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What nutrients should an energy gel contain?

 

PREFATORY REMARKS REGARDING INDIVIDUAL BIOCHEMISTRY & THE COMMON PHYSIOLOGY OF EXERCISE METABOLISM
The answer to this question depends on length of the event for time necessary to transit for depleted/stressed macronutrients and micronutrients. In an endurance event lasting 12 hours or less, fluids, carbohydrate fuels and specific electrolytes may have performance-limiting effects if not replenished. In those events lasting longer than 12 hours, it is required that the athlete replenish depleted macronutrients and micronutrient during the event, proportionate to time, rate, and individual athlete's biochemical makeup, in order to postpone failure.

1. CARBOHYDRATES ARE THE PERFORMANCE LIMITING ENDURANCE FUEL
Carbohydrate fuel glycogen stores are the first to go within 60-85 minutes. Pro-Trainer Jim Bruskewitz suggests recovery losses from post-exhaustive training as follows [1, 2, 3]:

Removal of 90% lactic acid from a muscle cell
1 1/2 minutes
Repayment of a lactic acid oxygen debt
5 minutes
Repayment of lactic acid debt
30-60 minutes
Removal of lactic acid from muscle and blood
1-2 hours
Restoration of muscle glycogen
10-48 hours
Restoration of vitamins and enzymes
24 hours
Recovery from high intensity strength training
2-3 days

An event lasting 12 hours or less will not permit adequate restoration of vitamins, some of the enzymes or complete recovery. The science of nutrition in relation to sports performance has progressed from empirical studies investigating the effects of dietary manipulations, such as restriction and supplementation, to the direct investigation of the physiological basis of the specific nutritional demands of hard physical exercise. One such review is based on the premise that the best clues to ideal nutrition for athletic performance come from what comes out rather than what goes in. Various aspects of the physical demands of athletic exercise are viewed as stresses that induce specific biochemical, and hence nutritional, strains in the athlete.

Training is the predominant demand in the athletic lifestyle. This is characterized by acute bouts of high power output. During one hour of hard training an athlete may expend 30% of his or her total 24-hour energy output. These high power outputs have important implications for energy substrate and water requirements. Carbohydrate, specifically muscle glycogen, is the obligatory fuel for the high power outputs demanded by athletic sports. Muscle glycogen is a limiting factor in hard exercise because it is held in limited amounts, and utilized rapidly by intense exercise. Fatigue occurs when muscle glycogen is depleted to low levels in the active muscles. Liver glycogen may also be exhausted by hard exercise and low blood glucose contributes to fatigue. High sweat rates are demanded during severe exercise and large water deficits commensurate with energy expenditure are incurred during extended periods of hard training and competition. Salt, potassium and magnesium are lost in nutritionally significant amounts in the sweat, but vitamins and trace elements are not.

Carbohydrate fuel (CHO) is a performance-limiting or performance-enhancing macronutrient fuel in all forms of endurance exercise. Carbohydrate misuse, overuse, under use, timing and confusion continue to plague endurance athletes, interfering with their maximal performance. Misinformed, athletes continue to errantly misuse simple sugars or too much complex carbohydrates prior to exercise, during exercise and after exercise.

2. WHAT TYPE OF SUGAR DO WE USE?

Hammer Nutrition & HAMMER NUTRITION LTD. ADDS "NO SIMPLE SUGARS" TO THE MACRONUTRIENT PRODUCT PROFILE
The carbohydrate profile of the long chain complex carbohydrates used in these products contains no added simple sugar sweeteners. The long chain maltodextrins selected for Hammer Gel presents a 7.4% mono- and di- saccharides, which are interpreted as simple sugar content compared to 92.6% long-chained carbohdyrates.

Simple sugars such as sucrose, fructose and galactose double the osmolality, draw fluids and electrolytes from the exercising athlete's system, across the stomach lining, often inducing gastric stress, cramps, flatulence and premature fatigue. Sugar is defined as a monosaccharide or a disaccharide. The shorter the chain length a carbohydrate is, the higher it raises the solution osmolality in the stomach. Simple sugar must be mixed in weak 6-8% solutions or they will sit undigested in the stomach and not pass the gastric lining, possibly creating sour stomach, cramps or flatulence. Maltodextrin is a multiple of sugars hooked together, allowing from 18% to 24% solution immediately in transit to the liver where it is turned back to the energy cycle as muscle glycogen. The Amylose-Amylopectin content of maltodextrin and potato starch are very similar in their chemistry to human stored glycogen. Therefore the gold-standard carbohydrate source for energy drinks, bars or gels originates from longer-chain carbohydrates (Maltodextrins) because more caloric volume crosses gastric lining with less distress to the competing athlete. Body fluid osmolar pressures change when the temperature and humidity excrete endogenous electrolyte stores. During hyperthermic conditions (above 70 degrees & 70% humidity) electrolyte loss or imbalances induce dilutional hyponatremia.

Adding the right combinations of electrolytes with Vitamin B-6 and L-Tyrosine may enhance absorption. Diluting CHO mixtures lower than body-fluid osmolar levels further induces a positive transition rate of gastric emptying, especially when stressed sodium electrolytes are lost in evaporative cooling. Simple sugars such as sucrose and fructose double the osmolality, draw fluids and electrolytes from the exercising athlete's system, across the stomach lining, often inducing gastric stress, cramps, flatulence and premature fatigue.

3. HOW SHOULD A PERSON REPLACE ELECTROLYTES AND FLUIDS DURING ENDURANCE EFFORTS?

LIMITED ELECTROLYTE DEPLETION IS TIME-INDUCED, WET-BULB TEMPERATURE-DEPENDENT

With the application of a low sodium electrolyte replacement, the body is permitted to adapt by trial and error using a sodium intake of 80-240 mg. per hour when accompanied by complimentary electrolytes. One rationale argues for including chloride, potassium, magnesium, manganese, L-Tyrosine, and Vitamin B-6 in order to reduce sodium depletion rate by enhancing natural body hormones to spare fluids and sodium simultaneously.[7] When conditioning has achieved both fitness and hyperthermic acclimatization, the use of a hypotonic solution of long chain carbohydrates at the rate of 240-280 calories per hour in a 16-24 fluid ounce solution each hour with a low-sodium electrolyte form may sustain endurance performance rate indefinitely at a 60-75% VO2 Max aerobic pace.

Sodium is a mineral. The main dietary source of sodium is common table salt (sodium chloride) which is 40% sodium and 60 chloride, but regular unprocessed foods contain natural sodium as well. Meat, fish, poultry, eggs, milk and cheese all contribute sodium. The dietary guidelines for healthy American adults recommend limiting dietary intake to less than 2400 milligrams (mg) per day. (1 teaspoon of salt contains about 2400 mg of sodium) The human body needs very minute amounts of sodium to function normally. We need only 250 mg of sodium each day, athletes maybe 500 mg., which is easily supplied by natural, unprocessed foods; however, the average American consumes approximately 6000 to 7000 mg per day. In Asian diets, the sodium intake can climb to over 8000 mg per day. High sodium intake is linked to high blood pressure. For some people, high sodium diets can also cause fluid retention and swelling in the feet, face, eyes and hands. Humans regulate water, salt and H+ balances primarily through kidney functions. Reabsorption in distal tubule (summarized as variations in sodium) is controlled by aldosterone hormone release. As adrenal cortical hormones increase, renal reabsorption of sodium ions and water increases body sodium and water. Chloride follows passively, while water volume recirculated and controlled by the hormone, vasopressin, which is released from the anterior pituitary neurons with cell bodies in the hypothalamus (in the paraventricular and supraoptic nuclei) secrete vasopressin from their terminals on blood vessels in the posterior pituitary. The sodium and other electrolytes required may differ greatly. Evidence has been reviewed and is on file from a variety of blood lab values taken before and after an ultramarathon substantiating one athlete's need for one electrolyte per hour while other athletes require six to eight of the same supplement in order to avoid electrolyte depletion. The adaptation of human physiology to electrolyte losses in extreme endurance events is sensitive, predictive and must be replenished for resolution. The highest endurance athlete's intake of sodium observed over the past 17 years was a ultramarathon runner who reported the need to take 1000 mg. sodium per hour during the last half of a 100-kilometer ultramarathon. The lowest endurance athlete's intake of sodium observed was one ultramarathoner runner who reported taking only 13.3 mg. sodium per hour all they way through a 100-mile ultramarathon. The later finished well, while the former won the race. This demonstrates successful individual upper and lower sodium tolerances by a factor of 10X! Most athletes perform successfully using from 80-300 mg. sodium per hour in prolonged endurance events. Why is this and what are the mechanisms which support replenishing electrolyte losses with a low-sodium formula?

MECHANISMS REGULATING SODIUM EXCRETION IN KIDNEYS
They are very complex and lengthy, but follows some of those mechanisms in which a low-sodium electrolyte is shown not to interfere with hormonal regulatory influences but rather supports the body's natural biochemistry. Adrenocorticotropin hormone (ACTH) is secreted by the basophillic corticotrophs that are usually situated in the anteromedial part of the pituitary gland. ACTH stimulates the production of glucocorticoids, mineralocorticoids and androgenic steroids. These are collectively known as corticosteroids. The mineralocorticoids are secreted from the parenchymal cells of the zona glomerulosa which function in maintaining a normal metabolite balance.

ALDOSTERONE
It is the most potent mineralocorticoid as it counts for 95% of activity in this class of corticosteroids. They aid in controlling electrolyte homeostasis by acting on the distal tubule cells of the kidney to increase sodium re-absorption and decrease potassium resorption.

PHYSIOLOGY RATIONALLY SUGGESTS A LOW SODIUM ELECTROLYTE.
The following function in maintaining the osmotic balance in the urine and prevent serum acidosis:

  1. Control of filtration rate in kidney
    1. Increasing filtration rate causes an increase in Na+ filtration and hence Na+ excretion; water is excreted along with the Na+, so extracellular fluid(ECF) volume decreases.
    2. decrease in filtration rate leads to decrease in Na+ filtration and excretion; Na+ and associated water conserved, which leads to an increase in ECF volume.
  2. Control of Na+ reabsorbed in kidneys
    1. In proximal tubule and loop of Henle, a constant percentage of filtered Na+ is reabsorbed, regardless of the absolute amount present.
    2. In the distal tubule, Na+ reabsorption is regulated.
    3. Primary positive regulation system is the renin-angiotensin-aldosterone system.
  3. If Na+ levels fall (which causes a decline in ECF volume and blood pressure), the juxtaglomerular apparatus secretes the hormone renin into the blood.
  4. Renin activates angiotensinogen by converting it to angiotensin I, which is then converted to--->#3.
  5. Angiotensin II by angiotensin converting enzyme produced by the lungs.
  6. Angiotensin II then stimulates the adrenal cortex to secrete 5.aldosterone, which increases Na+ reabsorption in the distal and collecting tubules by adding more Na+-K+-ATPase pumps to the basolateral membranes.
  7. This promotes Na+ retention, and so increases ECF volume and arterial blood pressure
  8. Angiotensin II also is vasoconstrictor, stimulates thirst and stimulates vasopressin (which induces water retention by the kidneys) which result in an increase in ECF volume and arterial blood pressure.

CONTROLLING WATER BALANCE IS ALSO PART OF THE OSMOLAR PRESSURE MECHANISM AND IS CLOSELY RELATED TO THE SODIUM ELECTROLYTE BALANCE ISSUE

(ECF=Extracellular Fluids, ICF=Intercellular Fluids)
Regulation of ECF Osmolarity: Controlling Water Balance A. Purpose: Regulation of ICF Osmolarity B.How ECF osmolarity (mg solutes/ml fluid) affects ICF osmolarity.

  1. ECF hypertonicity (usually by dehydration) leads to ICF hypertonicity because water moves from ICF to ECF by osmosis. This causes cells to shrink which can lead to mental impairment and circulatory shock.
  2. ECF hypotonicity (usually overhydration) leads to ICF hypotonicity because water moves by osmosis from ECF to ICF. This can lead to brain dysfunction and muscle weakness.
  3. Isotonic fluid loss (usually by hemorrhage) occurs when water and solutes are lost together. This does not impact ICF volumes, but does lead to a decline in ECF volume.

MECHANISMS OF WATER REGULATION

  1. Hypothalamic osmoreceptors monitor ECF osmolarity and initiate responses.
  2. High osmolarity = hypertonic (too little water) a.Vasopressin released and thirst stimulated; the vasopressin causes the kidneys to reabsorb more water so less is lost in the urine, and being thirsty causes you to drink more water. Urine still produced, but it has a very high concentration of solutes (maximum of 1200 mosm/l).
  3. Low osmolarity = hypotonic (too much water) a.Vasopressin release inhibited; thirst inhibited and reabsorption of water in the kidneys slowed or discontinued. Urine produced has a low concentration of solutes (minimum of 100 mosm/l).

A SIMPLIFIED VERSION FOR ENDURANCE APPLICATION.
The average 154 lb. person has two compartments filled with 85 lbs.(total) of fluids that must be kept in constant osmotic balance. Inside our cells where potassium ions are 15 times higher than outside, 25 liters of water (53 lbs.) is stored in homeostatic balance with more water stored outside cell walls. Outside the cells, sodium ions are ten times higher than inside, an additional 15 liters or 32 more lbs. of water are stored. When the temperature is high a runner can lose up to 2.2 pounds of water per hour, which is two percent of a tiny 110 lb. person or one percent of the larger athlete! Symptoms that have been observed when a percentage body water weight is lost are as follows [5]

0%
normal heat regulation and performance
1%
thirst is stimulated, heat regulation during exercise is altered, performance declines
2%
further decrease in heat regulation, increased thirst, hinders performance
3%
more of the same (worsening performance)
4%
exercise performance cut by 20 - 30%
5%
headache, irritability, "spaced-out" feeling, fatigue
6%
weakness, severe loss of thermoregulation
7%
collapse is likely unless exercise is stopped
10%
comatose
11%
death likely

When an athlete loses up to three percent body water weight of their valuable life-giving fluids from evaporative sweat cooling, performance begins to suffer dramatically. After a five percent water-weight loss, mental concentration is impossible, following a ten percent body weight loss of fluids the athlete loses consciousness; a loss of an additional 1 percent could result in death.

Exercise in thermic conditions dramatically effects our normal tissue-fluids state of being [6, 7]:

NON-EXERCISE
EXERCISE IN THE HEAT
INTAKE
URINE -1400 ml.
-500 ml.
FLUIDS+1500 ml.
SKIN -350 ml.
-350 ml.
FOOD + 800 ML.
BREATHING -350 ml.
-650 ml.
SWEAT -100 ml.
-5000 ml.
 
FECES -100 ml.
-100 ml.
TOTAL -2300 ml.
-6600 ml.
+2300 ml.(Normal)
TOTAL FLUID LOSSES = -4300 ml.(Exercise-induced)

Normal activity shows a daily balance, but add exercise to the model, resulting in a nine lbs. water weight deficit or nearly six percent of the original 154 lb. athlete's total body weight! Dr. David C. Nieman, Ph.D. describes a six percent loss as very serious, causing impairment in temperature regulation and rapidly increasing heart rate.[8] Water is most efficiently replaced by distilled water or water that has been precisely modified with a low-sodium electrolyte profile. Sodium is lost more rapidly than fluid volume.

The more fluid lost, the more sodium and electrolyte stores are depleted. Rapid replacement of sodium neutralizes the body's hormonal defenses, allowing water replenishing to dilute sodium content. A high sodium electrolyte supplement is temporal and contradictory to natural physiological serum electrolyte control. High sodium or high electrolyte fluids are also held longer in the vascular compartments than the lower sodium-electrolyte composite. One reason salt tablets were eliminated from professional athletic training kits is that shortly after a sodium-depleted athlete would slug a few salt tablets, stomach cramps would bend them over double. One report suggests however, that total correction or over correction of sodium solution may result in irreversible damage to the brain.[9] Why is this and what causes these pressure gradients to occur?

BODY FLUID OSMOLAR PRESSURES CHANGE IMPACT PERFORMANCE
Equilibrium solutes concentrations of osmotic pressures occurs at 300 milliosmoles per liter(mOsm/l.) When a change in the pressure of the solutes or electrolytes vary, correction of the pressure deviance will occur in a single cell in less than 60 seconds! When the whole body is out of equilibrium with as little as a three percent fluid loss, it takes up to 30 minutes of NO activity at normal body temperatures, using a perfect fluid-electrolyte replenishment drink to restore osmolarity to 300 mOsm/l to the human body's 40-liter intra- and extra-cellular fluid content inside a typical 154 lb. athlete exercising in thermic conditions.

The internal biochemistry of each individual differs based on genetics, fitness, acclimatization, core body temperatures, blood-serum fluid volume and electrolytes. Kidneys filter 180 liters of the body vascular fluids per day, but returns 99% of its filtrates, while eliminating only 1-1.5 liters as waste water. These magnificent filters help us maintain a constant internal 300 mOsm/l osmolarity. When body biochemistry senses a + or - 3three percent solute change, the following mechanisms may be called upon to assist the kidneys in osmolarity balance:

  1. The Pituitary secretes ADH (Anti-Diuretic Hormone) enabling water to be re-absorbed, sensing it is too concentrated.
  2. The adrenal glands secrete aldosterone when sodium concentration in plasma is low, causing sodium to be reabsorbed producing a more diluted urine.
  3. An osmolarity rise of one percent may cause a thirst craving for drinking fluids and diluting blood serum-urine concentrates.

All of these control mechanisms are sensitive to a + or - three percent deviation in sodium and a + or -7% deviation in potassium, while calcium levels are also monitored in the extracellular fluids within a few percents by secretions of the parathyroid. It's interesting to note that normal healthy body fluids in saliva, gastric juices and small intestine produce a 7:3 ratio** of potassium to sodium, similar to the number deviation which triggers control mechanism restoring normal electrolyte-fluid osmotic balance. Under normal conditions (during non-exercise) intake of a liter of water will cause eight times the normal urine output within 45 minutes lasting up to 120 minutes after intake. Want to know if you are properly pre-race hydrated? To measure hydration before an exercise or after, consume a liter of water, then measure urine output from 45-120 minutes. Dehydration signs present proportionate to darkness scale of urine color.

OTHER BODY FLUID ELECTROLYTE PROFILES[6]
(8 fluid ounces=240 ml.)

  1. SALIVA is produced at the rate of 800-1500 ml./day, composed of 3000-4000 mg. Bicarbonate, 1170 mg. Potassium, and 877 mg. Sodium Chloride.
  2. GASTRIC JUICE is produced at the rate of 1500 ml/day composed of 5600 mg. HCL, 1120 mg. Potassium Chloride and 175 mg. Sodium Chloride.
  3. SMALL INTESTINE requires Pure Water 1800 ml/day from Extracellular fluids. All three require low amounts of sodium replenishment.

MAXIMAL ELECTROLYTES RATE LOSS-(g/L./HOUR)
Sweat losses generate large losses in sodium and chloride, which are re-circulated by a positive feedback loop monitored closely through hormonal receptors throughout the body. It is interesting to note that the adaptively-trained, acclimatized athlete loses considerably less sodium than the unfit, unacclimatized person, evidence for the adaptive feedback loop in action.

FIT-ACCLIMATIZED
FIT-UNACCLIMATIZED[7, 10]
SODIUM 1.8 g/l
2.60 g/l
CHLORIDE 0.9 g/l
1.10 g/l
POTASSIUM 0.1 g/l
0.15 g/l
MAGNESIUM 0.1 g/l
0.10 g/l

With the application of a low sodium electrolyte replacement, the body is permitted to adapt by trial and error using a sodium intake of 80-240 mg. per hour when accompanied by complimentary electrolytes. One rationale argues for including chloride, potassium, magnesium, manganese, L-Tyrosine, and Vitamin B-6 in order to reduce sodium depletion rate by enhancing natural body hormones to spare fluids and sodium simultaneously.[7] When conditioning has achieved both fitness and hyperthermic acclimatization, the use of a hypotonic solution of long chain carbohydrates at the rate of 240-280 calories per hour in a 16-24 fluid ounce solution each hour with a low-sodium electrolyte form may sustain endurance performance rate indefinitely at a 60-75% VO2 Max aerobic pace.

REFERENCES
[1, 2, 3]-Courtesy of Mr. Jim Bruskewitz, ep@home.com, professional trainer.

  1. A-Bompa, T.O. (1994), Theory and Methodology of Training. Dubuque, Iowa: Kendall/Hunt Publishing Inc.
  2. B-Fry, R.W., R. Morton, and D. Keast. (1991), "Overtraining in Athletics." Sports Medicine, 2(1):32-65.
  3. Kuipers, H. and H.A. Keizer. (1988), "Overtraining in Elite Athletes: Review and Directions for the Future," Sports Medicine,6:79-92.
  4. Nutrition and Sports Performance. Brotherhood JR, Sports Med 1984 Sep-Oct 1:5 350-89.
  5. Grandjean & Ruud, Clinics in Sports Med. Vol 13(1);235-246. Jan 1994.(Nutrition for Cyclists)
  6. TEXTBOOK OF MEDICAL PHYSIOLOGY, AL Guyton, WB Saunders, 1991.
  7. Misner WD, NUTRITION FOR ENDURANCE: FINDING ANOTHER GEAR, Dolezal & Associates, Livermore, Calif.,1998: 264-274.
  8. Nieman DC, SPORTS MEDICINE FITNESS COURSE, Bull Publishing, Palo Alto Calif., 1986.
  9. Knochel, JP, Hypoxia Is the Cause of Brain Damage in Hyponatremia, JOURNAL OF AMERICAN MEDICAL ASSOCIATION, 1999;281:2342-2343.
  10. Verde T, et al., Sweat composition in exercise and heat, J Appl Physiol, 53{6}:1541-1543.


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