|If rely on the results of the most recent study from Australia, the answer to the above question probably reads "Yes, to a certain degree it does".|
Does vitamin D build muscle?
I guess all of you will tell me that, in view of the results of pertinent studies (cf. Girgis. 2013a), the answer is "no, it doesn't, but deficiency seems to hamper muscle growth and impair skeletal muscle function". This conclusion is hard to debate, especially in view of the fact that we don't even know what exactly vitamin D does in human muscle cells.
Exactly this, i.e. the question "what exactly happens, when muscle cells are exposed to vitamin D" must have been bother Girgis et al., too. Therefore they devised a very simple yet interesting in-vitro study in the course of which they treated C2C12 cells, which are a commonly used model (see bottom line for a comment on this) for human skeletal muscle with both, the active 1,25(OH)2D and inactive 25(OH)D form of 'vitamin D' and observed the effects on cell proliferation and growth.
|Figure 1: Number of live cells (10^4/dish; middle) and images of the cells w/out & w/ 25(OH)D2 (Girgis. 2013b)|
Ok, enough of the enzymes what about "getting big"?
Let's briefly forget about the mechanisms and return to the actual effects on growth and proliferation. Effects such as the 30-50% increases in G0/G1, a gene that's responsible for arresting the cell cycle, and the 30% and 20% decreases in Myc and Cyclin-D1 the scientists observed in response to both 25(OH)D and 1,25(OH)2D.
In view of the fact that these genes are necessary for the progression of the cell cycle, it is not surprising that the exposition to both forms of vitamin D brought the cycle to a screeching halt. In the end, this is yet a long-known phenomenon. The antiproliferative effects of 1,25(OH)2 D in muscle cells were first described in 1985 and are, as Girgis et al. point out, ...
"[...] they are consistent with antiproliferative effects of 1,25(OH)2 D in a number of other cells and tissues including skin, cancer cells and immune cells ." (Girgis. 2013b)What's news though, is that the researchers were able to confirm that even 25OHD, the "prohormone" (Girgis. 2013b) to 25(OH)D2, displays antiproliferative effects in C2C12 cells.
|Don't forget the "Underestimated Vitamin D Sources: Especially Eggs, But Also Chicken, Pork, Fish & Dairy Contain an Overlooked, Physiologically Relevant Amount of Ready-Made 25OHD" | read more|
"What? Vitamin D kills muscle growth?"
At first sight the cell-cycle arrest really suggest that high, and not the often cited low vitamin D levels should have anti-anabolic effects. Since muscle does not necessarily depend on proliferation, or more specifically cell devision, to grow this is yet not the case. At least up to a volume time-point your muscle cells and with them your total muscle volume can grow by simply taking up more protein. This process is called hypertrophy and it works quite nicely until a certain threshold is reached and myostatin pulls the emergency break (if you read my previous article "Getting Big Means Growing Beyond Temporary Physiological Limits" you will know that this is the point, when the activation and incorporation of satellite cells becomes important; learn more)
|Figure 2: There may be less live cells, but once the cell cycle arrests, the cells that are bathed in serum with high amounts of acvite vitamin D 1,25(OH)2D grow like crazy, but probably only until they are 'ready to burst' (Girgis. 2013b)|
- Girgis, Christian M., et al. "The roles of vitamin D in skeletal muscle: form, function, and metabolism." Endocrine reviews 34.1 (2013a): 33-83.
- Girgis, Christian M., et al. "Vitamin D Signaling Regulates Proliferation, Differentiation and Myotube Size in C2C12 Skeletal Muscle Cells." Endocrinology (2013b): en-2013.
- Halevy, Orna, and Orna Lerman. "Retinoic acid induces adult muscle cell differentiation mediated by the retinoic acid receptor‐α." Journal of cellular physiology 154.3 (1993): 566-572.
- Kotliar, N., and P. F. Pilch. "Expression of the glucose transporter isoform GLUT 4 is insufficient to confer insulin-regulatable hexose uptake to cultured muscle cells." Molecular Endocrinology 6.3 (1992): 337-345.
- Langelaan, Marloes LP, et al. "Advanced maturation by electrical stimulation: Differences in response between C2C12 and primary muscle progenitor cells." Journal of tissue engineering and regenerative medicine 5.7 (2011): 529-539.