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Much of our current understanding of age-related declines in mobility has been aided by decades of investigations on the role of muscle–tendon units spanning major lower extremity joints (e.g., hip, knee and ankle) for powering locomotion. Yet, mechanical contributions from foot structures are often neglected. This is despite the emerging evidence of their critical importance in youthful locomotion. With the rapid growth in the field of human foot biomechanics over the last decade, our theoretical knowledge of young asymptomatic feet has transformed, from long-held views of the foot as a stiff lever and a shock absorber to that of a versatile system that can modulate mechanical power and energy output to accommodate various locomotor task demands. In this perspective review, we predict that the next set of impactful discoveries related to locomotion in older adults will emerge by integrating the novel tools and approaches that are currently transforming the field of human foot biomechanics. By illuminating the functions of the feet in older adults, we envision that future investigations will refine our mechanistic understanding of mobility deficits affecting our aging population, which may ultimately inspire targeted interventions to rejuvenate the mechanics and energetics of locomotion. Full article

Sarcopenia, defined as the loss of muscle mass, strength, and function with aging, is a geriatric syndrome with important implications for patients and healthcare systems. Sarcopenia increases the risk of clinical decompensation when faced with physiological stressors and increases vulnerability, termed frailty. Sarcopenia develops due to inflammatory, hormonal, and myocellular changes in response to physiological and pathological aging, which promote progressive gains in fat mass and loss of lean mass and muscle strength. Progression of these pathophysiological changes can lead to sarcopenic obesity and physical frailty. These syndromes independently increase the risk of adverse patient outcomes including hospitalizations, long-term care placement, mortality, and decreased quality of life. This risk increases substantially when these syndromes co-exist. While there is evidence suggesting that the progression of sarcopenia, sarcopenic obesity, and frailty can be slowed or reversed, the adoption of broad-based screening or interventions has been slow to implement. Factors contributing to slow implementation include the lack of cost-effective, timely bedside diagnostics and interventions that target fundamental biological processes. This paper describes how clinical, radiographic, and biological data can be used to evaluate older adults with sarcopenia and sarcopenic obesity and to further the understanding of the mechanisms leading to declines in physical function and frailty. Full article