β-Hydroxy-β-methyl butyrate (HMB) is a metabolite of the amino acid leucine, known for its ergogenic effects on body composition and strength. Despite these benefits, the magnitude of these effects remains unclear due to variability among studies. This umbrella review aims to synthesize meta-analyses investigating the effects of HMB on body composition and muscle strength in adults.
A comprehensive literature search was conducted in Scopus, PubMed and Web of Science without date or language restrictions until August 2024. The study protocol was registered at Prospero (No. CRD42023402740). Included studies evaluated the effects of HMB supplementation on body mass, fat mass (FM), fat-free mass (FFM), muscle mass and performance outcomes. Effect sizes (ESs) and 95% confidence intervals (CIs) were calculated, and a random-effects model was used for meta-analysis. Standard methods assessed heterogeneity, sensitivity and publication bias. The methodological quality of included studies was assessed using the AMSTAR2 tool.
Eleven studies comprising 41 data sets were included, with participants aged 23–79 years. HMB supplementation significantly increased muscle mass (ES: 0.21; 95% CI: 0.06–0.35; p = 0.004), muscle strength index (ES: 0.27; 95% CI: 0.19–0.35; p < 0.001) and FFM (ES: 0.22; 95% CI: 0.11–0.34; p < 0.001). No significant changes were observed in FM (ES: 0.03; 95% CI: −0.04 to 0.35; p = 0.09) or body mass (ES: 0.09; 95% CI: −0.06 to 0.24; p = 0.22). The quality assessment revealed that five studies were of high quality, three were of low quality and three were of critically low quality.
HMB supplementation may benefit individuals experiencing muscular atrophy due to physiological conditions, particularly enhancing muscle mass and strength without significant changes in fat mass or body weight.
Despite muscle power derived from the 5-rep sit-to-stand (STS) test having been demonstrated to be a valuable biomarker in older individuals, there is limited information regarding muscle power derived from the 30-s STS test, a widely used test in the clinical setting. This study aimed (i) to compare relative 30-s STS power values between older men and women, (ii) to identify cut-off points for low relative 30-s STS power, (iii) to compare the prevalence of low relative STS power between sexes and (iv) to evaluate the association of low relative 30-s STS power with adverse conditions in older people.
A total of 1475 community-dwelling older adults (65–98 years; 45% men) from the Toledo Study for Healthy Aging were included. Relative STS power was assessed using the 30-s STS test and the Alcazar's equation. Adverse health conditions considered encompassed frailty, depression, disability in basic (BADL) and instrumental activities of daily living (IADL), cognitive impairment and low habitual gait speed (HGS).
Relative STS power decreased linearly at an average rate of 1.0% year−1 in men and 1.5% year−1 in women. The cut-off points for low relative STS power were 2.53 and 2.01 W·kg−1 for men and women, respectively. The prevalence of low relative STS power was significantly lower in older men compared with older women (43.5% vs. 50.0%, respectively; p = 0.005). In men, low relative STS power was associated with frailty (OR [95% CI] = 4.4 [2.4–8.0]), cognitive impairment (OR [95% CI] = 1.7 [1.0–2.7]), disability in BADL (OR [95% CI] = 4.5 [1.5–13.8]) and low HGS (OR [95% CI] = 3.4 [1.9–5.9]). In women, low relative STS power was associated with frailty (OR [95% CI] = 5.2 [3.5–7.7]), disability in BADL (OR [95% CI] = 4.3 [1.8–9.9]) and IADL (OR [95% CI] = 3.1 [2.2–4.3]) and low HGS (OR [95% CI] = 6.1 [2.8–13.1]). No associations were found between low relative STS power and disability in IADL or depression in men, nor between low relative STS power and cognitive impairment or depression in women.
Relative STS power decreased with increasing age in both men and women. The provided sex-specific cut-off points for low relative STS power using the 30-s STS test adequately identified older people with frailty and were associated with an increased risk of experiencing adverse conditions.
Falls and sarcopenia are significant public health issues in Vietnam. Despite muscle strength being a critical predictor for these conditions, reference data on muscle strength within the Vietnamese population are lacking.
To establish the reference ranges for muscle strength among Vietnamese individuals.
The study involved 4096 individuals, including 1419 men and 2677 women aged 18 years and above, from the Vietnam Osteoporosis Study. Muscle strength was assessed using a Baseline hand dynamometer for handgrip strength and a Back-Leg-Chest dynamometer for leg strength. We calculated mean values, standard deviations, interquartile ranges, and peak muscle strength (pMS) for both handgrip and leg strength across various ages. Reference curves were created with the Generalised Additive Model for Location Scale and Shape, and polynomial regression models were employed to analyse the relationship between muscle strength and age.
Advancing age was significantly associated with lower muscle strength. Peak muscle strength typically occurred between ages 30 and 40, with earlier peaks in women, especially in leg strength. Men consistently showed higher muscle strength than women, with variations depending on the measurement site. Specifically, average handgrip strength was 36.4 kg ± 8.4 (mean ± SD) for men and 23.2 kg ± 6.0 for women (p < 0.001). Leg strength averaged 63.9 kg ± 27.2 for men and 29.5 kg ± 13.9 for women (p < 0.001). Additionally, we produced a percentile chart illustrating muscle weakness ranges based on the 25th percentile of muscle strength and the appendicular skeletal muscle mass index (ASMI) for the Vietnamese population.
These data provide reference ranges for evaluating muscle strength in the Vietnamese population, offering crucial insights for identifying individuals at risk of falls or sarcopenia in clinical settings.
Adeno-associated virus (AAV) 8 and 9 are in clinical trials for treating neuromuscular diseases such as Duchenne muscular dystrophy (DMD). Muscle consists of myofibres of different types and sizes. However, little is known about the fibre type and fibre size tropism of AAV in large mammals.
We evaluated fibre type- and size-specific transduction properties of AAV8 and AAV9 in 17 dogs that received systemic gene transfer (dose 1.94 ± 0.52 × 1014 vg/kg; injected at 2.86 ± 0.30 months; harvested at 20.79 ± 3.30 months). For AAV8, two DMD dogs and three carrier dogs received an alkaline phosphatase (AP) reporter vector, and five DMD dogs received a four-repeat microdystrophin (uDys) vector. For AAV9, one normal and one DMD dog received the AP vector, and five DMD dogs received a five-repeat uDys vector. Association between AAV transduction and the fibre type/size was studied in three muscles that showed mosaic transgene expression, including the biceps femoris, teres major and latissimus dorsi.
Transgene expression was detected in 30%–45% of myofibres. In the AP reporter vector–injected dogs, neither AAV8 nor AAV9 showed a statistically significant fibre type preference. Interestingly, AP expression was enriched in smaller fibres. In uDys-treated DMD dogs, slow and fast myofibres were equally transduced. Notably, uDys-expressing myofibres were significantly larger than uDys-negative myofibres irrespective of the AAV serotype (p < 0.0001). In AAV8 uDys vector–injected dogs, the mini-Feret diameter was 15%, 16% and 23% larger in uDys-positive slow, fast and hybrid fibres, respectively; the cross-sectional area was 30%, 34% and 46% larger in uDys-positive slow, fast and hybrid fibres, respectively. In AAV9 uDys vector–injected dogs, the mini-Feret diameter was 12%, 13% and 25% larger in uDys-positive slow, fast and hybrid fibres, respectively; the cross-sectional area was 25%, 28% and 59% larger in uDys-positive slow, fast and hybrid fibres, respectively.
Our studies suggest that AAV8 and AAV9 transduce fast and slow myofibres at equivalent efficiency. Importantly, uDys therapy effectively prevented dystrophic myofibre atrophy. Our study provides important insight into systemic muscle AAV delivery in large mammals and supports further development of uDys gene therapy for DMD.
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