McKenna 2022 J Appl Physiol (1985)

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Publications in the MiPMap
McKenna CF, Salvador AF, Keeble AR, Khan NA, De Lisio M, Konopka AR, Paluska SA, Burd NA (2022) Muscle strength after resistance training correlates to mediators of muscle mass and mitochondrial respiration in middle-aged adults.

Β» J Appl Physiol (1985) 133:572-84. PMID: 35834627 Open Access

McKenna Colleen F, Salvador Amadeo F, Keeble Alexander R, Khan Naiman A, De Lisio Michael, Konopka Adam R, Paluska Scott A, Burd Nicholas A (2022) J Appl Physiol (1985)

Abstract: Skeletal muscle aging is a multidimensional pathology of atrophy, reduced strength, and oxidative damage. Although some molecular targets may mediate both hypertrophic and oxidative adaptations in muscle, their responsiveness in humans and relationship with functional outcomes like strength remain unclear. Promising therapeutic targets to combat muscle aging like apelin, vitamin D receptor (VDR), and spermine oxidase (SMOX) have been investigated in preclinical models but the adaptive response in humans is not well defined. In an exploratory investigation, we examined how strength gains with resistance training relate to regulators of both muscle mass and oxidative function in middle-aged adults. Forty-one middle-aged adults [18 male (M), 23 female (F); 50 Β± 7 yr; 27.8 Β± 3.7 kg/m2; means Β± SD] participated in a 10-wk resistance training intervention. Muscle biopsies and plasma were sampled at baseline and postintervention. High-resolution fluo-respirometry was performed on a subset of muscle tissue. Apelin signaling (plasma apelin, P = 0.002; Apln mRNA, P < 0.001; apelin receptor mRNA Aplnr, P = 0.001) increased with resistance training. Muscle Vdr mRNA (P = 0.007) and Smox mRNA (P = 0.027) were also upregulated after the intervention. Mitochondrial respiratory capacity increased (Vmax, oxidative phosphorylation, and uncoupled electron transport system, P < 0.050), yet there were no changes in ADP sensitivity (Km P = 0.579), hydrogen peroxide emission (P = 0.469), nor transcriptional signals for mitochondrial biogenesis (nuclear respiratory factor 2, Gapba P = 0.766) and mitofusion (mitochondrial dynamin-like GTPase, Opa1 P = 0.072). Muscular strength with resistance training positively correlated to Apln, Aplnr, Vdr, and Smox transcriptional adaptations, as well as mitochondrial respiratory capacity (unadjusted P < 0.050, r = 0.400-0.781). Further research is required to understand the interrelationships of these targets with aged muscle phenotype.

Although some therapeutic targets may ameliorate hypertrophic and oxidative dysfunction with muscle aging in preclinical models, their responsiveness in human muscle remains unclear. We demonstrated that resistance training concurrently upregulated therapeutic targets of muscle aging and mitochondrial respiratory capacity, which positively correlated to strength gains. Specifically, we are the first to demonstrate that apelin and spermine oxidase are upregulated with resistance training in humans. Our work corroborates preclinical observations, with future work required for clinical efficacy. β€’ Keywords: Aging, Apelin, Sarcopenia, Spermine oxidase, Vitamin D receptor β€’ Bioblast editor: Plangger M β€’ O2k-Network Lab: US WI Madison Konopka A

Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Coupling state: LEAK, OXPHOS, ET  Pathway: NS  HRR: Oxygraph-2k, O2k-Fluorometer 

2022-09, AmR 

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