We and others have reported that vitamin D receptor (VDR) null mice have impaired muscle strength. The expression of VDR in muscle has been controversial, and the role of vitamin D in muscle development and function is unclear.

To address this question, we created myocyte-specific VDR null mice by breeding VDR floxed mice with human skeletal actin-Cre mice (HSA-Cre). HSA-Cre is expressed in skeletal but not cardiac myocytes.

mVDR mice breed normally, and are born in normal Mendelian ratios. They have normal body weight and overall growth trajectories. However, from 8 weeks of age (the earliest time tested to date) they have impaired strength, with a ~15% decrease in grip strength. Interestingly, the defect persists to at least 17 weeks without obvious change in severity. There was a tendency for shorter voluntary running distance in mVDR mice compared to their floxed controls.

Despite impaired grip strength, at sacrifice, mVDR mice have increased quadriceps and gastrocnemius weight per gram of bodyweight. Fibre typing shows a marked increase in Type IIa fibres. Consistent with the role of VDR as a transcription factor, there were many changes in gene expression in mVDR versus control mice.

Together, these data show a direct role for myocyte VDR in muscle function.