Nutrition/Metabolism Capstone Review

Optimal nutritional management of geriatric horses.

-Feed to maintain BCS -Monitor and adapt to dentition -Adjust form of feed as needed (pellets, soaked food, be cautious with older horse on pasture).

What are post-mortem characteristics of starvation?

1. Dead animals with atrophy of fat stores: grossly fat atrophy manifest as "serous atrophy fat" = watery quality and slightly dark tint imparted to fat stores. Look for this on epicardial grooves, perirenal fat stores, surface of thoracic wall. Also dirt and debris may be present and indicate animal was foraging for food.

What are appropriate interventions for canine "urine burn" of grass lawns?

1. Feed high BV (biological value) protein dog food - less urea. 2. Increase water intake to dilute the urea in urine: canned dog food, moistened dry dog food, add salt to food (careful, increased blood volume is touch on older hearts). 3. Change the turf to more resistant grasses. 4. Train dog to pee in certain areas.

What are the advantages and disadvantages for the various methods of enteral feeding tube placement in critical care patients, including risks and contraindications?

1. Nasopharyngeal - should not go into stomach; can buildup fluids that will lead to stricture healing of esophagus. Can only use liquid diets; does not require general anesthesia for placement. 2. Pharyngostomy - same cons as nasopharyngeal 3. Esophagostomy - same as the first two 4. Gastrostomy - used with patients with a functioning GI tract who cannot/won't eat on their own; and if anorexia expected to last for weeks/months; requires anesthesia for placement --> can be placed endoscopically or surgically; well-tolerated by most patients. 5. Enterostomy - need to bypass the stomach; vomiting, surgery or pancreatitis patients. Place in duodenum or jejunum; done during exploratory laparotomy; requires liquid diets.

The metabolic adaptations to a high-fat diet in the canine athlete

Ingestion of high fat diet during training alters metabolism to favor endurance. Increased circulating FFA, increased VO2 max, increased max rate fat oxidation, increased mitochondrial density, muscle glycogen sparing. Dogs fed high fat diet can run faster and longer than dogs fed a low fat diet.

What is the dietary management of patients with cutaneous adverse food reactions (CAFR)?

It is best to use a novel protein/carb - either commercial or homemade. Hydrolyzed proteins - breakdown of proteins so that the body doesn't react to it - cannot crosslink. Or use anallergic diets which eliminates epitopes. Elimination diets require a minimum of 8 weeks, and is considered a diagnostic test (what are you NOT feeding?).

Clinical signs of exocrine pancreatic insufficiency

diarrhea, weight loss, polyphagia

Discuss the causes and signs of hypophosphatemic rickets in young New World Camelids

Rickets is another disease characterized by hypophosphatemia. Clinical signs: - lameness - inactivity Causes: - camelids at lower elevations and with pigmented skin are unable to get UV light and are unable to activate vitamin D precursors. Treatment: - Supplemental Vitamin D - more is not better!!

What are diagnostic methods that can be used to diagnose CAFR?

Signs mimic non-seasonal atopy - pruritis, otitis, secondary infections, +/- GI disturbances, urticarial. It is mostly a diagnosis of exclusion - check for ectoparasites, mites, FAD, and use elimination diets (>8 weeks).

Discuss pathogenesis and clinical signs of pregnancy toxemia in ruminants.

"Twin lamb disease" -another disease state caused by chronic negative - energy drain here is the fetuses. -70% of fetal growth takes place in last 40-50 days (the last trimester) -energy drain most pronounced with twins, triplets. -little room in abdominal cavity for the rumen. -This disease occurs when late pregnant ewe or doe cannot or does not eat enough to meet energy demands (fed low energy feeds or anorectic from another disease process). -Same process of ketone production, only it's caused by fetuses instead of lactation. Clinical signs: -Any ill ewe or doe in the last 6 weeks gestation is a possible pregnancy toxemia case. -separated from flock -star-gazing -glassy-eyed -weak -recumbent -poor/no appetite -*severe hypoglycemia* -so much ketone production occurs that they influence acid-base balance in ECF - ketoacidosis can occur. -left untreated the fetuses will die and ewe or doe soon after. Serum chemistries: -BG = low -blood FFAs = high -ketones = high -insulin = low -glucagon = high

Dietary management of liver disease

1. Energy: high palatability, high energy density, small meals frequently. Fat - 20-50% of dietary calories. Carbs - maximum of 45% of dietary calories, complex carbs 2. Protein: High quality, highly digestible, low in copper (beef, cheese, eggs), >20% of dietary calories. Restrict nly in hepatic encephalopathy 3. Fiber: moderate amounts, preferably soluble (effect on bacterial overgrowth; lessens NH3 absorption - may lessen hepatic encephalopathy) 4. Vitamins and minerals: increased vitamin B and E, moderate sodium restriction (lessens ascites), adequate potassium, restricted copper (lessens accumulation) 5. Antioxidants: increased zinc, increased vitamin E, increased vitamin C (also and appetite stimulant), increased taurine.

Dietary management of renal disease.

Azotemia = elevation of BUN, creatinine or both. Classification = Pre-renal = dehydration, USG >1.030 (dog). Renal = USG <1.030 (dog) Post-renal = obstruction, hyperkalemia. Keep these patients eating to slow progression of disease. Diets: BUN control - highly digestible, low protein. Acidosis control - alkalinizing diets Phosphorous control - secondary renal hyperparathyroidism Potassium wasting - supplementaion indicated Make sure they are eating! Use phosphate binders if diets fail to control. These target CA and PO4 product <70 Watch appetite and stool character.

How can nutritional management prevent or treat certain forms of colic?

Colic = abdominal pain. There are many causes, and is impossible to eliminate. If a farm has a high incidence of colic check: diet, parasite control program, dentition maintenance program. Nutritional consideration: Impaction - LI, often palpable. Caused by inadequate water intake, low digestibility forage (high bulk, slow passage), ingestion of foreign material. Prevention: increase water intake and quality of forage; soak feeds that swell, divide ration into 3-4 meals (beet pulp, wheat bran, linseeds, pelleted feeds), have adequate salt intake to prevent pica. Gas colic = LI, can palpate Etiology = overfermentation in LI (lush forage, high grain diet) Sand colic = LI, difficult to palpate Suspect when exposure to sand, or sand is found in feces. Prevention: free access to water, reasonably digestible forage, slow adaptation to new diet, don't overfeed grain or lush pasture, don't feed within 1 hour of exercise or when horse is excited, good oral health

Discuss causes and signs of copper deficiency in ruminants.

Copper is a cofactor for superoxide dismutaste (present in all mitochondria). It destroys superoxide (O2-) in mitochondria, and has influence on immune system and productivity/fertility. Cinical signs: - thin body condition - low rates of gain - as copper status declines, animal shows reduced disease resistance, poor productivity, reduced fertility = the most common type of trace mineral nutrition problem! - copper is also a cofact for tyrosine conversioin to create melanin = hypopigmentation - cofactor for lysyl oxidase - collagen synthesis - with severe deficiency the animal will have growth plate inflammation and micro fractures. - severe deficiency = anemia (copper is also involved with iron mobilization within cells). Causes: - high iron content impairs the bioavailability of copper.

What are concurrent health conditions (stress, exercise, etc) that influence the amount of insulin needed to control diabetes mellitus?

Exercise increases # of GLUT4 channels in cell membrane - brings insulin into cells and reduces need for exogenous insulin. Stress - releases stress hormones leading to HSL (hormone sensitive lipase) (inhibited by insulin, stimulated by stress) and is catabolic process - forces FFAs out of cell and into vasculature where it ends up in liver.

Dietary methods to minimize the risk of developmental orthopedic disease in predisposed breeds of dogs.

Fast growth is associated with increased risk of skeletal disease in large breeds - these animals should gain 3.5-4 lbs/week. Giant breeds = 4-4.75lbs/weeks. Protein may actually be protective, no risk of feeding high protein, but hard to separate high protein from high energy. Use large breed foods. Excessive energy and mineral intake can be problematic.

What are methods of dietary management in dogs and cats with hepatic and renal disease?

Hepatic encephalopathy - restrict protein, use soluble fiber to lessen NH3+ absorption; with hepatic encephalopathy you see seizures, blindness, head pressing --> seen with shunt dogs or older dogs in liver failure after they eat a meal. Correct precipitating factors: hypokalemia, GI hemorrhage, infection, restrict protein (<12-16% of dietary calories), modify protein quality (veggie or dairy proteins); adjunctive lactulose (converts NH3 to NH4 and locks in intestines), antibiotics changes flora that make NH3; *protein restriction diet only with clinical signs* Renal failure - keep them eating and slow progression. Diets: BUN control - high digestible, low protein; acidosis control - alkalinizing diets; phosphorous control - secondary renal hyperparathyroidism; potassium wasting - supplementation indicated. BUN = cannot excrete proteins, so low protein diets are best. Acidosis control = cannot eliminate renal acids, platelets go down, bicarb is used, patient feels bad, use alkalinizing diets. Phosphorous control - use phosphate binders if diets fail to control; target CA and PO4 product <70. Restriction prolongs life in CRF dogs. Potassium supplementation - use even if cat is low normal

Discuss pathogenesis and clinical signs of hepatic lipidosis.

Hepatic lipidosis "Fatty Liver"/Fat Cow syndrome: -A disease that results from prolonged negative energy balance occurring immediately after calving (at the onset of lactation). -Tends to affect *overweight/overconditioned* cows. -All cows have some degree of reduced appetite around time of calving, so mobilization of body fat occurs at this time in *all* cows. -Overweight cows: tend to go completely off feed near calving; tend to go off feed longer than non-obese cows. More fat is mobilized in these cows, and an avalanche of fatty acids are sent to liver. When the pathway to ketones is saturated, the FFAs to go somwhere, as they affect blood pH. So enzymes are activated to grab FFAs, reesterify them and redeposit as intracellular fat. The hepatocyte begins to look like an adipocyte and liver can't function. These cows often develop other diseases (metritis, mastitis, abomasal displacement) and respond poorly to treatment. Clinical signs: -depression, anorexia, weight loss (especially with a history of being overweight prior to calving) -ketosis, hypoglycemia - plus symptoms of other diseases. Treatment: -same as with ketosis, but they are hospitalized for IV glucose needs for 4-5 days. Feed them via stomach tube and try to restart propionate.

What are the expected clinical signs of hypocalcemia in ruminants, horses and dogs?

Hypocalcemia = impaired insulin release (Ca++ is needed for insulin release from pancreas). Ca++ is also needed for NT release in CNS (ACh and norepinephrine). Severly low Ca++ in ECF can result in coma in some species. Ruminants: Periparturient paresis "milk fever"; usually occurs within 48 hours of calving. Clincial signs: -Stage 1 (axonal hyperirritability): irritability, hyperesthesia; tongue protrusion with jaw open; trembling, jerking motions, spasms; very brief duration. -Stage 2 (NMJ and muscle effects predominant 2 & 3): head may be turned back into the flank; infrequent or absent gut sounds; bloat, constipation, urine retention, dilated pupils, slow to constrict to light, heart muscle strength is decreased - pulses feel weak; but HR increases due to sympathetic drive to maintain CO; subnormal body temp, cool extremeties. -Stage 3: Coma - death soon follows, respiratory/cardiac arrest, bloat or aspiration of rumen contents. -Treatment: Calcium salts *slowly via IV* too fast = stone heart -Prevention: add acidifying agents to ration 2-3 weeks prior to calving to make cow's blood more acidic; *calcium stores are mobilized under acidic conditions* Hypocalcemia in small animals: - Puerperal eclampsia: rigidity, tremors, panting, may progress to convulsions (especially in small breed dogs with big litters; less common in cats). -Risus sardonicus - contracture of facial muscles that occurs in diseases that cause tetany (eclampsia and tetanus). - Clinical hint: *tetany, hyperthermia, and/or convulsions in a dog or cat wiht a functional mammary chain!* Horses: - "Lactational tetany" - signs similar to dog, cat, human. More often seen in draft breeds.

What are the effects of insulin on metabolism and electrolyte balance?

Insulin = anabolic, increased storage (glucose, fatty acids, amino acids). Metabolic actions of insulin: -Transport of Glucose, aa, K+ into cells. -Stimulate protein synthesis -Inhibit protein degradation -Activate glycogen synthase -Inhibit gluconeogenic enzymes -Increase mRNA for lipogenic enzymes

What is the expected response of a diabetic animal to insulin therapy?

Insulin is anabolic, so it will pull things into cell. Transport of glucose, AA, K+ into cell. Stimulate protein synthesis; inhibit protein degradation; activate glycogen synthase; inhibit gluconeogenic enzymes; increase mRNA for lipogenic enzymes.

Discuss the pathogenesis and clinical signs of ketosis.

Ketones serve to spare precious glucose for other needs, as it is an alternate energy source for heart, kidney, skeletal m., mammary glands. Some ketone synthesis is normal in heavily lactating dairy cows, ewes/does carrying triplets who can't eat enough to meet energy demands. Fat mobilization exceeds carb intake. But in high concentrations, ketones can suppress appetite, and cause altered CNS function. Ketosis occurs when fat is mobilized to serve as energy. FFAs sent to to hepatocyte. Acetyl CoA produced from fat mobilization. Supply of Oxaloacetate is limited, so TCA cycle is not efficient. The acetyl CoA builds up in the cell and is chemically unstable, so it is rapidly converted to ketones (which are the result of incomplete oxidation of fatty acids). Clinical signs: -gradual reduction in appetite -lethargy, glassy eyed stare -*decreased milk production* -acetone odor to breath -signs of underlying disease that made them anorectic to begin with. Treatment: -give propylene glycol - converts to proprionate -give IV glucose -goal is to get oxaloacetate back up! Fix whatever the physcial problem is so she starts eating again, then she can start making more substrates. Or give propylene glycol to restart proprionate production in rumen; also give dextrose IV to give liver a break. Blood concentrations for ketosis: BG = low ketones = high insulin = low glucagon = high blood FFAs = high cellular oxaloacetate = low Ketoacidosis rarely occurs though because the glucose drain of lactation will shut off.

Discuss the pathophysiology and nutritional strategies for prevention of laminitis in horses.

Laminitis = inflammation of the sensitive lamellae of the foot. Characterized by lameness and pain. Can be physcial or consussion - impact founder; or acute toxicity - infection, toxin, nutritional. Excessive intake of soluble carbs (grain, concentrate, lush pasture) overwhelms SI capacity for digestion/absorption, leading to excessive fermentation products (lowering pH), bacterial die off - bacterial toxins absorbed, increased TPR, fatal colic 12-16 or laminitis 20-24 hours post ingestion. Treatment: within 12 hours of ingestin of offending nutrients: stop or slow fermentation - mineral oil, laxatives, walk to increase GI motility unless TPR is elevated, antiinflammtory and toxin binding drugs (be careful with NSAIDs).

Optimal nutritional management of gestating horses.

Maintain BCS at 5-6 -more issues with under rather than over nutrition -no increase necessary until last trimester of pregnancy -during last trimester (16 weeks) increase 12-20% -for quarterhorse/thoroughbred mares this = 150-200lbs gain in BW during pregnancy Protein: -maintenance first 2 trimesters (8% ok) -increase to 10% for last trimester -legume-grass or legume hay should be ok -grass hay may need grain with 12% protein Minerals: -major minerals requirement is ~2 fold maintenance - Ca 0.4-.45% - P 0.3% - if grass hay 1% CaCo3, 1% dicalcium phosphast or grain with 0.55% Ca. - with legume Ca OK but may need P supplement Minor minerals: - Se 0.1-0.2 ppm - Cu 10 ppm

Discuss the dietary causative factors, clinical signs, treatment options, and methods for prevention of hypomagnesemia in grazing ruminants.

Mg++ is biologically active form. (70% bone, 30% soft tissues). 1. Enzyme cofactors (kinases, ATPases, GTPases, cyclases, AChase), critical cofactor in PTH release - Mg nutrition impacts Ca++ homeostasis. Without adequate Mg++, cows can't release PTH, and can induce low blood [Ca]. -Mg increased demands by fetus and lactation. - No hormone system dedicated to homeostasis - GI tract is main source! Must ingest it and absorb it! Absorbed from rumen of ruminants. Feed and soil factors greatly influence Mg absorption. High levels of N and K lead to reduced Mg absorption. "Grass tetany" - hypomagnesemia during ingestion of lush pasture. Best to add salt/sugar blocks with Mg salt to supplement their diets. -Treatment: MgSO4 enema: 200mL hot water + 60mL epsom salt into rectum. Will likely need Mg and Ca IV slowly. -Prevention: Dust forages with Mg

What are the advantages and risks of parenteral feeding of critical care patients?

Parenteral = administration of nutrient without using the GI tract; can be used 3-10 days in animals. All essential amino acids, fat and water soluble vitamins, micronutrients, more nutrients compounded, more chance for incompatibilities. Used dedicated lines so it doesn't need to be broken down often. GI sepsis occurs due to GI bugs, NOT skin bugs.

Optimal nutritional management for lactating horses.

Protein: - requirement is 13% - if grass hay is fed, grain should be 16-18% protein - if legume hay is fed, grain can be as low as 12% grain Minerals - same as gestation

Optimal nutritional management of starved/neglected horses.

Re-feeding: -*Don't overfeed!* - leads to GI problems, laminitis - If BCS >3 can feed ad libitum (6-7 weeks to recover) - Otherwise take 3-4 days to build from 70% to 100% MER - Increase protein intake amounts to levels recommended for growth (12-14%) unless contraindicated by presence of disease - supplement B vitamins - re-establish mineral and electrolytes WNL (K, Mg) -feed small amounts frequently -use fresh palatable food and remove old food within 2 hours -change structure of the food if necessary (pellet, mash, fresh grass) -watch for food aversion -treat physical problems that may make eating difficult or painful -feed around other horses that are eating at the same time

How do horses and camelids response to metabolic and serum biochemical responses to chronic negative energy balance contrast with ruminants?

Some subtle differences in how these species respond to negative energy balance, but remember as for all other species *insulin = low; glucagon = high; if pain or illness, cortisol and epinephrine = high* Nutrient stores will be mobilized: NEFAs (FFAs) released; protein breakdown - amino acids released; glycogenolysis - glucose released. Common scenarios for negative energy balance disorders: -overweight dams in late prenancy or early lactation -chronic illness in adult of any age -underlying primary disease: dental disease, heavy parasite burden, laminitis, injury. Horses have variable blood levels of glucose - they have a poorly developed ketogenic pathway, so they tend to re-package mobilized FFAs and export them as lipoproteins. Camelids: mobilized FFAs go to liver and some ketogenesis (like ruminants); some hepatic fat deposition (like ruminants and horses), some fat export as lipoproteins (like horses), can be *hyperglycemic* - develop severe insulin resistance and make very little insulin anyway, so they may have supped up gluconeogenesis. BG ultimately depends on whether or not thaty have a glucose drain. When stressed by an underlying disease, camelids tend to show prolonged *hyperglycemia* (their stress hormones and glucagon cause mobilization of glycogen reserves. Summary of NWCs: - they show features seen in both ruminants and equids: -ruminants - high blood NEFAs, ketogenesis, hepatic lipid deposition -equids - high blood NEFAs, hepatic lipid deposition, hyperlipidemia -*hyperglycemia* a unique feature to NWCs

Describe the pathogenesis, clinical signs, and expected laboratory findings of renal hyperparathyroidism of dogs and cats.

Stems from a calcium deficiency - secondary hyperparathyroidism stimulates the secretion of parathyroid hormone, increases productin of calcitriol (active vitamin D). PTH + Calcitriol = bone resorption - leads to skeletal fractures. Controlling phosphorus is important because the retention of phosphorus leads to lower calcium levels which stimulates PTH, pulls calcium from bones, and results in "rubber jaw".

Optimal nutritional management for growing horses.

Suckling foals require energy: milk, mare's grain, creep feed, and pasture/forage. Creep feed: corn, oats, barley - 14-16% protein (soybean meal, skim milk) - 0.8% Ca - 0.55% P - 30 ppm Cu - Feed 1lb/month of age/day starting at 1-3 months Weanling foals: - feed to BCS 4 - never want foals to be fat - leads to DOD! - protein - 14% - Ca 0.6-0.8%, P -0.45% - Grain or concentrate - Cu 30ppm, Zn 75-100ppm, Se 0.2ppm

Discuss homeostatic mechanisms involved in maintenance of normal ionized calcium concentration in ECF.

The biologically active form is ionized calcium - the form closely regulated in the body. The pools for calcium homeostasis is dietary Ca in GI tract and bone. Losses/drains = fetus and lactation. Calcium in ECF/blood: -55% ionized form (Ca++) - 35% loosely bound to albumin -10% complexed to citrate, phosphate, oxalate, and other anions The pH of body fluids influences calcium homeostasis. -Alkalosis (alkalemia) = high pH in the blood and ECF. -Severe alkalosis can cause signs of low [Ca++] and can occur with repetitive vomiting. -Acidosis renders bone mineral *more* soluble - Ca++ is released more readily from bone under conditions of acidosis. Osteoclasts use acid to release calcium from bone. PTH: -Stimulus for release = low ECF [Ca++] -In bone, PTH mobilizes bone mineral "resorption" by osteoclasts - liberates Ca from bone and increases ECF [Ca++]. Age influences this response - older bones respond more slowly than younger bones. -Effect on kidney: Promotes saving of calcium (resorption) by nephrons. Phosphate is lost in urine, this results in less complexing of phosphate with calcium in blood. *PTH puts the P in pee* Promotes activation of 25-OH, vitamin D3, stimulates 1 alpha hydroxylase in kidney, end product: 1,25 di-OH vitamin D3 - helps PTH to mobilize bone mineral; increases absorption of Ca and P from gut. Net effect = increases [Ca++], {phosphate] in ECF.

Discuss causes and signs of thiamin deficiency in cats.

Thiamine (B1) deficiency leads to encephalopathy in a variety of species. Usually induced by thiaminases in the diet or thiaminases produced by gut microflora. Clincial signs: - characteristic ventroflexion of the neck and convulsions (ventroflexion occurs during convulsive activity). - thiaminase in cats: raw fish, esp. tuna and salmon; also shellfish. It is NOT mercury poisoning!

Describe pathogenesis, clinical signs, and expected lab findings in nutritional secondary hyperparathyroidism in horses.

This is called Bran disease. Bran is hulls of grain, so no Ca++ absorption occurs because high diet phosphorous competes with Ca++ for intestinal uptake. There's low Ca++ in blood that triggers chronic elevations of PTH. We see weakened bones that suffer from microfractures (lameness, bone remodeling with fibrous tissue - esp. mandible), can see osteopenia and microfractures in maxilla also.

Discuss the environmental, dietary, and climatic factors that might cause the incidence of ketosis to increase on a dairy.

Types of ketosis: - primary = ration is deficient in carbs - secondary = diet is fine, but animal has another disease that makes it anorectic. Ketosis then occurs secondary to disease-induced anorexia (this is much more common than primary). - Nervous ketosis - CNS signs predominate - apparent blindness, stupor, occasionally hyperesthetic and aggressive clinical signs: - gradual reduction in appetite - lethargy, glassy-eyed stare - decreased milk production - acetone odor to breath - signs of underlying disease tha made them anorectic to begin with Diagnosis: - hypoglycemia (low BG) - measure blood, milk or urine for [ketones] - blood - easiest to mesure is beta hydroxybutyrate (BHB or BHBA) Cows at greatest risk: - Fresh cows (because cows make more milk than heifers) - sometimes heifers if there are social issues with them eating enough food for energy needs.

Discuss the causes and signs of vitamin/Se deficiency in livestock and horses.

Vitamin E: - requirement = 50mg/kg DM - protects against lipid peroxidation in the cell membrane - pasture usually adequate, oxidizes with storage, transferred to neonate in colostrum and milk, will need to be supplemented especially in draft and race horses. Se: -requirement = 0.1ppm - acts in the cytosol to "clean up lipid peroxides and protects against proliferation of free radical damage. Vitamin E and Se work synergistically so a deficiency in one increases the need for the other - usually administered together. Deficiency is most often seen in foals because they are rapidly growing. - degenerative myopathies - white muscle disease --skeletal muscle, cardiac muscle, smooth muscle --may involve tongue and impair swallowing - inhalation pneumonia -steatis - yellow fat disease with firm gritty granules Clinical signs: - aspiration pneumonia is common if laryngeal/pharyngeal muscles are weakened. -unable to curl tongue to suckle Treatment: - Vitamin E and Se injection at birth IM for foals at risk - Se and Vitamin E in creep feed - Se supplementation 3mg/mare/day increases IgG production and transfer Prevention: - Ensure adequate Vitamin E and Se intake by mare during pregnancy Excess: - Vitamin E is well tolerated, risk is dimished absorption of Vitamins A, D and K - Se tolerance range is very low: 5-10 times requirement is toxic!

Dietary methods to support the energy needs of working dogs.

Working dogs generate measurable amounts of free radical end products. The antioxidants studied so far decreases some but not all of the commonly measured parameters of free radical damage. Antioxidant supplementation may be more beneficial during performance than training.