Bone Cell Repair: How Long Does It Take
Bone cell repair is both an interesting (as you will see in the next posts), and crucial question for our horses. The more I read and look at this the more I'm certain there is a small amount of insignificant damage in (trained) bone with each hard gallop. To determine how soon we can safely go on requires an understanding of the process of repair.There is of course a science to this that covers chapters which fortunately can be summarized for the basics.
We know that bone contains blood vessels and lymphatic channels that transport molecular nutrients and carry away waste products. Additionally the bone collagen cells also secrete materials directly at the damage site. Finally, in the event of larger damage, specialized bone cells arrive that aid in reconstruction.
The materials and nutrients involved are pretty much what you'd think: calcium, minerals, proteins, various catalysts, ionic activity with protons and electrons at the atomic level involved in constructing mineral lattice and so on.
How does it all work? If we have a single bone cell (and note the misnomer "bone cell" since each cell closely connects to the next to be almost indistinguishable), that e.g. has it's matrix 50% crushed, what we may imagine occurs forthwith is tight encasement of the damaged section of the single cell matrix by bone glue proteins. My thinking is that the pressure created in the gallop will squeeze and move the proteins into any microscopic vacuum created by a crushed matrix. Were the space left by the damage large enough we'd initially get fluid that would later congeal. BUT, I'm thinking in trained bone WE MERELY GET A SHIFT OF BONE GLUE PROTEINS ENCASING THE DAMAGE.
The end result post breeze will thus be numerous diffuse microscopic "spots" at the damage sites throughout the bone consisting of the remnants of the damaged matrix encased in sticky proteins with their microscopic bonds having the following (hypothesised) relative strength:
1. Undamaged matrix cell strength = 10 (rating).
2. Damaged matrix cell without being encased by bone proteins = 5 rating.
3. Damaged matrix cell encased by bone proteins = 7.5 rating.
Thus, what's necessary post breeze is that the damaged encased cell remineralize. Remineralization, by all info, is quick. I'll try to break this down next post.
Training:
Tues. 9/9: Only the frogs are happy at the farm. They're enjoying all the nice rain puddles. Arrived last night intending tack work, but there's Art limping on a sprung shoe, left rear. Shoe replaced, still limping, so Art rests. Looked like a one day thing, bruise from the springing of the shoe, and indeed Art was fine this morning 9/10. Too dark, by the time we replaced shoe,for tack work with Rod, and so he galloped hard riderless in the mud for 10 min. Something also is unwell with Rod as for last two workouts he's refusing to extend his gallop on the leftlead but is fine galloping on the right lead. We're without outward injury signs so I'm thinking hoof and am (very) worried about shoulder. Could also be a pulled muscle. I'll have to figure out this one later.
posted by rather rapid at
8:31 AM
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4 Comments:
While trying to dig up an answer to "How fast does bone remodel?' I came across the below which is a quote from the late Dr Mel Siff and another poster on a physiology forum. This is related to muscles not bones but some of the concepts seemed to mesh nicely with your bone exhumation...
KH
"Below are comments from Dr Siff regarding this topic:
Growth with and without Damage
In other words, genetic mechanisms can remodel tissues either to
facilitate normal growth, growth stimulated by mechanical effort or
growth to repair damage. The above example, therefore, suggests that
one should be cautious before implicating damage as a central and
necessary process which can explain all hypertrophy. After all, it
would appear to be unnecessarily inefficient and stressful for the
training athlete always to be in a state of damage. Does it sound
logical that damage should be the primary stimulus for all biological
growth? Would it not be preferable to implicate cellular
restructuring orchestrated by genetic programmes in response to
environmental and endogenous stresses (such as increase in tissue
tension).
Then, again, the frequent occurrence of macroscopic tissue injuries
(manifesting as partial or complete tissue ruptures or lesions) among
sports competitors would seem to corroborate the theory that
accumulating micro-injuries and damage are the fundamental cause of
many injuries which are not caused by traumatic impact or accident.
Possibly we need to distinguish carefully between several different
categories of growth and abandon the hypothesis that all growth is
stimulated by damaging tissue through exercise:
. Growth occurring as part of the normal maturation process
. Growth to replace tissues depleted by daily living and ageing
. Growth regulated by the mechanical stimulation of effort
. Growth to repair damage caused by excessive levels of tissue stress
. Growth to repair damage caused by disease or disuse
.....
Sure, strenuous resistance training can produce damage of muscle
fibrils and cells, but it's never been proven that this is a
necessary and sufficient condition for muscle hypertrophy and
strength increase. If this were true, it would mean that all serious
athletes are perpetually in a state of constant muscle damage, and
it's illogical that biological adaptation should rely solely on a
destructive mechanism like this.
In an attempt to refute the above deduction, someone might quote
research that the bones, for instance, are constantly being broken
down and rebuilt by specific chemical processes, thereby proving that
destruction and construction, analysis and synthesis, are the ways in
which adaptation always occurs. They would be perfectly correct, but
they would be ignoring the fact that this type of "adaptive
reconstruction" (the Russian term used in "Supertraining") is not
accompanied by pain.
Adaptation, as opposed to repair, doesn't involve tissue damage and
pain—it depends on painless reconstruction and modification of muscle
cells via communication of the coding mechanisms inside the cell and
the cell membrane. For example, the work of Goldspink shows that
muscle genes are regulated largely by mechanical stimulation, not
mechanical damage (The brains behind the brawn. New Scientist 1 Aug
1992: 28-33).
Txs KH. I do find it (after all my reading) a little humerous to see more than myself speculating instead of knowing. i might suspect since 1992 they might have some answers to questions posed by the professor, 'eh? Interesting question though, whether muscle cells grow in response to excercise due to accumulated damage or other factors.
I don't know if I buy into the argument that athletes would be in a CONSTANT state of destruction.
Wouldn't the tearing and growth of muscle only occur at stresses above what the tissue/bone is already used to? Once it accomodates a certain stress level then it just adapts to that after its growth/healing phase.
If that level is not maintained then it atrophies but maintaining that level would not necessarily continuously tear tissue.
I don't know.
winston, ya, but in the body building community, after you achieve adaptation you just go on to more weight and destruction-?? i doubt we ever work our horses hard enough to cause muscle cell damage, and, as i noted, with respect to transferring the professor's thinking to bone, i probably agree that "destruction" of bone cells has little to do with increasing bone strength and growth. there's be more on that here soon.
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