In midlife, women experience hormonal changes due to menopausal transition. A decrease especially in estradiol has been hypothesized to cause loss of muscle mass. This study investigated the effect of menopausal transition on changes in lean and muscle mass, from the total body to the muscle fiber level, among 47–55-year-old women. Data were used from the Estrogenic Regulation of Muscle Apoptosis (ERMA) study, where 234 women were followed from perimenopause to early postmenopause. Hormone levels (estradiol and follicle stimulating hormone), total and regional body composition (dual-energy X-ray absorptiometry (DXA) and computed tomography (CT) scans), physical activity level (self-reported and accelerometer-measured) and muscle fiber properties (muscle biopsy) were assessed at baseline and at early postmenopause. Significant decreases were seen in lean body mass (LBM), lean body mass index (LBMI), appendicular lean mass (ALM), appendicular lean mass index (ALMI), leg lean mass and thigh muscle cross-sectional area (CSA). Menopausal status was a significant predictor for all tested muscle mass variables, while physical activity was an additional significant contributor for LBM, ALM, ALMI, leg lean mass and relative muscle CSA. Menopausal transition was associated with loss of muscle mass at multiple anatomical levels, while physical activity was beneficial for the maintenance of skeletal muscle mass.

To evaluate the evidence on the effectiveness of myofascial release therapy to relieve chronic musculoskeletal pain and to improve joint mobility, functioning level, and quality of life in pain sufferers. Randomized controlled trials were systematically gathered from CENTRAL, Medline, Embase, CINAHL, Scopus, and PEDro databases. The methodological quality of articles was assessed according to the Cochrane Collaboration’s domain-based framework. In addition, the effect sizes of main outcomes were calculated based on reported means and variances at baseline and in follow-up. Of 513 identified records, 8 were relevant. Two trials focused on lateral epicondylitis (N = 95), two on fibromyalgia (N = 145), three on low back pain (N = 152), and one on heel pain (N = 65). The risk of bias was considered low in three and high in five trials. The duration of therapy was 30–90 minutes 4 to 24 times during 2–20 weeks. The effect sizes did not reach the minimal clinically important difference for pain and disability in the studies of low back pain or fibromyalgia. In another three studies with the high risk of bias, the level of minimal clinically important difference was reached up to two-month follow-up. Current evidence on myofascial release therapy is not sufficient to warrant this treatment in chronic musculoskeletal pain.

Background: In women, metabolic health deteriorates after menopause, and the role of physical activity (PA) in mitigating the change is not completely understood. This study investigates the changes in indicators of metabolic health around menopause and evaluates whether PA modulates these changes. Methods: Longitudinal data of 298 women aged 48–55 years at baseline participating in the ERMA and EsmiRs studies was used. Mean follow-up time was 3.8 (SD 0.1) years. Studied indicators of metabolic health were total and android fat mass, waist circumference, waist-to-hip ratio (WHR), systolic (SBP) and diastolic (DBP) blood pressure, blood glucose, triglycerides, serum total cholesterol, and high- (HDL-C) and low-density (LDL-C) lipoprotein cholesterol. PA was assessed by accelerometers and questionnaires. The participants were categorized into three menopausal groups: PRE-PRE (pre- or perimenopausal at both timepoints, n = 56), PRE-POST (pre- or perimenopausal at baseline, postmenopausal at follow-up, n = 149), and POST-POST (postmenopausal at both timepoints, n = 93). Analyses were carried out using linear and Poisson mixed-effect models. Results: At baseline, PA associated directly with HDL-C and inversely with LDL-C and all body adiposity variables. An increase was observed in total (B = 1.72, 95% CI [0.16, 3.28]) and android fat mass (0.26, [0.06, 0.46]), SBP (9.37, [3.34, 15.39]), and in all blood-based biomarkers in the PRE-POST group during the follow-up. The increase tended to be smaller in the PRE-PRE and POST-POST groups compared to the PRE-POST group, except for SBP. The change in PA associated inversely with the change in SBP (−2.40, [−4.34, −0.46]) and directly with the change in WHR (0.72, [0.05, 1.38]). Conclusions: In middle-aged women, menopause may accelerate the changes in multiple indicators of metabolic health. PA associates with healthier blood lipid profile and body composition in middle-aged women but does not seem to modulate the changes in most of the studied metabolic health indicators during the menopausal transition.

For women, menopausal transition is a time of significant hormonal changes, which may contribute to altered body composition and regional adipose tissue accumulation. Excess adiposity, and especially adipose tissue accumulation in the central body region, increases women's risk of cardiovascular and metabolic conditions and affects physical functioning. We investigated the associations between menopausal progression and total and regional body adiposity measured with dual‐energy X‐ray absorptiometry and computed tomography in two longitudinal cohort studies of women aged 47–55 (n = 230 and 148, mean follow‐up times 1.3 ± 0.7 and 3.9 ± 0.2 years, mean baseline BMI 25.5 kg/m²). We also examined associations between menopausal progression and skeletal muscle fiber characteristics, as well as adipose tissue‐derived adipokines. Relative increases of 2%–14% were observed in regional and total body adiposity measures, with a pronounced fat mass increase in the android area (4% and 14% during short‐ and long‐term follow‐ups). Muscle fiber oxidative and glycolytic capacities and intracellular adiposity were not affected by menopause, but were differentially correlated with total and regional body adiposity at different menopausal stages. Menopausal progression and regional adipose tissue masses were positively associated with serum adiponectin and leptin, and negatively associated with resistin levels. Higher diet quality and physical activity level were also inversely associated with several body adiposity measures. Therefore, healthy lifestyle habits before and during menopause might delay the onset of severe metabolic conditions in women.

Aims: We studied the changes in the circulating metabolome and their relation to the menopausal hormonal shift in 17β-oestradiol and follicle-stimulating hormone levels among women transitioning from perimenopause to early postmenopause. Methods and results: We analysed longitudinal data from 218 Finnish women, 35 of whom started menopausal hormone therapy during the study. The menopausal transition was monitored with menstrual diaries and serum hormone measurements. The median follow-up was 14 months (interquartile range: 8–20). Serum metabolites were quantified with targeted nuclear magnetic resonance metabolomics. The model results were adjusted for age, follow-up duration, education, lifestyle, and multiple comparisons. Menopause was associated with 85 metabolite measures. The concentration of apoB (0.17 standard deviation [SD], 99.5% confidence interval [CI] 0.03–0.31), very-low-density lipoprotein triglycerides (0.25 SD, CI 0.05–0.45) and particles (0.21 SD, CI 0.05–0.36), low-density lipoprotein (LDL) cholesterol (0.17 SD, CI 0.01–0.34) and particles (0.17 SD, CI 0.03–0.31), high-density lipoprotein (HDL) triglycerides (0.24 SD, CI 0.02–0.46), glycerol (0.32 SD, CI 0.07–0.58) and leucine increased (0.25 SD, CI 0.02–0.49). Citrate (−0.36 SD, CI −0.57 to −0.14) and 3-hydroxybutyrate concentrations decreased (−0.46 SD, CI −0.75 to −0.17). Most metabolite changes were associated with the menopausal hormonal shift. This explained 11% and 9% of the LDL cholesterol and particle concentration increase, respectively. Menopausal hormone therapy was associated with increased medium-to-large HDL particle count and decreased small-to-medium LDL particle and glycine concentration. Conclusions: Menopause is associated with proatherogenic circulating metabolome alterations. Female sex hormones levels are connected to the alterations, highlighting their impact on women’s cardiovascular health.

Physique athletes lose substantial weight preparing for competitions, potentially altering systemic metabolism. We investigated sex differences in body composition, resting energy expenditure (REE), and appetite-regulating and thyroid hormone changes during a competition preparation among drug-free physique athletes. The participants were female (10 competing (COMP) and 10 nondieting controls (CTRL)) and male (13 COMP and 10 CTRL) physique athletes. COMP were tested before they started their diet 23 weeks before competing (PRE), during their diet one week before competing (MID), and 23 weeks after competing (POST), whereas CTRL were tested at similar intervals but did not diet. Measurements included body composition by dual-energy X-ray absorptiometry, muscle size, and subcutaneous fat thickness (SFA) by ultrasound, REE by indirect calorimetry, circulating ghrelin, leptin T3, and T4 hormone analysis. Fat mass (FM) and SFA decreased in both sexes ( p < 0.001), while males ( p < 0.001) lost more lean mass (LM) than females ( p < 0.05). Weight loss, decreased energy intake, and increased aerobic exercise ( p < 0.05) led to decreased LM- and FM-adjusted REE ( p < 0.05), reflecting metabolic adaptation. Absolute leptin levels decreased in both sexes ( p < 0.001) but more among females ( p < 0.001) due to higher baseline leptin levels. These changes occurred with similar decreases in T3 ( p < 0.001) and resting heart rate ( p < 0.01) in both sexes. CTRL, who were former or upcoming physique athletes, showed no systematic changes in any measured variables. In conclusion, while dieting, female and male physique athletes experience REE and hormonal changes leading to adaptive thermogenesis. However, responses seemed temporary as they returned toward baseline after the recovery phase. ClinicalTrials.gov (NCT04392752).