Vitamin D deficiency may cause poor muscle function, particularly in older adults, according to a new study. Photo by PublicDomainPictures/Pixabay
April 16 (UPI) -- Lacking sufficient levels of vitamin D in the bloodstream may negatively affect muscle function, particularly in older adults, due to a reduction in energy production, a study published Friday by the Journal of Endocrinology found.
In experiments using mice, those with vitamin D deficiency had about a 40% decline mitochondrial function in their muscles, possibly impacting their ability to convert energy from food and limiting muscle performance and recovery, the researchers said.
Mitochondria are structures within cells that process energy obtained from food, and it is possible they need vitamin D to function optimally, they said.
The findings suggest that preventing vitamin D deficiency in older adults could help maintain muscle strength and function and reduce age related muscle deterioration, although additional research is needed, according to the researchers.
"Our results show there is a clear link between vitamin D deficiency and oxidative capacity in skeletal muscle," study co-author Andrew Philp said in a statement.
"They suggest that vitamin D deficiency decreases mitochondrial function, as opposed to reducing the number of mitochondria in skeletal muscle," said Philp, who heads diabetes and metabolism research at the Garvan Institute of Medical Research in Darlinghurst, Australia.
Vitamin D is a hormone that plays an important role maintaining bone health and preventing joint and muscle diseases such as osteoporosis and sarcopenia, or age-related muscle loss, according to the National Osteoporosis Foundation.
Up to 60% of adults in the United States are believed to be deficient in the nutrient, the National Institutes of Health estimates, potentially increasing their risk for these conditions as well as COVID-19, cancer and diabetes.
For this study, Philp and his colleagues used mice to determine the effects of diet-induced vitamin D deficiency on skeletal muscle mitochondrial function.
The mice were either fed a diet with normal quantities of vitamin D, or with no vitamin D to induce deficiency, for a period of three months, the researchers said.
Tissue and blood samples were collected from the mice monthly to measure vitamin D and calcium concentrations and to assess markers of muscle mitochondrial function.
After three months of diet-induced vitamin D deficiency, skeletal muscle mitochondrial function was found to be impaired by up to 37%, although it is unclear how lacking the nutrient disrupts this process, the researchers said.
They said they plan to explore the relationship further in future research.
"We are particularly interested to examine whether this reduction in mitochondrial function may be a cause of age related loss in skeletal muscle mass and function," Philp said.