PMID- 37410905 OWN - NLM STAT- MEDLINE DCOM- 20230728 LR - 20230728 IS - 1522-1601 (Electronic) IS - 0161-7567 (Linking) VI - 135 IP - 2 DP - 2023 Aug 1 TI - The importance of serial sarcomere addition for muscle function and the impact of aging. PG - 375-393 LID - 10.1152/japplphysiol.00205.2023 [doi] AB - During natural aging, skeletal muscle experiences impairments in mechanical performance due, in part, to changes in muscle architecture and size, notably with a loss of muscle cross-sectional area (CSA). Another important factor that has received less attention is the shortening of fascicle length (FL), potentially reflective of a decrease in serial sarcomere number (SSN). Interventions that promote the growth of new serial sarcomeres, such as chronic stretching and eccentric-biased resistance training, have been suggested as potential ways to mitigate age-related impairments in muscle function. Although current research suggests it is possible to stimulate serial sarcomerogenesis in muscle in old age, the magnitude of sarcomerogenesis may be less than in young muscle. This blunted effect may be partly due to age-related impairments in the pathways regulating mechanotransduction, muscle gene expression, and protein synthesis, as some have been implicated in SSN adaptation. The purpose of this review was to investigate the impact of aging on the ability for serial sarcomerogenesis and elucidate the molecular pathways that may limit serial sarcomerogenesis in old age. Age-related changes in mechanistic target of rapamycin (mTOR), insulin-like growth factor 1 (IGF-1), myostatin, and serum response factor signaling, muscle ring finger protein (MuRFs), and satellite cells may hinder serial sarcomerogenesis. In addition, our current understanding of SSN in older humans is limited by assumptions based on ultrasound-derived fascicle length. Future research should explore the effects of age-related changes in the identified pathways on the ability to stimulate serial sarcomerogenesis, and better estimate SSN adaptations to gain a deeper understanding of the adaptability of muscle in old age. FAU - Hinks, Avery AU - Hinks A AUID- ORCID: 0000-0002-1809-1006 AD - Department of Human Health and Nutritional Sciences, College of Biological Sciences, University of Guelph, Guelph, Ontario, Canada. FAU - Hawke, Thomas J AU - Hawke TJ AUID- ORCID: 0000-0003-4974-4820 AD - Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada. FAU - Franchi, Martino V AU - Franchi MV AUID- ORCID: 0000-0003-3165-4536 AD - Department of Biomedical Sciences, Neuromuscular Physiology Laboratory, University of Padua, Padua, Italy. FAU - Power, Geoffrey A AU - Power GA AUID- ORCID: 0000-0003-2604-0740 AD - Department of Human Health and Nutritional Sciences, College of Biological Sciences, University of Guelph, Guelph, Ontario, Canada. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20230706 PL - United States TA - J Appl Physiol (1985) JT - Journal of applied physiology (Bethesda, Md. : 1985) JID - 8502536 SB - IM MH - Humans MH - Aged MH - *Sarcomeres/physiology MH - Mechanotransduction, Cellular MH - Muscle, Skeletal/physiology MH - Aging MH - *Musculoskeletal Physiological Phenomena OTO - NOTNLM OT - aging OT - focal adhesion kinase OT - force-length relationship OT - titin OT - ultrasound EDAT- 2023/07/06 19:12 MHDA- 2023/07/28 06:42 CRDT- 2023/07/06 15:13 PHST- 2023/07/28 06:42 [medline] PHST- 2023/07/06 19:12 [pubmed] PHST- 2023/07/06 15:13 [entrez] AID - 10.1152/japplphysiol.00205.2023 [doi] PST - ppublish SO - J Appl Physiol (1985). 2023 Aug 1;135(2):375-393. doi: 10.1152/japplphysiol.00205.2023. Epub 2023 Jul 6.