Added: Ercia Otani - Date: 24.12.2021 19:44 - Views: 11192 - Clicks: 1962
Aging, even in healthy elderly people, is accompanied by a reduction in muscle mass and muscle strength 1 — 3. The gradual loss of muscle strength below a certain threshold in functional impairment 4 , 5 , the need for assistance in the performance of daily activities 6 , 7 , and an increased risk of falling and nonvertebral fractures 8. Therefore, the preservation of muscle strength in the elderly is of major importance. Vitamin D deficiency is associated with muscle weakness 9 and is common in elderly people Older people are prone to develop vitamin D deficiency because of various risk factors: decreased dietary intake, diminished sunlight exposure, reduced skin thickness, impaired intestinal absorption, and impaired hydroxylation in the liver and kidneys 11 — Muscle weakness due to vitamin D deficiency is predominantly of the proximal muscle groups and is manifested by a feeling of heaviness in the legs, tiring easily, and difficulty in mounting stairs and rising from a chair; the deficiency is reversible with supplementation 15 — Muscle atrophy—particularly of type II fibers—has been described histopathologically 17 , 19 , In this review we focused on the relation between vitamin D deficiency, muscle function, and falls in elderly people to determine whether vitamin D supplementation can improve muscle strength and functional ability in this population.
In the skin, under influence of ultraviolet radiation, 7-dehydrocholesterol is photoconverted to previtamin D 3 , which is converted to vitamin D 3 cholecalciferol. Its production and subsequent degradation is under tight metabolic control by various feedback systems, which are presented in Figure 1 22 — Feedback and regulation in vitamin D metabolism. In addition to being photoconverted in the skin, vitamin D can be obtained from the diet through ingestion of vitamin D—containing products eg, fatty fish , from vitamin D—fortified milk or margarine, and from the use of multivitamins.
The vitamin D ingested via this route is metabolized in the same manner as is endogenously produced vitamin D. Because 1,25 OH D 3 exerts its influence on distant target tissue, mediated by a vitamin D receptor VDR , it is considered to be a hormone rather than a vitamin The serum concentration of 25 OH D 3 is times that of serum 1,25 OH D 3 , and this excess concentration constitutes a storage facility similar to that of other steroid hormones. Although it is generally agreed that vitamin D status is most accurately reflected by serum 25 OH D 3 concentrations, evidence regarding adequate serum concentrations is inconclusive.
An elevated serum parathyroid hormone concentration is a common indicator of vitamin D deficiency. Physical inactivity increases bone turnover and serum calcium concentrations, which prevents an elevation in serum parathyroid hormone, even in the presence of vitamin D deficiency Thus, caution should be exercised when an elevated serum parathyroid hormone is used as an indicator of vitamin D deficiency. In addition, caution is needed in comparisons of from studies that used different assay techniques to determine serum 25 OH D 3 Apart from the classic target organs for maintaining body calcium homeostasis intestine, kidney, bone, and parathyroid gland , other target sites for vitamin D metabolites have been identified ie, skin, muscle, pancreas, immune system, hematopoietic system, and reproductive organs , and new actions have been discovered Birge and Haddad 38 , in the mids, were the first to show that 25 OH D 3 directly influences muscle phosphate metabolism in the diaphragms of vitamin D—deficient rats.
Since then, several studies have shown that vitamin D metabolites affect muscle cell metabolism through various pathways. It is beyond the scope of this article to present these mechanisms in detail, which are thoroughly described elsewhere 39 , Vitamin D metabolites have been found to affect muscle metabolism in 3 ways: 1 by mediating gene transcription, 2 through rapid pathways not involving DNA synthesis, and 3 by the allelic variant of the VDR.
Both in animal models 41 and in humans 42 , 43 , a VDR has been found in skeletal muscle cells that specifically binds 1,25 OH D 3. After transportation to the nucleus, this ligand-receptor interaction is modulated by various transcription factors and biochemical processes, resulting in a final transcription complex In cultured myoblasts, this genomic pathway was found to influence muscle cell calcium uptake, phosphate transport across the muscle cell membrane, and phospholipid metabolism and to mediate cell proliferation and subsequently differentiation into mature muscle fibers 40 , 43 — Vitamin D supplementation induces rapid changes in calcium metabolism of the muscle cell that cannot be explained by a slow genetic pathway.
Evidence indicates that 1,25 OH D 3 , possibly through a vitamin D membrane receptor 47 , 48 , acts directly on the muscle cell membrane. On 1,25 OH D 3 binding, several interacting second-messenger pathways were activated in the muscle cell, resulting in enhanced calcium uptake within minutes , both through voltage-dependent calcium channels 49 , 50 and calcium release—activated calcium channels Finally, muscle strength appears to be influenced by the genotype of the VDR in the muscle cell.
With the use of specific restriction endonucleases, several VDR polymorphisms have been determined. In the past decade, various cases of both young 15 , 17 , 19 and elderly 16 , 53 adults have been described in which prolonged vitamin D deficiency was associated with severe muscle weakness, often leading to marked disability 15 , 16 that improved within several weeks of vitamin D supplementation.
However, few studies have been conducted in which muscle strength was objectively quantified in relation to vitamin D status in elderly people. However, a causal relation cannot be inferred from cross-sectional studies. Other conditions may cause muscle weakness and impair mobility, thereby preventing elderly persons from going outside. Nevertheless, evidence from intervention studies does indicate causality.
Both knee extension strength and walking distance improved ificantly in the women, whereas no improvement was observed in a vitamin D—replete control group who received no therapy. However, the high prevalence of severe comorbidity present in this population likely affected functional performance as well.
In a healthy, vitamin D—replete, elderly population 70—90 y of age , no correlation was found between serum 1,25 OH D 3 concentration and knee-extension strength, although both declined with age Although muscle strength declined by 1. In addition, bone mineral density improved ificantly by 2.
Although not stated by the authors, the fewer of falls in the supplemented than in the placebo group might have contributed to the lower incidence of hip fracture in the supplemented group Vitamin D deficiency has been reported to affect predominantly the weight-bearing antigravity muscles of the lower limb, which are necessary for postural balance and walking 67 , and a ificant correlation between serum 25 OH D 3 concentration and the occurrence of falls in elderly people has been reported 55 , Although the increase in bone density was twice as large with estrogen than with calcitriol therapy, the subjects who took calcitriol experienced fewer fractures from falls than did the group who took estrogen odds ratio: 0.
Improvement in lower extremity muscle strength and balance with vitamin D supplementation explains the reduced of fall-related fractures. The aims of this review were to clarify the effect of an inadequate vitamin D status on muscle function in elderly people and to determine the rationale behind vitamin D supplementation for the preservation of muscle strength and functional ability. A comparison of from various studies is somewhat hampered by differences in subject demographics, study de, and outcome variables. Nevertheless, evidence indicates that muscle function in elderly people is affected by an inadequate vitamin D status 54 — Supplementation in this population improved muscle strength, walking distance, functional ability 57 — 59 , and body sway These findings and the observed improvements in bone density after vitamin D supplementation 67 , 72 provide an explanation for the association between vitamin D supplementation and fewer falls and nonvertebral fractures in elderly people 69 , However, vitamin D deficiency is merely one condition that affects muscle function in elderly people 73 , 74 , which is illustrated by the fact that even in healthy, vitamin D—replete, elderly people, muscle strength declined with age 61 , which was not prevented by vitamin D supplementation 62 , Moreover, severe comorbidity and subsequent immobility may cause muscle weakness and functional impairment, which cannot be improved by treating a coexisting vitamin D deficiency Experimental studies showed that muscle tissue is a direct target site for vitamin D metabolites and offer biochemical evidence for the association between vitamin D deficiency and muscle weakness Although 1,25 OH D 3 is considered to be the active metabolite affecting target sites, including muscle 41 , clinical studies reported a relation between serum 25 OH D 3 and muscle strength 55 , 68 and functional ability Two mechanisms might explain these findings.
Activation of 25 OH D 3 locally in target tissues may be involved in regionally controlled cell function In conclusion, vitamin D deficiency is a condition that may cause muscle weakness in elderly persons. Although only a few intervention studies with vitamin D have been conducted in elderly people, the available evidence indicates that vitamin D supplementation preserves muscle strength and functional ability in high-risk groups, eg, frail, mostly homebound elderly people.
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How to Regain Muscle Mass at Any Age