TY - JOUR
T1 - Muscle strength after resistance training correlates to mediators of muscle mass and mitochondrial respiration in middle-aged adults
AU - McKenna, Colleen F.
AU - Salvador, Amadeo F.
AU - Keeble, Alexander R.
AU - Khan, Naiman A.
AU - De Lisio, Michael
AU - Konopka, Adam R.
AU - Paluska, Scott A.
AU - Burd, Nicholas A.
N1 - Funding Information:
This study was funded in part by the Margin of Excellence Student Research Program, Division of Nutritional Sciences, University of Illinois (to C.F.M.).
Funding Information:
Parent study funded by the Beef Checkoff. Beef Checkoff sponsor was only involved in financial support of the parent
Publisher Copyright:
© 2022 the American Physiological Society.
PY - 2022/9
Y1 - 2022/9
N2 - 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 ± 7 yr; 27.8 ± 3.7 kg/m2; means ± 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.
AB - 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 ± 7 yr; 27.8 ± 3.7 kg/m2; means ± 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.
KW - aging
KW - apelin
KW - sarcopenia
KW - spermine oxidase
KW - vitamin D receptor
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U2 - 10.1152/japplphysiol.00186.2022
DO - 10.1152/japplphysiol.00186.2022
M3 - Article
C2 - 35834627
AN - SCOPUS:85137124339
SN - 8750-7587
VL - 133
SP - 572
EP - 584
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 3
ER -