Nunamaker/PETA/Dr.Peterson
As my search for optimal frequency of breezing/racing in terms of injury prevention proceeds--and note while I believe I know that speed work every three or 4 days will get the job done, the answer to the question in terms of minimal frequency i.e. the least we can get away with, remains unknown to me--I am, chronologically in terms of posting--at the point where we have the horse back at the barn after a race wondering how soon we need to go again for injury prevention, and how frequently thereafter.
Answering these questions presupposes an understanding of the bone remodeling process beyond my 2/19 post which summarized what happens within the cannon bone during the breeze.
I'd hoped to begin this with a summary of the present state of equine research, but was reaching a dead end as it seems we only have Nunamaker's work in the late '80s involving the Maryland Shin studies.
Eventually however the squirrel finds the nut. If you google, with low expectations, the subject: "Equine bone remodeling photos" you're as likely to find the name of Julio Canani's bail bondsman or a listing of this blog as actual equine research. Yet, this time, there embedded in of all things the PETA "Horse Lover's Forum" is a superb article by Robin Peterson DVM bringing up to date the work of Nunamaker et. al. regarding bone remodeling.
To avoid interrupting the flow of this article and its meticulous thoroughness, I'll print it in its entirety. It is long, but excellent. You may also follow it just by reading the highlighted bold sections and my comments in italics. There's some repetition here, but also much I've previously omitted that is new/old. Read closely e.g. and you'll get a scientific explanation of the grave danger of moving a horse trained on synthetics quickly to dirt.
Robin Peterson DVM
"The equine world is indebted to David Nunamaker, VmD PhD, an orthopedic surgeon and head of the University of Pennsylvania's New Bolton Center, for information on the role exercise plays in the formation of bone. Aided by grants from the U.S. Dept. of Ag., the New York Chapter of the HBPA, Grayson Jockey club, and the National Institute of Health (where are they now?), Nunamaker and his associates carried out in-depth research on bone development beginning in the late 1980s and continuing to the present (I clicked New Bolton and Nunamaker. Unable to see anything of note being carried on to the present.) that provided a great deal of information about the role played by exercise. Heavily involved in the early research with N. were Bill Moyer, DVM, formerly at New Bolton and today head of the Large Animal Medicine and Surgery Dept. Texas A&M, and John Fisher, DVM a horse training veterinarian (note Fisher's importance below.)from Maryland, who was the first to try Nunamaker's suggested approach for building strong bones in young racehorses.
The focus of their research involved bucked shins, but what they learned also provided enlightening information about exercise-induced development of bone.
(some bucked shin info omitted here)
Nunamaker's research revealed early on that casual, or light, exercise (she's calling 2 min. gallops light exercise) did not have a profound effect on growing and developing bone, but that more strenuous exercise did.
In an early segment of the study, four yearlings were purchased shortly before becoming two years of age. Two of them were turned out and never ridden. the other two were put into training that consisted primarily of two minute gallops nearly every day, but they were never ridden at speed.
At the conclusion of that phase of the study, the bones of the four horses were examined. There was no difference in the structure of the bones. The horses which had done nothing but roam a pasture had bones as strong as the horses which had galloped two miles on an almost daily basis. (Hence the term: RAFR, race appropriate fracture resistance.)
This indicated that galloping horses was not appropriate exercise to strengthen and prepare bones properly for the stress of racing.
Later research would reveal that working the young horses at speed periodically early in their careers would strengthen or remodel bone so that it could withstand racing stress. More about that later.
First, a look at how bones grow and develop.
Start with Cartilage.
Cartilage is a specialized connective tissue in which the collagen (a protein) matrix between cells is formed at positions of mechanical stress. In cartilage, the fibers are laid down along the lines of stressin long parallel arrays. This process results in a firm and flexible tissue that has great tensile strength. Cartilage binds together the bones that meet in joints, such as the knee and ankle.
Bone is a special form of cartilage in which the collagen fibers are coated with calcium phosphate salt. Healthy bone is a substance that is strong, but not brittle.
One comparison to bone is fiberglass (she's about to give a Paul Hansma type explanation). Fiberglass is composed of glass fibers embedded in epoxy glue. the individual glass fibers are rigid and strong, but they also are brittle. The epoxy component is flexible, but weak. The composite, however, is both rigid and strong. When a glass fiber breaks because of the stress and a crack starts to form, the crack runs into glue before it reaches another fiber. The glue distorts and reduces the concentration of the stress, and the adjacent fibers consequently are not exposed to the same high stress. In effect, the epoxsy glue acts to spreads the stress over the many fibers.
Bone is constructed in similar manner. Small needle-shaped crystals of a calcium-containing mineral, hydroxyapatite, surround and impregnate the collagen fibrils ) a small filament of fiber) of bone. Within bone, the collagen is laid down along lines of stress. No crack can penetrate far into bone without encountering a myriad of hydroxyapaite crystals in a collagenous matrix. Bone is more rigid than collagen just as fiberglass is more rigid than epoxy glue.
(an explanation of the structure of spongy bone at end of bones omitted.)
New bone is formed by cells called osteoblasts, which secrete collagen fibers on which calcium subsequently is deposited. Bone is laid down in thin concentric layers called lamellae. The lamellae are laid down as a series of tubes around narrow channels called Haversian canals, which run parallel to the length of the bone. The Haversian canals are interconnected and carry blood vessels and never cells. The blood vessels provide a lifeline of living bone-forming cells and the nerves control the diameter of the blood vessels and thus the flow through them.
With that rather pedantic, textbook explanation of bone as a basis, we can look into what happens to it as a result of exercise. We return to information provided by the New Bolton research.
Bone responding to Stress
In addition to learning that mild exercise had no real effect on bone development, the researchers also discovered that bucked shins weren't what many had thought the condition to be. The general consensus for years was that bucked shins were microscopic fissure fractures of the cannon bone that occurred when young, growing bone was placed under stress, such as race training.
Nunamaker found that bucked shins actually are the result of the bone training to respond quickly to the strains placed upon it. The result is that bone, when stressed, seeks "immediately" to form new a new layer of bone at the point of stress on the cannon bone. The "quickly" formed bone is periosteal or fiber bone and is more porous, and thus weaker, than the dense lamellar bone that is formed slowly over a longer period. In the process of the relatively rapid formation of bone, the periosteum is lifted and becomes inflamed and the horse is afflicted with bucked shins. (note importance of the words "immediately" and "quickly")
'We found that a horse chances the shape of its bone in response to training,' Nunamaker said, 'and, depending on what the training is like, you can just about change the bone in any direction you want. The way most conventional (race) training is conducted, a horse changes its bone in an abnormal way and not in the way it should change the bone.'
When you take a specimen of anything, he said and you cycle it for a long enough time, it eventually will break. this is called fatigue failure. When you take a piece of bone and cycle it, what happens first of all is that it starts to lose stiffness and bends more. As it starts to bend more there are higher strains on the bone, then suddenly something happens.
To accommodate the strains the bone tries to change shape and make itself larger. There is a fourth power involved in the equation here, and it takes only a little larger bone mass for it to become very much stronger. (Noted!!!!!)
Continue this next post.
Training:
3/2 and 3/3 off due to frozen bumpy ground and crusty snow. Luckily we were able to get in speed work on 3/1 and so, under Burch type training, if we can do more speed work 3/4 we'll maintain condition!
Answering these questions presupposes an understanding of the bone remodeling process beyond my 2/19 post which summarized what happens within the cannon bone during the breeze.
I'd hoped to begin this with a summary of the present state of equine research, but was reaching a dead end as it seems we only have Nunamaker's work in the late '80s involving the Maryland Shin studies.
Eventually however the squirrel finds the nut. If you google, with low expectations, the subject: "Equine bone remodeling photos" you're as likely to find the name of Julio Canani's bail bondsman or a listing of this blog as actual equine research. Yet, this time, there embedded in of all things the PETA "Horse Lover's Forum" is a superb article by Robin Peterson DVM bringing up to date the work of Nunamaker et. al. regarding bone remodeling.
To avoid interrupting the flow of this article and its meticulous thoroughness, I'll print it in its entirety. It is long, but excellent. You may also follow it just by reading the highlighted bold sections and my comments in italics. There's some repetition here, but also much I've previously omitted that is new/old. Read closely e.g. and you'll get a scientific explanation of the grave danger of moving a horse trained on synthetics quickly to dirt.
Robin Peterson DVM
"The equine world is indebted to David Nunamaker, VmD PhD, an orthopedic surgeon and head of the University of Pennsylvania's New Bolton Center, for information on the role exercise plays in the formation of bone. Aided by grants from the U.S. Dept. of Ag., the New York Chapter of the HBPA, Grayson Jockey club, and the National Institute of Health (where are they now?), Nunamaker and his associates carried out in-depth research on bone development beginning in the late 1980s and continuing to the present (I clicked New Bolton and Nunamaker. Unable to see anything of note being carried on to the present.) that provided a great deal of information about the role played by exercise. Heavily involved in the early research with N. were Bill Moyer, DVM, formerly at New Bolton and today head of the Large Animal Medicine and Surgery Dept. Texas A&M, and John Fisher, DVM a horse training veterinarian (note Fisher's importance below.)from Maryland, who was the first to try Nunamaker's suggested approach for building strong bones in young racehorses.
The focus of their research involved bucked shins, but what they learned also provided enlightening information about exercise-induced development of bone.
(some bucked shin info omitted here)
Nunamaker's research revealed early on that casual, or light, exercise (she's calling 2 min. gallops light exercise) did not have a profound effect on growing and developing bone, but that more strenuous exercise did.
In an early segment of the study, four yearlings were purchased shortly before becoming two years of age. Two of them were turned out and never ridden. the other two were put into training that consisted primarily of two minute gallops nearly every day, but they were never ridden at speed.
At the conclusion of that phase of the study, the bones of the four horses were examined. There was no difference in the structure of the bones. The horses which had done nothing but roam a pasture had bones as strong as the horses which had galloped two miles on an almost daily basis. (Hence the term: RAFR, race appropriate fracture resistance.)
This indicated that galloping horses was not appropriate exercise to strengthen and prepare bones properly for the stress of racing.
Later research would reveal that working the young horses at speed periodically early in their careers would strengthen or remodel bone so that it could withstand racing stress. More about that later.
First, a look at how bones grow and develop.
Start with Cartilage.
Cartilage is a specialized connective tissue in which the collagen (a protein) matrix between cells is formed at positions of mechanical stress. In cartilage, the fibers are laid down along the lines of stressin long parallel arrays. This process results in a firm and flexible tissue that has great tensile strength. Cartilage binds together the bones that meet in joints, such as the knee and ankle.
Bone is a special form of cartilage in which the collagen fibers are coated with calcium phosphate salt. Healthy bone is a substance that is strong, but not brittle.
One comparison to bone is fiberglass (she's about to give a Paul Hansma type explanation). Fiberglass is composed of glass fibers embedded in epoxy glue. the individual glass fibers are rigid and strong, but they also are brittle. The epoxy component is flexible, but weak. The composite, however, is both rigid and strong. When a glass fiber breaks because of the stress and a crack starts to form, the crack runs into glue before it reaches another fiber. The glue distorts and reduces the concentration of the stress, and the adjacent fibers consequently are not exposed to the same high stress. In effect, the epoxsy glue acts to spreads the stress over the many fibers.
Bone is constructed in similar manner. Small needle-shaped crystals of a calcium-containing mineral, hydroxyapatite, surround and impregnate the collagen fibrils ) a small filament of fiber) of bone. Within bone, the collagen is laid down along lines of stress. No crack can penetrate far into bone without encountering a myriad of hydroxyapaite crystals in a collagenous matrix. Bone is more rigid than collagen just as fiberglass is more rigid than epoxy glue.
(an explanation of the structure of spongy bone at end of bones omitted.)
New bone is formed by cells called osteoblasts, which secrete collagen fibers on which calcium subsequently is deposited. Bone is laid down in thin concentric layers called lamellae. The lamellae are laid down as a series of tubes around narrow channels called Haversian canals, which run parallel to the length of the bone. The Haversian canals are interconnected and carry blood vessels and never cells. The blood vessels provide a lifeline of living bone-forming cells and the nerves control the diameter of the blood vessels and thus the flow through them.
With that rather pedantic, textbook explanation of bone as a basis, we can look into what happens to it as a result of exercise. We return to information provided by the New Bolton research.
Bone responding to Stress
In addition to learning that mild exercise had no real effect on bone development, the researchers also discovered that bucked shins weren't what many had thought the condition to be. The general consensus for years was that bucked shins were microscopic fissure fractures of the cannon bone that occurred when young, growing bone was placed under stress, such as race training.
Nunamaker found that bucked shins actually are the result of the bone training to respond quickly to the strains placed upon it. The result is that bone, when stressed, seeks "immediately" to form new a new layer of bone at the point of stress on the cannon bone. The "quickly" formed bone is periosteal or fiber bone and is more porous, and thus weaker, than the dense lamellar bone that is formed slowly over a longer period. In the process of the relatively rapid formation of bone, the periosteum is lifted and becomes inflamed and the horse is afflicted with bucked shins. (note importance of the words "immediately" and "quickly")
'We found that a horse chances the shape of its bone in response to training,' Nunamaker said, 'and, depending on what the training is like, you can just about change the bone in any direction you want. The way most conventional (race) training is conducted, a horse changes its bone in an abnormal way and not in the way it should change the bone.'
When you take a specimen of anything, he said and you cycle it for a long enough time, it eventually will break. this is called fatigue failure. When you take a piece of bone and cycle it, what happens first of all is that it starts to lose stiffness and bends more. As it starts to bend more there are higher strains on the bone, then suddenly something happens.
To accommodate the strains the bone tries to change shape and make itself larger. There is a fourth power involved in the equation here, and it takes only a little larger bone mass for it to become very much stronger. (Noted!!!!!)
Continue this next post.
Training:
3/2 and 3/3 off due to frozen bumpy ground and crusty snow. Luckily we were able to get in speed work on 3/1 and so, under Burch type training, if we can do more speed work 3/4 we'll maintain condition!
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