Musculoskeletal Aging Overview

Principles

Definition

Musculoskeletal aging is the complex biological process involving progressive structural and functional changes in muscle, bone, cartilage, and connective tissues over time. As a research concept, it investigates the underlying cellular and molecular mechanisms driving this age-related decline, its systemic impact on mobility, strength, and stability, and strategies for the prevention and treatment of associated conditions such as sarcopenia, osteoporosis, and osteoarthritis, which significantly affect healthspan and quality of life.

Ontological type

Interventions

Cellular Mechanisms

Risk Factors

Key developments

Key Figures

Mitochondrial Energy Decline era

Elena Volpi [1] conducted research across Washington University in St. Louis [3] and the University of Arkansas for Medical Sciences [4] during the Mitochondrial Energy Decline era (2002-2008). Her key contribution was showing that the paper 'Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging' [7], a finding that linked energetic constraints to impaired anabolic signaling and underscored the potential for exercise and nutrition to partially restore metabolic transcriptional programs. Blake B. Rasmussen [2] was active with the University of Texas Medical Branch at Galveston [5] and the University of Southern California [6] during this era. His co-authorship of the same study 'Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging' [7] highlighted the central role of energy metabolism in aging muscle and reinforced the importance of combining resistance exercise with amino acid nutrition to mitigate mitochondrial energy decline.

Anabolic-Catabolic Signaling era

Todd M. Manini [1] is a scholar whose work in the Anabolic-Catabolic Signaling era spans institutions such as University of California, San Francisco [3] and Stanford University [4]. His contributions in this era center on mitochondrial aging effects in skeletal muscle, as exemplified by the paper 'The impact of aging on mitochondrial function and biogenesis pathways in skeletal muscle of sedentary high- and low-functioning elderly individuals' [5], which highlighted how aging alters mitochondrial biogenesis and function and the integration of mitochondrial quality-control pathways into anabolic–catabolic signaling, a key theme for muscle mass and proteostasis in this era. Marco Pahor [2] is a key figure associated with University of California, San Francisco [3] and Stanford University [4] during this era. His contributions in this era, as captured by the same paper [5], emphasize functional heterogeneity among aging individuals and the role of mitochondrial and bioenergetic pathways in mediating anabolic–catabolic signaling, illustrating why these molecular regulators matter for muscle mass preservation in aging.

Metabolic-Neuromuscular Integration era

Mariangela Rondanelli [1] is a scholar active in this era, with affiliations at Baylor College of Medicine [3] and Thomas Jefferson University [4]. Her key contribution in this era is the paper Whey protein, amino acids, and vitamin D supplementation with physical activity increases fat-free mass and strength, functionality, and quality of life and decreases inflammation in sarcopenic elderly [7], which demonstrated that targeted nutrition and exercise can restore lean mass and functional capacity in aging muscle, linking metabolic milieu to neuromuscular performance. Christopher S. Fry [2] is a scholar active in this era, with affiliations at The University of Texas Medical Branch at Galveston [5] and the University of Kentucky [6]. His contribution is the paper Fourteen days of bed rest induces a decline in satellite cell content and robust atrophy of skeletal muscle fibers in middle-aged adults [8], which illustrated how short-term immobilization disrupts satellite cell dynamics and accelerates muscle atrophy, underscoring the metabolic–neuromuscular integration essential for aging muscle.