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Some vitamin D is stored in skeletal muscles – multiple studies

Unfortunately, none of the studies appear to mention what % of 25(OH)D (Calcidiol) is stored in muscles


Vitamin D and Skeletal Muscle: Current Concepts From Preclinical Studies - Dec 2021

JBMR® Plus (WOA), Vol. 5, No. 12, December 2021, DOI: 10.1002/jbm4.10575
Christian M. Girgis1,2,3© and Tara C. Brennan-Speranza1,4,5
1 Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia 2Department of Diabetes and Endocrinology, Westmead Hospital, Sydney, NSW, Australia 3Department of Endocrinology, Royal North Shore Hospital, Sydney, NSW, Australia 4School of Medical Sciences, University of Sydney, Sydney, NSW, Australia 5School of Public Health, University of Sydney, Sydney, NSW, Australia

Muscle weakness has been recognized as a hallmark feature of vitamin D deficiency for many years. Until recently, the direct biomo- lecular effects of vitamin Don skeletal muscle have been unclear. Although in the past, some reservations have been raised regarding the expression of the vitamin D receptor in muscle tissue, this special issue review article outlines the clear evidence from preclinical studies for not only the expression of the receptor in muscle but also the roles of vitamin D activity in muscle development, mass, and strength. Additionally, muscle may also serve as a dynamic storage site for vitamin D, and play a central role in the maintenance of circulating 25-hydroxy vitamin D levels during periods of low sun exposure.
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The Role of Skeletal Muscle in Maintaining Vitamin D Status in Winter - July 2019

Current Developments in Nutrition, Volume 3, Issue 10, October 2019, nzz087, https://doi.org/10.1093/cdn/nzz087
Rebecca S Mason, Mark S Rybchyn, Myriam Abboud, Tara C Brennan-Speranza, David R Fraser

The status of vitamin D is determined mainly by its formation in skin by the photochemical action of solar UVB light (wavelength 290–320 nm) on the precursor 7-dehydrocholesterol. Because of seasonal variation in intensity of solar UV light, vitamin D status falls in winter and rises in summer. It has been presumed that there is no functional store of vitamin D. Thus, to avoid deficiency, a nutritional supply would be required in winter. However, there is now evidence that the main circulating metabolite of vitamin D, 25-hydroxyvitamin D, accumulates in skeletal muscle cells, which provide a functional store during the winter months. The mechanism is mediated by muscle cell uptake of circulating vitamin D–binding protein (DBP) through a megalin-cubilin membrane transport process. DBP then binds to cytoplasmic actin to provide an array of high-affinity binding sites for 25-hydroxyvitamin D [25(OH)D]. The repeated passage of 25(OH)D into and out of muscle cells would account for its long residence time in blood.
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Skeletal Muscle and the Maintenance of Vitamin D Status - 2020

Nutrients 2020, 12(11), 3270; https://doi.org/10.3390/nu12113270
by Mark S. Rybchyn 1ORCID,Myriam Abboud 1,2ORCID,David A. Puglisi 1,Clare Gordon-Thomson 1,Tara C. Brennan-Speranza 1,3,Rebecca S. Mason 1ORCID andDavid R. Fraser 4,*ORCID

Vitamin D, unlike the micronutrients, vitamins A, E, and K, is largely obtained not from food, but by the action of solar ultraviolet (UV) light on its precursor, 7-dehydrocholesterol, in skin. With the decline in UV light intensity in winter, most skin production of vitamin D occurs in summer. Since no defined storage organ or tissue has been found for vitamin D, it has been assumed that an adequate vitamin D status in winter can only be maintained by oral supplementation. Skeletal muscle cells have now been shown to incorporate the vitamin D-binding protein (DBP) from blood into the cell cytoplasm where it binds to cytoplasmic actin. This intracellular DBP provides an array of specific binding sites for 25-hydroxyvitamin D (25(OH)D), which diffuses into the cell from the extracellular fluid. When intracellular DBP undergoes proteolytic breakdown, the bound 25(OH)D is then released and diffuses back into the blood. This uptake and release of 25(OH)D by muscle accounts for the very long half-life of this metabolite in the circulation. Since 25(OH)D concentration in the blood declines in winter, its cycling in and out of muscle cells appears to be upregulated. Parathyroid hormone is the most likely factor enhancing the repeated cycling of 25(OH)D between skeletal muscle and blood. This mechanism appears to have evolved to maintain an adequate vitamin D status in winter.
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