How Acute and Chronic Exercise Regulate Muscle Atrophic Genes to Mitigate Sarcopenia: A Narrative Review.

Area of Science:

• Muscle physiology and molecular biology
• Gerontology and chronic disease research
• Exercise science and rehabilitation

Background:

• Muscle atrophy, characterized by reduced muscle mass and strength, stems from decreased muscle fiber size and protein content.
• It is exacerbated by physical inactivity, aging, starvation, immobilization, and chronic conditions like cancer and diabetes, leading to diminished quality of life.
• Physical inactivity is a primary driver, increasing inflammatory factors and glucocorticoids, disrupting signaling pathways (GH/IGF-1, testosterone, myostatin), and promoting atrophy gene expression (ATROGIN-1, MuRF-1).

Purpose of the Study:

• To review the molecular mechanisms underlying muscle atrophy, focusing on the genes ATROGIN-1 and MuRF-1.
• To examine how exercise, both acute and chronic, influences the expression of these atrophy-related genes.
• To explore other regulators involved in muscle remodeling in response to exercise.

Main Methods:

• This narrative review synthesizes findings from experimental and clinical studies.
• It analyzes molecular mechanisms involving gene expression, protein degradation (ubiquitin-proteasome system), and signaling pathways (mTOR, Akt/FoxO).
• The review discusses differential gene expression patterns of ATROGIN-1 and MuRF-1 in response to various exercise interventions.

Main Results:

• Physical inactivity triggers signaling cascades that lead to the activation of ATROGIN-1 and MuRF-1, promoting muscle protein degradation via the ubiquitin-proteasome system.
• Exercise interventions demonstrate the potential to counteract muscle atrophy by activating muscle protein synthesis (e.g., via mTOR) and suppressing the expression of atrophy-related genes.
• Specific molecular pathways and regulators involved in exercise-induced muscle remodeling are highlighted.

Conclusions:

• Muscle atrophy is a complex process driven by molecular signaling, significantly influenced by physical activity levels.
• Exercise emerges as a key intervention to mitigate muscle wasting by modulating both protein synthesis and degradation pathways.
• Understanding these mechanisms provides a basis for targeted therapeutic strategies to combat muscle loss in various populations.