Background: Essential amino acids (EAA) and aerobic exercise (AE) acutely and independently stimulate skeletal muscle protein anabolism in older adults.
Objective: In this Phase 1, double-blind, placebo-controlled, randomized clinical trial, we determined if chronic EAA supplementation, AE training, or a combination of the two interventions could improve muscle mass and function by stimulating muscle protein synthesis.
Methods: We phone-screened 971, enrolled 109, and randomized 50 independent, low-active, nonfrail, and nondiabetic older adults (age 72 ± 1 years). We used a 2 × 2 factorial design. The interventions were: daily nutritional supplementation (15 g EAA or placebo) and physical activity (supervised AE training 3 days/week or monitored habitual activity) for 24 weeks. Muscle strength, physical function, body composition, and muscle protein synthesis were measured before and after the 24-week intervention.
Results: Forty-five subjects completed the 24-week intervention. VO2peak and walking speed increased (p < .05) in both AE groups, irrespective of supplementation type, but muscle strength increased only in the EAA + AE group (p < .05). EAA supplementation acutely increased (p < .05) muscle protein synthesis from basal both before and after the intervention, with a larger increase in the EAA + AE group after the intervention. Total and regional lean body mass did not change significantly with any intervention.
Conclusions: In nonfrail, independent, healthy older adults AE training increased walking speed and aerobic fitness, and, when combined with EAA supplementation, it also increased muscle strength and EAA-stimulated muscle protein synthesis. These increases occurred without improvements in muscle mass.
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http://dx.doi.org/10.1093/gerona/gly109 | DOI Listing |
PLoS Biol
January 2025
Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
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January 2025
Department of Psychology, The University of Tennessee Knoxville, Knoxville, Tennessee, USA.
Long-term effects of social play on neural and behavioral development remain unclear. We investigated whether just 1 h of juvenile social play could rescue the effects of play deprivation on stress-related behavior and markers of neural plasticity. Syrian hamsters were reared from postnatal days 21-43 in three conditions: peer isolation, peer isolation with daily social play sessions (dyadic play), or group-housed with littermates.
View Article and Find Full Text PDFFuture Cardiol
January 2025
BridgeBio Pharma, Inc., San Francisco, CA, USA.
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View Article and Find Full Text PDFAutophagy
January 2025
Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Postmitotic skeletal muscle critically depends on tightly regulated protein degradation to maintain proteomic stability. Impaired macroautophagy/autophagy-lysosomal or ubiquitin-proteasomal protein degradation causes the accumulation of damaged proteins, ultimately accelerating muscle dysfunction with age. While studies have demonstrated the complementary nature of these systems, their interplay at the organism levels remains poorly understood.
View Article and Find Full Text PDFHypertension
January 2025
Cardiology Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA. (X.Z., Q.X., A.V., Z.L.).
Background: Recent studies show that hyperactivation of mTOR (mammalian target of rapamycin) signaling plays a causal role in the development of thoracic aortic aneurysm and dissection. Modulation of PP2A (protein phosphatase 2A) activity has been shown to be of significant therapeutic value. In light of the effects that PP2A can exert on the mTOR pathway, we hypothesized that PP2A activation by small-molecule activators of PP2A could mitigate AA progression in Marfan syndrome (MFS).
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