Sarcopenia

Overview

Sarcopenia — age-related loss of muscle mass and strength — begins in the fourth decade and accelerates after 60. It is a major driver of frailty, falls, metabolic decline, and mortality in older adults. Peptide therapy addresses the primary drivers: GH/IGF-1 axis decline, mitochondrial dysfunction, inflammation, and myostatin overexpression. Resistance training remains the essential foundation for any sarcopenia intervention.

Recommended Peptides

MOTS-C – mitochondrial peptide that functions as an exercise mimetic; improves muscle metabolism, glucose uptake in muscle tissue, and fatigue resistance
CJC-1295 / Ipamorelin – restores pulsatile GH secretion that drives IGF-1-mediated anabolism; most studied GH peptide combination for body composition
Tesamorelin – GHRH analogue with favorable body composition effects; particularly reduces fat while preserving lean mass
SS-31 – preserves mitochondrial function in aging muscle; reduces sarcopenic muscle atrophy driven by mitochondrial ROS
Follistatin 344 – myostatin antagonist that inhibits the primary brake on muscle growth; can produce significant lean mass increases but carries regulatory caution
5-Amino-1MQ – activates AMPK and SIRT1 pathways; improves muscle metabolic efficiency and may partially mimic exercise adaptation

Protocols

Related Conditions

Research Summary

CJC-1295 maintains pulsatile GH secretion and increases IGF-1 in humans (PMID-17018654). Ipamorelin is the first selective GH secretagogue (no cortisol/prolactin effects) and counteracts glucocorticoid-induced bone loss with 4-fold periosteal formation increase (PMID-11735244). MOTS-C reversed age-dependent physical decline in aged mice and is exercise-regulated in human skeletal muscle (PMID-33473109). NNMT inhibition (5-Amino-1MQ class) activated senescent muscle stem cells in 24-month-old mice with ~2-fold greater fiber area (PMID-30753815).

#condition #musculoskeletal