Abstract
The extracellular matrix (ECM) plays an essential role in the development, growth and repair of skeletal muscles and serves to transmit contractile force. However, its regulation is poorly understood. This study investigates the age-specificity of the effects of acute resistance exercise on ECM gene expression. To this purpose, five young (YM, 23.8 ± 2.2 yrs.) and 5 elderly (EM, 66.8 ± 4.1 yrs.) men performed one session of unilateral leg press and leg extension exercises. Six hours post-exercise, biopsies were taken from the vastus lateralis muscles of both legs. A PCR array was used to profile the expression of 84 ECM-related genes, of which 6 were validated by qPCR. The PCR array found 9 and 4 ECM-associated genes to be selectively altered (>1.5-fold change) in YM or EM only. Four further genes were upregulated in YM but downregulated in EM. Of the 6 genes validated on individual samples MMP9 expression increased in YM (9.7-fold) and decreased (0.2-fold) in EM. MMP15 was downregulated in EM only (0.6-fold). A significant correlation between leg extension 1 RM and changes in COL7A1 expression (ρ = 0.71) suggests a potential influence of fitness levels. In conclusion, acute resistance exercise affects ECM gene expression at least partly in an age-specific manner. The altered expression of genes encoding matrix metalloproteinases (MMP3, MMP9, MMP15) highlights the role of remodelling processes in the response to an acute bout of resistance exercise. Larger studies are required to verify the age-associated differences in gene expression profiles and establish their functional implications.
Highlights
Skeletal muscles are characterised by a remarkable capacity to respond and adapt to different types of exercise
This study investigates the age-specificity of the effects of acute resistance exercise on extracellular matrix (ECM) gene expression
Screening for several genes involved in ECM organization, development and degradation we identified some matrix metallopeptidases (MMP3, MMP9, MMP15), ADAM metallopeptidases (ADAMTS1, ADAMTS8), collagens (COL7A1, COL1A1), integrins (ITGB3, ITGAL), laminins (LAMB3, LAMA1), and other cell adhesion molecules (CD44, CDH1, SELE, SELL, CTNND2, SPP1) as candidates for being selectively down- or upregulated (>1.5-fold change) in either young or older subjects
Summary
Skeletal muscles are characterised by a remarkable capacity to respond and adapt to different types of exercise. In order to explain the mechanisms underlying these changes, the majority of studies have focused on examining molecular pathways inherent to skeletal muscle cells (Hoppeler, 2016). Many other cell types are embedded in or recruited to skeletal muscles upon stimulation and it is evident that efficient muscle remodelling requires the interplay between these and skeletal muscle cells. Tightly regulated inflammatory processes involving neutrophils, macrophages, mast cells, eosinophils, cytotoxic T cells, and T-regulatory lymphocytes contribute to exercise adaptations (Peake, Neubauer, Della Gatta, & Nosaka, 2017). Less is known about the exact role of fibroblasts which have been shown to directly stimulate the proliferation, differentiation and fusion of myogenic precursor cells (Mackey, Magnan, Chazaud, & Kjaer, 2017). Fibroblasts and other adherent cells are sensitive to mechanical strains in their extracellular matrix (ECM) environment and able to transduce mechanical into chemical
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