Vitamin D receptor expression and associated function have been reported in various muscle models, including C₂C₁₂, L6 cell lines and primary human skeletal muscle cells. It is believed that 1,25-hydroxyvitamin D₃(1,25(OH)₂D₃), the active form of vitamin D, has a direct regulatory role in skeletal muscle function, where it participates in myogenesis, cell proliferation, differentiation, regulation of protein synthesis and mitochondrial metabolism through activation of various cellular signalling cascades, including the mitogen-activated protein kinase pathway(s). It has also been suggested that 1,25(OH)₂D₃and its associated receptor have genomic targets, resulting in regulation of gene expression, as well as non-genomic functions that can alter cellular behaviour through binding and modification of targets not directly associated with transcriptional regulation. The molecular mechanisms of vitamin D signalling, however, have not been fully clarified. Vitamin D inadequacy or deficiency is associated with muscle fibre atrophy, increased risk of chronic musculoskeletal pain, sarcopenia and associated falls, and may also decrease RMR. The main purpose of the present review is to describe the molecular role of vitamin D in skeletal muscle tissue function and metabolism, specifically in relation to proliferation, differentiation and protein synthesis processes. In addition, the present review also includes discussion of possible genomic and non-genomic pathways of vitamin D action.

To evaluate the reproducibility and validity of a previously constructed FFQ to assess the usual diet of patients with type 2 diabetes mellitus (T2DM). Cross-sectional survey using two quantitative FFQ (1-month interval) supported by a food photograph portfolio, a 3 d weighed diet record (WDR) and urinary N output measurement (as a biomarker of protein intake). Group of Nutrition in Endocrinology, southern Brazil. Out-patients with T2DM. From a total of 104 eligible T2DM patients, eighty-eight were included in the evaluation of FFQ reproducibility and seventy-two provided data for the validity study. The intakes estimated from the two FFQ did not differ (P > 0·05) and the correlation coefficients were significant (P < 0·01) for energy and nutrients, ranging from 0·451 (soluble fibre) to 0·936 (PUFA). Regarding the validity evaluation, data from the FFQ were higher than those from the WDR for total (28·3%), soluble (27·4%) and insoluble fibres (29·1%), and SFA (13·5%), MUFA (11·1 %) and total lipids (9·2%; all P < 0·05). There were significant correlation coefficients between the FFQ and WDR for most nutrients, when adjusted for energy intake and de-attenuated. Also, the Bland-Altman plots between the FFQ and WDR for energy and macronutrient intakes showed that the FFQ may be used as alternative method to the WDR. The validity coefficient (using the method of triads) for the FFQ protein intake was 0·522 (95% CI 0·414, 0·597). This quantitative FFQ was valid and precise to assess the usual diet of patients with T2DM, according to its validity and reproducibility.

Keywords swimming; energy intake; food intake; sports nutrition; athletes.