This article is interesting [Payne et al., 2007: (http://www.ncbi.nlm.nih.gov/pubmed/17408874)], and the authors suggest that physical exercise may increase the bone marrow density and that very sedentary lifestyles may contribute to the development of unexplained anemia, particularly the state of so-called "anemia of chronic disease." In anemia of chronic disease, pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), among others, are thought to be released from monocytes and endothelial cells (and adipocytes, even), etc., and suppress hematopoiesis. There are ways of helping to diagnose anemia of chronic disease by examining the ratio of soluble transferrin receptor (sTfR), which is not the same as serum transferrin (sTf), to serum ferritin. There are these algorithms for interpreting the ratio and drawing guarded conclusions from it.
I think the most interesting factor, from a mechanistic standpoint, that the authors discuss is the regulation of bone marrow mesenchymal stromal cell differentiation by growth hormone (GH) and other factors that are released in response to resistance exercise. Evidently GH (and presumably IGF-1) may be able to promote the osteogenic (osteoblastic) differentiation of stromal cells [Moerman et al., 2004: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1850101&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/15569355)], to some extent, and may be able to increase the numbers of osteoblasts. Gevers et al. (2002) [Gevers et al., 2002: (http://endo.endojournals.org/cgi/reprint/143/10/4065)(http://www.ncbi.nlm.nih.gov/pubmed/12239118?dopt=Abstract)] also suggested that lipids, mobilized from bone marrow adipocytes, could serve as an energy source for hematopoietic cells. Gimble et al. (1996) discussed the same concept, and those authors are basically saying the yellow marrow isn't necessarily completely undesirable. I think that GH release and the whole set of responses of growth factors to resistance exercise would be the type of thing that could help to lend credence to the article by Payne et al. (2007). Obviously, the mechanical stress from the resistance exercise would be necessary also, and mechanical stress activates localized growth-factor responses in osteoclasts and osteoblasts. But the proportion of bone marrow that's "yellow marrow" increases substantially between the ages of 17 and 21 or something, and it sort of corresponds to the decline in GH output and to the end of physical growth, etc. Gevers et al. (2002) also discuss the fact that decreases in bone mass (i.e. decreases in bone density, due to aging or immobility) are associated with increases in the numbers of bone marrow adipocytes (yellow marrow), and that's the type of thing that Payne et al. (2007) discuss. Gevers et al. (2002) note that there's generally an inverse relationship between the numbers (i.e. density) of osteoblasts, in parts of the bones, and the numbers of bone marrow adipocytes.
It's strange the way there's not much research on factors influencing the density of the red marrow, and the bone marrow is presented and viewed as if it's this invoilable and immutable organ with an almost endless capacity to adapt to any physiological challenge. It's obviously more or less true that the bone marrow has this "vast regenerative capacity" to recover from damage, etc. But there hasn't been much of an attempt to address the factors, apart from pharmacological interventions, that would allow that regeneration to occur. It's interesting that the hematocrit (i.e. percentage of the blood volume that is red blood cells) is known to be positively associated with the lean body mass (i.e. muscle and bone) [I think this is one of the many articles that shows that: Muldowney, 1957: (http://www.ncbi.nlm.nih.gov/pubmed/13414148)]. I think the assumption is that it's a result of a higher rate of oxygen consumption into cells (higher resting metabolic rate, etc.), but maybe the effect is partially due to changes in the red marrow in response to resistance exercise. There's probably a lot of research that discusses this in more depth, but I haven't really looked into it. This type of effect of resistance exercise could be important in the context of aging or atherosclerosis, given that one might expect a higher hematocrit to be accompanied by higher numbers of circulating potentially-antiatherogenic, CD34+ endothelial progenitor cells [this isn't all that good an example, but the point is that hematocrit seems to correlate positively with the numbers of circulating endothelial progenitor cells: Bahlmann et al., 2003: (http://www.nature.com/ki/journal/v64/n5/pdf/4494070a.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/14531796)].
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