Effectiveness of Protein-enriched oral nutritional supplements on muscle function in middle-aged and elderly women: A randomized controlled trial

Zhou Z., Tian X.

This study aimed to examine the prevalence of type 2 diabetes (T2D) and the independent and joint associations of sleep duration and different volumes of physical activity (PA) with T2D in the China Health and Retirement Longitudinal Study (CHARLS). The prevalence of T2D among the Chinese population aged 45 years and older was estimated for the years 2011, 2013, 2015, 2018, and 2020. Data from 2020 were used to examine the independent and joint associations of sleep duration and different volumes of PA with T2D. Sleep duration was classified into three categories: short (< 6 h/day), normal (6–8 h/day), and long (> 8 h/day). PA volumes were classified based on the IPAQ recommendations as follows: light-volume PA (LPA, < 600 MET-minutes/week), moderate-volume PA (MPA, 600–3000 MET-minutes/week), and vigorous-volume PA (VPA, > 3000 MET-minutes/week). The data were statistically analyzed using a t-test and analysis of variance (ANOVA). Multivariate logistic regression models were used to examine the independent and joint associations of PA and sleep duration with T2D. The prevalence of T2D in the LPA and short sleep groups increased from 13.35% (95% CI = 10.41–16.75) and 11.52% (95% CI = 10.01–13.15) in 2011 to 17.27% (95% CI = 15.09–19.62) and 16.28% (95% CI = 15.34–17.25) in 2020, respectively. Compared with LPA, VPA was associated with lower odds of T2D (Model 3, OR = 0.82, 95% CI = 0.69–0.97). Compared to individuals with normal sleep duration, those with short sleep duration had a higher likelihood of T2D (Model 3, OR = 1.10, 95% CI = 1.08–1.22), whereas long sleep duration did not show a significant association (Model 3, OR = 1.03, 95% CI = 0.86–1.23). The risk of developing T2D was approximately 35% lower for individuals with LPA and normal sleep duration compared to those with LPA and short sleep duration (Model 3, OR = 0.65, 95% CI = 0.46–0.91). In the VPA group, the mitigation effect of exercise on T2D was observed regardless of sleep duration (Model 3, short: OR = 0.73, 95% CI = 0.56–0.95; normal: OR = 0.65, 95% CI = 0.51–0.85; long: OR = 0.63, 95% CI = 0.45–0.89). The prevalence of T2D among middle-aged and older adults in China increased substantially from 2011 to 2020. Short sleep duration is associated with higher odds of developing T2D. However, engaging in VPA mitigates this risk, even in those with insufficient sleep.

Ooi H., Welch C.

Ni Lochlainn M., Bowyer R.C., Welch A.A., Whelan K., Steves C.J.

Abstract Background Sarcopenia, characterised by an accelerated loss of skeletal muscle mass and function, is associated with negative outcomes. This study aimed to evaluate factors associated with skeletal muscle strength, mass and sarcopenia, particularly protein intake, and to assess whether shared twin characteristics are important. Methods This study utilised cross-sectional data from a study of community-dwelling twins aged ≥60 years. Multivariable logistic regression and between- and within-twin pair regression modelling were used. Results Participants (n = 3,302) were 89% female (n = 2,923), aged a mean of 72.1 (±7.3) years and composed of 858 (55%) monozygotic, 709 (45%) dizygotic twin pairs and 168 individual lone twins. Using optimal protein intake as the reference group (1.0–1.3 g/kg/day), there was no significant association between protein intake (neither high nor low) and low muscle strength, or between low protein intake and sarcopenia (odds ratio (OR) 0.7; 95% confidence interval (CI) 0.39–1.25; P = 0.229) in unadjusted models. High protein intake (&gt;1.3 g/kg/day) was associated with low muscle mass (OR 1.76; 95% CI 1.39–2.24; P &lt; 0.0001), while low protein intake was protective (OR 0.52; 95% CI 0.40–0.67; P &lt; 0.0001). High protein intake was associated with sarcopenia (OR 2.04; 95% CI 1.21–3.44; P = 0.008), and this was robust to adjustment for demographic, anthropometric and dietary factors. The association between muscle strength and weight, body mass index, healthy eating index, protein intake and alpha diversity was not significantly influenced by shared twin factors, indicating greater amenability to interventions. Conclusions High protein intake is associated with sarcopenia in a cohort of healthy older twins.

Pellegrino A., Tiidus P.M., Vandenboom R.

Human menopause is widely associated with impaired skeletal muscle quality and significant metabolic dysfunction. These observations pose significant challenges to the quality of life and mobility of the aging population, and are of relevance when considering the significantly greater losses in muscle mass and force-generating capacity of muscle from post-menopausal females relative to age-matched males. In this regard, the influence of estrogen on skeletal muscle has become evident across human, animal, and cell-based studies. Beneficial effects of estrogen have become apparent in mitigation of muscle injury and enhanced post-damage repair via various mechanisms, including prophylactic effects on muscle satellite cell number and function, as well as membrane stability and potential antioxidant influences following injury, exercise, and/or mitochondrial stress. In addition to estrogen replacement in otherwise deficient states, exercise has been found to serve as a means of augmenting and/or mimicking the effects of estrogen on skeletal muscle function in recent literature. Detailed mechanisms behind the estrogenic effect on muscle mass, strength, as well as the injury response are beginning to be elucidated and point to estrogen-mediated molecular cross talk amongst signalling pathways, such as apoptotic signaling, contractile protein modifications, including myosin regulatory light chain phosphorylation, and the maintenance of muscle satellite cells. This review discusses current understandings and highlights new insights regarding the role of estrogen in skeletal muscle, with particular regard to muscle mass, mitochondrial function, the response to muscle damage, and the potential implications for human physiology and mobility.

Griffen C., Duncan M., Hattersley J., Weickert M.O., Dallaway A., Renshaw D.

To determine the individual and combined effects of 12 weeks of resistance exercise (RE) and whey protein supplementation on skeletal muscle strength (primary outcome), mass and physical function, and hormonal and inflammatory biomarkers in older adults.

Ooi D.S., Ling J.Q., Ong F.Y., Tai E.S., Henry C.J., Leow M.K., Khoo E.Y., Tan C.S., Chong M.F., Khoo C.M., Lee Y.S.

Background: Branched chain amino acids (BCAA) supplementation is reported to aid in lean mass preservation, which may in turn minimize the reduction in resting metabolic rate (RMR) during weight loss. Our study aimed to examine the effect of BCAA supplementation to a hypocaloric diet on RMR and substrate utilization during a weight loss intervention. Methods: A total of 111 Chinese subjects comprising 55 males and 56 females aged 21 to 45 years old with BMI between 25 and 36 kg/m2 were randomized into three hypocaloric diet groups: (1) standard-protein (14%) with placebo (CT), (2) standard-protein with BCAA, and (3) high-protein (27%) with placebo. Indirect calorimetry was used to measure RMR, carbohydrate, and fat oxidation before and after 16 weeks of dietary intervention. Results: RMR was reduced from 1600 ± 270 kcal/day to 1500 ± 264 kcal/day (p < 0.0005) after weight loss, but no significant differences in the change of RMR, respiratory quotient, and percentage of fat and carbohydrate oxidation were observed among the three diet groups. Subjects with BCAA supplementation had an increased postprandial fat (p = 0.021) and decreased postprandial carbohydrate (p = 0.044) oxidation responses compared to the CT group after dietary intervention. Conclusions: BCAA-supplemented standard-protein diet did not significantly attenuate reduction of RMR compared to standard-protein and high-protein diets. However, the postprandial fat oxidation response increased after BCAA-supplemented weight loss intervention.

Nakayama K., Saito Y., Sanbongi C., Murata K., Urashima T.

The purpose of this study was to examine whether long-term ingestion of low-dose milk protein supplementation causes a greater increase in muscle mass and strength of older adults during low-to-moderate intensity exercise training intervention than isocaloric carbohydrate. In a randomized, double-blind, and placebo-controlled design, 122 healthy older adults (60–84 year) received either an acidified milk protein drink containing 10 g of milk protein (MILK; n = 61) or an isocaloric placebo drink (PLA; n = 61) daily throughout 6 months of body weight and medicine ball exercise training. Measurements before and after the intervention included body composition, physical performance and blood biochemistry. Lean body mass significantly increased in the MILK group (+ 0.54 kg, p < 0.001), but did not change in the PLA group (− 0.10 kg, p = 0.534). The increases in the MILK group were significantly greater than in the PLA group (p = 0.004). Fat mass (− 0.77 kg) and plasma uric acid levels (− 0.3 mg/dL) significantly decreased only in the MILK group (p < 0.001), with a significant group difference (p = 0.002 and p < 0.001, respectively). Most of the physical performance tests significantly improved in both groups, but no group differences were found. We conclude that low-dose milk protein supplementation (10 g of protein/day) combined with low-to-moderate intensity exercise training is associated with increased muscle mass, but not improved physical performance compared to carbohydrate combined with exercise in healthy older adults. This study was registered in the UMIN Clinical Trials Registry (UMIN000032189).

Haaf D.S., Eijsvogels T.M., Bongers C.C., Horstman A.M., Timmers S., Groot L.C., Hopman M.T.

BACKGROUND: An inadequate protein intake may offset the muscle protein synthetic response after physical activity, reducing the possible benefits of an active lifestyle for muscle mass. We examined the effects of 12 weeks of daily protein supplementation on lean body mass, muscle strength, and physical performance in physically active older adults with a low habitual protein intake (

Kim M., Won C.W.

This study aimed to compare 4-m usual gait speed obtained with different protocols and to determine the prevalence of slowness using different diagnostic criteria in a large cohort of community-dwelling older adults.A total of 1177 non-disabled community-dwelling older adults aged 70-84 years were assessed for 4-m usual gait speed using four different testing protocols: (1) automatic timer (ultrasonic sensor), dynamic start; (2) manual timer (stopwatch), dynamic start; (3) automatic timer, static start; and (4) manual timer, static start. To assess agreement between usual gait speed and the testing protocols, linear regression and Bland-Altman analyses were performed.There was systematic bias (i.e., difference between automatic timer and manual timer methods), with underestimation of usual gait speed (bias 0.0695 m/s for dynamic start; bias 0.0702 m/s for static start) by the manual timer. There was systematic bias in start conditions, with underestimation of usual gait speed with a static start using both timer methods, compared with that in dynamic start assessment (P < 0.001). The prevalence of slowness ranged from 2.3 to 4.7% in men and 5.9-11.1% in women for

Larsson L., Degens H., Li M., Salviati L., Lee Y.I., Thompson W., Kirkland J.L., Sandri M.

Sarcopenia is a loss of muscle mass and function in the elderly that reduces mobility, diminishes quality of life, and can lead to fall-related injuries, which require costly hospitalization and extended rehabilitation. This review focuses on the aging-related structural changes and mechanisms at cellular and subcellular levels underlying changes in the individual motor unit: specifically, the perikaryon of the α-motoneuron, its neuromuscular junction(s), and the muscle fibers that it innervates. Loss of muscle mass with aging, which is largely due to the progressive loss of motoneurons, is associated with reduced muscle fiber number and size. Muscle function progressively declines because motoneuron loss is not adequately compensated by reinnervation of muscle fibers by the remaining motoneurons. At the intracellular level, key factors are qualitative changes in posttranslational modifications of muscle proteins and the loss of coordinated control between contractile, mitochondrial, and sarcoplasmic reticulum protein expression. Quantitative and qualitative changes in skeletal muscle during the process of aging also have been implicated in the pathogenesis of acquired and hereditary neuromuscular disorders. In experimental models, specific intervention strategies have shown encouraging results on limiting deterioration of motor unit structure and function under conditions of impaired innervation. Translated to the clinic, if these or similar interventions, by saving muscle and improving mobility, could help alleviate sarcopenia in the elderly, there would be both great humanitarian benefits and large cost savings for health care systems.

Granic A., Mendonça N., Sayer A.A., Hill T.R., Davies K., Adamson A., Siervo M., Mathers J.C., Jagger C.

Low protein intake has been linked to reduced muscle strength and physical performance in older adults but little is known about how it may affect muscle health and subsequent functional decline in the very old (aged 85+), who are at enhanced risk of malnutrition and loss of muscle mass and strength.To investigate the associations between low protein intake, defined as the intake of

Park Y., Choi J., Hwang H.

ABSTRACTBackgroundAge-related loss of muscle mass and function is a major component of frailty. Nutrition supplementation with exercise is an effective strategy to decrease frailty by preventing sarcopenia, but the effect of protein alone is controversial.ObjectiveThe present study was performed to investigate a dose-dependent effect of protein supplementation on muscle mass and frailty in prefrail or frail malnourished elderly people.DesignA 12-wk double-blind randomized controlled trial was conducted in elderly subjects aged 70–85 y with ≥1 of the Cardiovascular Health Study frailty criteria and a Mini Nutritional Assessment score ≤23.5 (n = 120). Participants were randomly assigned to 1 of 3 groups: 0.8, 1.2, or 1.5 g protein · kg–1 · d–1, with concealed allocation and intention-to-treat analysis. Primary outcomes were appendicular skeletal muscle mass (ASM) and skeletal muscle mass index (SMI) measured by dual-energy X-ray absorptiometry.ResultsAfter the 12-wk intervention, the 1.5-g protein · kg–1 · d–1 group had higher ASM (mean ± SD: 0.52 ± 0.64 compared with 0.08 ± 0.68 kg, P = 0.036) and SMI (ASM/weight: 0.87% ± 0.69% compared with 0.15% ± 0.89%, P = 0.039; ASM/BMI: 0.02 ± 0.03 compared with 0.00 ± 0.04, P = 0.033; ASM:fat ratio: 0.04 ± 0.11 compared with −0.02 ± 0.10, P = 0.025) than the 0.8-g protein · kg–1 · d–1 group. In addition, gait speed was improved in the 1.5-g protein · kg–1 · d–1 group compared with the 0.8-g protein · kg–1 · d–1 group (0.09 ± 0.07 compared with 0.04 ± 0.07 m/s, P = 0.039). There were no significant differences between the 1.2- and 0.8-g protein · kg–1 · d–1 groups in muscle mass and physical performance. No harmful adverse effects were observed.ConclusionsThe present study indicates that protein intake of 1.5 g · kg–1 · d–1 has the most beneficial effects in regard to preventing sarcopenia and frailty compared with protein intakes of 0.8 and 1.2 g · kg–1 · d–1 in prefrail or frail elderly subjects at risk of malnutrition. This trial was registered at cris.nih.go.kr as KCT0001923.

Nilsson A., Montiel Rojas D., Kadi F.

The role of dietary protein intake on muscle mass and physical function in older adults is important for the prevention of age-related physical limitations. The aim of the present study was to elucidate links between dietary protein intake and muscle mass and physical function in older women meeting current guidelines of objectively assessed physical activity. In 106 women (65 to 70 years old), protein intake was assessed using a 6-day food record and participants were classified into high and low protein intake groups using two Recommended Dietary Allowance (RDA) thresholds (0.8 g·kg−1 bodyweight (BW) and 1.1 g·kg−1 BW). Body composition, aerobic fitness, and quadriceps strength were determined using standardized procedures, and self-reported physical function was assessed using the SF-12 Health Survey. Physical activity was assessed by accelerometry and self-report. Women below the 0.8 g·kg−1 BW threshold had a lower muscle mass (p < 0.05) with no differences in physical function variables. When based on the higher RDA threshold (1.1 g·kg−1 BW), in addition to significant differences in muscle mass, women below the higher threshold had a significantly (p < 0.05) higher likelihood of having physical limitations. In conclusion, the present study supports the RDA threshold of 0.8 g·kg−1 BW of proteins to prevent the loss of muscle mass and emphasizes the importance of the higher RDA threshold of at least 1.1 g·kg−1 BW to infer additional benefits on constructs of physical function. Our study also supports the role of protein intake for healthy ageing, even in older adults meeting guidelines for physical activity.

Liguori I., Russo G., Aran L., Bulli G., Curcio F., Della-Morte D., Gargiulo G., Testa G., Cacciatore F., Bonaduce D., Abete P.

Chung E., Mo H., Wang S., Zu Y., Elfakhani M., Rios S.R., Chyu M., Yang R., Shen C.

Skeletal muscle disorders including sarcopenia are prevalent during the complex biological process of aging. Loss of muscle mass and strength commonly seen in sarcopenia is induced by impaired neuromuscular innervation, transition of skeletal muscle fiber type, and reduced muscle regenerative capacity, all attributable to chronic inflammation, oxidative stress, and mitochondrial dysfunction. Current literature suggests that vitamin E molecules (α-, β-, γ-, δ-tocopherols and the corresponding tocotrienols) with their antioxidant and anti-inflammatory capabilities may mitigate age-associated skeletal dysfunction and enhance muscle regeneration, thus attenuating sarcopenia. Preclinical and human experimental studies show that vitamin E benefits myoblast proliferation, differentiation, survival, membrane repair, mitochondrial efficiency, muscle mass, muscle contractile properties, and exercise capacity. Limited number of human cross-sectional observational studies reveal positive associations between serum tocopherol level and muscle strength. Several factors, including difficulties in validating vitamin E intake and deficiency, variations in muscle-protective activity and metabolism of diverse forms of vitamin E, and lack of understanding of the mechanisms of action, preclude randomized clinical trials of vitamin E in people with sarcopenia. Future research should consider long-term clinical trials of with adequate sample size, advanced imaging technology and omics approaches to investigate underlying mechanisms and assess clinically meaningful parameters such as muscle strength, physical performance, and muscle mass in sarcopenia prevention and/or treatment.