The problem with stretches like the medieval rack or sitting/sleeping with ankle weights is that they stretch more the cartilage and ligaments than the bones themselves. Sky of easy height was working on a program that stretched the bone. Unfortunately, Sky disappeared before sharing his data.
If your tie a rope around the top of your ankle and then load the bottom of the rope with iron plates, your leg is being stretched down and out(being lengthened). If you then tie a rope around the bottom of the ankle and then tie the middle of the rope around a bar; and then load that rope with iron plates your leg is being stretched upwards and out. If you do both of these at the same time with equal amounts of force then the up and down forces cancel out and your bone is only being lengthened outwards.
You could also alternate between pulling your ankle up and down which would proceed to lengthen your bone in a zig-zag motion. We know that bone is elastic and that bone has the ability to microfracture. If you stretch your bone and microfractures occur in a stretched state then the bone should maintain some of that elasticity. Pull a pencil apart, when you do microscopic damage occurs in the length of the pencil. The pencil is now longer than before. Unlike a pencil however, bone has the ability to heal those microfractures. So you distract the bone cause microfractures, the microfractures heal, and then you distract the bone again. Gradually, becoming taller and taller over time.
One element of Sky's multitude of experiments that he has kept in his new Shinbone Version 2011 is cycling with ankle weights(with a raised saddle). The hypothesis of why cycling with ankle weights would work is that you are stretching your leg bone forcing your leg bone to reach lower and lower. Now if Sky does have a method of performing cycling to properly put a stretching force on the leg bone then it could work.
There are a couple of problems involved with the heavy iron plates method however. You are putting load on your tendons and ligaments. You have to find some way to nullify the tendons and ligaments. If you perform this method say around the ankle then you are probably only going to stretch the tibia and not the fibula. The iron plates method would probably best be used in parts of the limb where there is only one bone such as the femur and humerus.
Essentially, a bone stretching method could work. In contrast to LSJL, you would want the load slightly below the growth plate(you only want to stretch your cortical bone in contrast to LSJL where you are trying to deliver red bone marrow stem cells into your growth plate). You would then have to find a way to perform it without putting all the strain on your tendons/ligaments. You would then have to find a way to equally push the bone down from the top and the bottom. You would have to make sure that you were causing microfractures during the process. If you read the last study, you can see why it may be worth it to perform bone stretching while doing LSJL.
Osteodistraction of the maxilla in transverse deficiency in adults: Analysis of the literature and clinical case.
"Osteogenic distraction is a bone regeneration and reconstruction technique. [Osteogenic distraction is] "the process of creating new bone by stretching"[bone stretching can best be analyzed by tensile strain, however this seems to be a different form of stretching]. Disjunction entails separating two anatomical structures at their junction system and, therefore, at a suture[so they're not stretching the bone they're separating the junctions between the bone]. Usually, it involves separating two semi-maxillae in the transverse dimension by means of an osteotomy[osteotomy refers to bone cutting so they are cutting the bone but now it seems like they are separating two separate bones and not cutting the bones itself]. Transverse maxillary distraction appears to offer an alternative of choice to orthognathic surgery alone, which is frequently prone to relapse. The greatest benefit of osteogenic distraction lies in its greater potential for expansion and concurrent growth of the soft tissues. Among other things, this technique increases arch length, thus precluding tooth extractions in cases of maxillary crowding, and appears to provide more stable results than conventional surgical intermaxillary disjunction."
If osteodistraction does work by stretching between the bones then perhaps something that stretches the cartilagenous area of the knee could help you to grow taller.
Effects of osteoinduction on bone regeneration in distraction: results of a pilot study.
"Rate and frequency of distraction as well as stimulatory effects transmitted by growth factors and local gene therapy have a decisive influence on bone regeneration. In a pilot study we tested the effect of four different morphogenetic and mitotic proteins and a genetically transferred vector system on bone healing in continuous osteodistraction in a large animal experiment on 24 Goettingen mini-pigs. For this purpose bone morphogenetic protein (BMP-2), BMP-7, TGF-beta, IGF-1 and a liposome vector were instilled into the distraction gap. The animals were killed after 1-4 weeks of consolidation. Histological and radiological evaluations showed maximum bone formation after the application of BMP-2/7, whereas the application of TGF-beta, IGF-1 and the liposomal vector had only a limited effect on bone regeneration. The quantitative analysis demonstrated an average amount of bone in the distraction gap of 50% and 61% after instillation of BMP-2 and 7, respectively. The BMP-2 expression, however, was maximal after induction with the non-viral vector. Only after BMP-2/7 application could physical, radiographic and histological evidence of bone union be detected. In bone distraction with a short observation period the application of morphogenetic proteins seems to enhance bone regeneration significantly. Before application in humans further studies are necessary to measure the dose-effect relationship, the mode of application and the efficacy of different inductive proteins. The combination of osteodistraction with osteoinduction, however, could shorten treatment times dramatically."
If you look in this picture you can see that the bone grew back without any compounds like BMP-2/7 or TGF-Beta1
"Within the context of ossification, cellular elements with increased BMP-2 expression were found both in the distraction zone, and in the consolidated osseous area close to the osteotomy region. A reduced BMP-2 expression was found in the central distraction zones of those animals, where induction did not stimulate bone regeneration in the distraction region"<-so bone does not seem to form without BMP-2 in the distraction region in this study
"Labelled bone marrow stem cells are systematically mobilized and attracted to fracture sites from remote cell depots"<-Stem cells are still involved. Also remember that a callus might generate hydrostatic pressure.
In the article on limb lengthening surgery, we learned that stretching Type I Collagen might cause a mechanotransduction based signal that results in the increase of the size of the micronuclei of bone cells thus causing bone hypertrophy. This would mean that there would be no need for the fracture and that all you'd need is for tensile strain on Type I Collagen.
Limb bud mesenchyme cultured under tensile strain remodel collagen type I tubes to produce fibrillar collagen type II.
"In this work, we studied the effects of tensile strain on limb bud mesenchymal cells (MSC) cultured on a collagen type I tubular scaffold. A novel bioreactor was designed to culture the cells while subjecting the tubular scaffold to tensile stress and strain. Control samples included unseeded and MSC-seeded tubes cultured for 2 weeks under unloaded, no-strain conditions, and unseeded tubes subjected to prolonged tensile stress and strain. Mechanical properties of tube specimens were measured under oscillatory compressive stress. Following mechanical testing, scaffolds were fixed for immunohistochemistry or frozen for mRNA extraction. The storage modulii of both seeded/unstrained and seeded/strained tubes were significantly less than that of unseeded tubes, suggesting that MSC disrupted the structure and elasticity of the tubes' collagen type I. At a frequency of 1.0 Hz, the loss tangent of seeded/strained tubes was more than 2.5 times greater than that of seeded/unstrained tubes, and almost 6 times greater than that of unseeded tubes. Confocal microscopy and qRT-PCR results demonstrated that collagen type II and aggrecan expression was upregulated in the seeded/strained tubes. Culture under tensile strain induces MSC to remodel the collagen type I tube with collagen type II and aggrecan expression into fibrils dispersed throughout the matrix[so basically tensile strain on the mesenchyme encourages removal of bone and the creation of cartilagenous, possibly growth plate like structures. Note there is mesenchymal tissue in the bone marrow]. The seeded/unstrained tubes manifested less collagen type II with a more random expression pattern. Compared to seeded/unstrained tubes, qRT-PCR for collagen type II in the seeded/strained tubes showed a 4-fold increase in the message for collagen type II and a 13-fold increase in the message for aggrecan. These results demonstrate that MSC cultured for at least some period under tensile strain are able to remodel collagen type I scaffolds to produce a more viscous construct having many of the mechanical and biological features of engineered cartilage."
"In the knee, static compression of the joint creates hydrostatic stress, and movement of the joint creates shear stresses. However, because the knee is a non-conformal surface, the cartilage will also experience a directional tensile stress and strain during use"<-We use static compression in LSJL to create hydrostatic pressure on the bone marrow of the epiphysis.
So tensile strain involved in limb lengthening surgery may stimulate cartilage formation by tensile strain on the mesenchymal tissue itself. Here's the effects of tensile strain directly on the Type I Collagen.
Deformation-dependent enzyme mechanokinetic cleavage of type I collagen.
"Collagen is a key structural protein in the extracellular matrix of many tissues. It provides biological tissues with tensile mechanical strength and is enzymatically cleaved by a class of matrix metalloproteinases known as collagenases. Collagen enzymatic kinetics has been well characterized in solubilized, gel, and reconstituted forms. However, limited information exists on enzyme degradation of structurally intact collagen fibers and, more importantly, on the effect of mechanical deformation on collagen cleavage. We studied the degradation of native rat tail tendon fibers by collagenase after the fibers were mechanically elongated to strains of epsilon=1-10%. After the fibers were elongated and the stress was allowed to relax, the fiber was immersed in Clostridium histolyticum collagenase and the decrease in stress (sigma) was monitored as a means of calculating the rate of enzyme cleavage of the fiber. An enzyme mechanokinetic (EMK) relaxation function T(E)(epsilon) in s(-1) was calculated from the linear stress-time response during fiber cleavage, where T(E)(epsilon) corresponds to the zero order Michaelis-Menten enzyme-substrate kinetic response. The EMK relaxation function T(E)(epsilon) was found to decrease with applied strain at a rate of approximately 9% per percent strain, with complete inhibition of collagen cleavage predicted to occur at a strain of approximately 11%[but is inhibition of collagen cleavage good or bad for height growth?]. However, comparison of the EMK response (T(E) versus epsilon) to collagen's stress-strain response (sigma versus epsilon) suggested the possibility of three different EMK responses: (1) constant T(E)(epsilon) within the toe region (epsilon<3%), (2) a rapid decrease ( approximately 50%) in the transition of the toe-to-heel region (epsilon congruent with3%) followed by (3) a constant value throughout the heel (epsilon=3-5%) and linear (epsilon=5-10%) regions. This observation suggests that the mechanism for the strain-dependent inhibition of enzyme cleavage of the collagen triple helix may be by a conformational change in the triple helix since the decrease in T(E)(epsilon) appeared concomitant with stretching of the collagen molecule."
"Collagen degradation is a mechanism for extracellular matrix (ECM) remodeling and maintenance[the possibility for remodeling Type I Collagen into Type II Collagen which is the cartilage of the growth plate], and in response to trauma, disease and inflammation. Collagenases-1, 2 and 3 are the primary enzymes that act to degrade interstitial collagens (types I, II and III) in humans and animals. These collagenases are part of a larger family of enzymes (matrix metalloproteinases or MMPs) characterized by a zinc dependency for catalytic activity. MMPs are secreted by the cell as inert zymogens in response to the cell being activated by inflammatory cytokines, such as growth factors (interleukin-1) and mechanical loads. In order for collagen cleavage to occur, the collagenase (MMPs-1, 8 and 13, respectively) gains access to the collagen triple helix by binding to the enzyme’s attachment domain along the α-chains, followed by separation (unwinding) of the α-chains to expose the cleavage site, and then cleavage of the α-chain by the enzyme’s catalytic domain[tensile strain of 11% or greater(which means that the bone is stretched to 11% of it's original length) results in the in ability for collagen cleavage]. Collagenases contain two protein domains joined by a linker (hinge), a hemopexin C domain to which the collagen molecule attaches, and a catalytic domain responsible for the α-chain cleavage. MMP-1, 8 and 13 will cleave all three α-chains of interstitial collagens by a single scission at a specific site, located 3/4 from the N terminal and 1/4 from the C terminal, which is characterized by a Gly775-Ile776 or Gly775-Leu776 peptide bond, resulting in two fragments of the collagen molecule. Following this initial cleavage other MMPs (mainly gelatinases and stromelysins) can collectively further degrade the collagen fragments. However, the mechanism of the initial cleavage of the collagen molecule must originate with collagenase binding, triple helix unfolding and ¾-¼ scissoring."
"increasing tensile strain up to 4% (grip-to-grip) resulted in a decrease in the rate of enzymatic degradation, while strains above this (to 7%) caused an increase in the rate"<-Thus perhaps why limb lengthening surgery only stretches by 1mm a day which is well below 4%.
"mechanical deformation of type I collagen fibers caused by an axial strain (elongation) applied to the fiber will result in a significant decrease in the rate of collagen degradation by bacterial collagenase"<-This could cause height growth, if production of Type I Collagen outweighs degradation of Type I Collagen then bone could become longer.
It's possible that hydrostatic pressure is involved and that decreased cleavage results in increased hydrostatic pressure.
"Due to the self assembly nature of collagen, there appears to be a long range attraction which prevents molecules from coming too far apart and which induces the self assembly where hydrogen water bridges surrounding the molecule act as specific recognition sites for attracting other collagen molecules[So collagen attracts water to form water bridges]. More important, however, is that an exponential increase in the interaction energy (forces between triple helices) occurs as the α-chain separation distance decreases[as the Type I collagen fibers get farther apart the interaction cost increases]. Heightened hydration interaction forces are observed nearing the last 10-20 angstroms of α-chain separation (osmotic stress as high as 1000 MPa have been measured)[Increased hydration interaction forces due to increased distrace results in increased hydrostatic pressure]. This increased interaction force is [possibly] due to the energy required to rearrange the hydrogen bonding network near the molecular surfaces of macromolecules, such as might occur as the collagen molecule’s diameter is reduced as the molecule is stretched in response to an axial tensile load[tensile strain lowers the collagen molecule's diameter thus increasing the energy for hydrogen bond interaction]. Alterations in the ionic strength will also effect electrostatic interactions (<1 MPa at 15-60 Å). When the collagen molecules come into close proximity the van der Waals forces (<1 MPa at 10-25Å separation) result in an attraction or repulsion dynamic. Thus, a high concentration of repulsion ionic character will position the molecules further away from neighboring molecules creating a greater separation distance and ultimately a larger diameter. Conversely, attractive ionic character would link the molecules with a greater affinity, resulting in smaller diameters."
Stretching Type I Collagen lowers the diameter resulting in an increased energy required to rearrange the hydrogen bonding network. This increases hydrostatic pressure. So again it all leads to hydrostatic pressure.
So bone stretching may help during LSJL by lowering Type I Collagen fibril diameter thereby increasing hydrostatic pressure.
An exponential law for stretching–relaxation properties of bone piezovoltages
"Bone can change its mass, shape and density to adapt its external environment"
Ways to alter bone modeling include pizeoelectric potential, streaming potential, and fluid-generated shear stress.
"the piezoelectricity of bone arises from the organic components (mainly collagen)"
"Collagen molecules are filled and coated by platelet like tiny mineral crystals, which form the mineralized collagen fibril. A group of collagen fibrils embedded in the mineral crystals form a hierarchical structure of collagen fiber"
" Based on the hypothesis the deduced main reason for the stretching-exponential behavior is the triple helices structure of collagen fibrils distributed randomly in bone, which suffer relatively large deformation, under external loads, including self-deformations and relative slipping between molecule chains. The relative slipping movements may change the dielectric constants and resistances of bone, which leads to multiple relaxation time behaviors during deformation of bone."
Body height changes with hyperextension.
"The purpose of this study was to determine if the overall body height, as measured by a stadiometer, could be increased by brief episodes of hyperextension rather like a stretch that people frequently employ when arising. The subjects were loaded with 10 kg and the recovery with quiet sitting was compared to hyperextension 'stretches'. 15 s of hyperextension caused a significant temporary height increase [due to disc rehydration]."
"lifts up to 32 kg, and lateral bending with lifts up to 10 kg [were performed], the following parameters were estimated: lumbosacral angle and elongation, contribution of each lumbar segment to the lordosis reduction, relative pelvic/spine motion, and trunk velocity. "
-6.33mm was lost after 5 minutes of sitting.
"unloaded sitting with five hyperextensions resulted in an average height gain of +5.05 mm"
Exercise and the height of horses.
Exercise and the height of horses.
"The heights of 89 horses were measured at the withers before and after half a furlong of trotting exercise. The mean (+/- sd) height increase after exercise was 1.75 +/- 0.86 cm and the horses returned to their resting height within seven minutes. There was no linear relationship between gain in height and pre-exercise height."
Couldn't get this full study and it would be important before drawing conclusions.