The Nitty Gritty: Bone Cells During The Breeze

Probably my boys would like to avoid racing against Go Country Grip, but for the present I'm more interested in what happens when the lead leg of that speed ball smacks into the ground. When you're on board you hear the smack followed shortly thereafter by the jarring and vibration as the weight of the horse shifts on the follow through. You can pick this up visually with some effort at slow mo.

In terms of what occurs there's a lot to consider. If you look at a leg bone attention is first drawn to the macro level, the bending, contortion and expansion and contraction of the whole bone. But, absent overbearing torsional force perhaps in the form of the bad step, the bone as a whole generally holds together.

At the micro level we consider the various part of the leg bone as illustrated below:

I believe we're primarily concerned with areas:
1. The cancellous spongy bone that we'll find near the blood vessels in the interior portion.
2. The cortical or hardened bone as we go outward which is the maturing mineralized matrix.
3. The thin outer layer of unmineralized collagen beneath the periosteal membrane..

And, of course, there's this primary area of concern:
which would be the condylar or end aspects of the bone which for our youngsters contain the still developing ephysial plates as well as developing spongy bone. Here's another view:

Considering the force that applies to the bone as microscopic structure and what we know about how they hold together, which includes:

1. the manner of the layering of the cells.
2. the mineralized connections.
3. the proteins which make up the bone glue and their bonds which also include the sacrificial bonds which lengthen with pressure and come back together with the release of pressure

possibly we can conjure what occurs to single bone cells while the horse is running. You get, if you think about it, is a single bone cell that's undergoing momentary intense pressure and contraction, and then release, repeated 230 times over the mile .

Next post I'll look at what's happening in a single bone cell in the areas of concern.

Training:
Thurs. 7/31 still a total mess from the 2.1 inches of rain 2 days ago, but, the paddock is just dry enough for riderless work. 10 min of slow trot-gallop then the two year old was removed. Art then did 2 x 4f as fast as conditions allowed, probably 14-15 sec/f, it was a good workout considering the horse was motoring through the mud. We skipped tack work due to conditions.
Fri. 8/1 still quite wet, the horses did 2.5 miles of trot-slow gallop without stopping. Then 10 min. of walk under tack for each horse.

The Lead Leg Of Got Country Grip

Above is "Got Country Grip", a Paint Horse featured in this week's Blood Horse videos setting a world record for 350 yards en route to 15 straight wins, and once again the illustration of the forces working on the horse at these speeds. (Left click for better view.)

I watched Grip's lead leg hitting the track in both in real time and at slo mo at these much faster speeds than you see in thoroughbred races. We're looking here for hoof hitting track surface and deciphering what we see visually as this contact occurs. For any single clean hit on a pristine surface we consider the questions of severity and degree of forces operating and the manner in which the leg seems visually to adjust to these forces. It's a bit of a "stop action" thing as consider exactly what's going on.

The visual impression (at world record Paint Horse speed) is more the hoof "flicking" the ground instead of "hits" or "pounds". While I'll note that the impression of "flicking" fades just a bit in slow mo because there you can see that momentary instance where there is some jarring, the overall visual impression you get from watching the lead leg hit the track is more one of fairly easy absorption instead of overbearing force that might cause real damage.

BUT, this is only a visual inspection of a single hoof strike. I've noted before there are other ways to judge the event including being on the horse and "feeling" and "hearing" the degree of force from every stride. Note that feeling and hearing the strike give an impression of a much greater degree of force than you are able to pick up visually. I'd go as far as to say what you see with your eyeballs in a hoof strike almost makes no sense compared to what you feel and hear in terms of degree of force.

So, between watching, feeling and hearing any single hoof strike, where's the reality? I'll elaborate later, but I'd be surprised if there's any damage either at the macro or micro level from any single hit. I'd said you get 90 of those per mile race. I was mistaken. It's actually 230 hoof strikes per race--15 strides per furlong. Even if we conclude that any single hoof strike is unlikely to damage our horse, when we consider 230 of those it becomes a different ball game. I'll take a look at this at the cellular level and systemically in the next posts.

Training: It rained 11 or 12 days in July including the last 5 days straight. 2.1 inches Tues and Wed. We've given Rod off time over the last week as he seems to be in a growth spurt. I avoid exercise during growth spurts. Thus, the below is only for Art the three year old, though Rod did a little light galloping and trotting here and there.
Fri. 7/25: 6F riderless at max speed with warm up and warm downs.
Sat. 7/26: trotted 1 mile under tack.
Sun. 7/27: Off. Rain
Mon: 7/28: 2 miles riderless slow + 1 mile trot under tack
Tues. 7/29: Rain threatens but we get in 6f riderless near all out with warm ups and warm downs. Nice work for Art.
Wed. 7/3o Off. 2.1 inches of rain.

Cannon Bone During The Breeze

Nice photo showing front lead legs in flight. As those hoofs slam into the track and are pulled through the stride the cannon bone will be subject to several concussive forces working simultaneously in quick sequence.

Initially as the hoof hits the ground considerable force would be sent quickly upward, and then with the horse pulling the leg on through (in rearward motion) pressure would hit directly on the front of the cannon pulling that material backward.

Thereafter comes the largest force from above directly downward as the weight of the horse centers over this lead leg.

As these forces come together in the cannon bone what happens at the cellular/molecular/atomic level during the stride, and what is the condition of the bone immediately post race would be the questions. Hopefully we can then imagine the extent of damage post breeze and consider how low long the repair process will take before we may safely breeze again.

I found a few more illustrations of bone (posted below) which give a good idea of structure, for anyone interested. (Left click on them to enlarge.)

Training:
Fri. 7/25: half an inch of rain today, everything a mess. The horses were galloped riderless in the paddock 3 x 6f as fast as the conditions allowed. Probably close to :15 sec/f speed. Nice cardiovascular work for our 2 yr. old, who needs it.

Momentary And Repeating Force

This photo accurately shows the right front lead leg at the height of the downward arc that will end with the hoof striking the track. Notice the left leg perpendicular to the track carrying most of the weight of the horse at this point.

Again, the height of the front right at this point seems insufficient to me to generate that 12,000 lbs/sq. inch of supposed force on the cannon bone regardless of the muscular strength that slams the hoof to the track surface, but possibly you get that amount of pressure in the short moment when the entire weight of the horse will shift to the front right leg during the follow through of the stride as in the image of the front right (outside horse) below.

I'm thinking the photo catches the black horse above just after the point of maximum pressure on the right front. Notice the right front is the only leg touching the ground. For a short moment that right front carries the entire weight of the horse, and significantly this moment occurs almost simultaneously (just after) the hoof thuds into the track. And so you have the concussive effect of the hoof strike hitting onto the track radiating back up the cannon bone at the exact (or almost exact) moment the entire weight of the horse is coming down from above. It's probably for that 1/2 second when these two forces coming in opposite directions coalesce that the 12,000 lbs./sq. inch. of concussive force on the cannon bone comes into play as supposed .

This process repeats over and over then about 230♦ times in a mile run, and thus on our bone cells and molecules we have a half second of maximum force that is "momentary and repeating".

What effect on the cannon bone? I tried to simulate by striking my arm, palm open, on an air mattress repeating strike after strike. What I noticed is that this striking results in "pressure" on the arm bones, and in particularly pressure on the surface of the bone. So that for our horse and the bone cells we have this interesting sequence:

Momentary + Repeating + Pressure

This understanding might allow us then to conceptualize what happens in this process within the cannon bone in my next post.

Training:
Tues 7/22: riderless fast 3 x 2f all out. Skipped tack work.
Wed. 7/23: Off.
Thurs. 7/24 As I hit the farm the Hurricane Dolly rain was almost upon us. We hustled them out of the pasture hoping to get in some riderless stuff before the skies opened and we accomplished 2 x 6f at a 2 min. clip with some faster spurts. The total volume was over 2 miles but we allowed a rest after the 6f. The rain held off and we got in some tack work: Rod trotted 1/2 mile, Art trotted 1 mile. I like to trot due to rider weight when it's been three days since the last tack work.

Horses Breezing: How Much Force

As they come down the stretch watch the lead leg hit the ground through each stride and it hardly looks like all that big a deal. There's an appearance of concussion, to be sure, as the hoof strikes the ground but it's far less than the bone shattering effect you expect reading my last series of posts.

Keep in mind that mostly down the stretch they're going in :13s which differs markedly in intensity from a sprinter doing :11s. Stride style also affects as low choppy striders will hit the ground less efficiently but also with less force than the long flowing outward reaching stride. In any event, regardless of speed you wonder where the supposed 12,000 lbs/sq. inch of concussion comes from.

It's there, be assured, but you have to observe really really close to see it. First, I'll note as in prior posts, if you're on the horse at speed the amount of concussion is quite obvious. You both hear a thud at speed as the front legs strike, but you can feel the force of impact reverberating through the horse. Its of such force that when I'm on I'm planning an exit with every stride. the sensation is that scary.

What really happens--where the 12,000 lbs./sq. inch applies in the flowing stride as the front leg reaches out and down as in the illustration of the lead horse in the photo, is that at some point after the hoof hits the ground and while still in contact with the ground on the follow through the entire weight of the horse balances on that one leg. This happens only for an instant, quite luckily, but for that second all of the force is there. It's probably in that split moment of full weight bearing contact that we need to consider what's occurring in our cannon bone.

Training:
Wed. 7/23/08 The Woodlands closes. I'll comment on this soon. After yesterday's speed work the horses were off.

Mineralization In The Cannon Bone

To visualize what's going on in the cannon bone during the breeze we have to consider how the canon is constructed at that point in time. Particularly we are interested in the strength and state of maturity of mineralization, which is an ongoing process, as we go from the interior of the bone on outward.

Last post I noted that the mineralization takes about two weeks to establish itself and then (presumably) continues to mature until you have the a crystallized lattice completely encompassing the remnants of the living bone proteins and collagen fibrils of the matrix.

The initial part of this process (I'm guessing) would be the laying down of calcium crystals in and around the bone proteins and collagen fibrils that make up the immature cells of the matrix (live bone material). Eventually this crystallization process will "encase" those proteins and collagen fibrils, and finally the collagen itself begins to mineralize until you get that final layer of material that has the strength of reinforced concrete.

In our young horse age 3 I'm presuming only the interior sections of the canon bone have completed this process and that as you go outward from the interior to the periosteum membrane that covers the outer bone surface the state of mineralization is less and less mature as you proceed outward until you reach (at some point) live matrix cells where mineralization has yet to begin.
May we presume the outer surface of the cannon bone just below the periosteum consists of unmineralized bone matrix. This unmineralized outer layer is being constructed by Osteoblasts and is called the Osteoid, per below.

With this background I'm ready to discuss what's happening during the breeze and more importantly the state of the Osteoid surface and inward immediately post breeze.

Training:
Mon. 7/21: Tack work for Art--1.5 miles trot with some short gallops. We'd no more thrown Nob up on Rod when we noticed a missing front shoe and a severely lacerated heel bulb. Work canceled, shoe reapplied. Luckily we had only a bulb injury. Idiot.
Tues. 7/22: Fast work day. RR outsmarts himself. The original plan was tack work then fast, but go to the farm and the youngsters were fighting and already into it, so thought I'd do light riderless fast then tack work after. The riderless faster work turned into 3 x 2f all out for Art. He looked good, but too fast to risk tack work after in case of any injury. Rod was allowed to trail with his heel bulb injury. We will wait to after Sept. to press the 2 year old.

Mineralization

Profound stuff from the The Journal of Endocrinology and Metabolism:

"Bone is made in two stages; matrix is formed first and about 2 weeks later (in children) it begins to mineralize; the delay is longer in the adult skeleton. The process of adding mineral to matrix is referred to as "bone mineralization" "

(we know that matrix is composed of a combo of proteins (bone glue) and collagen.)

"It is important this this term not be used for the quite different process of adding bone to the growing skeleton". (This latter statement presumably refers to bone growth from the ephyseal plates.)

Let's sharpen this up a bit:

"Mineralization of bone--essential for its hardness and strength--involves a well orchestrated process in which crystals of calcium phosphate are produced by bone-forming cells and laid down in precise amounts within the bone's fibrous matrix or scaffolding. If the process is not properly regulated, the result can be too little of the mineral or too much....inorganic pyrophosphate is involved in controlling the right rate, the right pace of calcification in the normal skeleton."

and then, from the National Institute of Arthritis:

"Although chemical and physical analyses have revealed many details of the structure and organization of mineral in bone, much remains unclear about the process by which calcium and phosphate ions are sequestered from the soluble phase to form crystals in association with the bone matrix."

"In bone formation, osteoblasts first secrete the proteins of the bone matrix, or osteoid, which acquires mineral after forming as a histologically distinct layer. Several proteins have been identified which the property of inhibiting matrix mineralization, suggesting that the potential for precipitation of mineral is inherent in the physiological milieu, and that a counterbalancing inhibition is required to prevent inappropriate formation of insoluble crystals. ..Yet it remains unclear whether mineralization of bone principally reflects passive chemical processes, requiring only the presence of appropriate local concentrations of the precipitating ions, or instead, involves active biological processes, requiring higher-order functions of cells and their macromolecular components."

How fast mineralization proceeds and also the manner seem important questions.

Training:
Sun. 7/19 Tack work after yesterday's speed work: Rod walk/trot 10 min, about 1/2 each and Art 1.4 miles trot.

Fracture Process At The Molecular Level

For our horse there is actually a physical observable process of fracture that we would like to avoid. But, to avoid, do we first have to understand the process?

Above left an illustration of "cross linking". Solid materials at the molecular level hold together by certain mechanisms. Spider web molecules (fromHansma website, ) hold together both by a successive looping of molecules in terms of their arrangement and molecular cross linking as in the illustration, i.e. an assembly of molecules of some sort.

As force applies to this spider web material Hansma (through Atomic Force Microscope Imaging) notes the material contains sacrificial bonds and hidden length that reform quickly if the protein is allowed to relax after it is extended.

As force increases to rupture Hansma uses such terms as "rupture peaks" and "successive rupture peaks" along the molecular matrix. The cross linking springs and molecular loops give way molecule by molecule breaking the sacrificial bonds.

In bone collagen the process is similar. From Hansma: "We found that collagen molecules can rupture sacrificial bonds at constant values of the distances they are stretched. We observed two patterns of rupture: After applying forces greater than 500pN, several ruptures would occur for every 78+3nm the molecule was stretched. (IT TAKES FORCES OF OVER 1000pN TO BREAK A COLLAGEN BACKBONE)" Note that the number of ruptures is related to the distance the molecules are stretched + force applied.

The two patterns of rupture Hansma observed here involved, merely, different degrees of force, one much greater than the other. With application of weaker force, increasing it slowly as you go, they note the breaking of the bonds still occurs as force continues to increase but the breaking process is barely detectable.

The conclusion is logically exactly what you'd expect. The individual subunits rupture sequentially AND less and less peak force is necessary to continue the rupture process because the backone of the collagen begins to break and so less force is needed to rupture the remaining molecules.

One may imagine for our breezing/racing horse the various degrees of force that may apply depending on circumstance. As in Hansma's example we might have weaker forces working on already damaged bone, stronger forces rupturing healthy bone or any sort of combo.

Our interest of course is in making sure the bone is healthy before our next breeze. We need to understand precisely what's happened, and what will occur before we breeze again.

Training:
Thurs 7/17 tack work after yesterday's speed work. Rod walked 10 min and Art trotted the pasture course 1.4 miles.
Fri. 7/18 Rain again. 1/2 inch. unbelievable. Off.
Sat. 7/19 RR getting disgusted with the weather. What's new? Unable to gallop due to wet conditions so we settle on riderless fast work. The horses went 4 x 2f as fast as the muddy conditions allowed. Nice work by the 3 yr. old, less so by Rod who we're declining to press due to the state of his physical development at the moment.

AFM

You're guessing this the Mars Lander but actually it's the the Atomic Force Microscope (AFM) used in the Paul Hansma Labratory at UC Santa Barbara where they're studying fracture resistance both in solid materials and human bone. I returned to the Hansma website to review it before continuing with my wild speculation that our breezing youngster will be "rearranging" the molecules on the surface of his cannon bone instead of creating microscopic fissures. And, indeed, the latest is that Hansma now has developed a tiny probe that can view microscopic bone in a living being. You might think the Jockey Club Eight Belles Committees would be hot on this trail.

But here, I'll try to focus in and ferret out from Hansma's lab what might apply to the thoughts of my prior posts, and ask any reader to understand that this is highly technical, though fascinating stuff.

You have to start with the understanding that there are three types of bone materials:

collagen fibrils
mineral plates
a matrix of unmineralized, non-fibrillar organic material made up of proteins called "bone glue" by Hansma

These are shown in the 500nn images below, A,B,C and D:


"A" shows collagen fibrils coated with bone glue.
"B" shows unmineralized colagen fibrils.
"C" shows mineralized collagen fibrils.
"D" shows crack formation in the "non-fibullar organic matrix.

Now, Hansma's group is studying what happens when you apply force to each of these materials, and, to sum up a long dissertation, most interesting, Hansma uses phrases such as "the gliding effect within the fibrils", cross linking and more to describe what's going on.

Hansma takes us through precisely what happens at the molecular level in solid materials such as bone as force is first applied and then withdrawn, next post.

Training:
Wed 7/16 I improvised my prior plans a bit. Scratched Art's planned riderless 3 x 3f at max speed for a far less strenuous workout that would permit us to go on without a day of rest on Thurs. We did about 6 x 3f riderless mostly slow with some short bursts of speed with both horses. Art then trotted 1.35 miles under tack in the pasture. The welder was out to do the trailer floor. The wood flooring hopefully goes back in tonight and we're in business.

More Thoughts On Post Breeze Microfracture

Were the red arrow points and on down indicates the post breeze area of cannon bone concern. I've never breezed a horse any distance without getting heat on the outer surface of both front cannons. This heat may dissipate in as little as a few hours in extremely conditioned animals. If it lasts more than 48 hrs. I become very concerned.

My worry in this regard is/has been possible micro fractures resulting from the breeze/race, and how long it takes to heal them and allow us to continue, i.e. the most basic question in racing, how much time will have to elapse before we can safely go again.

Last post I speculated that: with CONDITIONED bone possibly my post breeze concern for micro fracture may be misplaced in that a breeze or race that has been progressive in nature may fail to produce any tissue tearing or gaps at all. Rather, what happens on application of force is a slight rearrangement of material at the molecular level.

But, force applies over the whole bone, and so the idea of mere "rearrangement" of live tissue in a particular area simplifies the real problem since since rearrangement of tissue given a specific quantity of force probably varies depending on the location of the application of force. Look at below illustration and consider that tissue moving and rearrangement may differ depending on location.


To get a final answer whether we get microfractures or mere rearrangement post breeze, perhaps we have to consider the areas of the bone in details.

Will soldier on with this next post. I'm reading the latest from Paul Hansma. Conclusions coming~!


Training:
Mon. 7/14 Still wet. Art gets the day off after yesterday's fast work. Rod has been given some time off due to a growth spurt and this evening he's shorter than he was before. Somehow they manage to shrink. Art trotted riderless gently for about 10 minutes with very little stopping.

Rearrangement (Continued)

When I'm in a strenuous breezing schedule as last summer and into the Woodlands meet with my Groovin' Wind, were there were 45 breezes over a period of 4 months, subsequent to each breeze there is concern as to the condition of the cannon bone in terms of microfracture, and whether these would heal for the next breeze two days hence. When you're going all out every third day in multiple heats as was Wind, the reader will have to trust me that the degree of concern here weighs rather heavily, particularly when the evaluator of this process is also the rider of the horse.

However, as I'm thinking about this process of tearing down and rebuilding of bone, or post-breeze microfracture repair, I'm considering that my fears may have simply been wrong and misplaced. In fact, as I'm considering all this now, in conditioned bone, post-race microfracture may be a misplaced concern.

Why? It has to do with the idea of "reararrangement" of bone substance at the molecular level in response to application of force. Instead of microscopic tears and gaps being left by the 12,000 lbs./sq. inch of momentary pressure, I'm more thinking now that the fluid/solid bone materials shown in the electron microscopic images above merely rearranges itself like waves in the ocean and while each molecule post breeze might be in a slightly different position vis a vis it's neighbors, the material composed of these molecules remains substantially the same, i.e. without microscopic fractures.

The above is a bit of a simplicfication, and I'll try to nail it down next post.

Training:
In KC we continue to get hammered by weather. It's slowing down the race prep. BUT, as soon as the trailer floor repair is complete, we're off to the track. I'd say race training has begun for Art, though Rod is still in the pre-training phase.
Sat. 7/12: rained out by 1 inches of rain.
Sun: 7/13 Art does riderless speed work in the muddy paddock. This horse has the look. Hope I'm seeing things right. Probably was about 5 x 3f as fast as conditions allowed, then 10 min. walk under tack. Rod got the day off as he seems to be in a growth spurt.

Rearrangement: A Key Concept

Busy week, but back to fracture resistance. Txs to Bill for comments last post.

As I continue to think on this I might have just realized something that is going to change my conceptions quite a bit, an epiphany perhaps! Prior posts as our horse breezes down the racetrack noted what might be happening and the forces involved. Focus on a small portion of cannon bone tissue maybe the size of a dime. Will consider what's happening at the electron microscope level on out.

First, think of the leg bone of a chicken. I'd suspect human bones, and certainly large animal bones are far more calcified then our feathered friend, but, we see in the consistency of chicken bone the effect of collagen on the bone structure. There is quite obviously mixed into the mineral lattice a significant amount of live tissue.

Thus, when we consider what happens as the hoof strikes the racetrack at speed, and I noted:

1. heat buildup.
2. movement or oscilation at the cellular/molecular level.
3. damage and squeezing here and there.

But, as I'm visualizing what might actually be happening my thoughts trend in a different direction. Forces working on the lattice of a dead, solid object are going to create some mollecular movement. The molecules buttress each other, and unless the force overwhelms the final result probably is the molecules pretty much retain their position.

BUT, when we throw in the live tissue in the bone lattice I think we might get an entirely different result BECAUSE we have a different sort of bonding.

Imagine our cannon bone is constructed of water molecules. Then, let's harden it up a bit, but gradually. We have a substance slighter harder then water. The next substance is harder yet. The next substance harder and so on until perhaps we have a material as thick as pudding. We keep hardening the substance and finally we get something as thick as collagen.

I'm suspecting that forces acting on collagen instead of oscillating the molecules or causing them to vibrate instead act in a similar manner as when force is applied to water in that "waves" of material are REARRANGED. As the substance thickens there is less and less movement and the waves become shorter and shorter, but, the principle remains the same in that force merely rearranges very similar molecules vis a vis each other SO THAT THE END RESULT IS MATERIAL EXTREMELY SIMILAR TO WHAT WAS THERE BEFORE THE FORCE WAS APPLIED.

This seems to me a key concept for bones and fracture resistance. I'll expound, next post.

Training:
We're working on putting a new floor in the horse trailer. As soon as that's done we're off to the race track. This interfered with training a bit this week.
Wed 7/9: Both horses ran riderless in a still muddy paddock. We did very fast and very short spurts as the ground was ideal for that. Probably a total of nine 1/2f spurts with the horses galloping into and out of them. Nice, albeit short, speed work.
Thurs. 7/10: Art trotted 1.5 miles under tack. Rod walked 7f. He was a bit feisty and the cowardly Nob afraid to go into the trot.
Fri. 7/11 Tack work sacrificed to working on the trailer floor. The horses were galloped riderless 1.5 miles with speed work planned for tomorrow.

Vector Forces At The Breeze

Our youngster motors down the track quite easily, giving us an illusion of invincibility and strength. As the horse moves we're considering, as a matter of course, what's happening within the bone structure even as we may for the moment be distracted by the grace and speed of our horse.

What's happening to those cannon bones can be illustrated easily by a simple experiment that anyone can conduct, as follows:

Put on a pair of soft running shoes and go out for a brisk walk. As you walk begin concentrate on your tibia. You will feel immediately a surprising amount of force operating with each and every one of your strides. With myself I feel the largest amount of force just below knee cap which emanates on down as I swing through the walk. At the same time I feel a lighter force at the ankle which seems to move up and coalesce with what's coming down from the knee. Again, you will be surprised at the amount of this force.

In consideration of this we think of what's going on in the cannon bone of our speeding horse. I have trouble imagining this since supposedly the force exerted is three times the force on human leg bones at speed (4000 lbs/sq. inch in humans; 12,000 lbs./sq. inch in the horse.)

But there's something else to consider also, which is that the "amount" of the force is only one factor that plays on the atoms/molecules/cells of the cannon bone. When force hits, we also have operating the vector, direction, and intensity of the force, as in the puppy illustrations above. 12,000 lbs. per square inch will differ in effect depending whether said force is applied head on or at an angle, and also whether after application the leg remains stationary or immediately begins to swing through a stride. In this regard the nature, shape and speed of the stride will also affect the degree of force applied on any single molecule of the the bone.

Interestingly, in terms of the moving horse the application of force might differ in a horse with an efficient, graceful stride (see Big Brown) as opposed to a chop chop stride, or, significantly, in a tiring horse that loses its action.

Complex, but stuff we need to be aware of in imagining, per last post, what's happening in this process at the molecular level. I'll try tomorrow to combine the thoughts of the these last two posts as to what exactly happens to the bone tissue at the mollecular level during the breeze.

Training:
Sun 7/6 After yesterday's speed work, Art trotted a mile under tack and Rod walked 5f under tack.
Mon. 7/7 both horses galloped 1.5 miles riderless after warm up. Art then trot-galloped 1.25 miles under tack. The gallops in this were very short as Mr. Nob (the rider) attempts to get this youngster under control at the gallop. No bucking today in the first gallop in a week, but still having a lot of trouble getting the left lead. The horse is responding well to rein work though in terms of changing his diagonal at the trot. Rod does his first trotting under tack which makes 7/7/08, I'm supposing, a significant day for Rod.
Tues. 7/8 the planned speed work gets rained out, again. Atypical wet weather for our area continues.

The Microscopic View

We presumably know the basics--bone remodeling, osteoclasts and osteoblasts, mineralization, growth in response to stress, but all that happens before or after the breeze.

This post will try to imagine what occurs during the breeze itself, and per last post we understand there may be differing effects depending on whether we're talking live tissue (collagen, etc.) or mineralized dead tissue or a combo.

The first thing that happens at speed is that there's a hard hoof strike and then 3 pauses before the next strike as the horse flies through the air. I'm assuming that the 12,000 lbs per square inch of the strike that dissipates on through the entire structure causes a couple of things, and we may imagine these by striking together two solid objects or perhaps a limb of a live tree against a solid object.

First there is obvious "vibration". At the cellular/molecular level we may imagine this as oscillation or simply, movement. The cells and molecules move (at whatever distance) vis a vis each other, and said movement is restricted both by the proximity of millions of molecules stuffed into the lattice, and also by the bonding and inherent structure. You can see some of the bonding material in the electron microscopic image above. Without the forces which hold the molecules together, they would simply fly apart.

The second thing that occurs (that I'm able to think of) is heat build up. Chemists and physicists understand that heat is a function of movement--a speed up of electrons, neutrons, etc.--and increases exponentially if it is trapped as when millions of molecules closely encased move in unison. In large animals there is also of course systemic heat build up which contributes.

(Edit 7/9) There is also a third thing that probably occurs, which would be "damage or reshaping of individual molecules/cells" at certain points.

Pretty basic stuff until we consider that:
1. Heat build up weakens bonding material and structure. (picture hard plastic melting).
2. Oscillation and vibration offer minimal harm until the speed overcomes the forces of the bonds.

Continue next post.

Training:
Sat: 7/5: riderless 3 x 2f at 85% speed. They went faster then planned. Both horses walked in the paddock under tack afterwards.
Sun: 7/6 Art trotted 1 mile under tack. Rod walked 5/8 mile under tack.

Anatomy 101

Amid firecrackers, nice weather and barbecue smells emanating from my neighbor's yard I might better be out celebrating the weekend, but, I'm locked up in the office clearing off a few things including a malware invasion of my computer. Should have avoided clicking on that video of Alex Rodriguez's wife. Thank goodness for Spybot Search and Destroy, and where the heck was my Norton 360.

But, on to the big stuff. Our youngster's cruising down the track and we're leaning over the rails thinking what's holding those front legs together. Knee carpals, sesamoids, metacarpals of the pastern, even the splint bone, but I'd think Dr. Cruz (last post) U of Ontario researchers are looking at cannon bone structure assuming the principles will apply across the board, and thus, so will I.

We know (from diligent reading of this blog), the cannon consists of collagen and mineral lattices in various stages of mineralization as well as significant enervation, blood vessels and various canals permeating the outer bone structure. We may find more collagen as opposed to mineralized bone in our youngster compared to my 13 year old retiree.

How strong is this bone, and what may it withstand? We go back to that image of Nunnamaker et. al. striking and bending cadaver bones to discover the breaking points. What confuses our conceptions here is the mixture in the bones of dead and live tissue. Is e.g. bone more akin to the strength of rock or steel (somebody compared it to reinforced concrete), or perhaps, as I'm thinking, a similarly sized limb of a tree?

To give a little more perspective, we're talking here bones and "fracture resistance", but fracture resistance is also a mechanical engineering concept that applies to all solid materials and becomes relevant in such inquires as the Minnesota bridge collapse. We know e.g. that many solid materials(absent weakness and cracks) will resist fracture until they reach a point of breakage where the particular bonding material will simply give way all at once.

To investigate this process a look at the atomic/molecular/cellular level is necessary, and we pull out our electron microscope. The inquiry will include the recognition that in mixed live/dead materials such as tree limbs and horse bones there will be a differing fracture effect on the ossified or dead wood portions than the collagen or living plant cells. You'd think the live stuff would "tear" in the fracture process whereas the more ossified materials might "explode" with sufficient stress.

Complex stuff because we also in bone look at the effect of stress on both live and dead substance and a mixture of the two. Now, I'm back to the barbecue until I investigate this further.

Training:
Wed 7/3: the horses went a slow riderless 1.5 miles yesterday in prep for today's speed work. Never happened. 3.17 inches of rain instead. Unknown that I've ever seen that much at once. It was about 9 inches in the buckets. Started just as I was leaving the office to go train.
Thurs. 7/4 Farm under water. Off for the second day.
Fri 7/5 Thanks to some sun we're back in business. It's been a questionable 5 days of training. Weather again. 15 minutes of riderless play for both to get back into it. Went something like 8 x 3f slow with rests between in the mud.

Some Preliminaries

I've had some trouble with this next post for in the typing, my mind keeps straying to my personal disgust over racing's approach both to catastrophic injury and injury in general. The blog is about to get to the central stuff and what I consider one of the three or four biggest problems in racing which is that our trainers with their methods are both injuring their horses and in process driving owner after owner out of the game.

I've been now 25 years in the sport. I continue my personal amazement that the powers that be in racing seem unable to concentrate on or comprehend the central problem of injury and its effects. Even now with Eight Belles it's more whips, genetics and horse shoes than any recognition of the real causes. If you fail to understand or disagree, perhaps take a look at the Research Archive of the Grayson Jockey Club where you'll find exactly zero studies of the type of inquiry going on right now on this blog. Why would we be surprised at the George Washingtons and Eight Belles when the primary research arm of the sport fails us to this degree? It's a scandal.

But, just as I was giving up finding any horse related research as to the state of cannon bones during breezing I remembered the gentleman pictured above, Dr. Antonio Cruz, and that some good work indeed is going on right now at the Veterinary College, University of Ontario.

The Ontario project seems to have started in 2004. Here is a description:

"Identification and prediction of canon bone fractures in 2 and 3 year old race horses (Projects 2004-2005): Dr. M. Hurtig. This project is part of a more comprehensive program designed to reduce musculoskeletal injuries at Ontario racetracks by improving the monitoring of horses and racetrack surfaces. In previous work, the Comparative Orthopaedic Research Group has established the utility of using accelerometers for monitoring shoeing and track conditions. The current proposal expands the examination of horses presented from the Ontario Racing Commission Death Registry program to establish the incidence and location of micro fractures in the canon bones. Quantitation Ultrasound, a non-invasive technology that can be used on living horses for assessment of bone quality, will be correlated with three-dimensional imaging to link speed of sound measurements with bone pathology."

This has matured in 2007-2008 as follows:

"Non-invasive surveillance of cannon bone and joint health in racehorses by quantitative ultrasound and bio markers: Dr. A. Cruz.
This project is part of a larger ongoign program to identify and prevent catastrophic bone failure in thoroughbred racehorses. The project will investigate and monitor the cannon bones and joint health of 2 and 3 year old racehorses and will determine their response to exercise. (Wow! Finally!). In the last two years we have identified from post-mortem specimens quantitative ultrasound locations in the cannon bone of racehorses that could predict bone failure and abnormal remodelling. Our findings showed severe joint disease of over 70% associated with subchondral bone disease in the fetlock joint. The present study will use the techniques and knowledge acquired from the previous study and evaluate the cannon bones of 32 two and three year old racehorses on a monthly bases during racing for 2 consecutive years."

The website indicates Dr. Cruz is studying such things as frequency and duration of training, number of races, racetrack design, identifying potential risk factors and identifying the effect of various training programs. Interestingly, he is using portable ultrasound to identify cannon bone quality from commencement of training to immediately identify horses at risk.

So, at U of Guelph, Ontario they're researching and you'd expect some solid info reasonably soon. Tomorrow I'll get on with the speculation here and look at what happens to the cannon bones at speed.

Training:
Mon. 6/30 Off.
Tues. 7/1 Nob is awol again. In prep for Wed. speed work both horses after warm up galloped riderless slow 1.5 miles.