Relationship of menopause to skeletal and muscle mass

Relationship of menopause to skeletal and muscle mass.

relationship of menopause to skeletal and muscle mass

Menopause leads to the cessation of ovarian estrogen production The effects of estrogen on skeletal muscles are not yet well known. Decreased lean body mass and muscle loss by decreased muscle protein . correlation between follicle stimulating hormone (FSH) and bone resorption has. Metabolic bone diseases; Muscle strength; Sarcopenia; Body mass index Thus , the present study had the objective to identify the relationship among BMD.

Discussion Highlight the mechanisms that predispose older postmenopausal women at risk of fractures may corroborate to create more efficient preventive strategies to prevent this. Although, aging is one of the most important risk factors for osteoporosis, recent studies have demonstrated that the most fractures in postmenopausal women occur in subjects with normal BMD or osteopenia [ 166 ].

With respect of this, the present study evaluated the relationship between BMD, anthropometric characteristics, years of postmenopausal, strength, muscle mass and the performance on functional tests in up 10 years postmenopausal women. The osteoporosis is a multi-factorial bone diseases and it is controversial in the literature what are the anthropometric and physical characteristics that most influence BMD [ 1017 ]. The mechanical load may lead to bone strengthening with mobility-induced weight-bearing stress [ 3 ].

Thus, our results are in accordance to previous studies that demonstrated that weight loss may increase the bone turnover, suggesting that body weight enhances the differentiation of osteoblasts and increase osteoblastic bone formation besides attenuates osteoclastic activity [ 13141518 ].

Previous studies suggested that low weight or BMI might be an important risk factor for lower BMD [ 2410161719 ], pelvis and femur fractures [ 6 ] and the correlation is stronger over time for nonhispanic whites [ 18 ]. In this context, the femoral neck BMD varies each 0. In addition, previous studies suggested that fat mass is associated with whole body BMD in older women, independent of lean mass [ 15 ].

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The relationship between body composition and endocrine control is related to the production of peripheral gonadal hormones by adipose tissue.

With respect to this, in obese subjects this hormonal changes may affect bone turnover and BMD, protecting the adverse effects of estrogen deficiency after menopause [ 31014 ] and attenuating the bone loss. The leptins, the adipokine most studied in relation to bone, increase proliferation and differentiation of osteoblasts and they also regulate osteoclast development. Additionally, the secretion of boneactive pancreatic beta cell hormones like insulin, indirectly, amylin and preptin also seems more prevalent in obesity and they are direct stimulators to osteoblast growth and inhibiting osteoclastic bone resorption [ 1021 ].

Other authors suggest that the weight body is significantly correlated with skeletal muscle mass because heavier subjects require greater muscle mass for movement and would be expected to have more muscle [ 919 ].

Consistent with the statement that lower strength or low muscle mass or RSMI may induce a lower contraction and mechanical stress on bone, a lower osteogenic stimulus in osteocytes resulting in a lower BMD development and possible higher risk of osteoporotic fracture in elderly people [ 461322 - 24 ]. In addition previous observational data suggested that increasing lean mass could constitute a preventive measure against bone loss and possibly musculoskeletal aging [ 213 ].

Additionally it is unclear which measure should be used to sarcopenia [ 722 ], associated to the fact that decrease of muscle mass by itself seems an inconsistent predictor of mobility limitation [ 7 ] or functional ability [ 25 ]. The present study did not find correlation between physical performance and RMSI. Consistent with some authors, modest reductions in skeletal muscle mass with aging do not cause functional impairment and disability [ 26 ], however others have demonstrated the clinical risk factors as a indicate of low BMD and fracture [ 27 ].

Regarding TUG test, the results are similar to those expected for the same age [ 12 ].

Relationship of menopause to skeletal and muscle mass. - Semantic Scholar

These functional performance results may be explained by the fact that the evaluated women did not present sarcopenia. Our sample did not meet the muscle mass criteria below 5. Previous studies supported the idea that intervention strategies designed to preserve muscle mass should be initiated by the fifth decade of life, because although the prevalence of sarcopenia increased from the third to sixth decades of life, it remained relatively constant thereafter [ 29 ].

Our data corroborate the studies about the effect of weight and BMI on BMD, however it is important to emphasize that higher BMI is significantly associated with a number of comorbidities, including asthma, emphysema, diabetes, reduced physical activity, co-medications, increased risk of falls, higher morbidity and economic costs associated with fractures because of a greater risk of non-union, postoperative complications, comorbidities, and slower rehabilitation [ 32432 ,].

Furthermore, the BMI and hip fracture seems to have nonlinear correlation. Although the lower BMI is a higher risk factor for fracture, the higher BMI not seems a higher protect factor comparing with normal BMI, thus obesity should not be a protective factor for hip fracture risk [ 33 ].

Additionally, the increased prevalence of overweight in older US women appears unlikely to be accompanied by a significant reduction in osteoporosis prevalence [ 26 ] suggesting that protective factors to avoid BMD decrease should be further studied and recommendations on the benefits of BMI should be cautious for post-menopausal women. Finally, the screening and prevention of bone loss and a specific orientation about weight body in younger postmenopausal women may be an effective way to prevent or delay fractures in postmenopausal women.

Although the menopause occurs around 50 years old and the rate of BMD loss accelerates in the peri-menopause and in the first yeas after menopause [ 10 ], the women before 60 or 65 years old do not meet current national guidelines for osteoporosis treatment [ 1034 - 38 ].

Understanding the influence of different body composition on BMD or on fractures, as well as the importance of increasing lean mass as a strategy for preventing bone loss seem relevant. Limitations of this study include the fact that we chose to use HGS, TUG and FTSTS tests to measure respectively muscle strength and performance because they could be easily applied in clinical practice. However, we do not know whether these results would be similar if we had used different evaluation methods to measure muscle strength and performance such as isokinetic or isometric strength tests for lower limb muscles, self-reference gait speed or power stair climbing test.

Summary of effects of physical exercise on menopause-related health problems. Changes in body composition Regular physical activity is beneficial in preventing weight gain, improving body composition, strength development and functional capacity.

Relationship of menopause to skeletal and muscle mass.

In a review of exercise in postmenopausal women, a more optimal body composition, including lower adiposity and higher lean mass, was associated with higher levels of physical activity [ 44 ]. Regular exercise of any type, even activities such as brisk walking, reduces body weight and body fat [ 4546 ]. Resistance training, preferentially at high intensity, appears to be the most appropriate physical exercise modality to improve muscle mass [ 47 ].

Therefore, postmenopausal women would maximally benefit from combining daily aerobic activity with a resistance training programme [ 4448 ].

relationship of menopause to skeletal and muscle mass

Regular physical activity causes metabolic adaptations in skeletal muscle, possibly promoted by cumulative effects of transient gene responses to exercise sessions. Repeated, episodic bouts of muscle contraction cause functional adaptation and remodeling in muscle [ 49 ]. Training-induced adaptations include changes in contractile proteins, mitochondrial function, metabolic regulation, intracellular signaling and transcriptional responses [ 49 ].

These include genes which are myogenic regulators, genes of carbohydrate and lipid mobilization, transport and oxidation, mitochondrial metabolism and oxidative phosphorylation, and transcriptional regulators of gene expression and mitochondrial biogenesis [ 49 ]. Cardiovascular disease Regular physical activity and exercise offers cardiovascular protection in both genders in all age groups by modifying the CVD risk factors and improving vascular function. Evidence is scarce as to whether physical activity and exercise influence the increased CVD risk posed by menopausal transition per se.

A systematic review of randomized controlled trials RCT s in postmenopausal women concluded that a combination of aerobic and resistance exercise may improve hypertension and dyslipidaemia [ 44 ]. Interventional trials in postmenopausal women with aerobic exercise alone, resistance training alone and a combination of aerobic exercise and resistance training have shown improvements in lipid profile including the lowering of total cholesterol, triglycerides and low density lipoprotein—cholesterol LDL-Cincrease of high density lipoprotein—cholesterol HDL-C and improvements in glycaemic control and insulin resistance [ 50 - 52 ].

Exercise training has been shown to be an effective antioxidant and anti-atherogenic therapy in relation to CVD risk and disease [ 53 - 55 ].

Exercise training reverses endothelial dysfunction and improves coronary blood flow in subjects with coronary artery disease [ 5657 ] and promotes endothelium-dependent vasodilation in healthy subjects [ 58 - 61 ].

Aerobic exercise training in pre and postmenopausal women of comparable ages decreased diastolic blood pressure and increased biomarkers of vascular function i. Although there is a dose-response effect between physical activity and reduced CVD risk and disease, even less-vigorous exercise such as walking reduces CVD risk in postmenopausal women [ 6364 ]. Vasomotor symptoms Exercise appears to have varying effects on VMS. Other RCTs [ 66 ], longitudinal studies [ 67 ] and cross sectional studies [ 6869 ] have described similar findings.

Menopause and Exercise: Linking Pathophysiology to Effects

Two systematic reviews on the effectiveness of yoga for menopausal symptoms [ 7071 ] and a more recent RCT [ 72 ] revealed no significant impact of yoga on VMS. Contrastingly, a recent review concluded that physical activity and structured exercise reduced VMS [ 73 ].

Other studies support this finding, showing that both short bouts of exercise and prolonged aerobic training improved VMS to varying degrees [ 7475 ]. A recent RCT reported a significant improvement in VMS in participants of weekly minute yoga classes combined with daily at-home practice compared to subjects engaged in individualized facility-based aerobic exercise training 3 times a week [ 76 ].

Several plausible mechanisms explain the effects of physical exercise on VMS. Vagal tone increases as a response to aerobic exercise training [ 77 ]. With exercise training, hour urinary norepinephrine decreases, possibly due to increased vagal tone [ 24 ].

relationship of menopause to skeletal and muscle mass

The influence of stress hormones such as cortisol and catecholamines that could precipitate hot flushes may be counteracted by parasympathetic activation during exercise training [ 24 ]. Higher endorphin levels decrease the frequency and amplitude of LH levels and regulate gonadotropin-releasing hormone GnRH levels [ 31 ]. Such effects are postulated to stabilize the thermoregulatory centre and reduce the incidence of VMS [ 2431 ].