Bone Density, Exercise and Supplements
by John Tuckfield | February 28, 2011
Shin soreness, a condition of the third metacarpal bone (McIII), is a very common
condition in young horses and usually occurs during the first year of training. A study of
30 two year olds entering race training found that those that went shin sore (5) did not
produce as much McIII bone as unaffected horses (25). The reasons for the difference
was not apparent as all the horses were similarly managed. (The Relationship
Between Shin Soreness, Blood Parameters And Cannon Bone Measurements In
Thoroughbreds Being Prepared For Two Year Olds In Training Sales, J.D. Pagan
et al.)
Thus improved bone density appears to be a distinct advantage. A further study of 15
yearlings by most of the same researchers from Kentucky Equine Research (Skeletal
Adaptions With Onset Of Training In Thoroughbreds) showed confinement and
minimal exercise reduced bone mineral content, which then increased as exercise levels
increased to an intense level of training, when it reached pre-training levels. The horses
consumed fortified feed and grass hay throughout the study, but not additional nutrient
supplementation.
From this it can be deduced that both exercise and fresh pasture are important to the
development of bone density, but that full time stabling and inactivity may require the
use of a supplement to maintain its intensity.
Vitamin K (VK) supplements are now widely available and a paper presented at this
months recent Australian Equine Science Symposium on the Gold Coast has
outlined the results of a study on their efficacy in the promotion of bone density
(Vitamin K Function And Bone Density Of Growing Horses, J.R. Biffin et al).
VK has long been know to have a role in blood clotting but is now also known to have a
major role in bone metabolism.
The normal source of VK for a horse is its forage. VK deficiency due to the horse not
consuming enough is claimed to have never been reported, however, the consumption
of substances that work against VK and make it unable to do its job have been
associated with symptoms of deficiency. An example of such an antagonist is
dicoumarol, which is produced by mouldy sweet clover. Further, the therapeutic use of
warfarin can interfere with the metabolism of VK .
VK toxicity from over consumption has not been reported in horses and it is estimated
that the horse need ingest at least 1,000 times the daily recommended intake. However,
in one study every horse administered with a single dose of synthetic VK by injection
developed renal failure.
The naturally occurring primary source of VK in the forage is phylloquinone, a transient
instantaneous product of photosynthesis in live green leaves, which is destroyed in cut
leaves by light. The VK level falls more quickly the higher the UV index (UVI). At UVI of
5, half is gone in 7 hours; at UVI 10, half is gone in 4 hours. A study has shown that VK
levels in fresh-cut rye grass was 8.9 mg/kg compared with 2.3 mg/kg after 2 days sundrying.
Furthermore VK, being a fat soluble vitamin, is poorly absorbed (12%), especially
in low fat diets.
Another Biffin et al. study (Osteoclacin carboxylation, vitamin K and bone integrity
in thoroughbred yearlings) found that 7 mg VK/day was required by a 500 kg horse in
a bioavailable solution to produce greater bone density. It is simply impossible to get
such amount from hay, grain and seed alone.
The amount of VK in pasture has been measured in a wide variety of pasture stages and
climate. A rough guide is the appearance of the pasture. Brown grass contains almost
none; yellow-green grass a little more and deep green grass with a tinge of blue the
most. A horse grazing fresh green pasture will get sufficient VK, a stable- fed horse will
not and require supplement.
In short the results of all these studies "suggest that many horses may receive
suboptimal intakes of VK and further research is required to determine equine VK
requirements in different management systems and the efficacy of different forms of the
vitamin".
Other questions requiring clarification include:
1. If a supplement has been used to promote bone density, would exercise still cause
even greater density, or would the supplement have produced the maximum density that
the horse can lay down?
2. Are there any long term effects on the bone from the use of the supplements?
3. What happens when the supplement is discontinued?
4. Is there a maximum bone density achievable that can not be surpassed no matter
how much supplement is provided?
(Ed's note: I am yet again indebted to Larry Greetham of Piplyn Lodge for
suggesting this topic and for the questions that his ever enquiring mind raises)
