Thursday, February 18, 2010

Running and Microfractures and Height

I mentioned in an earlier blog entry about how bone density scans(Dual energy X-ray absorptiometry) also detect changes in size.  Researchers define volumetric bone mineral density as the mass divided by volume(we of course are striving to increase the volume, so an increase in bone size can actually lead to the same levels of vBMD if both mass and volume increase at the same rate).  vBMD can be useful for our purposes as a sign of trabecular microfractures because if you don't cause trabecular microfractures you're not going to cause microfractures in the cortical bone. 

Proximal tibia volumetric bone mineral density is correlated to the magnitude of local acceleration in male long distance runners.

"Male runners present generally higher BMD than sedentary individuals. We postulated that the proximal tibia BMD is related to the running distance as well as to the magnitude of the shocks (while running) in male runners."

Running at minimum causes trabecular microfractures and increases bone mineral content.  The theory was that the amount of microfractures caused is related to the force of impact generated while running and the duration of exercise.

"Several measurements were performed at the proximal tibia level: volumetric BMD (vBMD), cortical index (CI) i.e. an index of cortical bone thickness and peak accelerations (an index of shocks during heel strike) while running (measured by a 3-D accelerometer)."

The cortical index could be very useful to us as a measurement tool to determine when cortical microfractures have occurred.

"CI and vBMD a) increase with running distance to reach a plateau over 30 km/wk, b) are positively associated with peak accelerations over 30 km/week."

"CI and vBMD are associated with the magnitude of the shocks during heel strike in runners."

The faster you run and the harder you strike the ground the more microfractures you cause.  The fact that cortical index leveled off over time goes against our microfracture theory.  As you should always be able to cause microfractures(unless there's a performance issue where you're not able to run as hard or fast or there's an adaptation issue where over time the same impact no longer causes cortical microfractures). Perhaps the cause of the increase in cortical bone size is by other factors than microfracture healing.

Note however that the sedentary individuals are actually the tallest and that the more the individuals ran per week the shorter they tended to be.  This could be due to proteoglycan depletion and other factors from articular cartilage.  It could also be due to shorter individuals enjoying going running more.  There would have to be a longitudinal study done to know the true effect of running on height. 

Bone mass and geometry of the tibia and the radius of master sprinters, middle and long distance runners, race-walkers and sedentary control participants: a pQCT study. 

Note in this study the control group also tended to be taller than the runners but there was seemingly no correlation between height and distance ran like in the other study.

"As hypothesised, tibia diaphyseal bone mineral content (vBMC), cortical area and polar moment of resistance were largest in sprinters, followed in descending order by middle and long distance runners, race-walkers and controls. When compared to control people, the differences in these measures were always >13% in male and >23% in female sprinters (p<0.001)."

Diaphysis is the midshaft section of the bone.  The healing of microfractures induced by running would increase bone mineral content in that area.  The use of the terminology cortical area rather than cortical volume alludes to the fact their was no increase in height.

"Similarly, the periosteal circumference in the tibia shaft was larger in male and female sprinters by 4% and 8%, respectively, compared to controls (p<0.001)."

Sprinting creates a strong enough chemical and mechanical signaling to increase periosteal width. Periosteal width is different from the deposition of new bone beneath the periosteum.

"Epiphyseal group differences were predominantly found for trabecular vBMC in both male and female sprinters, who had 15% and 18% larger values, respectively, than controls (p<0.001)."

So trabecular microfractures were caused first, followed by cortical microfractures, and followed by an increase in periosteal width.

This study did not take place over a duration of time so it could not have studied a change in bone length.

What we learned though is that sprinting is sufficient to cause cortical microfractures by the fact that cortical area increased.  There's no basis as to why if cortical length and width can increase that cortical height can't increase as well(unless sprinting causes microfractures in a way that only results in an increase of length or width of the bone when the microfractures are healed).  However, there doesn't tend to be cortical bone in the epiphysis.  The reason why periosteal width can increase with some stimulus and the epiphysis can't is that they are different tissues.  To increase the height of the epiphysis requires special stimulation.  The healing mechanisms for bone differ from how the cortical bone is aligned as cortical bone tends to increase in width rather than height(likely due to the OPG/RANKL gradient).
Note that the long distance runners had the greatest epiphyseal area.  This could however be due to less modeling into cortical bone.

Growth and adaptation to mechanical loading of immature bone and articular cartilage

"The osteogenic response due to different running modes was greatest in the femoral metaphysis. In particular, solely downhill running with high proportions of eccentric loadings was able to increase femoral trabecular bone mineral density in the metaphysis, while level running with similar amounts of concentric and eccentric loadings failed to induce an osteogenic response in this area. In contrast, neither in the dia- nor in the epiphysis any running mode-related structural alteration could be found. Moreover, downhill running increased femoral cartilage height and COMP staining height in a site-specific manner, while level running was insufficient to induce such alterations. These changes were not accompanied by any signs of degeneration. In contrast, cartilage thickness, mechanical properties, and expression of major cartilage network proteins (i.e., collagen II, collagen IX, COMP, and matrilin-3) in tibial cartilage remained unaffected by the different running modes. Growth was associated with high modeling of the morphology, biochemical composition, mechanical properties of articular cartilage, and structure of subchondral bone. COMP showed a profound redistribution throughout the cartilage. Moreover, growth diminished cartilage thickness, distribution and amounts of the matrix proteins collagen II, collagen IX, and matrilin-3 and related to this decreased its compressive properties. Functional condensation of the subchondral trabecular bone and subchondral plate due to enchondral ossification was also found to occur with increasing age, which did not seem to affect cartilage mechanical properties. In conclusion, these are the first in vivo data illustrating the effect of different running modes with different proportions of eccentric and concentric loadings on immature bone and articular cartilage in such a physiological and systematic manner."

This study was in a foreign language and I could not get the full thesis. 

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