1. Feeding horses –horses need nutrients –feeds supply nutrients
The NRC determines requirements -No safety factor.
Energy is not a nutrient , it is the fuel for all metabolic activity.
Derived from nutrients –Energy is the number one metabolic need for horses next to water. Other nutrient needs are sacrificed for energy if deficient.
Use ideal weight to determine energy needs.
Energy needs vary -Breed differences, Work level , environment , health issues. The type of exercise, temperament, reproduction and lactation or growth. Or Stress ? Must he gain or lose weight?
A body condition score of 5 is ideal.
How do we feed properly?

2. Forage is number one!-the horse is a hind gut fermenter with unique needs.
Maximize hay/forage and pasture.
The digestive tract is not suited to high concentrate feeding metabolically, physiologically, or mentally.
The bacteria in the hind gut can provide the energy needed for maintenance and low level work by fermenting fiber to volatile fatty acids used by the horse for energy.
Adequate forage will maintain the population of bacteria that ferment fiber. These bacteria keep the hind gut healthy.
The stomach is small and the small intestinal tract is short and not suited to high levels of true sugars and starch . The normal diet of the horse , native range is not usually high in simple sugars and starch.
Feed a minimum of 1.5% BW as forage.
Horses usually eat from % of BW as forage. This can support maintenance to light work.

3. Feed forage for gut health
Lack of forage and over use of grains results in sugar and starch moving through the digestive system into the hind gut.
Result is the growth of bacteria that thrive on sugars and starch .
These harmful bacteria produce lactic acid (LA) lowering gut pH creating acid conditions.
LA/low pH is harmful to the fiber fermenters creating die off of friendly fiber fermenters. They release factors that can be toxic to the horse such as endotoxin, vaso active amines and other compounds harmful to the horse.
The harmful bacteria also produce exotoxins and enzymes and substances that can be toxic or damaging to the gut lining to the point of causing digestive upset and laminitis.
Experts suggest a maximum of grams starch per 100 kg BW per meal and a maximum of two meals per day minimum 6 hours apart.

4. Chewing-critical. Breaks open plant cells to help digestion.
Forage encourages more chewing.
Maximum chewing stimulates the production of saliva.
Saliva moistens the bolus and adds a mucous to aid swallowing of the bolus.
The saliva also contains a high level of bicarbonate which helps buffer the stomach.
Unlike humans, saliva has relatively low levels of the enzyme amylase so not as efficient at digesting starch compared to humans and other animals.
Proper forage levels ensure more water . Water intakes are about 3-5 to one for forage as opposed to to one for grains.
Water helps dilute acid in the stomach. Water hold more weight and ballast in the intestinal tract and helps prevent colic.

5. Feed forage for gut health
Choke-avoid hard dry feeds. Maintain proper hydration
Horses without feed do not produce saliva in large volume but do produce acid in the stomach 24/7. Natural grazing is hours per day. Horses are nibblers.
Ulcers -5 hours rule if without feed ulcers may occur. Coarse forage may cause ulcers.
The saliva is unique having little Amylase to help start starch digestion.
Watch for salivary gland issues and mandibular joint issues with seniors. Wear increases with age. Minis may have issues chewing.
Adult horses may secrete up to liters / day with a pH of This is very alkaline.
Horses do not chew poor forage better!

6. Chewing –The palate requires tactile stimulation & good hydration
Chewing -60,000 sweeps on pasture .
Hay- half hour per 2 lb vs grain 10 minutes per 2 lb. Adequate forage relieves boredom .
Hay-4000 chews /kg vs grain 850 chews /kg forage encourages more saliva production.
Chewing grains not a full jaw sweep so sharper edges on teeth. Seniors are special needs horses as are minis.
Horses may seek out anything they can to buffer stomach acid without adequate forage.
Coarse forage may cause ulcers (new data).
Minis may have issues chewing.
Minis should not get coarser hays as they are prone to impaction colic.
Adult horses may secrete up to liters / day saliva with a pH of This is very alkaline.
Horses do not chew poor forage better!

7. Esophagus to stomach usually a one way system-
Esophagus inches long . No mucous protection for lining, can choke.
Relatively small stomach at 8-12 liters or 8-9% of the GIT
They eat little and often. Many small meals throughout the day naturally.
Does not hold feed very long . Food may only stay minutes.
Naturally never full, best if only ¾ full maximum.
May move food on to the small intestine at 2/3 rds full even if not properly digested in the stomach.
A layered effect with a mat on top having a higher pH and more alkaline with the lighter fibrous forage and grass particles and with the smaller denser particles on the acidic bottom area .
Produces acid and the enzyme pepsin 24/7 to start protein digestion
Acid production stops fermentation in the upper portion from the initial intake.

8. Stomach-two areas-sqaumous and glandular
sqaumous portion-non glandular-saccus caecus –
squamous epithlial cell lining similar to the lining of esophagus- more susceptible to acid damage.
Fermentation can occur here if excess grain fed or on rich grasses if turned out empty.
A horse cannot belch to get rid of excess gas. The stomach is small and vulnerable to rupture.
The stomach is not visible so care in assessing issues.
Lacks the protective mucus/bicasrbonate layer and prostaglandins that enhance mucosal blood flow and secretion of mucus and bicarbonate present in glandular portion.
Glandular area –fundic area and with pyloric area secreting gastrin the hormone stimulating secretion of HCL and pepsinogen/pepsin, and a small amount of lipase and amylase.
Pasture feeding is associated with the lowest incidence of ulcers. Grass colic can occur.

9. The stomach
Feeding more grain and less hay and withholding feed are associated with higher incidence of ulcers , lower stomach pH and higher blood gastrin levels .
There are effects of exercise independent of feeding.
Horses on a TM showed gastric compression caused by increased abdominal pressure which may enhance exposure of the sqaumous mucosa to acidic gastric contents.
Horses fed the same diet before and after exercise had higher gastrin levels during training.
Horses in pain or stress will have higher gastrin production. Stress ulcers are more in the glandular area for foals .
Fermentation in the stomach is a concern as it is small and cannot be seen :
An empty stomach may allow back flushing of doudenal / bile salts and acids which may cause ulcers.

10. The stomach
Fermentation may occur here on high Sugar and Starch diets or rich grasses.
Never turn an empty horse out on rich spring grass.
(eg grass colic.). You cannot see the stomach.
Pasture is ideal for prevention of colic and ulcers .
Feed hay before grain.
Feed some alfalfa a natural buffer. Time it for exercise.
Ulcers
70-90% of race horses
75% of 3DE horses
50-75% of western performance horses and
52% of dressage horses
10-30% of horses in 5 Swiss barns survey - ridden for pleasure .
10-30% of wild horses.
42-70% of foals.

11. The small intestine 25% of digestive tract capacity
About feet long
Enzymatic digestion of carbohydrates, fats, protein, macro minerals and trace minerals, and vitamins.
Relatively short , food spends only about 1 hour, possibly why relatively poor at digesting starch .
Also glucose transfer to the circulation seems less efficient.
Also possibly partly why slower to
reload glycogen the carbohydrate storage energy form in muscle.
Horses are unique in requiring about 72 hours to reload glycogen . Humans can reload using carb loading in 24 hours.
A portion is not anchored to the body cavity so it may be prone to colic.

12. Insulin release Related primarily to post prandial glucose levels.
However, equids differ in their insulin response compared to humans.
Where insulin resistance occurs, the pancreas can produce high levels of insulin for a long time keeping blood glucose at normal levels (euglycemia). Called compensated IR.
Recent research shows horses also respond to the entero-insular effect of incretin hormones.
These hormones like GIP and GLP are secreted by cells in the small intestine in response to the presence of nutrients like glucose. An oral dose of glucose will trigger and insulin response 2-3 times that of an iv dose of the same amount.
Also since high insulin alone can trigger laminitis in healthy equids with normal blood glucose levels, this may be an area of future research to prevent laminitis.
Breeds susceptible to high insulin /IR seem to have high incretin levels
High NSC /sugar and starch diets can reduce insulin sensitivity in mature horses and young horses in the absence of increased adiposity.

13. Large intestine:
65% of capacity
Cecum and colon. Cecum is a blind sac 30 l -feed stays about 7 hours. Easily impacted with poor feed.
Enlargement to promote Microbial fermentation of plant fiber for Energy as volatile fatty acids (VFA’s) that are absorbed and used to provide most of the horse’s energy requirements.
Limit starch to prevent hind gut overload. Maintain the biome! Excess starch will cause acidosis and may lead to laminitis by changing hind gut fermentation.
The bacterial population is unique to the forage being fed and requires two weeks to adjust to major changes.
Max grain per meal 5 lbs and max grain per day 10 lbs for a 1000 lb horse. No closer than 6 hours. (Maximum grain 1% body wt) /day.
Feed hay first.
Twists turns and changes in volume create issues with digesta movent.
Horses need to move for proper digestion.
Hydration is critical .
Use good quality forage

14. Large intestine-large colon-75 liters
Microbial fermentation produces
VFAs , B vitamins, Vitamin K, and C
Absorption in large intestine
A water and electrolyte reserve for the horse, B vitamins produced by bacteria.
Electrolytes (Na, K, Cl)
Phosphorus (Bacterial Phytases help with phytates) Adult horses can easily tolerate a wider cal p ratio of 4 to 1.
Many twists and turns. A problem area. To small colon and fecal balls are formed here water is absorbed and the fecal balls are stored in the rectum
Fiber and water add ballast to prevent colic from displacement, twists and impaction.. Use some soluble fiber!

15. NRC requirement for Energy
500 kg x Mcals per kg =16.50 Mcals of energy for maintenance.
Light work x 1.20
Moderate work x 1.40
Heavy work x 1.60
Very heavy work =0.036 x BW 1.90
Counting calories!
Most hays are about 1.8 mcals/kg
A 500 kg horse at maintenance only needs 16.5 Mcals a day .
9.2 kg /day of Hay alone can meet the energy needs.
The problem is horses do not regulate energy intake very well and will eat well above this level.
Certain breeds are genetically prone to be easy keepers, the thrifty gene.

21. Body Condition
The condition over 5 is fat. Losing condition below 4.5 is probably muscle mass loss.
A score over 7 is considered obese leading to health and endocrine and metabolic issues including IR/HI and laminitis.
Horses needing weight require approximately 9 Mcals per day per lb of gain .
Horses that need to lose weight need to be restricted by 8 Mcals /lb of loss required.
Obesity (particularly regional adiposity, peripheral insulin resistance, dyslipidemia , and risk of endocrinopathic laminitis is called Equine Metabolic Syndrome EMS.
Over weight and obese horses are prone to developing insulin resistance and possibly laminitis. EMS the most common form of laminitis seen
More than 3 criteria correlated with PAL in ponies on high starch/sugar pasture.
The mechanism remains obscure.

22. Fat deposition Increases risks of IR/ID , EMS, and Laminitis
In stallions BF decreases with age. Females defend their weight more efficiently.
Surveys show obesity a problem with over 50% in some surveys over weight or obese.
Obesity induces an inflammatory state characterised by increased expression and secretion of proinflammatory cytokines , which play a key role in IR.
EMS welsh ponies had elevated serum IL-6 and TNF-alpha with macrophage infiltration and fibrosis in AT .
Plus suppressors of cytokine signaling are increased by proinflammatory cytokines and link inflammation and IR in liver.
IR in obese horses is called EMS.
Horses and ponies with EMS developed laminitis.

23. obesity
Clinically normal horses and ponies treated with high insulin developed laminitis. New direction!
Obesity was related to increased risks of IR in TB geldings.
HI and mild to moderare HG or compensated IR confirm the presence of IR.
Broodmares with EMS are commonly reported to be subfertile and often exhibit abnormal cycling. Leptin and T3 may be elevated.
Obesity can adversely affect metabolism. With accumulation of intracellular triglyceride , adipocytes enlarge and outgrow their vascular supply , resulting in hypoxia and necrosis of individual adipocytes. AT becomes IR. TG can increase in blood and the body and in muscle cells and liver cells.
The presence of these necrotic cells is associated with leukocyte infiltration into the AT, and this is highly correlated to IR. Most of these macrophages shift to a proinflammatory state. However, inflammation is not seen in Ems at least not at first.
Adiponectin an anti-inflammatory adipokine loses its effects with obesity.
Composition of the diet also has short term effects on systemic IS in the absence of obesity. TB geldings fed high grain over 8 weeks (obese ones had loer IS), Also in post foaled broodmares with IR fed sweet feed vs FF, in young growing horses ie weanling TB’s on pasture, and metabolic programming during gestation foals born to mares with high ss diets.

24. insulin
A marker and plays a direct role in EMS with obesity, Insulin signaling becomes dysfunctional.
Two systems or signalling cascades operate in cells: One controls normal energy metabolism (PI3K) The other is mitogenic controlling cell division and differentiation morphology. (MAPK) acting with AMPK.
High insulin may switch the effects of insulin turning on different genes.
IGF-1 may be enhanced with another enzyme being decreased in activity AMPK
Triglycerides released harm liver (and muscle) cell function making it unable to clear insulin, and failure to control liver gluconeogenesis occurs.
Incretins like GIP may increase linked to human obesity and horses too may have a higher insulin response to a meal due to incretins. Breeds with IR seem to have a higher incretin effect.
Insulin influences vascular function. ET-1 may overide NO during HI.
Insulin through IGF-1 and AMPK may change cytoskeletal structures and connections weakening the lammeallar interface. The result is a stretching of SEL and failure.
Inflammation is not a marker of EMSAL , it is slow and insideus and often laminitis is the first sign something is wrong and by then may be too late.
The result may relate to skin cancer in humans .
Not all obese horses are IR, Not all IR horses are obese and breeds genetically prone to IR may have a lean geneotype that is IR.

25. PAL High levels of water soluble carbohydrates are involved.
Ponies can ingest up to 5% dry matter per day on pasture or short chopped rich hay.
Horses can eat 3-3.5% dry matter on pasture
Ponies limit fed on pasture cam eat 30-41% of dry matter intake in 3 hours of turn out.
Fructan/nsc content can vary with grass type, sunshine, temperature, time of day shade on pasture, stress on grass. See grass section.
NSC in grass may vary from 15% in the AM to 30% in the PM
Levels as high as 40% dry matter noted.
Grazing high nsc pasture may promote IR or persistent HI.
Grazing high NSC pasture may result in peaks of insulin similar to a high starch diet.
This may lower the threshold for laminitis to be triggered.

26. PAL -2 Low risk-(e.g. Non-obese TB type horses in full work
Moderate risk-(e.g. An obese or IR pony) may require restricted access to pasture, especially at certain times of the year.
Implementation of countermeasures that target laminitis risk factors (e.g. IR, obesity) may be indicated.
High risk animals (recent episode of PAL or animals that have suffered recurrent episodes of PAL ) may require limited or no access to pasture.
Manage appropriately for risk factors, coordinate with the veterinarian to DIAGNOSE properly for EMS or PPID, ensure other issues are not at play.
How a threshold for laminitis induction can be lowered under certain situations

27. Special Needs
For easy keepers lower maintenance needs by 10%.
EG Heavy Horses , foundation quarter horses, ponies, Morgans.
For hard keepers increase maintenance needs by 10%.
Eg Thoroughbreds vs heart size .
Senior Horses-teeth stop erupting at 21 years of age .
Minis may need extra care re teeth, and are more prone to impaction colic , and are very efficient and easy to get over weight.

28. Always maximize forage usage to meet the nutrient needs of horses.
Horses also need forage to prevent boredom and ensure good buffering of the stomach and gut health.
No mold or dust .
Horses eat more alfalfa hay than grass hay.
Horses eat more of the same hay in cubed form than long form.
Careful with haylages and clostridium (mouse story) and colic issues.
All the horse may need is a mineral and salt or a ration balancer pellet if protein is needed. Trace minerals are usually low and selenium may be low in this area.
Higher quality hays can be consumed at higher levels so watch intakes.
Pasture intakes may be much higher.
Horses do not chew coarser hays more to maximize energy, they eat more up to a point then decrease intakes if very coarse.
Coarse hays may cause diarrhea in older horses, the squirts in all horses and increase ulcers ( new Danish research).

29. Feeding: Maximize Hay Use
grass hays are modest for calcium and phos and most trace minerals are lower than requirements for even maintenance.
Selenium in certain areas is a special case.
Because of low rainfall from the sea iodine is also a concern in hays from dry climates.
High rainfall removes calcium and phos in fact creating a reverse ratio where calcium may be lower than phos.
Iron can be very high in forages grown here or imported.
Energy may be low to quite high.
AND MOST VITAMINS ARE LOW in hays. Do not rely on hays for vitamins and omega three fatty acids .
EMND.

30. Hay Analysis
Moisture- hay over 15% moisture may be subject to mold and bacterial spoilage
Horses cannot tolerate mold and other toxins. The mouse story.
Look at protein –level of CP and lysine an amino acid which is a measure of protein quality.
Horse DE measures actual energy content as Mcals/kg or lb.
Other numbers to consider :
ESC =all true sugars
Starch plus ESC directly affect insulin. Keep below 10% DM ?
New research says consider the fructan fraction and the biome, LA production and overall yield of insulin.
WSC= All sugars including grass fructans (compound fructose sugar units ) .
NSC =WSC plus starch Keep below 10-12% for metabolic or endocrine issues .
Examine the fiber levels and lignin.

33. Alfalfa Does it make horses crazy? Advantages
Higher energy than lower quality/mature grass hays
High protein , lysine other amino acids and calcium
Horses eat more alfalfa than grass hays of the same maturity levels .
Research shows alfalfa will truly buffer the stomach beyond chewing effects.
Ideal for rehabilitation of starving horses.
Helpful for lactation rations and growing horses. Limit for training endurance horses but small amount on trail helpful.
Use it strategically for performance horses. Consider 1-2 lbs 1 hour before competition.

36. Maintenance Hay Only

37. Maintenanace and all p lite
Evaluate how hay meets NRC requirements fed at approximately 2% body weight or predicted intakes.
Predicted intakes are 23.6 lbs per day in example.

38. Light work all p lite

40. Selenium Most of B.C. Island, Okanagan-Central interior
An area generally deficient but local levels may vary., usually less than 0.1 ppm in the Okanagan. Be aware alkaline soils are more conducive to selenium uptake.
A major component of enzyme glutathione peroxidase. Protects cell membranes.
Required for the control of thyroid metabolism. Activates thyroid hormone.
For fertility, immune system, retained placenta,
Deficiency more pronounced in foals with WMD at birth.
Mature horses partly protected by other factors but these drop off with age.
recent mortality reported from Washington state U with mature horses showing myo-necrosis of head and skeletal muscles, subcutaneous edema, pleural effusion, and ulcerative glossitis (an ulcerative and inflamed tongue). Suggests a full body involvement. The glossitis probably from pica due to mineral deficiency. Mortality had occurred. Herd wide selenium deficiency and myodegeneration were found. Watch for ventral edema, weakness and death.

41. Trace Minerals in the Okanagan

42. Selenium levels

43. The horse is designed for speed and power

44. Energy Generation-
Muscular movement requires the transformation of chemical energy stored in substrates or fuels to the kinetic energy of muscular contraction.
All pathways integral to energy supply are concerned with the ultimate production of ATP the final carrier of energy utilized by muscle for contraction.
Energy is generated by the aerobic system utilizing oxygen to burn glucose /glycogen and to burn fatty acids for slow release but long term release of energy. Energy can also be generated by anaerobic metabolism using just glucose as the main fuel . Energy release is very fast but can only be sustained for a short while .
Fatty acids can provide most of the energy for rest and low level work or long slow distance work, but are slow release energy sources. Fatty acids do release a large amount of energy compared to glucose from blood and glycogen reserves.
CO2 and water are the end products of aerobic metabolism.
More carbohydrate is used as work increases until burning glucose/glycogen moves to the anaerobic system
Excess glucose is changed into glycogen and stored in liver and muscle and glycogen is the main source of glucose during exercise. Excess glucose is also changed into fat and stored mostly in adipose tissues but some in muscle tissue. The liver also stores glucose in the form of liver glycogen which also acts as an energy reserve.
Once energy needs accelerate and using fats is too slow and oxygen cannot be supplied to burn glucose fast enough with oxygen, , the muscle burns stops burning more fat and uses glucose/glycogen through a short quick method called anaerobic metabolism . This is faster but less efficient and the end product is lactic acid. Fatigue comes after a few minutes if mostly anaerobic metabolism.
Muscle LA production and eventually lower glycogen and blood glucose contribute to fatigue.HR indicates fuels used.

45. Anerobic threshold
The horse at rest and low levels of energy output uses “aerobic metabolism”.
Uses mostly fat for generating energy eventually using some muscle glycogen and blood glucose , along with oxygen .
The end products being CO2 and water.
Can be sustained over long periods of time .
As work intensity and duration increases and the production of energy using oxygen cannot meet demands , metabolism switches to producing energy using quicker but less efficient “anerobic metabolism “ which does not use oxygen.
The end products being lactic acid.
Fat cannot be used in this process . Glycogen and blood glucose are the energy sources.
This creates acidosis.
Anaerobic metabolism cannot be sustained very long.
Even fairly heavy work still uses some aerobic energy such as race horses who use about 60-70% aerobic energy.

46. The horse is superb athlete

47. The horse as athlete High maximal aerobic capacity. (VO2 max)
Large intramuscular stores of glycogen
High respiratory capacity of skeletal muscle
Splenic contraction, results in the oxygen carrying capacity of blood increasing by up to 50% soon after the onset of exercise.
Highly efficient and adaptable gait.
Well developed capacity for thermoregulation.
The type of work a horse does and his muscle type will affect the energy source used and the metabolic system for generating energy.

48. Most horses use a combination of aerobic /anaerobic metabolism.
Speed work like racing will be more “anaerobic”. The heart rate tells you the type of metabolism happening to generate energy.
HR over 155 BPM means oxygen can no longer supply the needs for more energy and the anerobic system kicks in to supplement the aerobic system and burning fat drops off.
Only glycogen and some quick release compounds in the muscle fiber itself and some blood glucose can supply energy quick enough for anaerobic metabolism.
The by product is LA and fatigue is due to acidosis in muscle and possibly a drop in blood sugar causing mental issues.
The horse in speed work uses all muscle fiber types especially the fast twitch muscle fibers which do not use fat , relying more on muscle glycogen , liver glycogen and some blood sugar.

49. Most horses use a combination of aerobic /anaerobic metabolism.
Aerobic metabolism spares the need to burn muscle glycogen and blood sugar.
For long slow distance work.
Muscle friendly as the product of this metabolism is CO2 and water , both easy to get rid of. It generates a low heat load.
Endurance horses usually operate in this zone as do steadily working horses like dressage horses.
Fatigue for these horses is more due to thermal regulation problems and fluid and electrolyte losses. Lameness may still be the number one cause of disqualifying endurance horses, and colic issues may occur.
Horses like endurance horses use what are called slow twitch muscles (type 1) and type 2A muscle fibers (combination oxygen or no oxygen) fast twitch muscle fibers burning oxygen and fat.

50. Most horses use a combination of aerobic /anaerobic metabolism.
They use type 2B muscle fibers (which are strictly anaerobic) if more anaerobic metabolism is used.
They still use some muscle glycogen over time and overall conditioning and care is needed to ensure peak performance.
Transporting horses may resemble an endurance ride (Aerobic) so energy costs should be covered to allow for transport.
Training has a major effect on aerobic exercise capacity. Oxygen delivery is enhance by training increasing heart size by 10%, plasma volume by 10% and muscle glycogen reserves will increase by 10% .
Genetics affect muscle fiber types and aerobic capacity-eg Arabians vs heart size and muscle type.