Exercise Interventions for the Management of Sarcopenia: Possibilities and Challenges

Figures & data

Figure 1. EWGSOP algorithm for case-finding, making a diagnosis and quantifying severity in clinical practice. Image adapted from Cruz-Jentoft et al.¹³

Table 1. SARC-F Questionnaire used to begin the EWGSOP diagnostic protocol for patients with suspected sarcopenia.

Component	Question	Scoring
Strength	How much difficulty do you have in lifting and carrying 10 pounds?	None = 0 Some = 1 A lot of unstable = 2
Assistance in walking	How much difficulty do you have walking across a room?	None = 0 Some = 1 A lot of unstable = 2
Rise from a chair	How much difficulty do you have transferring from a chair or a bed	None = 0 Some = 1 A lot of unstable = 2
Climb stairs	How much difficulty do you have climbing a flight of 10 stairs?	None = 0 Some = 1 A lot of unstable = 2
Falls	How many times have you fallen in the past year?	None = 0 Some = 1 A lot of unstable = 2

A score equal to or greater than four is predictive of sarcopenia and poor outcomes. Table adapted from Malmstrom et al.¹⁴

Table 2. Summary table of the anatomical, cellular, and molecular changes observed in aging and sarcopenia.

Anatomical changes	Cellular and molecular changes
Neurodegeneration	Anabolic resistance
Muscle atrophy	Altered proteostatis
Myosteatosis	Low-grade inflammation
Reduction in type II muscle fibers	Mitochondrial dysfunction (oxidative stress)
	Hormonal changes
	Altered satellite cell number/fucntion

Figure 2. Simplified mTOR1 pathway for muscle protein synthesis. Anabolic stimuli including insulin/IGF-1, exercise (mechanical stimulation), and BCAAs can induce the mTOR1 pathway for protein synthesis. Insulin/IGF-1 and exercise allow the phosphorylation of PKB/Akt. PKB/Akt phosphorylation stimulates mTORC1 activity via the phosphorylation of TSC2 and PRAS40, both negative regulators of mTOR activity. Exercise also induces mTOR1 activation via the binding of phosphatidic acid (PA) to mTOR1. Sensing of BCAA presence in the muscle cell leads to mTOR1 lysosomal translocation leading to its subsequent activation. Activated mTOR1 phosphorylates translation repressor 4E-BP1. mTOR1 also phosphorylates S6K1, which stimulates a second phosphorylation event by PDPK1 activating S6K1. Active S6K1 can, in turn, stimulate the initiation of protein synthesis.

Table 3. Summary table of the current barriers and future possibilities for exercise intervention to reverse muscle aging.

Current barriers to exercise intervention	Future possibilities for intervention
Delayed sarcopenia diagnosis leading to delayed intervention.	Implementation of early screening using EWGSOPˈs diagnostic criterion and the future development of sarcopenic biomarkers.
Staffing and infrastructure changes to provide exercise training to all diagnosed with or at risk of developing sarcopenia.	Introduction of patient organizations, community groups or third-sector exercise professionals to conduct exercise sessions.
Poor adherence to exercise programs.	Remove the barriers to exercise and exploit the ˈexercise motivatorsˈ by conducting free, face-to-face, social, and engaging exercise sessions. Alternatively, home- based exercise support can be provided by regular patient contact with clinicians or via a telehealth approach.

Cruz-Jentoft AJ, Bahat G, Bauer J, et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. Jan 1 2019;48(1):16–31. doi:10.1093/ageing/afy169.

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Malmstrom TK, Morley JE. SARC-F: a simple questionnaire to rapidly diagnose sarcopenia. J Am Med Dir Assoc. Aug 2013;14(8):531–532. doi:10.1016/j.jamda.2013.05.018.

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