R. Venter started Lateral Synovial Joint Loading on July 6, 2010. His age was 28 and his height was 5'5". He weight trains 3 times a week which would help by inhibiting myostatin and increasing his GASP-1 levels. He started out using a 10lbs hammer and loading the ankles and knees for 5 intervals of 20 seconds a piece. On July 13, 2010 he reported a growth of 2mm. Starting Week 2 of August he started using the 10" clamp. He gained another 1 mm on his right leg as of September 1, 2010 and no further gains in his left leg. As of October 14th, he reported a total growth of 1/4" in his right leg but no further growth beyond the 2 mm in his left.
So in about 3 months R. Venter grew 1/4" but what's interesting is that his left leg did not grow beyond 2mm.
This study here shows the various load pathways involved in LSJL. LSJL upregulates more genes in the ECM(extracellular matrix) than anything else. If you look at the growth plates under LSJL you can see the massive amounts of Matrix secreted(the white stuff). LSJL also increases levels of hyaluronan synthase which has been used as a carrier for BMP-2(which can encourage chondrogenic differentiation). LSJL also upregulates levels of MMP-3 which is involved in the vascularization and ossification of chondrocytes but also in the formation of cartilage canals.
R. Venter reported that he's always had issues with his left knee possibly due to the fact that his left knee is not secreting extracellular matrix properly.
LSJL can work by multiple mechanisms. One of the mechanisms could be bone deposition on the subchondral plate resulting in Venter's 2mm gain in his left tibia. Another could be differentiation of stem cells and periosteal progenitor cells into chondrocytes as a result of TGF-Beta, hydrostatic pressure, and hyaluronan-mediated BMP-2. These cells then form cartilage canals(thanks to MMP-3) through the perforating fibers of the periosteum, then these cartilage canals turn into new growth plates. LSJL also inhibits MMP-1 which degrades the extracellular matrix.
The seeming peak that occurs to LSJL could be due to myostatin(inhibited by exercise and other things), telomere length, and DNA Methylation. Also, cartilage likes hypoxic environments and most adult growth plates are already vascularized. Exercise increases hypoxia inducible factor-1 which would help cartilage grow. Also, bone is never completely vascularized allowing some cartilage to grow in the un-vascularized areas.
The diminishing returns of LSJL can also be due to an increase in bone vascularity inhibiting the formation of new cartilage canals.