cholecalciferol and Muscle-Cramp

Suboptimal mitochondrial function has been implicated in several disorders in which fatigue is a prominent feature. Vitamin D deficiency is a well-recognized cause of fatigue and myopathy. The aim of this study was to examine the effects of cholecalciferol therapy on skeletal mitochondrial oxidative function in symptomatic, vitamin D-deficient individuals.. This longitudinal study assessed mitochondrial oxidative phosphorylation in the gastrosoleus compartment using phosphorus-31 magnetic resonance spectroscopy measurements of phosphocreatine recovery kinetics in 12 symptomatic, severely vitamin D-deficient subjects before and after treatment with cholecalciferol. All subjects had serum assays before and after cholecalciferol therapy to document serum 25-hydroxyvitamin D (25OHD) and bone profiles. Fifteen healthy controls also underwent (31)P-magnetic resonance spectroscopy and serum 25OHD assessment.. The phosphocreatine recovery half-time (τ1/2PCr) was significantly reduced after cholecalciferol therapy in the subjects indicating an improvement in maximal oxidative phosphorylation (34.44 ± 8.18 sec to 27.84 ± 9.54 sec, P < .001). This was associated with an improvement in mean serum 25OHD levels (8.8 ± 4.2 nmol/L to 113.8 ± 51.5 nmol/L, P < .001). There was no difference in phosphate metabolites at rest. A linear regression model showed that decreasing serum 25OHD levels was associated with increasing τ1/2PCr (r = -0.41, P = .009). All patients reported an improvement in fatigue after cholecalciferol therapy.. Cholecalciferol therapy augments muscle mitochondrial maximal oxidative phosphorylation after exercise in symptomatic, vitamin D-deficient individuals. This finding suggests that changes in mitochondrial oxidative phosphorylation in skeletal muscle could at least be partly responsible for the fatigue experienced by these patients. For the first time, we demonstrate a link between vitamin D and the mitochondria in human skeletal muscle.

Topics: Adolescent; Adult; Cholecalciferol; Fatigue; Female; Humans; Longitudinal Studies; Magnetic Resonance Spectroscopy; Male; Middle Aged; Mitochondria; Muscle Cramp; Muscle, Skeletal; Oxidative Phosphorylation; Phosphocreatine; Phosphorus Isotopes; Treatment Outcome; Vitamin D Deficiency; Vitamins; Young Adult

Topics: Cholecalciferol; Female; Humans; Male; Mitochondria; Muscle Cramp; Muscle, Skeletal; Vitamin D Deficiency

We report a case of thyrotoxicosis with prolonged post-treatment muscle cramp and hypocalcemia. A 36 year-old woman with hyperthyroidism was treated with Methimazole (MMI). As plasma levels of T4 and T3 were normalized, hypocalcemia was noted and severe cramp of skeletal muscle appeared so that the patient was unable to walk. The cramp was gradually relieved as the levels of thyroid hormones re-increased by discontinuance of MMI, and recurred as the hormone levels were normalized by readministration of MMI. The plasma levels of free calcium ion was positively correlated with those of thyroid hormones, and the muscle cramp was worsened with lowering of the calcium level. Serum examination also revealed vitamin D-deficiency, which was probably due to an unbalanced diet of the patient. A therapeutic trial with 1 alpha-vitamin D3 and calcium lactate in addition to MMI improved both thyrotoxicosis and muscle cramp. These findings suggested that hypocalcemia due to vitamin D-deficiency was involved in the exceptionally prolonged muscle cramp associated with the treatment of hypothyroidism in this patient.

Topics: Adult; Cholecalciferol; Female; Humans; Hypocalcemia; Lactates; Lactic Acid; Methimazole; Muscle Cramp; Thyrotoxicosis; Vitamin D Deficiency