April 27, 2024

Vitamin D Deficiency Can Impair Muscle Function

Vitamin D deficiency might hinder muscle function due to a reduction in energy production in the muscles, according to a mouse research study published in the Journal of Endocrinology. Vitamin D lacking mice were discovered to have impaired muscle mitochondrial function, which may have implications for muscle function, recovery, and efficiency. Previous research studies indicate that impaired muscle strength in people with vitamin D shortage might be linked to impaired muscle mitochondrial function. Determining the role of vitamin D in muscle efficiency of older people is likewise hard, as they might suffer from a number of pre-existing health conditions that can also impact their vitamin D status. These findings recommend that vitamin D deficiency might impair mitochondrial function and decrease the quantity of energy produced in the muscles, which may lead to poor muscle function.

Vitamin D shortage might hinder muscle function due to a reduction in energy production in the muscles, according to a mouse research study released in the Journal of Endocrinology. Vitamin D lacking mice were found to have impaired muscle mitochondrial function, which might have ramifications for muscle recovery, function, and performance. This might suggest that preventing vitamin D shortage in older adults could help maintain better muscle strength and function and lower age-related muscle wear and tear, however further studies are required to confirm this.
Previous research studies suggest that impaired muscle strength in individuals with vitamin D deficiency might be linked to impaired muscle mitochondrial function. Identifying the function of vitamin D in muscle efficiency of older individuals is likewise hard, as they may suffer from a number of pre-existing health conditions that can likewise impact their vitamin D status. Previous research studies have been unable to figure out how vitamin D may directly impact muscle performance.

Dr. Andrew Philp and his team at the Garvan Institute of Medical Research in Australia, and teaming up universities, used a mouse model to determine the results of diet-induced vitamin D deficiency on skeletal muscle mitochondrial function in young, male mice. Tissue and blood samples were gathered monthly to quantify vitamin D and calcium concentrations and to assess markers of muscle mitochondrial function and number. After 3 months of diet-induced vitamin D shortage skeletal muscle mitochondrial function was found to be impaired by up to 37%.
” Our outcomes reveal there is a clear link in between vitamin D deficiency and oxidative capability in skeletal muscle. They recommend that vitamin D deficiency reduces mitochondrial function, as opposed to lowering the number of mitochondria in skeletal muscle.” Dr. Philp comments. “We are especially interested to analyze whether this decrease in mitochondrial function may be a cause of age-related loss in skeletal muscle mass and function.”
These findings suggest that vitamin D deficiency might hinder mitochondrial function and decrease the amount of energy produced in the muscles, which may cause poor muscle function. Preventing vitamin D deficiency in older people might help preserve muscle performance and lower the danger of muscle-related illness, such as sarcopenia. Further research studies that investigate the direct effect of vitamin D deficiency on muscle function and strength are essential to verify this.
Whilst this research study suggests that vitamin D shortage can change mitochondrial function in skeletal muscle, Dr. Philp and his group were unable to identify exactly how this procedure took place. For that reason, their future work intends to establish how vitamin D shortage changes mitochondrial control and function in skeletal muscle.
Recommendation: “Diet-induced vitamin D shortage minimizes skeletal muscle mitochondrial respiration” by Stephen P Ashcroft, Gareth Fletcher, Ashleigh M Philp, Carl Jenkinson, Shatarupa Das, Philip M Hansbro, Philip J Atherton and Andrew Philp, May 2021, Journal of Endocrinology.DOI: 10.1530/ JOE-20-0233.