Myopathy in Bone Loss of Ageing: Improvement by Treatment with 1α-hydroxycholecalciferol and Calcium

Abstract

1. Eleven patients with the bone loss of ageing were treated with the vitamin D analogue 1 alpha-hydroxycholecalciferol and calcium for 3--6 months. 2. Muscle biopsies were taken from the vastus lateralis before and after the treatment and the activity of several enzymes was measured. Succinate dehydrogenase and total phosphorylase activities, which are a measure of the oxidative capacity, were low and increased significantly with the treatment. The lactate dehydrogenase activity, which can be taken as a measure of the anaerobic metabolism, was normal and did not change with treatment. The phosphagen stores, ATP and creatine phosphate were low and increased to normal with treatment. 3. Histochemical classification of the fibre composition revealed that the treatment induced an increase in the relative number of fast-twitch a (FTa or type II A) fibres accompanied by a reduction of the fast-twitch b (FTb or type II B) fibres. The cross-sectional area of the FTa fibres also increased with the treatment. 4. The present findings indicate that treatment with the active vitamin D analogue, 1 alpha-hydroxycholecalciferol, and calcium improves the myopathy associated with the bone loss of ageing.

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“…First, the VDR is expressed in human muscle tissue, (37,38) although this was questioned recently, (39) and VDR activation may promote de novo protein synthesis in muscle. (40) Mice lacking the VDR show a skeletal muscle phenotype with smaller and variable muscle fibers and persistence of immature muscle gene expression during adult life. (34,41) Second, proximal muscle weakness is a prominent feature of the clinical syndrome of vitamin D deficiency.…”

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“…Sorenson et al showed that fast-twitch type II muscle fibers atrophy in the absence of 1.25(OH) 2 D 3 and reappear by treatment with alfacalcidol [35]. Analogues of 1.25(OH) 2 D 3 (D-hormone) have been shown to have an effect on muscle power and neuromuscular coordination [39,43,46,47,48].…”

“…Serum concentrations of 1.25(OH) 2 D 3 , which are significantly above the lowest defined normal value of 1.25(OH) 2 D 3 , respectively associated increases in iPTH serum levels, have been shown to have a negative impact on muscle strength and functional mobility [8,9] and have been related to myopathy [9,10,11,28,34]. Serum levels of 1.25(OH) 2 D 3 have been associated with decreased muscle strength, lower endurance [8,9,10,11,12], reduced functional mobility [13,14], and atrophy of fast-twitch muscle fibers [35]. Also, 1.25(OH) 2 D 3 is an effective treatment of the iPTH-related decrease of energy metabolism in skeletal muscle and proteolysis of muscle proteins [36,37,38].…”