional world, it has not been this way in the past. As part 2 of dietary intervention this article will shed some light on the role of protein and how important it really is.

Part 1 | Part 2

The Role Of Protein In Athletic Diets

Although proteins have become the center of attention in the nutritional world, it has not been this way in the past. Because proteins have little to do with energy production during activity, they are most often put on the side. Proteins do however have critical roles for intensely training athletes. This role primarily includes the basis of which training is performed.

In other words, it is the availability of various proteins and protein substrates that makes the rebuilding and regeneration process stimulated by training possible.

The structural component of proteins is amino acids. There are 20 amino acids required by the human body, nine of which are considered essential to the diet because they contain special carbon skeletons that can not be synthesized by the human body.

Amino acids, and thus proteins, differ from carbohydrates and lipids in that their basic structure involves an amine group containing nitrogen. In contrast, carbohydrates and lipids do not contain any nitrogen.

Through a variety of dietary protein sources involving sufficient total protein and the nine essential amino acids, the body can increase the chances that all 20 amino acids will be available through transamination. Transamination involves creating and transferring side chains of nonessential amino acids as metabolically required.

Although transamination is a metabolic safety net, limiting the requirement by consuming sufficient amino acid quantities through varied sources is a much more efficient process.

The Basics Of Amino Acid Metabolism.
This examination of proteins and amino acids will cover the metabolism of the protein we eat and catabolic situations in the body.
[ Click here to learn more. ]

Both plant and animal sources can provide vital amino acids. With ample protein consumption, the body can use transamination to produce some of the limiting amino acids in the diet. The essential amino acids must be consumed from dietary sources due to the body's inability to produce them.

The Variable Of Exercise

    Exercise however is a variable that alters protein metabolism and utilization. After all, it is the resultant changes, or alterations if you will, that are the goal of any training program. In general, the more activities an athlete is involved in creating greater levels of physical activity and work, the greater the requirement for protein.

    Tarnopolsky et al. (1992) discussed the body's ability to become physiologically accustomed to activities and therefore more efficient at using amino acids and other nutrients, for cellular repair and growth.

    Over time muscles become more efficient at using protein and the liver becomes better at exchanging amino groups. When we change the stimulus presented to our integrated systems the adaptation reaction must also be altered. Alterations can only be made at a certain rate which is partially dependant upon available protein and overall caloric intake. Too little protein and adaptations become limited because of the basic metabolic utilization of amino acids.

    Proteins are primarily utilized for structural components and enzymes. Although exercise may increase amino acid oxidation over baseline values, proteins play an extremely small role in energy production of healthy people during all intensities of exercise (Bowtell et al., 1998; Gibala, Hargreaves, & Tipton, 2000; Hargreaves et al., 1998; Lemon & Mullin, 1980).

    In return, a low protein intake will likely not directly effect immediate exercise performance, but rather may result in impaired recovery abilities and reduced strength levels over even a small training cycle (Tarnapolsky et al. 1992).

    Exercise, especially resistance training and long-duration exercise, may increase the dietary needs for protein (Berning, 2000; Tarnapolsky et al. 1992). The extra protein is needed for cellular repair and growth as a result of the exercise induced trauma. Tarnopolsky et al. (1992) stated that "a protein intake that is too low may result in sub-optimal strength and lean body mass accretion despite maintenance of a positive nitrogen balance" (p. 1986).

    In simple terms, without sufficient amino acid consumption the cytoskeleton damage, enzyme denaturation and reduced cell wall integrity which is resultant of intense training can not be sufficiently repaired between training sessions and a downward spiral begins.

    Tipton, Ferrando, Williams, and Wolfe (1996) found that net muscle protein synthesis is increased in women participating in one and one-half hours of high intensity intermittent swimming and approximately one hour of resistance training. The combination of the two exercise protocols significantly increased protein synthesis over the swimming and resistive training individually. It was hypothesized by the authors that it is the increased work load will lead to the greater protein requirements and not the relative intensities performed.

    Tipton, Ferrando, Williams, and Wolfe (1996) hypothesized that adding additional swimming or resistance training would have had added further to the amino acid requirements to further support the respondent greater levels of protein synthesis. Although this hypothesis has not been tested, it is congruent with the protein requirements for endurance athletes who participate in an extremely high physical activity work load. Past research has conclusively shown that as endurance athletes increase their workload, say from 20-to-30 miles per week, they also increase their protein requirement, and not just overall calories.

    The notion of workload and protein requirements should be simple when put in these terms.

    More Work = More Cell Damage = More Repair

    Protein is a primary constituent of cellular structural components which has been disrupted.

    More Repair = More Required

    Athletes who participate in strength training alone also require more protein than sedentary individuals. Tarnopolsky et al. (1992) tested the leucine kinetic and nitrogen balances of young male weight trainers when consuming 0.86, 1.4 or 2.4 grams of protein per kilogram per day.

    Results showed that the protein requirement of athletes participating in the resistance-training group was 98% higher than that of the sedentary control group. The resistance-training participants required 1.76 grams of protein per kilogram compared to the 0.89 for the sedentary group. In conclusion, active athletes require more than two times the amount of dietary protein intake than do their sedentary counterparts.

    How Much Protein Do You Consume?

      1 Gram x Bodyweight / Day
      1.5 Grams x Bodyweight / Day
      2 Grams x Bodyweight / Day
      Over 2.5 x Bodyweight / Day

    It is most likely rare that the body will require, or even be able to utilize, greater than 2.0 g/kg/day of protein for cellular and enzyme regeneration. (Berning, 2000). When greater than required intake of amino acids is consumed the excess will either be oxidized if glucose is still required or simply stored in adipose tissue. The guideline for participants in strenuous athletics is a protein intake of 1.2-1.8 g/kg/day.

    At this level negative results of excess protein intake will be avoided and almost always sufficient intake will be reached. When recommending protein intake to athletes, a general consensus in the literature is that it is better to shoot a bit high than low as long as the protein is not replacing required carbohydrates.

The Role Of Lipids In Athletic Diets

Lipids are the densest form of energy we consume. Fatty acids contain approximately nine calories per gram compared to only four for carbohydrate and protein. One 6-carbon glucose molecule can yield 38 ATP where as one 18-carbon fatty acid can yield 147 ATP. Although extremely dense in energy, fatty acids have major limitations when it comes to providing fuel for athletic performance.

Fat Metabolism!
Dietary fat is not an enemy. In fact, when adequate amounts of good fats (unsaturated) are consumed, it can improve one's health and athletic performance. Learn what these good fats are and how they keep the body function properly.
[ Click here to learn more. ]

The process of producing ATP via oxidative metabolism yields almost four times as much energy, but it requires 26 oxygen molecules to completely oxidize a 18-carbon fatty acid compared to the six oxygen molecules required to completely oxidize a 6-carbon glucose (Sherman & Leaders, 1995).

During most athletic activities oxygen is at a premium. Multiple sprint sports, such as soccer, football, and basketball push metabolic systems to maintain power output under severe metabolic strain; there simply is not enough oxygen present to allow sufficient utilization of fatty acids as a predominant fuel source.

Thus substrate utilization during high intensity exercise is effected with what appears to be a "coordination of effects on adipose tissue and muscle" (Coyle, Jeukendrup, Wagenmakers, & Saris, 1997, p. E272). There appears to be a relationship between free fatty acid (FFA) release from adipose tissue and glucose metabolism in the muscle cell. Romijn et al. (1993) studied the affects of exercise intensity upon endogenous fat and carbohydrate metabolism using trained subjects.

The Affects Of Exercise Intensity

    Results showed that as exercise intensity increases, the reliance upon lipids as an energy source decreases, exactly as we would expect. Muscles' reliance upon stored triglycerides and FFA was significantly less during physical activity at 85% VO2max as compared to 65% VO2max.

    During exercise at 85% VO2max, FFA become "trapped" in the adipose tissue by a variety of factors that also favor carbohydrate metabolism in the muscle cells (Romijn et al., 1993). Among these factors is the constriction of blood flow to adipose tissue by the body. As a natural and required reaction, fluids are channeled to muscles under the most metabolic distress.

    VO2 Max Calculator

    Enter the total distance covered in meters in 12 minutes and then press the 'Calculate' button.

      * 1600 meters = 1 mile
      * 5280 feet = 1 mile
      * 3 feet = 1 meter



    VO2 Max mls/kg/min

    Constriction of vessels limits the availability of oxygen to the adipose tissue for use in lipolysis as well as reduced blood plasma volumes to bind and transport the hydrophobic fatty acids. Shifting blood flow away from the adipose tissue thus increases the oxygen availability to the working muscles showing a hierarchy of needs at this intensity (Romijn et al. 1993).

    In contrast, during exercise at 65% VO2 max, muscle triglycerides and plasma FFA made a significant contribution to energy expenditure. At intensities of 65% VO2 max and less, working muscles generally are not in an oxygen deficit and are able to use the energy rich source of triglycerides.

    Muscle metabolism at moderate intensity relies more upon muscle triglyceride stores and plasma FFA than at higher intensities and in turn, the energy contribution from glycolysis is reduced (Coyle, Jeukendrup, Wagenmakers, & Saris, 1997; Romijn et al., 1993; Williams, 1999). Carbohydrate availability and utilization thus appears to somewhat regulate triglyceride release and oxidation during exercise (Coyle et al. 1997; Hargreaves, Kiens, & Richter, 1991; Romijn et al., 1993).

Increasing Circulating FFA

    Increasing levels of circulating FFA by intravenous methods was shown not to alter glycolysis, even at higher intensities (Hargreaves et al. 1991). Severely limiting lipid intakes by athletes beyond what is necessary for cardiovascular health in an attempt to improve carbohydrate metabolism appears to not present any beneficial effects upon muscle metabolism due to the natural control methods.

    Diets that have very low lipid profiles can have negative consequences on performance by limiting triglyceride stores within the body for use as fuel when needed, limiting absorption the absorption of specific vitamins, and by reducing required substrates for the production of hormones. (Berning, 2000).

    The four fat-soluble vitamins, A, D, E and K, may be absorbed in limited supply if dietary lipids are restricted severely (Combs, 2000; Williams, 1999). After longer durations of limited absorption, bodily stores of these fat-soluble vitamins may diminish and performance can slip or a clinical deficiency can develop.

    Lipids are vital to the formation of hormones, which act as physiological mediators within the body. One such hormonal mediator essential to health is eicosanoids. Eicosanoids are paracrine hormones produced in the local region of use (Ettinger, 2000). Omega-3 and omega-6 essential fatty acids (EFFA) are cleaved for the formation of an extremely large variety of eicosanoids. Dietary lipid consumption can influence the many processes in which these eicosanoids are involved, including inflammatory interleukins, cytokines, chemokines, clotting factors, growth factors, adhesion factors and possibly others that have not been identified (Ettinger, 2000).

    Excessively low or high levels of dietary lipids can have some extremely negative health consequences. It has been shown clinically many times that immune status can be negatively affected by a combination of strenuous exercise and a poor diet, including low lipid intake (Bishop, Blannin, Walsh, Robson & Gleeson, 1999; Venkatraman, Leddy & Pendergast, 2000). Shek, Sabiston, Buguet, and Rodornski (1995) studied the effects on the immune system of training at 65% VO2 max for 120 minutes.

    The results suggested a potential period of leukocytosis, especially during the post-exercise period. T-cells were plummeted to 60% of their pre-exercise level two hours post exercise. This period of decreased immune function potentially can leave the athletes open to infection, which can in turn reduce performance or restrict training capacity for future sessions.

Fatty Acids & The Immune System

    The value of fatty acids to immune system health has been vastly under appreciated in past decades. Most persons focused solely upon vitamins and antioxidants while in the low-fat diet craze of years past. As science has shown, it is the type of fats that reflects more upon the health of the system rather than the absolute total volume.

    Nutrient unavailability will affect virtually all processes within the immune system because the vast interrelationship of responses between multiple mechanisms (Bishop, 2000; Bishop et al., 1999; MacKinnon, 2000; Venkatraman et al., 2000). According to Venkatraman et al., "the role of lipids in the immune responses to exercise has been under appreciated" (p. S389). Realizing that athletes can use a significant amount of triglyceride stores during moderate and interval training, replenishing stores through proper dietary intake is a necessity. A diet lacking in proper lipid calories can exacerbate the period of post-exercise immune suppression.

    Regarding healthy intakes of lipids, the prevention of cardiovascular disease is of primary concern beyond maximizing performance. Types and quantity of dietary lipids potentially affect risk factors for coronary heart disease (CHD). Atherosclerosis, the major underlying cause of CHD, is a slowly progressing process involving primarily deposits of fat, oxidized low-density lipoprotein (LDL), cholesterol, and macrophages which combine to form plaque in the endothelium of blood vessels (Krummel, 2000). LDL is one of four primary lipoproteins circulating in blood transporting nutrients.

    The other three primary lipoproteins are chylomicrons, very-low density lipoprotein (VLDL), and high-density lipoprotein (HDL). Low-density and high-density lipoproteins have the largest implications to atherosclerosis. "Low-density forms of lipoproteins may predispose certain individuals to coronary heart disease whereas high-density forms may be protective (Williams, 1999, p. 137). LDL is approximately 45% cholesterol, which is only needed in limited supplies by cells. Excess cholesterol left in the circulatory system carried in LDL can become involved the plaque process (Williams, 1999).

    Athletes then should not alter significantly from the general health requirements of sedentary individuals in terms of fat consumption. Total caloric intake will most likely make the greatest implication to levels of fatty acid consumption. We can somewhat accurately decipher the required amounts of carbohydrates and amino acids. Once this information has been calculated, the remainder of calories can be consumed as fat as long as the value falls into the relative guidelines listed below.

Recommended Lipid Intakes
Total Fat Calories Monounsarated Fat Calories Polyunsaturated Fat Calories Saturated Fat Calories Cholesterol
15-30% of total calories 10-15% of total calories Up to 10% of total calories < 10% of fat calories <300 mg per day
Source: Jonnalagadda (2000)

Enter Your Total Daily Calorie Intake:

I Consume Calories A Day

Your Total Fat Intake Should Be Between
& Calories Per Day
& Grams Per Day

Your Total Monounsarated Fat Intake Should Be Between
& Calories Per Day
& Grams Per Day
Your Total Polyunsarated Fat Intake Should Be Up To
Calories Per Day
Grams Per Day
Your Total Saturated Fat Intake Should Be Between
& Calories Per Day
& Grams Per Day

The Role Of Vitamins & Minerals In Athletic Diets

A) Vitamins

    Vitamins are organic compounds that have multiple functions within the human body. The 13 classified substances are divided into two basic categories of; water-soluble and lipid-soluble. Water-soluble vitamins consist of the B-complex vitamins and vitamin C. Vitamins A, D, E, and K represent the lipid-soluble category. Vitamins are metabolically required only in relatively small amounts but are extremely crucial to bodily function and a deficiency can be apparent in as little as two to four weeks in hard training athletes (Combs, 2000; Williams, 1999).

    Vitamins are primarily involved in acting as coenzymes, antioxidants and hormone functions. These physiological processes become more active during and after exercise. Although vitamins are not "used up" during the process, they are subject to characteristic changes and therefore must be replenished. For example, enzymes consist of a protein and a cofactor, such as a vitamin. Each enzyme is specific and is not able to participate in any other reaction. Enzymes are not used up in the reaction process but rather act as catalysts that can become denatured. As enzymes and cofactors are used in reactions they may eventually become distorted or degraded, thus a continued supply is metabolically required.

    Free radicals are unstable byproducts of oxidative reactions within the body. These compounds react with cellular membranes causing damage to deoxyribonucleic acid (DNA) structure and may be part of developing various diseases such as cancer or cardiovascular disease. Vitamins are present in many enzymes that work to catabolize the damaging free radicals.

    All vitamins are essential, but there is major concern for athletes with regard to folate and the B-vitamins (Berning, 2000). Each of these vitamins is essential in processes used excessively during exercise and exercise recovery. Although there is concern for adequate supply, a dietary supplement may not be necessary, especially if no deficiency exists. Haymes and Clarkson (1998) concluded that unneeded supplementation, meaning there is no deficiency, will not have a major performance boosting effect.

    Consuming enough calories through a variety of foods, especially vitamin rich sources such as fruits and vegetables, seems to be the best way to ensure proper vitamin levels. The primary concern in modern food supply however is the declining vitamin content of mass produced food. A steady decline of natural vitamin content in our foods has been tracked over the past decade. Most processed foods contain some sort of vitamin supplementation in an attempt to replace what has been removed. Within this context, moderate levels of water soluble vitamin supplementation may be warranted for athletes especially.

    Keep in mind though that consuming toxic levels of vitamins is more easily done through supplementation than through food only. Excessive consumption of lipid soluble vitamins especially can pose an even greater risk than the water soluble types because they are withheld in the body attached to stored lipids. Thus, lipid soluble vitamins are also less easily removed from the body (Combs, 2000).

B) Minerals

    Minerals are inorganic elements that are collectively involved in both tissue formation and physiological regulation. Minerals are generally divided into two categories; macro minerals and micro minerals.

    Macro minerals are those which have a recommended daily intake (RDI) greater than 100 mg, or are stored in the body in amounts greater than 5 grams. Calcium, phosphorus, and magnesium are considered to be macro minerals. Iron, copper, zinc, chromium, and selenium are microminerals. According to Williams (1999, p. 241) "a diet that provides the RDI for iron, calcium and calories from a balanced selection of food throughout the different food groups will provide adequate amounts of both the major and trace minerals." Within athletic populations the minerals of major concern are calcium, iron and zinc.


      Calcium is a major mineral within the body composing a large percentage of skeletal mass as well as being essential to nerve function and muscular contractions. In total, calcium accounts for approximately 1.5% to 2% of total body weight and 39% of total body minerals stored at any given time within the body (Anderson, 2000).

      Prolonged periods of low calcium intakes may lead to a decreased bone mineral density because of the flux of calcium between the skeletal storage sites and the muscles. Calcium ions are essential to muscular contractions and low serum levels will impair proper function. Bones exist as dynamic tissues in which minerals are stored and then mobilized when needed elsewhere in the body (Anderson, 2000). Hormones within the body regulate the extraction of calcium from bone as needed (Williams, 1999).

      It is unlikely that muscle function will suffer, but impaired calcium metabolism can lead to diseases involving bones, colon cancer and hypertension (Williams, 1999). The guideline for calcium intake within intercollegiate athletic populations is the same as the recommended dietary intake for non-athletic individuals of the same gender and age.


      Iron is essential in processes that involve utilizing and transporting oxygen. Approximately 200-1500 mg of iron is stored in the body as either ferritin or hemosiderin. About 30% is stored in the liver and about 30% in bone marrow (Anderson, 2000).

      The major oxygen-binding compound within red blood cells is hemoglobin, an iron and protein compound, which is the most important transporter of oxygen in the cardiovascular system (Anderson, 2000; Williams, 1999). Myoglobin is a compound similar to hemoglobin and is located within cells. Both hemoglobin and myoglobin are vital for cellular function and low iron levels can lead to decreased aerobic performance and recovery by reducing available oxygen transporting capabilities (McDonanald & Keen, 1988; Weight, 1993).

      Iron is essential in other molecules within the body as well. Such metabolic proteins are cytochromes, which are involved in electron transport, catalase, which are responsible for the conversion of hydrogen peroxided to oxygen and water, iron-sulfur and metalloproteins, which are essential to oxidative metabolism, and tryptophan pyrolase, which are essential to the oxidation of tryptophan.

      It has been hypothesized that intense workloads, especially endurance runners, may have an increased need for iron as compared to their sedentary or moderately active counterparts (McDonanald & Keen, 1988; Weight, 1993). At the present time the exact duration, intensities and times of physical activity which increase the need for iron is unknown. Others believe that the presence of an athletic anemia is unique to each athlete and that it most likely develops for the same reasons as in non-athletic populations (Weight, 1993). It has also been hypothesized that zinc levels can become diminished in response to strenuous exercise (McDonald & Keen, 1988).


  1. Ainsworth, B., Haskell, W., & Leon, A. (1993). Compedium of physical activities: Classification of energy costs of human physical activities. Medicine & Science in Sports & Exercise, 25, 71-80.
  2. Anderson, J. (2000). Minerals. In Mahan, L. & Escott-Stump, S. (Eds.) Food, Nutrition, and Diet Therapy. Philadelphia, PA: WB Saunders Co.
  3. Balsom, P., Wood, K, Olsson, P. & Eckblom, B. (1999). Carbohydrate intake and multiple sprint sports: With special reference to football (soccer). International Journal of Sports Medicine, 20, 48-52.
  4. Bangsbo, J., Graham, R., Kiens, B. & Saltin, B. (1992). Elevated muscle glycogen and anaerobic energy production during exhaustive exercise in man. Journal of Physiology, 451, 205-227.
  5. Berning, J. (2000). Nutrition for sport and exercise. In Mahan, L. & Escott-Stump, S. (Eds.) Food, Nutrition, and Diet Therapy. Philadelphia, PA: WB Saunders Co.
  6. Bishop, N., Blannin, A., Walsh, N., & Robson, P. (1999). Nutritional aspects of immunosuppression in athletes. Sports Medicine, 28(3), 151-176.
  7. Bowtell, J., Leese, G., Smith, K., Watt, P., Nevill, A., Rooyackers, O., Wagenmakers, J., & Rennie, M. (1998). Modulation of whole body protein metabolism, during and after exercise, by variation of dietary protein. Journal of Applied Physiology, 85(5), 1744-1752.
  8. Combs, G. (2000). Vitamins. In Mahan, L. & Escott-Stump, S. (Eds.) Food, Nutrition, and Diet Therapy. Philadelphia, PA: WB Saunders Co.
  9. Coyle, E., Jeukendrup, A., Wagenmakers, A., & Saris, W. (1997). Fatty acid oxidation is directly regulated by carbohydrate metabolism during exercise. American Journal of Physiology, 273, E268-E275.
  10. Davy, B. (2000). Managing body weight. In Rosenbloom, C. (Ed.) Sports Nutrition: A Guide for the Professional Working with Active People. Chicago, IL: American Dietetic Association.
  11. De Lorenzo, A., Bertini, I., Candeloro, B., Piccinelli, R., Innocente, I., & Brancati, A. (1999). A new predictive equation to aclculate resting metabolic rate in athletes. Journal of Sports Medicine & Physical Fitness, 39(3), 213-219.
  12. Economos, C., Bortz, S. & Nelson, M. (1993). Nutritional practices of elite athletes: Practical recommendations. Sports Medicine, 16(6), 381-399.
  13. Ettinger, S. (2000). Macronutrients: Carbohydrates, proteins, and lipids. In Mahan, L. & Escott-Stump, S. (Eds.) Food, Nutrition, and Diet Therapy. Philadelphia, PA: WB Saunders Co.
  14. Food & Nutrition Board (1989). Recommended Dietary Allowances (10th ed.). Washington D.C.: National Academy of Sciences.
  15. Gaitanos, G., Williams, C., Boobis, L. & Brooks, S. (1993). Human muscle metabolism during intermittent maximal exercise. Journal of Applied Physiology, 75(2), 712-719.
  16. Gibala, M. & Hargreaves, M. (2000). Amino acids, proteins and exercise performance. Sports Science Exchange Roundtable, 11(4), 1-4.
  17. Gleeson, M. & Bishop, N. (2000). Elite athlete immunology: Importance of nutrition. International Journal of Sports Medicine, 21, Supplement 1, S44-S50.
  18. Guezennec, C., Satabin, P., Duforez, G., Koziet, J. & Antoine, J. (1993). The role of type and structure of complex carbohydrates response to physical exercise. International Journal of Sports Medicine, 14(4), 224-231.
  19. Hargreaves, M., McKenna, M., Jenkins, D., Warmington, S., Li, J., Snow, R. & Febbraio, M. (1998). Muscle metabolites and performance during high-intensity, intermittent exercise. Journal of Applied Physiology, 84(5), 1687-1691.
  20. Hargreaves, M., Kiens, B. & Richter, E. (1991). Effect of increased plasma free fatty acid concentrations on muscle metabolism in exercising men. Journal of Applied Physiology, 70(1), 194-201.
  21. Hausenblas, H. & Carron, A. (1999). Eating disorder indices and athletes: an integration. Journal of Sport & Exercise Psychology, 21, 230-258.
  22. Hawley, J., Schabort, E., Noakes, T. & Dennis, S. (1997). Carbohydrate-loading and exercise performance: An update. Sports Medicine, 24(2), 72-81.
  23. Haymes, E. & Clarkson, P. (1998). Minerals and trace minerals. In Berning, J. & Steen, S. (Eds.) Nutrition for Sport and Exercise. Gaithersburg, MD: Aspen.
  24. Johnson, R. (2000). Energy. In Mahan, L. & Escott-Stump, S. (Eds.) Food, Nutrition, and Diet Therapy. Philadelphia, PA: WB Saunders Co.
  25. Jonnalagadda, S. (2000). Cardiovascular disease and exercise. In Rosenbloom, C. (Ed.) Sports Nutrition: A Guide for the Professional Working with Active People. Chicago, IL: American Dietetic Association.
  26. Krummel, D. (2000). Nutrition in cardiovascular disease. In Mahan, L. & Escott-Stump, S. (Eds.) Food, Nutrition, and Diet Therapy. Philadelphia, PA: WB Saunders Co..
  27. Lemon, P. & Mullin J. (1980). Effect of initial muscle glycogen levels on protein catabolism during exercise. Journal of Applied Physiology, 48(4), 624-629.
  28. Leveritt, M. & Abernethy, P. (1999). Effects of carbohydrate restriction on strength performance. National strength & Conditioning Association, 13(1), 52-57.
  29. MacKinnon, L. (2000). Chronic exercise training effects on immune function. Medicine & Science in Sports & Exercise, 32(7), Supplement, S369-S376.
  30. McDonald, R. & Keen, C. (1988). Iron, zinc and magnesium nutrition and athletic performance. Sports Medicine, 5, 171-184.
  31. Mitchell, J., DiLauro, P., Pizza, F. & Cavender, D. (1997). The effect of preexercise carbohydrate status on resistance exercise performance. International Journal of Sport Nutrition, 7, 185-196.
  32. Pizza, F., Flynn, M., Duscha, B., Holden, J & Kubitz, E. (1995). A carbohydrate loading regimen improves high intensity, short duration exercise performance. International Journal of Sport Nutrition, 5, 110-116.
  33. Rankin, J. (2000). Dietary carbohydrate and performance of brief, intense exercise. Sports Science Exchange, 13(4), 1-4.
  34. Robergs, R., Pearson, D., Costill, D., Fink, W., Pascoe, D. & Benedict, M. (1991). Muscle glycogenolysis during differing intensities of weight-resistance exercise. Journal of Applied Physiology, 70(4), 1700-1706.
  35. Romijn, J., Coyle, e., Sidossis, L., Gastaldelli, A., Horowitz, J., Endert, E., & Wolfe, R. (1993). Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. American Journal of Physiology, 265, E380-E391.
  36. Roza, A. & Shizgal, H. (1984). The Harris-Benedict equation reevaluated: Resting energy requirements and body cell mass. American Journal of Clinical Nutrition, 40, 168-182.
  37. Shek, P., Sabiston, B, Buguet, A., & Radornski, M. (1995). Strenuous exercise and immunological changes: A multiple-time-point analysis of leukocyte subsets, CD4/CD8 ratio, immunoglobulin production and NK cell response. International Journal of Sports Medicine, 16, 466-474.
  38. Sherman, W. & Leenders, N. (1995). Fat loading: The next magic bullet? International Journal of Sport Nutrition, 5, S1-S12.
  39. Tarnopolsky, M., Atkinson, S., Phillips, S. & MacDougall, J. (1995). Carbohydrate loading and metabolism during exercise in men and women. Journal of applied Physiology, 78(4), 1360-1368.
  40. Tarnopolsky, M., Atkinson, S., MacDougall, J., Chesley, A., Phillips, S., & Schwarcz, H. (1992). Evaluation of protein requirements for trained strength athletes. Journal of Applied Physiology, 73(5), 1986-1995.
  41. Tipton, K., Ferrando, A., Williams, B., & Wolfe, R. (1996). Muscle protein metabolism in female swimmers after a combination of resistance and endurance exercise. Journal of Applied Physiology, 81(5), 2034-2038.
  42. U.S. Department of Agriculture (1992). The food guide pyramid. Home and Garden Bulletin No. 252. Washington, D.C.: U.S. Government Printing Office.
  43. Vandenberghe, K., Hespel, P., Eynde, B., Lysens, R. & Richter, E. (1995). No effect of glycogen level on glycogen metabolism during high intensity exercise. Medicine & Science in Sport & Exercise, 27, 1278-1283.
  44. Venkatraman, J., Leddy, J., & Pendergast, D. (2000). Dietary fats and immune status in athletes: Clinical implications. Medicine & Science in Sports & Exercise, 32(7), Supplement, S389-S395.
  45. Walton, P. & Rhodes, E. (1997). Glycaemic index and optimal performance. Sports Medicine, 23(3), 164-172.
  46. Weight, L. (1993). Sports anemia: Does it exist? Sports Medicine, 16(1), 1-4.
  47. Williams, M. (1999). Nutrition for Health, Fitness & Sport (5th ed.). USA: McGraw Hill.

Part 1 | Part 2