Image Map

by: Ryan Zeppelin
Performance Eating – Part II

In the first installment of Performance Eating, we looked at caloric requirements, caloric intake, and carbohydrate intake. In this installment, we will examine protein, fat, and hydration.

Part 4: Protein

Of all the nutrients, protein gets most of the press today, and for good reason. It is the nitrogen containing elements within that make them special. The structural component of protein is amino acids. There are 20 amino acids required by the human body for synthesis of bodyproteins. Nine are considered essential to the diet because they contain special carbon skeletons that cannot be synthesized by the human body. The essential amino acids must be consumed from dietary sources due to the body’s inability to produce them.

There are a variety of dietary sources from which proteins can be obtained. Both plant and animal sources can provide the essential amino acids if ample protein is consumed from a variety of foods. The body uses transamination to produce some of the limiting amino acids in the diet, except the nine that are considered nutritionally essential. This is a process in which amine groups are created and transferred to best meet the body’s requirements at the present time.

Amino acids, and thus proteins, differ from carbohydrates and lipids in that their basic structure involves an amine group containing nitrogen. The body can increase the chances that all 20 amino acids will be available when needed through a variety of dietary protein sources involving sufficient total protein and the nine essential amino acids.

Proteins function mainly as structural components and enzymes. Although exercise may increase amino acid oxidation, proteins play a very small role in energy production of healthy people during all exercise intensities [1-4]. Because of this fact, a low protein intake will most likely not directly affect exercise performance, but rather may result in impaired recovery abilities and reduced strength levels [5]. Exercise, especially resistance and long-duration exercise, may increase the dietary needs for protein [5,6]. The extra protein is needed for cellular repair and growth as a result of the exercise induced trauma.

For many years it was argued that increased protein intake above what was recommended for normal individuals, would have no impact upon growth. Many of these research studies failed to examine the overall training effect and the rationing of protein resources to the different bodily compartments. 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). When responding to a traumatic event, such as exercise, the body’s first response is survival and the second is growth. The body will use its positive nitrogen balance to repair the structures. When this is complete the remaining allotment, if any, will be used towards growth to resist future traumatic events.

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. The authors hypothesized that the increased work leads to the greater protein synthesis and not the relative intensities. Greater work performed generally increases the severity of the tissue trauma as a result of the activity, thus causing a greater demand to regain homeostasis and prevent future damage (growth). Tipton et al. also hypothesized that possibly adding additional swimming or resistance training would have had the same affect. 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 workload.

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 on either 0.86, 1.4, or 2.4 grams of protein per kilogram of body weight per day of dietary protein. The general recommendation by the American Dietetic Association is 0.8 g/kg per day for average individuals. 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 of body weight compared to the 0.89 for the sedentary group.

In general, the more activities an athlete is involved in causing a greater physical activity work level, the greater the requirement for protein. Tarnopolsky et al. (1992) also discussed the body’s ability to become physiologically accustomed to activities and therefore more efficient at using amino acids for cellular repair and growth. In essence, muscles become more efficient at using protein and the liver at exchanging amine groups.

Therefore, it is rare that the body will require higher than 2.0 g/kg/day of protein [6]. In general, a good guideline to follow regarding protein intake is 1.2-2.0 g/kg per day. A moderate exerciser will fall in the 1.2-1.5 g/kg range and the more intense athletes closer to 2.0 g/kg. Consuming protein above what is required for recovery and growth will not force the body to increase the level of muscle protein storage. Through hormonal regulation, the body dictates muscle growth — we only make it possible through nutrition.

During time periods of insufficient carbohydrate intake, the body, through reactions in the liver and kidneys, can create glucose or Krebs Cycle intermediates only from certain amino acids. This process, known as gluconeogenesis, is stimulated when the body senses a high glucagon to insulin ratio. Glucagon is a hormone responsible for the release of stored carbohydrates, where as insulin is responsible for increased storage. In response to insufficient circulating glucose, glucagon is released into the circulatory in an attempt to stimulate its release. As a survival priority, the body must use its limited amino acid pool, either free or that which is stored as muscle tissue, to create energy vital to CNS function.

Excess energy intake from carbohydrates, or also during periods of insufficient carbohydrate intake, the body can create fatty acids or ketone bodies for utilization. These substances are either utilized for energy production or stored for later use. As which is also the case regarding gluconeogenesis, only certain amino acids are available for these metabolic processes.

Protein quality is always of concern to athletes. This is very evident when examining the substantial protein powder industry that has developed over the past few years. There are a few methods of determining protein quality: Net protein utilization, Biological Value, Nitrogen Balance, Chemical score, and Protein efficiency ratio. Each of these uses a different method and thus different reference protein in determining quality. For example, the protein efficiency ratio uses casein and a chemical score compares to whole egg protein. The topic of proteins can be discussed for ages. Because complete proteins, which contain all of the indispensable amino acids in sufficient quantity, are most easily consumed from animal products, protein quality becomes a great concern regarding vegetarians, a topic within itself. One exception, gelatin, which is labeled as a protein and is from animal origin, is not a complete protein due to it lacking proper quantities of tryptophan. In the end, it is having the proper amino acids in sufficient quantities to repair and build tissue that is the critical issue. The best advice in this area is variety and quantity. Eat from a variety of sources in sufficient quantity and the body will develop.

Protein Sources

Mostly(Leanest complete protein choices.)
Sometimes(Higher saturated fat and/or cholesterol.)
Rarely(High fat and/or processing.)
Grilled/ baked chicken breasts
Round or sirloin beef/ buffalo/ VenisonBroiled/ baked/ boiled fishPork TenderloinTurkey breastEgg WhitesTuna, Salmon, Sardines, etc.


Whey & Casein Powders

Low Fat Cottage Cheese

80-90% lean ground. Meat
Chicken/ Turkey legs & thighsWhole Milk Cottage CheeseWhole EggsShellfish (Shrimp, lobster, crab)
Fried meats
Processed Luncheon MeatsNew York Strip & PorterhouseSausagesBaconBeef & Pork RibsPrime Rib


Part 5: Dietary Lipids

Lipids are the most concentrated forms of energy. Fatty acids contain approximately nine calories per gram compared to only four calories per gram for carbohydrate and protein. One 6-carbon glucose molecule when fully oxidized yields 38 ATP where as one 18-carbon fatty acid yields 147 ATP. This dense energy source has its limitations though. Fatty acids require aerobic metabolism to produce energy. The process of producing ATP via oxidative metabolism yields almost four times as much energy, but it requires 26 oxygen molecules to completely oxidize an 18-carbon fatty acid compared to the six oxygen molecules required to completely oxidize a 6-carbon glucose [8]. This affects substrate utilization during high intensity exercise with what appears to be a “coordination of effects on adipose tissue and muscle” (p. E272) [9]. There appears to be a relationship between free fatty acid (FFA) release from adipose tissue and glucose metabolism. Romijn et al. (1993) studied the affects of exercise intensity upon endogenous fat and carbohydrate metabolism using trained subjects. Results showed that as exercise intensity increases, the reliance upon lipids as an energy source decreases. 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 appear to be trapped in the adipose tissue by a variety of factors that also favor carbohydrate metabolism in the muscle cells [10]. Among these factors is the constriction of blood flow to adipose tissue by the body. This constriction limits the availability of oxygen to the adipose tissue for use in lypolysis 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 [10].

In contrast, during exercise at 65% VO2max, muscle triglycerides and plasma FFA made a significant contribution to energy expenditure. At intensities of 65%VO2max 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 [9,10,11]. Carbohydrate availability and utilization thus appears to somewhat regulate triglyceride release and oxidation during exercise [9,10,12].

Having relatively higher levels of FFA through intravenous methods was shown to not alter glycolysis, even at higher intensities [12]. 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 mechanisms of control. Long term diets that have very low lipid profiles could have negative consequences on performance by limiting triglyceride stores within the body for use as fuel [6].

Super low and high levels of dietary lipids can have many other negative health consequences. Lipids are major constituents in various bodily reactions. The four fat-soluble vitamins, A, D, E, and K, may be absorbed in limited supply if dietary lipids are restricted severely [11,13]. After longer periods 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 the eicosanoids. Eicosanoids are paracrine hormones produced in the local region of use [14]. Omega-3 and omega-6 essential fatty acids (EFFA) are the foundation for synthesis 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, and adhesion factors [14].

It has been shown that immune status can be negatively affected by a combination of strenuous exercise and a poor diet, including low lipid intake [15,16]. Shek, Sabiston, Buguet, and Rodornski (1995) studied the effects on the immune system of training at 65% VO2max for 120 minutes. The results suggested a potential period of leukocytosis, especially during the post-exercise period. T-cells were shown to be 60% of their pre-exercise level two hours post exercise. This period of decreased immune function potentially can leave athletes open to infection, which can reduce performance or restrict training levels.

Nutrient unavailability potentially can affect virtually all processes within the immune system because of the interrelated response of multiple mechanisms [15,16,18,19]. According to Venkatraman et al., “the role of lipids in the immune responses to exercise has been under appreciated” (p. S389). Realizing that athletes potentially 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. Types and quantity of dietary lipids potentially can affect risk factors for coronary heart disease (CHD). Atherosclerosis, the major underlying cause of CHD, is a slowly progressing process involving mainly deposits of fat, oxidized low-density lipoprotein (LDL), cholesterol, and macrophages which combine to form plaque in the endothelium of blood vessels [20]. LDL is one of four primary lipoproteins that travel in the blood stream 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 greatest implications to atherosclerosis. “Low-density forms of lipoproteins may predispose certain individuals to coronary heart disease whereas high-density forms may be protective (p. 137) [11]. LDL is approximately 45% cholesterol, which is required in limited supplies by cells. Excess cholesterol left in the circulatory system carried in LDL can become involved the plaque process [11].

Besides being a potential source of excess dietary calories, fats can have on impact on body composition through various factors. Hill et al. (1991) studied the effects of varied nutrient profiles on caloric expenditure. Each subject spent seven days each on three separate dietary profiles giving identical caloric intake: 60% calories from fat, 60% calories from carbohydrate, and 45% calories from fat. Results showed no alteration in caloric expenditure. However, each subjects’ metabolism showed an adaptation, or shift, more closely resemble the dietary intake. This study did not examine the effects of exercise, but prior evidence is clear that the activity energy requirements determine usage, not diet.

Because eating over 30% of calories from fats could be unhealthy to the cardiovascular, it is not recommended. This research does show that there is probably little difference between eating 15% calories from fats or 30% of calories from fats if the caloric intake is identical.

Another reason to limit caloric intake of lipids to less than 30% of calories is the corresponding results of the excess fat calories beyond what is needed. Horton et al. (1995) studied the effects of both excess carbohydrate and fat intake 50% above what was required. Overfeeding of carbohydrates resulted in 75-85% of the excess being stored where as 90-95% of the excess fat calories where stored. It appears that excess fat is more easily stored as adipose than excess carbohydrate. Even with a moderate shift in resting metabolism, it is easier for the body to store the lipids in adipose. The bottom line is to limit fats to a moderate level for health and a desired body composition make-up.

Because of the extremely anabolic nature of insulin, an understanding on lipids and their association with insulin sensitivity is warranted. Many research studies have surfaced in the past few years that show a relationship between the type of dietary fats consumed and insulin sensitivity.

Skeletal muscles appear to be the primary determinant regarding insulin sensitivity due to their very high role in caloric expenditure, and thus nutrient utilization. Modern research has shown a compounding relationship between saturated fats and a reduction in overall health. Not only can a high intake of saturated fats increase LDL and cholesterol levels, but they may also decrease muscular cell membrane insulin sensitivity.

Recently it has been reported that an increase in lipid membrane saturation is related to insulin insensitivity [23]. A decrease in insulin sensitivity can be associated with less substrate intake by the muscle cells and a subsequent greater amount of adipose storage. Vessby et al. (2001) studied this implication of dietary fatty acid intake on insulin secretion and sensitivity in 162 healthy human subjects for three months. Not only did the results show that a diet with a greater percentage of fat calories from monounsaturated sources to have result in higher insulin sensitivity, but also showed a decrease in LDL levels as compared to the higher saturated diets. These results were not recorded in higher fat diets over 37% of energy intake. Thus it appears that not only is the amount of calories consumed from fats important, but the type of fatty acids as well.
Cells can only use what they are supplied by the diet. If there is a very high level of saturated fats available, cellular structures will take on this orientation and in turn possibly reduce overall health.

Recommended Fat Intakes


Total Fat Calories
Monounsaturated Fat Calories
Polysaturated Fat Calories
Saturated Fat Calories
10-30% of total calories
10-15% of total calories
Up to 10% of total calories
< 5% of total calories
<100 mg per 1000 calories


Dietary Fat Basics

Some fatty acids, the basic unit of fat molecules, which are required by the body and are not able to be synthesized, and must be ingested in the diet. Linoleic acid and linolenic acid are two of these that are essential for normal cell growth and healthy skin. The best method of obtaining sufficient amounts of all types of fatty acids is to have plenty of variety in the food choices that are made.

There are five basic types of fatty acids highlighted; monounsaturated, polyunsaturated, saturated, omega-3, and trans-fatty acids.


  • Monounsaturated: These are fatty acids that are missing one hydrogen pair on their chemical chain and are generally considered important in lowering blood cholesterol levels. Foods with high levels are generally liquid at room temperature. Have a positive impact on insulin sensitivity and overall health and therefore is a preferred source of fat calories. Monounsaturated fats have a positive impact on HDL levels within the body.
  • Polyunsaturated: Foods with high levels are also generally liquid at room temperature. Polyunsaturated fats are missing two ore more hydrogen pairs on their chemical chains. Polyunsaturated is another preferred source for fat calories. Polyunsaturated fats have a healthy impact on LDL levels, but also tend to reduce HDL. For this reason, monounsaturated fats are preferred more over polyunsaturated.
  • Saturated: These fatty acids have all of the hydrogen possible and are generally firm at room temperature. Saturated fatty acids are known for their blood cholesterol raising properties. Primary sources are butter, meat, whole milk, and whole milk products. Saturated fats should be reduced for overall health and increased insulin sensitivity.
  • Omega-3: These fatty acids are highlighted, unlike Omega 6 and 9 oils, because they are typically consumed in the least amount in our diets. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) which are mostly found in higher fat seafood (albacore tuna, sardines, and salmon) and alpha-linolenic aid, found in lower amounts in some oils, such as flax and canola, omega-3 fatty acids are highly polyunsaturated. Most recently they have been highlighted for their heart healthy benefits of preventing vessel plaque build-up. Within the body, EPA and DHA can be synthesized from alpha-linolenic acid.
  • Trans-fatty: Formulated to increase shelf life and become solid at room temperature, trans-fatty acids are found primarily in margarine and vegetable shortening type products and also in baked goods. Although more research is needed, trans-fatty acids may be implicated in heart disease when consumed in excess.


The basic concept when it comes to dietary fat intake is to include a variety of sources, mostly in the form of monounsaturated and polyunsaturated fatty acids, and to limit the total intake to less than 30% of the total calories. Because of the required needs from carbohydrates and protein, most athletes will most likely naturally fall in the range of 10-20% of total calories, depending on caloric needs. Determine the total amount of calories to be eaten and then subtract the amount required from carbohydrates and proteins. The remainder of the calories may be obtained from fats, as long as it falls in the 10-30% range.


If you eat this many calories…

Fat calories no more than….

Fat grams no more than…



Fat Sources


(high mono/poly unsaturated; low saturated)
(moderate saturated fatty acids)
(high in saturated fatty acids)
*Canola Oil
Safflower Oil
Sunflower Oil
Soybean Oil
Cold Water Fish Oils
*Flax Oil
#Tub Margarine
#Stick Margarine
Peanut Oil
#Vegetable Shortening
Cottonseed Oil
Corn Oil
Chicken Fat
Palm Oil
Beef Fat
Cocoa Butter
Palm kernel Oil
Coconut Oil
Dairy Butter


* Best of the best! Highest alpha-linolenic acid contents.
Canola oil: 6% saturated fats, 22% linoleic acid, 10% alpha-linolenic acid, 62% monounsaturated fatty acids. Flax oil is 58% alpha-linolenic acid but has limited use in cooking due to poor heat stability and poor taste. Best used as a supplement.

# A case could be made to put these in the rarely category due to their traditionally high levels of partially hydrogenated fats. Look for items with low or no trans-fatty acids. Tub margarines have lower trans fatty acid contents than stick margarine or shortenings.

^ Dairy butter is a very poor choice of fats: 66% saturated fatty acids, 2% linoleic and alpha-linolenic acid, and 30% monounsaturated fatty acids.

Dietary and Blood Cholesterol

Technically cholesterol is not a dietary fat and does not contain any calories, but because it often appears with fat in meat and animal products, it becomes confusing. By using products consumed in the diet, our livers produce all the cholesterol that we need. Any extra cholesterol becomes converted into body fat or is left to buildup in the arteries. Dietary cholesterol does have an impact on blood cholesterol levels, but it appears that total fat and saturated fat intake can make an even greater impact. The best method to combat rising cholesterol levels is to eat a diet with a moderate to low total fat intake (10-30%), have a low saturated fat intake (less that 10% of fat calories), and to keep dietary cholesterol intake low (under 100mg/ 1000 calories). Plants do not produce cholesterol, so dietary cholesterol can only be ingested through products of animal origin. If you use any additional fats during preparation, the bast choices are low in saturated fat and are of plant origin. All of the oils listed in the “MOSTLY” category meet the criteria.

Part 6: Hydration

Water is vital to the function of the human body. About 40 to 60% of total body mass is water, with about 40% being within cells. Muscle mass is nearly 75% water, compared to only 50% of adipose tissue [24,25]. Within the body, the hypothalamus and kidneys are primary in regulating extracellular water osmolarity, and in turn, fluid homeostasis. Osmolarity refers to the balance of forces that control the movement of particles across membranes and is contingent upon the soluble products that are not able to freely permeate the membrane. The level of osmolarity is a signal for the regulatory systems that control hydration. When a decreased blood volume and increased osmolarity is detected, the systems respond by releasing a series of hormones, most notably anti-diuretic hormone, which increase the reabsorption of water and the sense of thirst. This demonstrates the fact that thirst is a good indicator of hypohydration, or dehydration, and to not wait until thirsty to consume liquids.

We receive water from three sources: foods, fluids, and as a metabolism byproduct. In a properly maintained system, fluid intake should constitute about one-half of water input. Water is lost through for general methods: urine, perspiration, exhaled air, and feces. During strenuous exercise and/or hot weather, perspiration through the skin can compromise 75% of the total output as compared to only 30-40% during normal temperatures with no exercise. This dramatic rise in perspiration is accompanied by a two to three fold increase in water output. This fact alone demonstrates the importance of proper hydration prior to physical activity.

The negative effects of improper hydration upon performance have been well documented. As early as the 1960’s and 1970’s exercise physiologists were establishing a relationship between poor hydration and decreases in performance within laboratory settings. More specifically, exercise physiologists noted decreased core temperatures and lowered heart rates during exercise when fluids were ingested within one hour of physical activity [26,27]. This is a direct result of a more efficient and productive period of physical activity.

In more recent times, the exact cause of hypohydration stress has been revealed. As the water deficit increases within both the intracellular and extracellular compartments, there is a decrease in cell tonicity and in blood volume [28]. These conditions, known as hypohydration and hypovolemia, decrease the body’s ability to disperse heat. As the body shuttles blood to the surface in an attempt to dissipate heat, there is a simultaneous reduction in cardiac output, metabolism, and therefore performance.

This same phenomenon has also been shown to reduce lactate threshold when hypohydration reached about 4% of bodyweight, even during thermally neutral environments with low humidity [29]. Participants showed not only an earlier lactate threshold, but it occurred with a lower VO2, ventilation equivalent, respiratory exchange ratio, rate of perceived exertion, and significantly lower blood lactate concentration. The reduction in ability to sustain a buffer to metabolic byproducts is an indication of increased strain leading to decreased performance.

Poor hydration status during exercise has been shown to decrease the extent of exercise-induced growth hormone (GH) release. Peyreign, C., Bouix, D., Fedou, & Mercier, J. (2001) showed significantly lower GH release after both 25 minutes and 40 minutes of sub-maximal cycling when no water was consumed during the activity. Besides its role in recovery and growth, growth hormone has been implicated in water retention at rest and sweat stimulation during exercise.

A similar fluid requirement may be needed in response to insulin growth factor 1 (IGF-1) release during physical activity [30]. When IGF-1 levels are high, as in response to exercise, blood viscosity decreases. This reduced fluidity is compounded by the concurrent reduction in hydration status due increased water output from sweating. These two factors may combine to limit the release of GH and thus the function of the GH-IGF-1 system.

To prevent the occurrence of hypohydration, it is critical for individuals to be properly hydrated prior to physical activity. Urine color seems to be the best method of tracking hydration status [31]. In a study by Armstrong et al. (1998), this method of tracking hydration worked just as well as other more technical measures. When proper hydration levels have been reached, urine should be a clear, relatively pale yellow color. The darker the yellow, the greater the hypohydration. It is important though to note the deficiency of this method during the post exercise period [32]. It appears that during the period up to 6-hours post exercise, the best method of insuring rehydration is to match body weight loss with fluid intake [33]. Simply weigh yourself both pre and post activity and match the difference with fluid intake.

It is also important to balance fluid intake with substrate and electrolyte intake. Due to the high loss of sodium and other electrolytes in sweat, the body will also suffer concurrent loses of vital nutrients. In conditions of excessive fluid loss, it becomes extremely vital to not only ingest water, but also sodium and other electrolytes. Sodium inclusion can decrease to fluid output and increase the rate of restoration [34].

In an attempt to combat the excessive fluid loss, the ingestion of water only can lead to hyponatremia. Clinical hyponatremia occurs when serum sodium levels fall below 136 mEq per liter. This generally only occurs during activities lasting 4-hours or more. Performance and recovery can be impaired as the body approaches this low level. Symptoms include headaches, confusion, and nausea. Severe sodium deficiencies can lead to seizures, coma, and even death.

Rehydration Strategies

Plain water appears not to be the ideal method to restore hydration status both during and post activity. The inclusion of carbohydrates and sodium has a positive effect upon fluid utilization and performance. First, the availability of energy substrates in the form of carbohydrates can maintain metabolic processes. Second, the inclusion of electrolytes will replace those lost from sweating and will aid in the absorption of the fluid [35,36]. This method showed greater recovery than from water alone.

When including carbohydrates, the level of solution is important to insure proper gastric emptying during activity. Murray et al. (1999) studied the effects of varied carbohydrate concentration upon gastric emptying during exercise. When concentration levels reached 8%, gastric emptying was significantly reduced as compared to 4% and 6% while cycling. Reduced gastric emptying will translate in possible uncomfortable feelings and reduced substrate availability. Many non-carbonated sports drinks are formulated to meet this standard.

Fluid Intake Guidlines



Non-Activity Period
Prior to Activity
During Activity

Drink at least 10-12 cups of water (about 1 oz. per kg of bodyweight) to
ensure proper functioning. Try to drink on more of a schedule, rather than
just when eating or thirsty.

16 oz water (part of the non-activity period) within one hour of activity

Drink 4-6 oz every 15 minutes, more if during hot and/or humid environment,
with electrolytes and a 2-8% concentration of simple carbohydrates
Match weight loss during exercise with equal amount of fluid ingestion: include electrolytes and carbohydrates



1. 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.

2. Gibala, M. & Hargreaves, M. (2000). Amino acids, proteins and exercise performance. Sports Science Exchange Roundtable, 11(4), 1-4.

3. 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.

4. Lemon, P. & Mullin J. (1980). Effect of initial muscle glycogen levels on protein catabolism during exercise. Journal of Applied Physiology, 48(4), 624-629.

5. 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.

6. 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.

7. 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.

8. Sherman, W. & Leenders, N. (1995). Fat loading: The next magic bullet? International Journal of Sport Nutrition, 5, S1-S12.

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. 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.

11. Williams, M. (1999). Nutrition for Health, Fitness & Sport (5th ed.). USA: McGraw Hill.

12. 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.
13. Combs, G. (2000). Vitamins. In Mahan, L. & Escott-Stump, S. (Eds.) Food, Nutrition, and Diet Therapy. Philadelphia, PA: WB Saunders Co.

14. 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.

15. Bishop, N., Blannin, A., Walsh, N., & Robson, P. (1999). Nutritional aspects of immunosuppression in athletes. Sports Medicine, 28(3), 151-176.

16. 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.

17. 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.

18. Gleeson, M. & Bishop, N. (2000). Elite athlete immunology: Importance of nutrition. International Journal of Sports Medicine, 21, Supplement 1, S44-S50.

19. MacKinnon, L. (2000). Chronic exercise training effects on immune function. Medicine & Science in Sports & Exercise, 32(7), Supplement, S369-S376.

20. Krummel, D. (2000). Nutrition in cardiovascular disease. In Mahan, L. & Escott-Stump, S. (Eds.) Food, Nutrition, and Diet Therapy. Philadelphia, PA: WB Saunders Co..

21. Hill, J., Peters, J., Reed, G., Schlundt, D., Sharp, T. & Greene, H. (1991). Nutrient balance in humans: effects of diet composition. American Journal of Clinical Nutrition, 54(1), 10-7.

22. Horton, T., Drougas, H., Brachey, A., Reed, G., Peters, J. & Hill, J. (1995). Fat and carbohydrate overfeeding in humans: different effects on storage. American Journal of Clinical Nutrition, 62(1), 19-29.

23. Vessby, B. (2000). Dietary fat and insulin action in humans. British Journal of Nutrition, 83(S1), S91-6.

24. Vessby, B., Unsitupa, M., Hermanse, K., Riccardi, G., Rivellese, G., Rivellese, A., Tapsell, L., Nalsen, C., Berglund, L., Louheranta, jA., Rasmussen, B., Calvert, G., Maffetone, A., Pedersen, E., Gustafsson, I., & Storlien, L. (2001). Sustituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU study. Diebetologia, 44(3), 312-9.

25. Groff, J. & Gropper, S. (2000). Advanced Nutrition and Human Nutrition (3rd ed.). Belmont, CA: Wadsworth.

26. McArdle, W., Katch, F. & Katch, V. (1996). Exercise Physiology. (4th ed.). USA: Williams & Wilkins.

27. Greenleag, J. & Castle, B. (1971). Exercise temperature regulation during hypohydration and hyperthermia. Journal of applied Physiology, 30, 847-85.

28. Moroff, S., & Bass, D. (1965). Effects of overhydration on man and physiological responses to work in the heat. Journal of Applied Pysiology, 20, 267.

29. Sawka, M., Montain, S. & Latzka, W. (2001). Hydration effects on thermoregulation and performance in the heat. Comparative Biochemistry and Physiology; Part A, Molecular and Integrative Physiology,128(4), 679-90.

30. Kenefick, R., Mahood, N., Mattern, C., Kertzer, R. & Quin, T. (2002). Hypohydration adversely affects lactate threshold in endurance athletes. Journal of Strength and Conditioning Research,16(1), 38-43.

31. Peyreign, C., Bouix, D., Fedou, C., & Mercier, J. (2001). Effect of hydration on exercise-induced growth hormone response. European Journal of Endocrinology, 145(4), 445-50.

32. Monnier, J. F., Benhadad, A., Micalief, J., Mercier, J, & Brun, J. (2000). Relationships between blood viscosity and insulin-like growth factor one status in athletes. Clinical Hemorheology, 22(4), 277-86.

33. Armstrong, L., Herrera, J., Hacker, F., Casa, D., Kavouras, S. & Maresh, C. (1998). Urinary indices during dehydration, exercise, and rehydration. International Journal of Sport Nutrition,8(4), 345-55.

34. Kovacs, E., Senden, J. & Brouns, F. (1999). Urine color, osmolality and specific electrical conductance are not accurate measures of hydration status during postexercise rehydration. Journal of Sports Medicine and Physical Fitness,39(1), 47-53.

35. Murray, R. (1998). Rehydration strategies- balancing substrate, fluid, and electrolyte provision. International Journal of Sports Medicine, 19 (supplement 2), s133-5.

36. Rehrer, N. (2001). Fluid and electrolyte balance in ultra-endurance sport. Sports Medicine, 31(10), 701-15.

37. Bilzon, J., Allsopp, A. & Williams, C. (2000). Short-term recovery from prolonged constant pace running in a warm environment: the effectiveness of a carbohydrate-electrolyte solution. European Journal of applied Physiology, 82(4), 305-12.

38. Galloway, S. & Maughan, R. (2000). The effects of substrate and fluid provision on thermoregulatory and metabolism response to prolonged exercise in a hot environment. Journal of Sports Science, 18(5), 339-51.

39. Murray, R., Bartoli, W., Stofan, J., Horn, M. & Eddy, D. (1999). A comparison of the gastric emptying characteristics of selected sports drinks. International Journal of Sport Nutrition, 9(3), 263-274.