The Conditioned Bone Cell Post Breeze

Here it is.

McCain: "We're offering a job that will take most of your time and attention. Can you handle that?"

Palin: "Well, let's see. I have 5 children, age 18 and under including a disabled newborn. Yes, I'll be proud to take the job and promise to devote all my time and attention.

They took the wind right out of Mr. Obama's sails, but might be interesting, how they'll handle the aforementioned problem of priorities, and, never mind that I personally have trouble with Veep candidates who probably can spell "potato" but enjoy killing fish. It's Alaska, I'm thinking.

But, on to horses and microscopic movement in bone cells. I was doing a run yesterday down by the Missouri River watching the whirling surface circulation and noting that the river constantly changes it's distribution but remains exactly the same river. This brought home to me again the concept of "rearrangement" of materials where liquids or hybrid liquid-solids such as bone glue proteins respond to application of force by moving or circulating somewhat but after the movement we have exactly the same material we had before. In the case of bone glue there probably also is the contraction and expansion of sacrificial bonds in response to stress.

The point is that though bone material subject to the intense pressure of a breezing horse probably undergoes fairly significant changes over the course of 240 blows in terms of total movement of material at the microscopic level, I'm thinking what you end up with, like the Mighty Mo River, is mostly precisely what you started out with, and in terms of practical effect we are without significant change in the bone cell material post breeze.

This is all totally speculation on my part as I try to rationalize what's happening particularly as to what might cause us concern. Next post will discuss in terms of all this whether there is any breakdown of material that we need to consider.

Training:
Wed. 8/27: Art did 1 mile trot gallop under tack. Rod trotted 1/2 mile under tack.
Thurs. 8/28: Art galloped 1.25 mile under tack with occastional trot due to lead change problems. Mr. Nob gets the horse to switch right to left sometimes, but never (yet) left to right. Luckily we can control which lead the horse takes off on from the trot, but at the gallop the common sight at lead change time is the horse veering off course with Nob swaying in the breeze, lol. Rod trotted 1/3 mile then aborted as the horse had something caught in his throat. Both horses then did 10 min. of intermittent riderless fast work at about 80% speed with some short full speed bursts. Rod starting to show some real speed as he matures.
Fri. 8/29: Off

Perspective on Bone Cells During The Breeze

The last days I've read the news instead of posting. What a distraction the Internet these days and all these Democrats or Dumocrats as my old Uncle delights to refer. Sometime before the election an RR political post coming.

But, horses and bone cells.

I love those You Tube Overdose(OD) videos and keep watching them over and over. Nice example to shoot for in your training, and, for here, to imagine what occurs to the OD bone cell motoring down the track.

You may left click to enlarge the dead cell images here that, were they live images from a moving OD, probably would be a bit more bloated and filled out instead of dead, dried out and contracted. We must project a bit as to what these would look like alive!

Does this material hold up both in single stride and with repeated concussion? Interject again here as you watch any race and focus your eyes on that front lead the lack of concern watching a single stride compared to how one's concern increases psychologically with repeat after repeat. Watch one and notice how you start to worry as the race goes on.

Another way to ask the question is whether the material remains static or whether there's any movement such as that postulated in the recent prior posts. I conclude there is indeed some movement with each strike, but we consdier the variables of this:

-nature of the material--organic, inorganic mineral matrix, collagen
-position of the cell within the whole bone
-direction, nature and quantity of force

and, extremely significant-- though probably at the tiniest microscopic level in our conceptions there IS movement of material, what really is the difference in practical terms between e.g. a 1nn (or less) distance of movement and the material remaining static??? Consider that electrons are spinning in every atom of our bodies at all times as a comparison. We might say there can be microscopic movement without any effect--almost.

We can say that there is "almost" zero practical effect from movement, rearrangement, gliding, sliding, expansion and contraction of bone cell material until we consider the phenomena of the "repeated blows." I'm imagining that with a single stride of a horse the quantity and significance of bone cell movement is almost nil, BUT as that along with the level of our own psychological concern as we watch repeated strides there is indeed something happening in real time at the bone cell level with repeated strikes.

What happens (for purpose of this blog) I'll describe as "loosening". I'll take the wild guess that the various materials simply fail to rebound completely within each stride although I'd suspect the amount of rebound after any single stride is at least close to complete. But, then we get less and less rebound with each succeeding stride until (possibly) after 60 strides on that lead the material is ever so slightly microscopically separated (or rearranged) from where began.

BUT, we take note, then the horse is off that lead and for the next 60 strides onto the other lead. Hence in our "strikes" on the bone cell, we have 60 strikes followed by a 60 stride pause. I'm thinking that this pause, probably gives the material time to nearly completely rebound before the next cycle commences.

Thus, this post postulates within the bone material some "movement" during the breeze, but movement over so small a distance that there's little difference to the material remaining static, though this relationship weakens as the horse continues to stride.

Hopefully I've hit here somewhat on what's actually happening. What may we conclude will follow.

Training:
Sun: 8/24: after yesterday's fast riderless Art trots a mile with a bit of gallop, tack. Rod is off with his healing mouth.
Mon. 8/25: Art under tack trot-gallops 1.25 miles, about 1/2 of it gallop. Rod walks under tack for 5 min. Both horse then do about 10 min. of riderless work at medium gallop.
Tues. 8/26: Off. Our trainer is awol today.
Wed. 8/27: Art tacks a 1 mile trot-gallop without about 3/4 of it gallop. Art has now galloped most of the .8 mile course but we've still yet to negotiate a couple of the difficult sections with gullies, and, leads continue to be a problem. Nob fails a lead change, and I remind, think Georgie Boy. RR Rule--fail to get the lead change, abort.

Woodlands Memories

The Woodlands closes today.

2008 Travers

The Travers was competitive, entertaining, and surprisingly true to expected form. Anyone notice the whips by the jocks in the stretch? Watch the contrast in whip use by G. Gomez and Albarado!

I noticed that by post time the betting public had figured out Colonel John. A bit of a no-brainer since CJ sported the best:

Owner
Trainer
Training
Jockey
Pedigree

And then won by half a nostril. Lol, occasionally things do turn out as expected. Was Neil Howard's horse on steroids? That will be a thankfully irrelevant question next year.

What happens here to the Breeder's Cup? The Pyro people will throw up their hands and figure (at long last) they have little to lose by training that horse like Curlin, and I'd might expect a healthy Pyro to make some noise Cup day but, unless there's a significant win in the works maybe in another race besides the Classic.

Colonel John will continue without doubt the steady training regimen of Eion Hardy, 5f breeze every 6 days that provides more appropriate work than any other Breeder's Cup horse is likely to get even if it's "light" training in reality. A healthy CJ with a couple more races I'd expect to be a very tough horse come November.

As to Curlin, how can big mouth Jess Jackson avoid the Breeder's Cup Classic with all this talk? Asmussen has to date done a nice job with this horse, and I'm wondering why breeding shed economics would be a concern for an 80 year old millionaire owner. I think Curlin will be there and we migth see whether the late 3 year old CJ can run down the late 4 year old Curlin who should be equally tough in terms of fitness. As of right now, I think CJ might do the job, but, we'll see how the training goes!

For Big Brown, formerly considered by me as the horse of the century in terms of talent, first I think BB may have outgrown his former ability. BB's thickened considerably and Dutrow has allowed the horse to gain a lot of weight. You are of course unable to starve an athlete in training, but certainly the training regimen should have been sufficient to prevent the 100 excess lbs. this horse has put on. So, without a chance to see the horse regularly, you'd have to expect that BB might have lost something since early in the year in terms of natural speed. It might also be otherwise and that with appropriate training and racing--at least 2 more races would be necessary--you could also see a Breeder's Cup runaway by Big Brown.

With a pretty decent trainer but truly creepy(to me) ownership, BB has become this year's wild card. Dutrow and Michelle Nevin screaming their lungs out as they enter the stretch will be worth the price of admission.

Tomorrow its on to look at bone cells post breeze.

Training:
Fri. 8/22: Off
Sat. 8/23 1/2 inch of rain eliminates any productive tack work. This is the easy day before the speed day and we choose to go riderless through the mud: 10 minutes, I never kept track but it was something like 8 x 4f all told at medium speeds for the most part. Pretty good workout. They were huffing and puffing due to the weight of carrying mud in their hoofs. The 2 year old is starting to look a little better in his work.

Compaction, Resistance, And Cushioning

Yesterday's Personal Ensign race video (NTRA website) nicely shows the tremendous cumulative concussive effect on the front lead legs as those fillies gallop all out to the wire. Some videos show it, and this one does. Ginger Punch, Lemon Drop Mom and a horse that sold for $4000 as a yearling finishing third. There is hope!

For our single bone cell in this situation I'm imagining what's left of the organic collagen cell(after mineralization) and encasing bone glue proteins undergo some squeezing and compaction that cushion the blow while simultaneously the mineral matrix of the individual cell that is also part of the larger mineral matrix of the whole bone resists and pushes back against the force according to some mathematical formula for inorganic solids from mechanical engineering similar to E=mc2 which proves the solid matrix resists and pushes back until the applied force becomes overbearing and commences to break or fracture the matrix.

This resistance is further aided by the organization of multiple bone cells in close proximity which further buttress, cushion and resist the force. You may see in the photo below, a microscopic image of contiguous bone cells, how few gaps or spaces appear in the material and the probable degree of cushion thus provided. Note -lower right -this is taken at 50 nm as opposed to Hansma's 5nm.
Under what conditions does this hold up? Next post.

Training:
Fri. 8/22 Horses are off. Vet day. Teeth, Shots, Coggins. Rod's tiny wolf teeth were removed. It turned out Art was without Wolfs. Must have removed them last year, but in the teeth right next to the Wolfs in the upper mouth Art had very sharp long prongs. I never got around to calling the vet in the spring, so this is what you have, and we're theorizing the prongs on these two teeth may have caused some gum laceration that caused him pain on application of the bit at the fast gallop. We'll see next gallop which will be after tonight since for the zillionth time this year we've had another .6 inches of rain this morning.

Signaling And The Methodology of Breakage

"Canaleculae and Lacunae of bone transducts mechano-chemical signals in bone cells".

Bone cells(apparently) get advanced warning of impending force and gird themselves in preparation by signals traveling through the Canals which permeate the material. Above note the Haversian Canals

In the next illustration the Lacuna which are the very thin lines separating the layering.

Below is a different view of these signaling mechanisms.

Thus, with the onset of force the matrix illustration at left will commence to "react" or resist both by pushing back against force and dissipating force by bending and swaying.

If we hit this matrix against a brick wall will it break or shatter? Obviously, if we hit it with enough force that will happen. The more interesting question for our horse is what happens in the case of a lesser but repeating force where we strike the matrix over and over again. We may imagine sixty strikes per lead change, sixty strides of much lesser force, then another sixty strikes at the next lead change.

I'm thinking that on strike there will be some compaction of this matrix, some resistance as the matrix pushes back, and then post strike the matrix will attempt to rebound to its original shape. If the force where sufficiently hard you'd suppose perhaps a connection here and there might come lose or be broken, though I doubt that occurs for our breezing horse.

Provided the matrix bears up against the initial strike, what happens on repeat?

I am thinking that possibly the matrix fails to rebound fully between strikes, and that with each succeeding strike, provided it comes soon enough, the matrix will compact more and more. You may imagine that with sufficient compaction that the degree of resistance or pushing back will at some point commence to diminish. Then, if you keep repeating at some point the matrix will be crushed. As Hansma notes, when one of those connectors break it takes less and less force to break the succeeding ones.

How do these general principals apply to horse bone cells, next post.

Training:
Tues. 8/19: Off.
Wed. 8/20: Tack work: Art 1.25 miles trot-gallop. Rod 1 mile trot.
Thurs. 8/21: The vet comes Friday to do teeth, remove wolf teeth, shots, coggins. In anticipation we decide on fast work. Art: Tack: 1.25 mile with about half of it as gallop. Nob for the first time says that Art probably also has a wolf tooth problem and that is why he's acting up on the left lead. Too dark for tack work with Rod. Both horses then do 7 x 2.5f riderless at about :14 sec/f with some faster spurts. Very energetic nice work at less than maximum speed.

How Does the Mineral Matrix React To Force

James Rooney DVM: "While much has been written about the treatment of fractures, very little attention seems to have been directed at the actual mechanism of fracture--how and why they occur."

Well, Doc, for horses little changed in 20 years since you wrote that. But several on-going "fracture resistance" studies for our species do help.

We're talking mineral here, rock, hard stuff, rigid, immovable material which on force application either holds together, maybe vibrates a bit, or blows apart. BUT, is there any "in between" here for our mineralized bone cells?

First we consider again in terms of materials the concept of "girding" or tightening against impending force. Muscle cells do this by expanding when squeezed, which in turn causes the little forks or phalanges sticking out from them and connecting to the neighboring cell to tighten. Tight, hard muscle cells break or tear much less easily than a slack cell at rest.

Can this same analysis be applied to an inorganic mineral matrix, i.e. on initial application of force does somehow this material sense the force and undergo any protective changes in response???

It seems so. "Fracture resistance" studies in terms of applied force refer to "load signals" or load signaling that causes reactions in the materials. These signals can cause either a "chemical" or a "mechanical" reaction withing the material which increases fracture resistance.

How does this work on the mineral matrix?
I am imagining that on application of pressure there is squeezing or compaction of the matrix which immediately resulting in backward resistance or pushing back against initial force. Mechanical inertia and energy then sustain this backward push and preserve the matrix, unless the force is "overbearing" causing breakage.

In addition to "backward resistance" (a term I just made up--unknown how a mechanical engineer might word this), I'm imagining the matrix can to a limited degree "bend" in several directions, which would further buffer and distribute and dilute the applied force.

In terms of how this applies to bone cells as few quotes located in my warm up post of August 15, 2007:

"...understanding the mechano-sensory bone system."

"Bone cells and/or cell network tend to adapt to external mechanical loads--they have a reaction to 'load signals'."

"Bone adaption depends on strain size, lasting time, frequency, history, type (pressure, tension) and strain distribution."

There is a vast body of evidence that the flow of fluids within the canaleculae and lacunae of bone is mostly responsible for the transduction of the mechano-chemical signal in bone cells."

This last statement is the clincher, and I'll have an illustration of a CANALeculae, next post.

Training:
Proving once again that you can find a needle in a haystack, last night as I was walking in the pasture on the 30 acres to "round them up" for training I walked right over my lost $400 cell phone with the 3.2 mega pixel camera lying there in the grass. What are the odds? The rain has destroyed it. Luckily I bought insurance.

Wed. night's work:
Rod: trotted a mile under tack. We're now 2/3 way around the pasture track with only the deer (lion in the bush) parts remaining. Hopefully we'll go all the way around tonight.
Art: 1.25 miles under tack--trot/gallop. Couple of sustained gallops but too dark to transverse the difficult parts. Sun dropping out of the sky like a rock this time of year.

Continuing With Bone Cells

Class is again called to order, and we'll have to sit through some pretty technical stuff to determine what happens to bone cells during the breeze, why the heck we get all that cannon bone heat for 12-24 hours post breeze, and how soon we can safely proceed to the next workout with our horse.

First I'll put out some NEW pertinent info concerning the single cannon bone cell extracted from mid bone. Hansma's website states the collagen is coated with mineral, whereas I just read from a Bone Journal that in fact on birth the collagen immediately begins mineralizing from the inside out and fairly quickly thereafter becomes completely calcified.

For understanding the exact process, nature, and end product of bone mineralization is extremely crucial for this reason: it is easy to visualize that pressure created by the forces during the breeze squeezing or compressing collagen and bone glue proteins, BUT how does compression affect a solid, rigid inorganic mineralized lattice illustrated above left?????? The puzzler becomes what happens to this lattice.

At 200nm (very small) Hansma's electron microscopy gives us this image of a bone cell:


You can visualize the above being squeezed together. But, what it really looks like is shown in another much larger Hansma image below:

This image shows mineralized bone to be very dense and solid, to the point that we have to wonder as the horse travels whether anything significant is happening at all. To answer this we have to really deconstruct and break down the process, and I'll get to this next post.

Training:
Tues. 8/19: Its the next day after a fast work. Off.

Monday

Sat. 8/16: Tack work: Art 1 mile trot. Rod 3/4 mile trot walk.
Sun. 8/17 Tack only: Art 1.25 mile trot/intermittent gallop. Rod 1 mile mostly trot.
Mon. 8/18. You never know with horses. This morning I'm rushing off to a mandatory meeting and Art shows light colic, refusing to eat, but gut sounds on both sides. I trotted him and administered banamine. I'm a pretty good judge of this stuff now believing he'd be fine and he was. No feed for today though, and thus we abandoned the planned tack work so I could monitor the colic situation by watching the horse work riderless.
5 x 2f fast with about 1/2f of each furlong full speed--remember we have a developing 2 year old in there. But, WOW! These boys are flashing some speed. We're starting to get excited. Racing is great, but this sort of stuff also makes your day! As a side note, the exercise gave the opportunity to get Art with his colic to drink. That's big--get 'em hot and they'll take some water and that will generally solve the problem!

Weekend Training

Next bone post, under construction. Our training for the weekend:
Fri. 8/15: Afternoon rain, and Mr. Nob awol Fri. night his unseemly skirt chasing. I'm sure she's cute. Not. This being a "fast" day we went riderless as fast as slippery conditions allowed--5 x 2f in :14s-15s, nice conditioning workout for both.
Sat. 8/16: Art: 1 mile trot under tack with some gallop. Rod 3/4 mile trot-walk on the pasture track--we're getting this youngster used to being alone in space with our "no risk to the rider" procedures. And, just as I'm thinking pulling the wolf teeth may be another old wives tale, Nob reports the youngster throwing his head at the trot due to the teeth. Art has his wolf teeth with zero problems. Could it be that Rod's teething. Time to call in the Vet.
Sun. 8/17: Art: energetic 1.25 mile trot-gallop. We're working with this horse on control at the gallop and getting leads. Good progress. Nob loves the horse. Art had been refusing his left lead at the gallop. But, Nob has trained him now with correct rein work to take either diagnonal at the trot and so Nob can control whether the trot is on the left or right diagnonal--easier said than done with some horses, but this one has a high IQ and picks things up accordingly. Even though Art is right footed in the extreme Nob can get him to motor along at the trot on the left diagnonal, and from there it's but a whip tap to commencing gallop on the left lead. Progress.
Rod: is now traversing about 1/2 of the pasture track. The parts were deer pop out of the woods are next. 1 mile mostly trot. Fast work for both horses tonight.

Pressure (Continued)

Now to continue the exciting analysis of what happens to a single bone cell as the front hoof of the two year old German horse Overdose strikes the surface of the race track, keeping in mind that the term bone cell covers a lot of territory in terms of the various cellular and molecular structures in the cannon bone.

Last post contained various matrix's, organic and inorganic, which illustrate the links or connections between bone materials microscopically. Then the question, when concussive or compressive force applies what precisely occurs? For our traveling horse we postulate that such forces come from all directions and that they are other than uniform.

But, the effect of any particular strain or force will work differently depending whether its:

1. a cell of collagen
2. calcified mineral lattice, or
3. the proteins of the bone glue.

For the bone glue proteins, below:
we may presume flexibility to the point of rubberiness. Materials science uses the term "ductile" as a synonym for malleable, and we know from Hansma's work these are characteristics of sacrificial bonds at work which lengthen and contract, ie. give, in response to stress.

I am supposing however, that concussive forces coming up from the track, and compressive forces coming down from the weight of the horse, mostly compress, squeeze or pressure proteins of the types illustrated above. Since the links are ductile instead of brittle one may presume them squeezing together in the manner of the springs of a mattress, as they are hit about 60 times with each change of lead. Whether any of the links will break or tear will be the next discussion.

As to the collagen fibrils that are encased by a mineral coat, I'm supposing very little happens here except again that they might be contracted somewhat to the extent permitted by the mineral coating around them. Without sufficient force--science calls it "critical strain"--I'm assuming very little happens to the collagen that comprises the larger volume of the total bone.

The unknown and concern is what happens to the mineral lattice in this process that is made of of calcium, phosphates and various other inorganic materials in smaller amounts which are more akin to solid rock than rubber.

For this I had to again google for some mechanical engineering stuff for this seems critical to me: what happens to the mineral lattice in the bone as the horse breezes?

Can e.g. the mineral lattice be squeezed in the manner of the organic material, or does it just hold solid and then break, shear or tear when we exceed critical strain?

Here are some relevant illustration of what we're looking at:

Ice crystals:
Glass crystals:
Rock:
An illustrations of atoms layers in a crystal:
Another illustration of a crystal:

Bang the above against a track surface 130 times at 12,000 lbs/sq. inch and what happens?

Some interesting terminology from Ceramics science:

Shear mode

Tear mode

Ductility--materials can be deformed without fracture.

the brittle-ductile transition zone

the stress intensity factor

the stability of the crack--cracks in the material are ok as long as they remain stable.

the energy release rate--

fracture resistance decreases as the number of thermal cycles increases

I'll try to put together some conclusions next post.

Training:
This post will mark the transition to making a separate training post for the particular day, which I'll continue below.

Training Thurs. 8/14

Wed. 8/13 off
Thurs. 8/14: Art trotted 1 mile under tack with a few steps of gallop here and there. Very energetic, as expected. Forgot to check the tendon afterwards. Still a slight bit of fleshiness this morning around the check ligament-splint area. We'll go easier for this reason in this cycle and make it 4 days instead of 3.
Rod: Trotted under tack about a mile back and forth on the 1/4 of the Pasture track. In the 15 minutes from the end of this work to the start of shoeing Rod--we put on one shoe a night--the horse managed to lose his shoe. And, sure enough there's a laceration on the back of the pastern where he was pawing at something in the dark. Luckily it's just skin deep, and with a little of the silver spray bandage applied we will go right on. The horse lost his shoe 10 minutes BEFORE we started shoeing instead of 10 min. AFTER. How fortuitous is that? Our luck possibly is changing.

Pressure (Continued)

I am now a bone cell in the front cannon of the 2 year old German horse, Overdose. I am located about mid-thickness in the illustration below.
What happens to me as Overdose motors down the track?

The many illustrations in this post hopefully will support the conclusions which are totally my own speculation. Bone cells as many materials hook or attach together in a matrix symbolized by the illustration below.
We see this sort of patterning in electron microscopic images of silicon, below:
Here are images of proteins in matrix. Notice the 5nm resolution that I'm presuming is rather small.
and, below, illustration of spider webb cells. Notice the hooks that hold them together.
and, finally, bone imaging. The below is "low resolution". Very unfortunately I was unable to copy the high resolution imaging of the same photo that appears in Journal of Bone. The high resolution of the below shows crisp perfect patterning of the matrix much as you see in the other images above.
and below, osteoperotic bone showing a similar pattern. One may imagine "pressure" working on this bone as opposed to the solid bone cells above.
This post continues below:

Pressure (Continued)

and then this 200 nm (larger) image of a bone showing collagen fibrils which have been mineralized "by being coated with knobby mineral plates of hydroxyapatite. " External to (i.e. on top of and surrounding) these mineralized fibrils is the(visible)protein matrix called bone glue that acts as an interface or bond between the fibrils.
Now, what happens to this cell as our horse breezes? A much larger image of the material appears below:

My point in the many illustrations is to emphasize first the lattice or matrix by which the bone materials are constructed and held together. You can see this patterning even in the larger image above, and we may imagine that initially the pressure of concussion caused by the hoof strike will compress the above materials, or will it? I'll continue next post.

Training:
Tues. 8/12: The third consecutive training night since Art's tendon injury, and in this workout we'll test the tendon to see if we get any swelling. As it turns out, we do. We're in race training now, and so note, significantly, we're doing tack work BEFORE the riderless work, whereas previously we'd done the reverse. Both horses trotted a .8 mile, and then (in near dark) were driven riderless at intermittent fast-slow speeds with the fastest at 14 sec/f. We wanted a fast workout with Art without doing too much. Afterwards we had slight upper tendon swelling (as I'd half way expected), and an hour later some significant thickening. BUT, the swelling disappeared as expected by the next morning. The tendon is still in a state of healing and we'll have to be careful.
Wed. 8/13 Off.

Pressure

Two year olds so good they leave the field come along once in a while. The
Doctor Ak-Sar-Ben in mid '80s got his own cap, and Arazi at right came along shortly, and now Overdose. If you've yet to watch the YouTube videos of Overdose, do.
If
I was also interested in the Overdose videos because they show more clearly than most the pressure undergone by the front lead leg as the horse motors down the track. Overdose is a bounder, elevates the lead unusually high, and with his speed and effort causes (from the videos) more than normal concussion.

If you have any interest, as you watch the above video focus your attention exclusively on the front lead leg. Initially your reaction will be "so what". Keep an eye directly on the lead as the race progresses. Your reaction will change.

What you see over time in the video is the front lead beating against the track over and over. One or two strides make little impression, but, as you see the multiple beatings on the thin legs, my reaction was to begin to worry. If you look closely you can see with each stride the moment of max concussion. The talented animal both runs fast an is pretty hard on himself, which is even more clear in some of the other YouTube videos.

In this respect I want to imagine a singe bone cell in the cannon of Overdose and imagine what's happening with that bone cell during the race.

The particular bone cell will come from the mature calcified matrix from the mid-interior portion. We'll presume (to the extent we can identify a single cell in this area), that the cell is part of the calcified lattice, i.e. mature, finished calcium crystals surrounding living collagen that is in itself in a particular state of calcifying.

Of particular importance here is the concept of "density" and whether there is any spacing between the crystals and collagen, or whether the material is tightly packed together. We'll assume, in our appropriately trained bone, that the material is dense, tightly packed and without spacing.

The question then becomes what happens to this cell when Overdose repeatedly hits it against the track surface.

Training:
Sun. 8/10: Art does his first post injury exercise. Both horses were trotted riderless with some gallop 6 or 7 minutes. Rod then walked-trotted a mile under tack walking for the second time on the pasture track.
Mon: 8/11 Both horses riderless--mostly play gallop for 10 min with plenty of stops. We're watching the tendon. Both trotted a mile under tack with stops, and Rod did his first trotting in the pasture. Race prep is around the corner. Tendon appears fine.

Mineralization/Mixing Concrete

The purpose is to know what occurs in the cannon bone during the breeze/race, and the amount of time necessary to repair the damage, if any. Our equine scientists seem to be without answers or interest at the moment, so we turn to human studies.

A few things for understanding before we get to the specifics:

(and, how new is this understanding--Article titled "Scientists Gain NEW Clues As To Bone Mineralization, dated 4/2006.)

they refer to Bone Mineralization as a "well orchestrated process".

Crystals of calcium phosphate are produced. (How?) (Where does the calcium come from?)

Answer: There are "bone forming cells" by which we surmise they mean "calcium producing cells" among other things, and we may surmise that the calcium arrives at its destination from the blood stream much as circulatory system transports nutrients throughout the body.

The bone forming cells are called Osteoblasts.

BIG NEWS: Osteoblasts are found on the outer surface of the bone BUT ALSO IN THE BONE CAVITIES. So, if our breeze creates any pores or spaces we'll have Osteoblasts on site to lay down mineral and bone!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

What do Osteoblasts lay down exactly in addition to calcium phosphate? e.g. Do they also produce collagen cells and bone glue(proteins)????? Unknown to me. I am assuming Osteoblasts produce collagen certainly at the surface of the bone, but that probably bone glue proteins are then secreted by the collagen cells possibly as waste products.

Science has identified precisely the molecules involved in laying down the calcium--i.e. the mineralization process--including how these molecules regulate themselves to produce exactly the correct quantity of material. I'm visualizing it sort of as MIXING CONCRETE on the molecular level.

For bone, what's mixed? It appears to be a combo of inorganic material, proteins some of which act as regulators of the mixing process, and the materials that will form the matrix which I'm presuming to include collagen cells. (as one e.g. how detailed these studies are "Levels of inorganic pyrophosphate--which inhibits abnormal calcification--are controlled by at least three other molecules: nucleotide pyrophosphate phosphodiesterase 1 (NNP1), which produces pyrophosphate outside the cells; ankylosis protein (ANK), which further contributes to the extracellular pool of pyrophosphate by transporting it from the cell's interior to the cell surface; and tissue nonspecific alkaline phosphatase (TNAP), which breaks down pyrophosphate in the extracellular environment, keeping its levels in check.)

Note above they speak of what occurs in the "extra cellular environment" i.e. in and around the collagen cells, and also of transporting materials in and out of the cells.

More concepts: at any one time 4% of the total bone is involved in this on-going process of mineralization that--in order to mix things properly--involves both tearing down of the old and laying of the new. The bone you had when you were born has been completely replaced.

We will be interested in the architecture and distribution of this bone mass, and the geometry of the bone.

Training:
Sat. 8/9/08: Art is off but the tendon is back to normal, without swelling. Dodged a bullet!
Rod: after considerable warm up that involved aiming several 60mph clods of dirt directly at his recalcitrantly lazy rump, several of which made well deserved contract, the youngster--who was running by himself as our oldster had lost a shoe-finally got the idea and did 4 x 1.5f at about :14/f. Rod then made his maiden voyage in the pasture under tack, without incidence, and walked 10 minutes.

Plans And Horses

The bone post is now done, and I'll post it tomorrow. I've been focusing quite a while exclusively on injury prevention, but since I interrupted this, thought I'd post today on what my stable is up to for anyone interested.

We have $6000 worth of horse flesh purchased from Fasig Tipton via the Internet. I bid on 'em 10 hours from Lexington sitting in my office chair. I'm happy with them, lucky I suppose, as I might as easily have ended up with two dogs buying them from afar without close inspection. Here's a brief summary:

Art is age 3. He's a Storm Cat grandson out of a Deposit Ticket mare. I'll be posting pictures soon. Art is nicely conformed, looks racy and flashes stuff here at the farm that hopefully will translate to the race track. I'd be surprised if this horse was uncompetitive. Art has a funny way of going probably due to his slightly long pasterns. But, he's reasonably quick and has a quality of tenacity. The main talent here is breathing ability. I've yet to have a horse that breathes this well. You have to do a lot with Art for this reason to get into him. His pop finished second in the Belmont, and I expect Art to be a very tough distance horse with this breathing ability, though he's built more as a miler.

Rod the two year old is a chunk. He looks good, gives an impression of strength, but so far shows absolutely nothing in his training. This is in part because Rod's been very slow to mature particularly in terms of body lengthening. He's still got a very short barrel and thus has yet to have an adult stride. His legs are long but body short and this unbalances him when he runs. The chief concern is the horse is lazy. He's without any desire to compete or keep up, and we generally have to drive him to do his work. His breathing is normal instead of exceptional. I've yet to give up the Derby plans though this horse is a pure sprinter type. He's got gaskins like Popeye the sailor man's form arms. I'll prepare him like his forbears for sprint racing, and then see if we can lengthen him. Rod will start serious prep Sept. 1. Unlike Art at the same age, he's big enough now for our rider.

With the Woodland's closing we're a little up the creek with our plans. I've got such a nice situation here, a farm 12 miles from the down town of a major city with some tracks reasonably close. But, I'd planned to give it all up as I'm recognizing KCMO weather has switched over the last years to constantly wet, making it near impossible to do consistent race training in our pasture track. The farm unfortunately is holding back the racing.

My present thought is, weather permitting, to gallop Art as fast as the farm allows through the first of October. We should have a very fit animal at that point with Rod coming along. We'll then have to go to a track to get to racing, and it'll probably be Eureka initially, and then, depending on how things go, maybe Oaklawn, if we can find some off track stabling. If the horses show little then we'd be looking at Will Rogers in Tulsa in early February with Prairie Meadows or Lincoln a possibility in the spring.

Pulling this off requires a dramatic change of life style, money, and determination. The determination part comes a little bit harder when you hit 60. We'll see.

Training:
Fri. 08/08/08: After three days off Rod did a riderless 5 x 4f with his older buddy who dragged him occasionally into some two minute stuff. I wanted to do some with the weighted Astride saddle, but the girth is now too small. Art is still off. After romping in the pasture he showed some slight swelling last night and again this morning. I've revised my diagnoses again as there's definitely tendon sheath swelling, and so were probably dealing with a bruised tendon sheath. Luckily no heat, no pain, no lameness. I think it's a minor problem whatever was the damned cause, and we'll have him back shortly.

A Growth Spurt And Injury Remedy

An injury update on Art while the next bone post is (still) being written. For posterity I'll detail the injury below

First, and for us quite significantly, in the last 10 days both my horses ages 2 and 3 have grown 1/2 hand. Art is now finally necessary 15' 3 1/2" to allow our enlarged Mr. Nob to breeze him. Rod has grown to the same size.

Is it coincidence that suddenly two horses including a middle 3yr. old simultaneously gain half a hand which also includes the overall increased scope that this entails? There's a big difference in total size between 15'3" and 15' 3.5".

I'm supposing in terms of bone growth"calcium matters". What's happened with the 10+ days of rain in July, my fields are covered with a sheet of clover which the horses ingest in the daily grazing. I feel certain this dramatically increases dietary calcium content which most likely is responsible for the present spurt. Would be interesting to know whether supplementing calcium would cause the same result. I have in the past induced growth spurts by providing sudden increases of alfalfa hay.

We finally have big enough horses which is so important for us.

ART'S INJURY

I'd thought the rap (hit) was on the tendon, but by day 4 with the swelling much reduced I see an enlarged fetlock and probably that's were the hit occurred. There's still significant heat on Thurs. night, and some significant swelling just above the fetlock in the tendon/suspensory/condylar area that THREATENS TO CALCIFY creating a hardened area above the fetlock. With calcification in this area and hardening the horse can still run pain free but this hardening of the lower tendon sheath is a permanent injury which compromises speed. You are unlikely to have a successful racehorse with such injury, and though I'm thankful we're without a bow, I'm very very concerned as I go to bed Thurs. evening.

While in Kentucky (Lexington in 97/98) witnessed all sorts of "remedies" for injury with most at first blush seemingly stupid. Over time there I began to develop a respect for "what works" and the accumulated knowledge of KY horse people.

One thing I learned in Lexington was how to create healing heat in the tendon area by putting furizone (the yellow Vaseline based topical antibiotic) over the area and covering it with plastic Saran wrap. This creates as much heat and therefore circulation in the leg as a heating pad.

And so, Thurs. night the furizone/plastic wrap was put on Art's tendon and fetlock. Fri. morning it was removed, and voila, swelling gone. (What a relief). There's still some very slight fetlock enlargement, but the area just above the fetlock is clean. Art, a horse that's impressing us, should be back in business by Sunday.

Training:
8/7/08 Thurs: Both horses were off for the 3rd day.

Short Farm Post

Apologies for the inconsistent blogging. Thanks to KH for the 8/3 comment. Gives me an excuse to write about the farm while I'm putting together the next bone post. I know everyone is waiting breathlessly for that. Art as an early two year old above. I'll have the camera back soon. He's a different horse now.

As to sending mine to a training center, that's a fair question. And, a thought, with the Woodlands closing. Doubt we'll go that route, unless we find a budding Dutrow, lol. Our best laid plans were to gallop into the Woodlands with 8 weeks of a real live race track to do the jock work, and then stable at Fairmont Park possibly considering Oaklawn or Will Rogers in Tulsa, depending.

With Woodlands gone, jeez, we're trying to figure Plan B and the price of gas, plus we had a rather revolting development yesterday. see below. My two truthfully have been held back by weather and immaturity and maybe a little more dawdling on my part than I'd like. But, I think they're about there now, and hope to be able to report from a race track in the next weeks.

As to Got Country Grip, KH, I'm unable to see what you referred to. Nor am I entirely sure I understood your point. But, agreed there's a lot of concern about youngsters and speed. I have it and am considering some interesting revisions to Burch training which I'll post eventually.


Training:
Tues. 8/5: Injury to Art today that I'd thought was a bowed tendon. Unbelievable. I'll archive the observation and the thought process. Let's say I was discouraged for a good while. Morning feeding time I see Art take one bad step. I'm in a hurry and see nothing else untoward, but all day at the office I'm thinking hmmm. Decide not to train Tues. night, one of those premonitions. Then, feeding in the dark, I injury check still worrying about that bad step, and sure enough a blown up front right from mid cannon down to the fetlock with a whole lot of heat emanating from one little area above the fetlock. I'm in disbelief because there's absolutely nothing this horse has done training wise to cause this. I'm starting to think rap instead of bow.

Tues. night the horse gets bute and by Wed. morning lots of swelling still. I look at it in daylight, and, interestingly, the appearance is much more of a rap than a bow. Unable to tell for sure as there's significant swelling now going all the way up the leg. But, that's good, i.e. the swelling is other than localized, we're without the fleshy feel of a bow, and #1 the horse is NOT lame at the walk. At this point I'm thinking very serious rap instead of bow. We're without kinks also.

Put leg in the water bucket for the few moments I've got before the office. Checked Art at 7 pm this evening, and, by jove, significant reduction in swelling. Unable to feel any heat. This might be only a one week thing. Upsets me to lose a week, but beats losing this horse. Verdict still out though, as I type. Rod had his second day off. (Edit--Thurs. morn heat is back. The youngsters were romping hopefully explains renewed heat. Swelling is way down, but above the fetlock it threatens to harden. Due to that I'm back to being very concerned.)

Bone Cells and Impending Force

This post I'd like to analyze what's happening in that front lead leg as the horse breezes since I'm thinking the whole process which involves the entire structure of the bone and the various forces working on that structure will give us some significant clues as to what we need to be doing to avoid injury. Again, I'm focusing on the cannon bone, though the inquiry will be much the same for each bone in the lower leg.

In any particular workout the bone is, of course, in a particular state of development that we need to consider in planning the workout. In my barn, e.g., we've been taking it easier the last two weeks as it appears both of my youngsters are in mini-growth spurts, and I'm assuming recently laid down collagen that might be damaged or destroyed by too much work pressure at this point. My 13 year old, on the other hand, could withstand almost anything we'd want to throw out, but, according to his present training.

The point is that the development of bone in the the cannon is in a particular state of being, as we head to the track, which changes from workout to workout. For this workout we'll assume that we've planned well, that there is appropriate development for what we're going to do, and that our cannon is without existing microfracture or other injury. The forces then that we'll encounter in the breeze will be working on healthy bone tissue of sufficient strength for what we're planning.

I've identified the forces to be encountered in the prior posts, but, let's indeed get down to the nitty gritty and look at precisely what we're about here.

Please note the entire stride as it involves the lead leg. The stride begins with the lead leg elevating itself into the air in preparation for the downward arc into the track. The height of this depends a bit on the conformation and stride type of the horse as well as speed. Bounders e.g. will have their front leads higher than horses that chop along in the manner of Got Country Grip. Interestingly, I believe the higher the elevation of the lead leg probably the more force is generated as the hoof slams into the track, BUT, if you think about it, the maximum force during the weight bearing phase (where the entire weight of the horse momentarily places on the lead leg), might last slightly longer in the choppers as opposed to the bounders. Perhaps the bounder types are a little easier on themselves in this regard and can stand more work in terms of structure.

The lead leg elevates and slams into the ground. Then, of enormous significance, if you watch this closely in slo mo video you'll see the leg acting as a pendulum with a certain degree of force operating on ground contact which increases to a maximum point and then lightens again just before the leg completes the stride. Maximum force therefore applies only after a short period of prep for that force so that in the stride in terms of amount of force we have something that looks like this:

initial force--increasing force--maximum force--immediate release of maximum force.

There is thus a short momentary prep of bone cells for max force. Analyzing this "prep" phase brings about the question: do bone cells like muscle cells gird themselves for impending force?

Continue next post.

Training:
Sat. 8/2: Off
Sun. 8/3: Light 2 mile riderless gallop without tack work.
Mon. 8/4: riderless: 6f warm up + 1.25 miles steady at about 15 sec/f. Tack work: Rod trotted 5/8, Art trotted 6/8.

Big Brown and Mineralized Collagen

Steroids right now cast a pall on everything for me. But, that was kind of a neat race in the Haskell today, even if I suspect that Big Brown was running against chemical Zito. But, a neat race that I played over and over. They avoided giving it to BB with that 1:35.1 mile. My impressions: BB's gained a lot of weight since those facile early season runaways. And, he's running clean and less dominant. You also might question a horse running 1 1/8 mile on 5/8 works. Will be interesting how Dutrow plays it from here on in. Me, the horse would be back on track (if he's ok after that drifting out), on Tuesday aiming for the Travers.

Back to bone cells. A couple pictured here--unidentified at left, a collagen fibril above right. You could simplify all this and say that in the weight bearing phase of the stride bone material is
squeezed or pressured. "Bone material" covers a lot of territory though, and we need to know what we're specifically talking about. Three main ingredients to our cannon bone:


1. collagen
2. mineralized lattice
3. sticky gunky proteins called bone glue.

I am imagining that bone in the fetus begins as collagen and commences mineralization. By the time of the outset of training you'd think there is a significant mineral lattice already in place, and that in the course of training the bone osteoblasts are laying down additional collagen surrounded by bone glue which gradually mineralize as we go. I was unable to find anything about how quick the mineralization process is, but, I think we can surmise that it's slow instead of fast. For a single collagen fibril to mineralize from creation to the time it's solidly encased and itself begins to mineralize, I'm thinking this process has to take at least two months, and probably more. I get that when I think how fast a broken bone mends. Broken bones take months before they're as good as new and I suspect this is because of the slow process of the mineralization.

So, what we have there at the outset of training is spongy bone at the interior near the blood vessels and on the condylar aspects, with a significant mature minerlized layer going out to the exterior of the bone and finally the ostoid consisting of recently layed down, unmineralized collagen.

What changes during training? We know from the photos that the mineralized portion of the bone grows thicker both inward and outward. Why this happens in response to exercise also gives a giant clue on what's happening with our bone material during the breeze itself, next post.

Training:
Sat. 8/2: I developed the intuition this night that the horses should lay off. I'm heading out now for Sun. and will do some tack work and then some short riderless spurts.