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Martial Arts Bone Conditioning and LSJL

LSJL is lateral loading of the synovial joints or possible the epiphysis of the bone to stimulate fluid flow to stimulate degradation(remodeling) of the cortical bone and creation of mesenchymal stem cell chondrogenesis through a favorable microenvironment.

Martial arts bone condition is another form of this as impact is a form of loading.  However impact loading would not stimulate the soft tissues surrounding the bone which are all connected to the bone this is an important distinction.  Axial loading does not really drive fluid flow so that elements punching as a studiable stimulus.  However, several martial artists do tapping of the bones of the leg and arm.

The different between this and an LSJL style tapping would be that the tapping would not necessarily be at the longitudinal ends of the bone so the bone would be more innervated and there would be less of a fluid pressure gradient than at the longitudinal ends of the bone.  The goal of martial arts bone conditioning is described as something like calcification or bone thickening which is not exactly what we want.

The other difference between LSJL and martial arts bone conditioning is the intensity of the load.  Short intense bursts is more osteogenic whereas longer less intense bursts of loading are more chondrogenic.  This is primarily because osteocytes respond to sudden changes in fluid flow but osteocytes(probably) cannot make you taller as osteocytes produce bone and bone is what blocks you from growing taller!  Soft tissue is what allows for interstitial growth.  So for LSJL style loading you would tap the longitudinal ends of the bone with more frequency and less intensity.

If the bones weren’t so innervated would you be able to grow via martial arts style loading?  Probably not by rolling a bottle up and down your leg.  But we know that martial artists fracture legs during kicks.

And fractures definitely result in longitudinal bone growth because the bone clot results in a lot of fluid stimulus and it removes the cortical bone impediment.

We also know that there’s a phenomenon known as stress fractures where bones can develop fracture over time to non-overly traumatic loads just as the bone is no longer able to recover.

But we want to know if it’s possible to induce the longitudinal bone growth stimulus without fracturing a bone.  And could it be possible with a tapping stimulus?  The key is to target a less innervated part of the bone which happens to be the epiphysis although there are some epiphysis where regions are fairly innervated.  Tapping the epiphysis also generates a fluid pressure gradient.

With these fluid pressures we want to stimulate bone degradation via osteoclasts(remodeling)[this process could be accelerated via HGH] but we don’t want bone deposition via osteocytes and osteoblasts we want cartilage deposition although it’s feasible that other fibrocartilage tissues could work so that’s why we want sustained loading pressures over time so consistent taps.  The stress fracture phenomenon is also beneficial for our purposes.  Microcracks are good at stimulating fluid forces.

Nerve issues are probably unavoidable but we want to choose the least nerved location.

Does anyone have any anecdotal evidence of martial artist effects on bone?

I know there’s not a lot of solid proof of anything here but basically I’m testing epiphyseal tapping over prolonged periods to generate bone degradation and creating a favorable microenvironment for replacement via soft tissues.  I wanted people to know what I’m working on as I haven’t posted here in a while.  I’m solely dependent on generating proof at this point so if anyone has any evidence of martial artists generating any kind of visible bone adaptation whatsoever that would be extremely helpful.

 

 

 

 

 

 

 

p-Coumaric acid<- potential height increasing supplement

According to the study it only increases IGF-1, but it may have other effects that are not known about.  Red Clover flowers contain p-Coumaric Acid.  I could only find p-coumaric acid available for scientific use.

p-Coumaric acid stimulates longitudinal bone growth through increasing the serum production and expression levels of insulin-like growth factor 1 in rats.

“The aim of the present study was to examine the effects of p-coumaric acid on the longitudinal growth of the long bone in adolescent male rats. Teatment with p-coumaric acid significantly increased the tibial length and the height of each growth plate zone and the ratio of 5-bromo-2′-deoxyuridine-positive cells relative to total proliferative cells. Expression of insulin-like growth factor 1 and its receptor in the proliferative and hypertrophic zones, and serum levels of growth hormone and insulin-like growth factor 1 were significantly increased as well in the p-coumaric acid-treated group. Via increasing both the serum level of insulin-like growth factor 1 and its expression, p-coumaric acid could promote cell proliferation in growth plate zones. These results suggest that p-coumaric acid has the potential to increase height and may be a feasible alternative to growth hormone therapy.“<-the statement that this may be a feasible alternative to growth hormone therapy makes this seem more powerful than just your typical supplement.

The study also mentions other supplements that have beneficial effects on chondrogenesis.  If you look at figure 1 and 2 you can see that there are differences between p-Coumaric Acid and Growth Hormone growth plates.  The scientists suggest that p-Coumaric acid upregulates IGF-1 and IGF-1R.

Ligaments constrain growth

The reason that the jaw can grow via stretching by forwarding positioning and bite-jumping appliances is that it is not as constrained by ligaments as other bones.  It’s possible that other movable joint regions like the wrists, fingers, and toes would also be stretchable.  The wrists would come under extreme stress due to the farmers walk so if this true there should be anecdotal evidence of longer arms due to the farmers walk.  It is possible that a new height increase method could be invented that causes enough tensile strain in the articular cartilage to activate endochondral ossification in that region.  The ligaments holding the bone together would constrain this.  This would also help explain why people with Marfan’s become taller as they have more flexible joints and therefore their growth is less constrained by ligaments.   Here’s another connective tissue disorder that may affect longitudinal bone growth.  It’s also possible that differences between condylar cartilage and articular cartilage allow this to happen in the mandible but not in other joints.

So if anyone could look for instances of longer arms due to heavy farmers walk.  This would be much easier to do than LSJL.  So any research on this would be a great boon to further the cause of height increase.

The adaptive remodeling of condylar cartilage—a transition from chondrogenesis to osteogenesis.

“Mandibular condylar cartilage is categorized as articular cartilage but markedly distinguishes itself in many biological aspects, such as its embryonic origin, ontogenetic development, post-natal growth mode, and histological structures. The most marked uniqueness of condylar cartilage lies in its capability of adaptive remodeling in response to external stimuli during or after natural growth. The adaptation of condylar cartilage to mandibular forward positioning{basically bringing your jaw forward} constitutes the fundamental rationale for orthodontic functional therapy, which partially contributes to the correction of jaw discrepancies by achieving mandibular growth modification. The adaptive remodeling of condylar cartilage proceeds with the biomolecular pathway initiating from chondrogenesis and finalizing with osteogenesis{so basically by stretching the articular cartilage you activate enchondral ossification enabling you to grow on the longitudinal ends of the bone}. During condylar adaptation, chondrogenesis is activated when the external stimuli, e.g., condylar repositioning, generate the differentiation of mesenchymal cells in the articular layer of cartilage into chondrocytes, which proliferate and then progressively mature into hypertrophic cells. The expression of regulatory growth factors, which govern and control phenotypic conversions of chondrocytes during chondrogenesis, increases during adaptive remodeling to enhance the transition from chondrogenesis into osteogenesis, a process in which hypertrophic chondrocytes and matrices degrade and are replaced by bone. The transition is also sustained by increased neovascularization, which brings in osteoblasts that finally result in new bone formation beneath the degraded cartilage.  The repositioning of the mandibular condyle in adult rats led to a reactivation of chondrogenesis in condylar cartilage which otherwise is at resting status, and finally results in increased bone formation{this is huge if as it means a bigger stronger jaw}”

“chondrogenic activity of BMP-2 in vitro involves the action of the cell-cell adhesion protein, N-cadherin, which functionally complexes with beta-catenin the change of condyle position relative to the glenoid fossa constitutes an important trigger for [the endochondral ossification related adaptation of the mandible].”

The deviation of the condyle from the glenoid fossa by mandibular forward translation is the basis for orthodontic functional therapy, which aims to enhance condylar growth and therefore to eliminate the discrepancy between upper and lower jaws.

“a decrease in compressive loading enhances condylar growth, whereas an increase in loading inhibits growth”

Note that they do say that condylar cartilage is distinct from articular cartilage.

Here’s another study:

Murine TMJ loading causes increased proliferation and chondrocyte maturation.

“The purpose of this study was to examine the effects of forced mouth opening on murine mandibular condylar head remodeling. We hypothesized that forced mouth opening would cause an anabolic response in the mandibular condylar cartilage. Six-week-old female C57BL/6 mice were divided into 3 groups: (1) control, (2) 0.25 N, and (3) 0.50 N of forced mouth opening. Gene expression, micro-CT, and proliferation were analyzed. 0.5 N of forced mouth opening caused a significant increase in mRNA expression of Pthrp, Sox9, and Collagen2a1, a significant increase in proliferation{These alone will not increase height except maybe the increase in proliferation}, and a significant increase in trabecular spacing in the subchondral bone, whereas 0.25 N of forced mouth opening did not cause any significant changes in any of the parameters examined. Forced mouth opening causes an increase in the expression of chondrocyte maturation markers and an increase in subchondral trabecular spacing.”

“The articulating surfaces of the temporomandibular joint (TMJ) are covered by fibrocartilage, which is composed of chondrocytes at various stages of maturation that are organized into four zones: (1) superior articular zone—cells in this zone express proteoglycan 4 (Prg4); (2) polymorphic zone—cells in this zone express SRY-box 9 (Sox9) and parathyroid-hormone-related protein (Pthrp); (3) flattened zone—the cartilage cells in this layer express collagen type II (Col 2a1); and (4) hypertrophic zone—the chondrocytes express collagen type X (Col 10a1)”

“Growth in the condylar cartilage proceeds from cells exiting the proliferative pool in the polymorphic zone and undergoing endochondral ossification in the inferior cartilage zones. The mandibular condylar cartilage is able to remodel its structure in response to mechanical strains”

F and G are both forced mouth opening with F and G to a higher degree.  C and D have longer bones but there is less separation between the two bones with C and D.  The fear with articular cartilage endochondral ossification is that you’ll decrease the joint space.

“Functional appliance therapy is believed to place the mandible in a protrusive position, causing the condyle to be unseated caudally and ventrally from the articular fossa, while forced mouth opening is believed to cause a compressive force between the articular eminence and the mandibular condyle”

“A possible explanation for both functional appliance therapy and forced mouth opening causing similar effects in the mandibular condylar cartilage is that the mandibular condylar cartilage responds similarly to different types of loading compression for forced mouth opening and tension for functional appliance therapy{another possibility is that both activate the lateral pterygoid muscle and that’s what pulls on the cartilage}. Another possible explanation is that forced mouth opening and functional appliance therapy influence the masticatory muscles in such a way that the actual deformational strains within the mandibular condylar cartilage are similar for both.”

Forward mandibular positioning enhances the expression of Ang-1 and Ang-2 in rabbit condylar chondrocytes

“Functional appliances correct dental malocclusion, partly by exerting an indirect mechanical stimulus on the condylar cartilage, initiating novel bone formation in the condyle. Angiopoietin is involved in the angiogenesis associated with novel bone formation. This study aimed to determine the expression of angiopoietin (Ang)‑1 and ‑2 following forward mandibular positioning (FMP) in the condylar chondrocytes of rabbits. Sixty rabbits (age, 8 weeks) were randomly allocated to the experimental and control groups (n=30 per group). In the experimental group, FMP was induced by a functional appliance. Five rabbits from the experimental group and the control group were sacrificed following 3 days and 1, 2, 4, 8 and 12 weeks, respectively. The right temporomandibular joints (TMJs) were collected and the expression of Ang‑1 and -2 was evaluated by immunohistochemical staining. The expression of Ang-1 increased at day 3 and reached a peak at 2 weeks, whereas Ang‑2 reached maximal expression 4 weeks after FMP. Subsequently, the expression of Ang‑1 and ‑2 gradually decreased. Thus, FMP enhanced the expression of Ang‑1 and Ang‑2 in condylar cartilage, which is related to angiogenesis in the process of endochondral ossification.”

“Autocrine Ang-1/Tie-2 modulates blood vessel plasticity and contributes to vascular maintenance. In addition, Ang-1 enhances survival, migration and network formation of endothelial cells in vitro, and induces neovascularization in vivo. Ang-2 is a naturally occurring antagonist of Ang-1 that inhibits Ang-1-induced activation of Tie2. Ang-1 and -2 are located at sites of endochondral bone formation in the growing skeleton”

“The appliances were worn for 24 h to produce a continuous forward and downward positioning of the mandible.”

Look at all the cartilage growth.  There seems to be some endochondral ossification going on in the longitudinal ends of bone which is very good for height growth.

Here’s a normal jointNotice how they are connected strongly by a ligament(Li)

Here’s Mandibular Condylar Cartilage as a Juvenile and as an adult:

Microcracks effect on fluid flow. Long term loading may be key for LSJL.

This study is important because it indicates that microcracks may be bad for fluid flow which stimulates bone growth but good for cartilage growth as if fluid is not flowing than it is building up pressure and pressure is more conducive to chondrogenesis.  This indicates that a method to induce fluid flow such as  clamping/tapping should be higher duration and more “fatigue loading” based to insure the induction of microcracks.  Fatigue loading is the act of inducing bone damage not by a sudden large damage but by sustained bouts of loading over time.

Influence of interstitial bone microcracks on strain-induced fluid flow.

“microcracks act as a stimulus for bone remodelling, initiating resorption by osteoclasts and new bone formation by osteoblasts.  Microcracks alter the fluid flow and convective transport through the bone tissue. [We evaluate] the strain-induced interstitial fluid velocities developing in osteons in presence of a microcrack in the interstitial bone tissue. Based on Biot theory in the low-frequency range, a poroelastic model is carried out to study the hydro-mechanical behaviour of cracked osteonal tissue. the presence of a microcrack in the interstitial osteonal tissue may drastically reduce the fluid velocity inside the neighbouring osteons{So maybe microcracks will increase hydrostatic pressure as hydrostatic pressure is the pressure exterted by a fluid at rest}. This fluid inactive zone inside osteons can cover up to 10% of their surface. Consequently, the fluid environment of bone mechano-sensitive cells is locally modified.”

“Cortical bone constitutes the outer shell of long bones. This live entity is continuously renewed by bone cells in response due to the loading generated by daily activity”

“microdamage occurring inside the osteonal volume may generate a cell-transducing mechanism based on ruptured osteocyte processes. Concomitantly, microcracks are likely to alter the fluid flow and convective transport through the bone tissue and thus modify the hydraulic vicinity of the sensitive cells”

“the drag force caused by the pericellular fibres is thought to activate the cellular biochemical response through the interactions with the cytoskeleton”

“the pressure inversely increases from its Haversian reference to reach its maximum in the interstitial tissues.”

“the presence of the microcrack strongly modifies the fluid flow velocities in the osteons located in the immediate vicinity of the damage. It may generate an “inactive zone” inside the osteon wherein the fluid velocities are relatively low and thus the osteocytes stimulation too”<-But even though fluid flow may be low hydrostatic pressure may be high which may be better for chondrogenesis.

Fatigue Loading may be important to LSJL

This paper shows that axial loading can induce an almost complete fracture line through the bone through one side to the other.  But the break is on the wrong axis.  If fatigue loading was induced via transverse loading (lsjl or lateral impact loading) it is very likely that the micorodamage would be along the right axis.  But to induce bone fatigue in this way would likely require heavier loads than inducing sufficient hydrostatic pressure to induce chondrogenesis as the goal of increasing fluid forces in the bone is to encourage bone decay and induce differentiation of tissues that are capable of interstitial growth.

Role of Calcitonin Gene-Related Peptide in Bone Repair after Cyclic Fatigue Loading

“We used the rat ulna end-loading model to induce fatigue damage in the ulna unilaterally during cyclic loading. We postulated that CGRP would influence skeletal responses to cyclic fatigue loading. Rats were fatigue loaded and groups of rats were infused systemically with 0.9% saline, CGRP, or the receptor antagonist, CGRP8–37, for a 10 day study period. Ten days after fatigue loading, bone and serum CGRP concentrations, serum tartrate-resistant acid phosphatase 5b (TRAP5b) concentrations, and fatigue-induced skeletal responses were quantified. cyclic fatigue loading led to increased CGRP concentrations in both loaded and contralateral ulnae. Administration of CGRP8–37 was associated with increased targeted remodeling in the fatigue-loaded ulna. Administration of CGRP or CGRP8–37 both increased reparative bone formation over the study period. Plasma concentration of TRAP5b was not significantly influenced by either CGRP or CGRP8–37 administration.”

“sensory innervation of bone may have regulatory effects on skeletal responses to bone loading”

“Periosteum, endosteum, and bone tissue are all innervated by nerve fibers. This innervation exhibits plasticity in response to mechanical loading, in that a single loading event results in persistent changes in neuropeptide concentrations in both loaded and distant long bones, as well as changes in the neural circuits between limbs”

“Individual bone cells are directly connected to the nervous system via unmyelinated sensory neurons. Bone cells express a range of functional neurotransmitter receptors and transporters, including those for calcitonin gene related peptide (CGRP)”

“12 rats were fatigue loaded until 40% loss of stiffness was attained, using an initial peak strain of −3,000 µε (Fatigue group). ”

“To induce fatigue, the load applied to the ulna was incrementally increased until fatigue was initiated, as indicated by increasing displacement amplitude from a stable baseline. ”

The break extends all along the bone but is on the wrong axis.
“Increased bone blood flow precedes bone repair in response to fatigue loading, and remodeling in response to decreased mechanical loading . Systemic administration of CGRP also decreases blood pressure in a dose-dependent manner””
“”treatment with CGRP8–37 may have increased intraosseus pressure, transcortical interstitial fluid flow, and associated bone formation””

Impact loading on mouse bone length

Normally, I wouldn’t draw attention to this first paper but it draws an interesting thought:  “That long term sustained loading is better for longitudinal bone growth, whereas short term intense loading is better for bone quality.”  This could be due to hydrostatic pressure being good for stimulating a cartilagenous(and thus a pro growth plate micro-environment) whereas rapid changes in fluid flow as induced by short term dynamic loading(like jumping) are better for changes in bone quality.  So I will be changing the way I will be performing LSJL, rather focusing on clamping as hard as possible I will not be clamping as hard but doing longer more sustained clamps.

Enhancement of bone quality and longitudinal growth due to free-fall motion in growing rats

“[We] investigate the synchronous phenomena between bone quality and longitudinal length in a same subject affected by landing exercise. Physical exercise on the ground induces external loading to human body due to resistance from ground which can activate bone generation or remodeling. Especially, when the impact stimulation is applied to bone, it may improve bone quality and lengthening.
6-week-old male Wistar rats were randomly allocated to one of two conditions: free fall from 40 cm-height (I40; n = 7), and control (IC; n = 7). The impact stimulations were administered to the free fall groups, 10 times/day, and 5 days/week for 8 weeks. Structural parameters and longitudinal length of tibia were measured to quantitatively evaluate the variation in morphological characteristics and bone length with maturing.
The landing impact seems to be commonly effective on the enhancement of bone quality as well as longitudinal growth. However, the extent of enhancement may be more dominant in bone quality than longitudinal growth. On the other hand, the ratio of longitudinal growth seems to be dependent on the duration of stimuli whereas the enhancement of bone quality does not.
This study verified that free-falls exercise can be effective on the enhancement of bone qualities and promotion of vertical growth in long bones. We expect that it might be possible for the moderate impact stimulation to be proposed as an aid for prevention of bone loss and promotion of bone lengthening.”

” Bone cells accommodate to a customary mechanical loading environment, making
them less responsive to routine loading “<-thus possibly needing to cycle on and off a method of bone stimulus.  Although our goal is to target stem cells to form new growth plates and not necessarily bone cells.

“In comparison between two groups, there is no significant [differnece] at 4 week, whereas the values in I40 group exhibited slightly but significantly higher than that in IC at 8 weeks”  So there was a change in limb length but it took 8 weeks to notice a difference.  It would be interesting to see if impact loading could have an impact on animals without functioning growth plates.  If it could increase longitudinal bone growth in some other way.

“the ratio of longitudinal growth seems to be dependent on the duration of stimuli whereas the enhancement of bone quality does not.”<-this is interesting maybe it’s more important to clamp for a long period of time than intensity of clamping.  This could a lot of sense if longitudinal growth is driven by fluid whereas bone mechanical parameters are driven by stimulation of osteocytes and bone cells.  Longitudinal bone growth could be driven by sustained hydrostatic pressure whereas bone quality could be driven by rapid changes in interstitial fluid flow.

Another study found “. observed significantly greater increase in bone length compared to the sedentary rats when they implemented the similar training 100 times/day in 5 days/week
on Fisher 344 rats of 3-month-old and 6-month-old for 8 weeks”

Here’s that other study:

Effects of Jump Training on Bone Hypertrophy in Young and Old Rats

“The effects of jump training on bone hypertrophy were investigated in 3, 6, 12, 20 and 27 month-old female Fischer 344 rats. The rats of all age groups were divided into jump training
(height: 40 cm, 100 times/day, 5 days/wkfor 8wks), run training (speed: 30 m/min, 1 h/day, 5 days/wk for 8wk) or sedentary group. Fat-free dry weights (FFW) of the femur and the tibia were significantly greater in the jump-trained rats than in the runtrained rats, and were significantly greater in the run-trained rats than in the sedentary rats. jump training significantly increased FNV of the femur and the tibia not only in young rats but also in old rats, while run training did not increase FFW significantly in old rats. In young rats, both jump training and run training significantly increased the length of the femur and the tibia and the diameter of the femur. The diameter of the tibia was greater in the jump-trained rats than in the sedentary and the run-trained rats in all age groups. The results of the present study indicate that jump training was a more effective training mode than run training for bone hypertrophy and that the effects were not limited by age. ”

According to the chart, Jump training increased length of the tibia and femur on rats younger than 12 months but actually decreased tibia and femur length on rats older than that.  So the compressive force actually denatured the tibia and femur such that it was shorter.

But in the study they do say ” In the 3 and 6 month-old rats, both jump training
and run training increased the length of the femur and the tibia and the diameter of the femur.”<-which is contrary to what the graph says.