Abstract
Sarcopenia is the age-related loss of skeletal muscle mass, strength, and function. It is associated with regenerative difficulties by satellite cells, adult muscle stem cells, and alteration of oxidative management, mainly the increase in superoxide anions (O2 •−). We aimed to investigate the relation between regenerative deficit in elderly and increase in O2 •− production along with mitochondrial alterations. Myoblasts and myotubes from skeletal muscle of young and elderly healthy subjects (27.8 ± 6 and 72.4 ± 6.5 years old) were measured: (1) superoxide dismutase activity and protein content, (2) mitochondrial O2 •− production levels, (3) O2 •− production variability, and (4) mitochondrial bioenergetic profile. Compared to young myoblasts, elderly myoblasts displayed decreased SOD2 protein expression, elevated mitochondrial O2 •− baseline levels, and decreased oxidative phosphorylation and glycolysis. Additionally, elderly versus young myotubes showed elevated mitochondrial O2 •− levels when stressed with N-acetyl cysteine or high glucose and higher glycolysis despite showing comparable oxidative phosphorylation levels. Altogether, the elderly may have less metabolic plasticity due to the impaired mitochondrial function caused by O2 •−. However, the increased energy demand related to the differentiation process appears to activate compensatory mechanisms for the partial mitochondrial dysfunction.
Highlights
Sarcopenia is defined as the age-related loss of muscle mass, strength, and function [1]
Activation and proliferation stages of satellite cells are characterized by the expression of myogenic regulatory factors (MRFs), and the phases of this process typically involve the sequential expression of proteins, including Pax3, myoD, and myogenin
The metabolic burst due to the onset of differentiation leads to a pronounced increase in glycolysis which does not occur in young myotubes
Summary
Sarcopenia is defined as the age-related loss of muscle mass, strength, and function [1]. In response to muscle damage, satellite cells, undifferentiated quiescent mononucleated cells present in muscle [3], which have properties of stem cells, are activated to proliferate as human primary myoblasts Proliferating myoblasts migrate to the damaged region of the fiber, where they differentiate and fuse to form myotubes via a similar process to that of myogenesis [4]. This capacity is reduced in the elderly, where satellite cells are unable to execute the complete repair process or they exhibit a slow recovery [5,6,7]. We previously demonstrated that the impaired regenerative potential in elderly primary myoblasts is related to dysregulation in myogenin and miR-1 and 133b
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