Impact of Resistance Training on Skeletal Muscle Mitochondrial Biogenesis, Content, and Function

Abstract

Skeletal muscle metabolic and contractile properties are reliant on muscle mitochondrial and myofibrillar protein turnover. The turnover of these specific protein pools is compromised during disease, aging, and inactivity. Oppositely, exercise can accentuate muscle protein turnover, thereby counteracting decay in muscle function. According to a traditional consensus, endurance exercise is required to drive mitochondrial adaptations, while resistance exercise is required to drive myofibrillar adaptations. However, concurrent practice of traditional endurance exercise and resistance exercise regimens to achieve both types of muscle adaptations is time-consuming, motivationally demanding, and contended to entail practice at intensity levels, that may not comply with clinical settings. It is therefore of principle interest to identify effective, yet feasible, exercise strategies that may positively affect both mitochondrial and myofibrillar protein turnover. Recently, reports indicate that traditional high-load resistance exercise can stimulate muscle mitochondrial biogenesis and mitochondrial respiratory function. Moreover, fatiguing low-load resistance exercise has been shown capable of promoting muscle hypertrophy and expectedly entails greater metabolic stress to potentially enhance mitochondrial adaptations. Consequently, fatiguing low-load resistance exercise regimens may possess the ability to stimulate muscle mitochondrial adaptations without compromising muscle myofibrillar accretion. However, the exact ability of resistance exercise to drive mitochondrial adaptations is debatable, not least due to some methodological challenges. The current review therefore aims to address the evidence on the effects of resistance exercise on skeletal muscle mitochondrial biogenesis, content and function. In prolongation, a perspective is taken on the specific potential of low-load resistance exercise on promoting mitochondrial adaptations.

Impact of blood flow‐restricted bodyweight exercise on skeletal muscle adaptations

“…In accordance, the impact of HRE on metabolic muscle adaptations has received relatively less attention (Groennebaek & Vissing, 2017). In accordance, the impact of HRE on metabolic muscle adaptations has received relatively less attention (Groennebaek & Vissing, 2017).…”

“…Importantly, improvements of muscle function do not exclusively rely on accretion of myofibrillar proteins, as proteins related to muscle metabolic properties also contribute to attainment of such improvements. In accordance, the impact of HRE on metabolic muscle adaptations has received relatively less attention (Groennebaek & Vissing, 2017). Yet, recent studies suggest that HRE can stimulate mitochondrial protein synthesis (Wilkinson et al, 2008) and mitochondrial respiration (Pesta et al, 2011;Porter et al, 2015).…”

Mitochondrial regulation in skeletal muscle: A role for non‐coding RNAs?

“…Mitochondria retain a unique conserved genome from prokaryotic ancestors, referred to as the mitogenome or mitochondrial DNA (mtDNA; Anderson et al., ; Groennebaek & Vissing, ). The human mitogenome is organized as a circular, covalently closed, double‐stranded DNA molecule made of 16,569 bp (Anderson et al., ; Andrews et al., ).…”

Chronic Inflammation in Rheumatoid Arthritis and Mediators of Skeletal Muscle Pathology and Physical Impairment: A Review

“…Endurance and resistance training improve body composition (i.e., increase lean mass and decrease adiposity) as well as physical function in individuals with RA (). The observed positive effects of endurance training could be due to increased mitochondrial biogenesis and respiratory function, blood flow, and insulin sensitivity (), but published studies on the cellular and molecular effects of resistance training in individuals with RA are almost nonexistent; we identified only 1 case report ().…”