Page 62 - 2018 Barrel Stallion Register

possible and keep exercising them. This trains the muscles to access the glycogen to burn it for fuel,” she says. Constant low levels of exercise are much more beneficial than sporadic exercise.
“The other thing exercise does is train the muscle to burn fat. When we add fat to the diet, horses can use this as an alternate form of energy during periods when they are having trouble accessing the glycogen,” she says.
“A high percentage of Belgians and Percherons have PSSM. About 10% of Quarter Horses have type 1 PSSM, and it’s also in Paints, Appaloosas, Morgans, Tennessee Walking Horses, Mustangs, Haflingers, and some warm- bloods,” she says.
Type 1 PSSM is most common in halter and pleasure horses and less common in more athletic disciplines. “Halter horses have been selected and bred for a lot of muscle and they don’t have to exert athletically, so PSSM may be overlooked unless they have a severe incident,” Valberg says. “When we’ve worked with PSSM horses on the treadmill, inability to access the glycogen in muscles makes these horses slower. They don’t need energy for traveling fast. These horses have
worked well for pleasure and halter horses, but if a person were to demand more from them, they are incapable of speed work with high demands on metabolism. About 14% of halter horses have both PSSM and HYPP (Hyperkalemic Periodic Paralysis),” explains Valberg.
“Once we located the gene for PSSM and looked again at all our muscle biopsies, we real- ized it didn’t account for all of the diagnoses. The ones in which we didn’t find the gene mutation we called type 2 PSSM, which is prevalent in lighter breeds and accounts for 80% of PSSM cases in warmbloods. We see it in some Quarter Horses, though the predominant form in Quarter Horses is type 1. In one study, we found that about 78% of PSSM cases in Quarter Horses, Appaloosas and Paints are due to type 1 PSSM and about 28% are due to type 2,” she says.
Both types respond to similar diet therapy. Horse owners who realize an animal is affected can minimize problems with careful diet and exercise. “But if it’s type 1 PSSM, they need to realize that if they ever breed that horse, no mat- ter what they breed to, there’s a 50% chance the foal will have this trait because it’s dominant.
It’s so common in draft horses that sometimes foals end up with 2 copies of this gene. Horses are much more seriously affected if they inherit mutations in both genes,” she explains.
Every animal has two copies of every gene— one from the sire and one from the dam. The inherited genes involving this aspect of muscle cell metabolism may be normal or mutant.
A horse may inherit a mutant gene from one
or both parents. Since the PSSM mutation is dominant, it only takes one copy of the mutant gene to cause PSSM; the foal will have PSSM
Hyperkalemic Periodic Paralysis (HYPP)
This genetic defect is found more often
in heavy-muscled halter horses and pleasure horses rather than speed horses. First identi- fied in 1985, this muscle disease is linked to Impressive. He was popular during the 1980’s, especially in halter horses, and his descendants now include Paints and Appaloosas as well as Quarter Horses. The defective gene is inherited as a dominant trait.
HYPP affects muscle metabolism and the transport of sodium in and out of muscle
The HYPP (Hyperkalemic Periodic Paralysis) muscle disease, which is linked to the 1969 Quarter Horse stallion Impressive (above), affects muscle metabolism and the transport of sodium in and out of muscle cells. Popular in the 1980’s with halter horses, Impressive has Quarter Horse, Paint, and Appaloosa progeny.
cells. The primary problem in the muscle is
in the sodium channel. The muscle is closer
to being contracted than a normal muscle fiber. If it takes x amount of influence to cause contraction of a muscle, a horse with HYPP needs only about half the influence required.
It is more susceptible to contraction and will contract sooner due to electrolyte abnormalities that occur at the cell membrane. The defec- tive sodium channel does not open and close properly to allow electrolytes inside and outside the cell to move in their normal manner, so the muscle contracts more readily.
Signs include muscle tremors and occa- sional prolapse of the third eyelid. The classic early sign before a tying up episode is muscle twitching. The skin seems to crawl with intermittent tremors, especially in the flank or muscles of the face. The horse has flared nostrils, sweats, and has elevated respiratory rate, often making a raspy sound as he inhales because muscles around the pharynx at the back of the throat collapse. Affected horses may drool because of the throat paralysis.
As the condition progresses, the horse collapses. No amount of encouragement can get him up and he is physically incapable of rising. He may lie there for an extended period and get up after several hours. Treatment with fluid therapy can shorten recovery time. Some horses cannot be saved; they simply collapse and die. Heavy sedation, such as for dental
work or surgery, may bring on an episode or result in death.
Horses die from this condition by asphyxia- tion, since the pharynx and larynx collapse and they can’t breathe, or because potassium levels become too high due to electrolyte imbalance. The heart muscle develops a fatal arrhythmia, blood pressure drops and the heart stops.
HYPP horses are likely to have muscle problems during exertion. Any stress can trig- ger symptoms—stress of transport, weather changes, illness, or exercise. Whether a horse ever shows symptoms may depend on whether he is H/H (2 copies of the gene) or N/H (one normal, one mutant gene). Being H/H can be fatal even to a foal. These horses may have to be on medication and have strict dietary manage- ment their whole lives. It is possible for an N/H horse, however, to live its life without a spasm, although it is always at risk. Most N/H horses can be managed by feeding low potassium diets and maintaining a steady work regime.
After the genetic aspect of this defect was discovered and a reliable DNA test established, breeders had a way to eliminate this gene. No more H/H offspring will be produced if the mutant gene is never doubled up. When breed- ing an N/H horse to a normal horse, half the offspring will be normal, and the bloodline can be continued with those. Thus, HYPP can be eliminated from affected bloodlines if breeders wish to do so.
60 SPEEDHORSE
equine health