It is generally accepted that the better than average racehorses tend to have heart sizes that are above average. However, heart size alone although a good indicator of racing ability does not guarantee racecourse success. Many successful horses have smaller than average sized hearts and many horses with large hearts were no good as racehorses. It seems easier to get away with a small heart at distances below 1600m and heart size becomes increasingly important as distance increases. Red Crest  (Melbourne Cup) a very good galloper a few decades back had a heart score of about 133-136, he managed to win a Melbourne Cup. His full brother a heart score of a 110, he managed a maiden highweight win at Paeroa. The very good sprinter Silver Wraith  a heart score of 110, he never won past a mile. One of the largest scores in New Zealand  at 140 was found in champion pacer Young Quinn , a little bit unusual as generally thoroughbreds have larger scores than standardbreds.

The most interesting and topical theory on large heart inheritance in horses is that of American Breeder and authoress Marianna Haun . Study of her theory, which is known as The X Factor, is recommended. Regardless of whether this theory is ultimately proven correct or wrong it is an example of how horse breeders can put rules of inheritance and genetic concepts to practical use.  Marianna Haun and her research partners have now measured more than 1000 horses and followed specific heart lines for four generations. Their studies suggest that there may be a mutated gene carried on the X chromosome that has resulted in exceptionally large hearts of some prominent stallions and mares. If you are unaware of this theory, it is fully detailed in her book The X Factor. Even if the theory is wrong, it is an example of why breeders should get some understanding of genetic concepts. The mares and stallions that have been identified by Marianna Haun are still going to be useful for any breeding plan. Large hearts are going to be useful and if these are the result of non-sex linked genes she has at least identified a number of horses that are possibly heterozygous  (Hh) or homozygous  (HH) for any potential large or normal heart gene.   

There is no doubt that heart size is an inherited trait and although environment can have an influence as to the efficiency of the heart and may alter size slightly no amount of conditioning will turn a small heart into a large heart. It would certainly suit me if this theory were eventually proven correct as I believe in breeding back to the X chromosome but do not attribute any specific trait to this chromosome. I do not dismiss the theory but have some major reservations. The reasons for not embracing the theory at this stage is due to personal experience and what I have read about myostatin that has an effect on what is commonly known as double muscling in certain breeds of cattle. A final reservation is related to inactivation in females of the X chromosome and the research suggests that the heart or heart genes are probably not on a sex-linked chromosome but may be inherited from either parent. That is, both the stallion and mare can pass on a large hearts regardless of the sex of the offspring,

My personal observations are very limited and with all small samples chance make these very unreliable. For example, the differences I have recorded between the colts and fillies seem to be greater than generally observed. No doubt, more readings would bring these figures more into line with those generally seen. I have had cardio graphed (measured heart size) of all horses I have intended racing. Primary reasons to make sure there are no irregularities than may cause problems and that the size indicates a reasonable heart size for the type the horse represents. A little motor in a compact can deliver the performance of a big motor in a Cadillac. The overall functioning of the heart is what really matters not just size. One consistent difference I have noticed is that all the colts have a heart score approximately 8-10 points higher than the fillies. All of the scores have tended to be above average but have been in a consistent range for both the fillies and colts.  An Australian study shows something similar, that colts tend to consistently have heart scores higher than the fillies. Note: because my personal experience is drawn from a small sample I have noted a larger difference in heart size between fillies and colts than would be the norm (3-5 points).

  In New Zealand,  a heart score of 100 would be considered low for any thoroughbred, for fillies 113 and for colts116 average to good, for fillies120 and for colts123 above average. You should be happy with scores in this range, as the heart will not be a factor in preventing your horse from performing at open class level. Probably not champion status but there is no heart reason why the horse will not be better than average.  Depending on how the readings are interpreted (an area of debate), for the more conservative vets 110 is about average for fillies and 113 for colts. Scores of 126-130 are well above average and not that common. Scores of about 135+ are rare and 140 exceptional.  

There does not appear to be any sex discrimination as to how heart size is inherited. Mares with above average scores tend to leave sons and daughters with above average hearts and though not common average sized hearts in some offspring have been found. Again not common but mares with average sized hearts can leave offspring of both sexes with larger than average hearts. Similar thing happens with sires. Some sires seem to leave both sons and daughters with above average hearts. For example, current New Zealand  stallion star Zabeel  appears to leave many offspring of both sexes with above average heart scores. It does not appear to be a sex-linked trait.  

In over 9000 cardiographs, the largest heart score measured by one of New Zealand ’s leading veterinarians, Jim Marks, is about 140. For another leading vet, Murray Brightwell, among the thousands he has done the 140 found in the champion pacer Young Quinn  is the highest he has recorded in any horse. Phar Lap ’s preserved heart of 14 lbs is the equivalent of a 140 heart score. This is well below the 150-160 heart scores found in some American thoroughbreds. The method of measuring heart scores is the same in New Zealand, Australia and the USA. If a mutated gene on the X chromosome were responsible for such a large heart scores it is surprising this has not shown up at least once in New Zealand or in Australia where the highest recorded is reportedly 143. This suggests that there is some other factor at play and the cause will not be genetic. This does not necessarily contradict the X Factor Theory. The American researchers have been tracing what they believe is a mutated gene and their research has not shown any variation depending on the sex of the offspring. The heart size is expressed the same regardless of the sex of the carrier or offspring. It is conceivable but unlikely that this mutated gene has not yet found its way to New Zealand  or Australia. All the exceptionally large scores identified to date (in the 150-160range) seem to have been found only in stock conceived and reared in America.  

A second reservation results from findings researchers have made when investigating the condition found in certain breeds of cattle known as double muscling. This condition found in Belgium Blue and Piedmontese cattle results in these animals having enlarged muscles including the heart. Researchers at AgResearch , Ruakura in New Zealand  have successfully isolated the cause of this condition, which is the result of a deletion in these cattle on the number 2 chromosome within the same interval as myostatin. This suggests that myostatin acts as an inhibitor of muscle growth. When this gene is present in its normal form heart and muscle size is normal. If a deletion is present then the double muscling occurs. Mice are similar and mice lacking a myostatin gene have increased muscle fiber numbers and size. Myostatin appears to be a negative regulator of growth. By some clever experimentation, which I do not understand John Bass  and his fellow researchers were able to show that myostatin not only affected skeletal muscle but also that, it is expressed in heart muscle.  

The research suggests that the large heart found in better gallopers might be attributable to something to do with myostatin , which is carried on the number 2 chromosome in cattle. This may be on the same chromosome or another non sex-linked chromosome in horses and could be inherited from both males and females and not a sex linked factor at all. Again this does not necessary contradict the X Factor theory as that relates to a gene mutation  that is believed to be on the X chromosome. The gene mutation may be different in cattle. However, these two factors give sufficient room for doubt not to embrace fully the X Factor Theory until definite genetic causes have been identified.  

The mosaic composition of females gives the greatest reason to doubt the X-Factor theory. It is difficult to understand how in female offspring, if a mutated gene carried on the X-chromosome is responsible; a large heart can be expressed in a single copy mare. I can understand how this might be passed to sons of a single copy mare that carries this gene mutation  but I have trouble understanding how a single copy mare might herself express this large heart. With male offspring, all genes on the X will be expressed regardless of whether this was recessive in females. This is not the case with females. They are a mosaic. In one cell, one X may be active and the other X inactive and this appears as a dark stain called a Barr Body .  In another cell the other X active and so on. It is difficult to see how a mutated gene can be dominant or recessive in a single copy mare. These mares have these large hearts but do not pass large hearts on to all their offspring.  Mothers of colour blind males are in fact colour blind in half the cells of their retina but are not colourblind themselves. Tortoise shell cats, always female, are another example. In a heterozygous  female different phenotypes are expressed.  

For the sake of argument, if we call the large heart gene H (produces a large heart cell) and the normal heart gene h (produces a normal heart cell). A single copy mare will be Hh (heterozygous ) for heart size. Therefore, in the hearts of these single copy mares in one heart cell H will be active and a large cell will result. In the next cell, the h may be active and a smaller cell results. In theory, a single copy mare should not exist because of the mosaic composition of females due to random inactivation of one of their X chromosomes in each cell. Single copy mares should not themselves express a large heart. This though has not been observed by the research done when tracing the X Factor through the generations. The researchers are definite that the heart size is either expressed or not expressed. This does not make sense in a single copy mare and in fact suggests that heart size is not a sex-linked characteristic. If the gene or genes responsible were on a non-sex linked chromosome, the observations made about single copy mares would make sense and be simply explained. The H gene is dominant to the h gene, which is recessive.

To illustrate using the normal hearted Mr Prospector  (h). He should have inherited a large heart from his dam Gold Digger  who was a daughter of the large hearted Nashua  (H) and the double copy mare Sequence  (HH) if the factor responsible for heart size is carried on the X chromosome. It is possible that Sequence has been wrongly classified and she was in fact only a single copy mare. This in turn means that Count Fleet must have been normal hearted or Miss Dogwood was a single copy mare (Hh) or possibly even (hh). However, if we assume that Sequence has been correctly classified the normal hearted Mr Prospector can be explained if this is a non-sex linked trait. It would also explain why Mr Prospector could be an outstanding sire but with a tendency for his offspring to excel over shorter distances yet still produce stock that can get a trip. There is plenty of evidence that heart size is increasingly important as distance increases. If it were a non-sex linked characteristic Mr Prospector would have inherited an H gene from Gold Digger and h gene from Raise A Native  (he in turn would be Hh or hh for heart size). This means Mr Prospector would be heterozygous  for heart size (Hh) even though his dam Gold Digger was homozygous  (HH) for this trait.

That the trait is not sex-linked makes it easier to explain apparent exceptions to the X Factor rather than saying that some large hearted horses may have been wrongly classified or some other factor is involved that switches the gene on or off. No further explanation is necessary if the gene or genes responsible are on a non-sex linked chromosome. If it is a dominant trait then when two homozygous (HH) carries mate, the trait will be expressed in all offspring. If two heterozygous carriers mate (Hh) then one in four offspring will display the trait. If two homozygous (hh) carriers mate the trait will never be expressed in the offspring. I would certainly like to embrace the idea that the large heart is the result of a gene carried on the X chromosome in certain females as I can see a definite pattern with female duplications in many of the better racehorses. More research is needed.

Even if the large heart theory is ultimately proven wrong and heart size is not a sex-linked trait, I do not think you will go far wrong in breeding to such a pattern. There is no doubt some mares make better mothers than others. It is possible that the large heart being traced is not a mutated gene on the X chromosome but reflects some families tend to produce mares with superior mothering abilities than other families.  These mares are excellent mothers and do their foals well and this in turn is passed on to the female offspring. When this is diluted, because of random recombination, by reintroducing a different strain this rejuvenates the mothering ability and better offspring including larger hearts result. All that is happening is important genes affecting mothering traits are carried on the X chromosome. By measuring hearts scores in the offspring of these superior mothers it appear heart size is inherited in a sex-linked manner whereas the actually gene or genes responsible for heart size are carried on a chromosome that can be inherited from either the stallion or mare. The better mothers just enable the heart gene or genes to be expressed to their full potential.  

I think the genes or genes responsible for heart size when found will be on a non-sex linked chromosome and merely influenced by factors carried on the X chromosome. If the theory is wrong the X factor supporters have successfully identified a number of horses that are homozygous  and heterozygous  for heart size and their observations can still be used to guess the probability of any given mating producing offspring with larger than average hearts. If the theory is correct and I am wrong then I will have an increased chance of getting this trait by default by breeding to my preferred pattern. Either way there are no losers. The research carried out by Marianna and her partners is invaluable information for all horse breeders. I am inclined to think their observations are correct so far as what horses have large hearts and rather than wrongly classifying certain horses they have attributed the trait to the wrong chromosome.  

To digress briefly the NZ Government has recently given approval for John Bass  and his fellow researchers at AgResearch  to breed double-muscled sheep. They will do this by knocking out the myostatin gene, which should result eventually in a herd of sheep that are leaner and have approximately 40% more body muscle. It will be interesting to see what results from this ongoing research as there are potentially huge implications for humans. They hope to get a better understanding of how muscle develops and what role myostatin may play in muscle wastage. To date research shows that myostatin appears in high levels in the cells of sheep that have had heart attacks and may play an important role in preventing cell death. This may have major implications for diseases such as muscular dystrophy and aids.

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An Email Sent to me by Terry Lee - April 26, 2003