Abstract

Here, we investigate changes in inflammation-related gene-expression in peripheral mononuclear blood cells (PBMC) by strength training. A total of 14 women aged ≥65 years were randomized into 3 months of either 3×/week intensive strength training (IST: 3×10 rep at 80% 1RM), strength endurance training (SET: 2×30 reps at 40% 1RM) or control (CON: 3×30 sec stretching). Differentially expressed genes (fold change ≤0.67 or ≥1.5) were identified by targeted RNA-sequencing of 407 inflammation-related genes. A total of 98 genes (n = 61 pro-inflammatory) were significantly affected. IST and SET altered 14 genes in a similar direction and 19 genes in the opposite direction. Compared to CON, IST changed the expression of 6 genes in the same direction, and 17 genes in the SET. Likewise, 18 and 13 genes were oppositely expressed for, respectively, IST and SET compared to CON. Changes in gene expression affected 33 canonical pathways related to chronic inflammation. None of the altered pathways overlapped between IST and SET. Liver X Receptor/Retinoid X Receptor Activation (LXR/RXR) and Triggering Receptor Expressed On Myeloid Cells 1 (TREM1) pathways were enriched oppositely in both training groups. We conclude that three months IST and SET can induce changes in CLIP-related gene expression in PBMC, but by affecting different genes and related pathways.

Highlights

  • Ageing is accompanied by elevated levels of circulating inflammatory biomarkers, described as a chronic low grade inflammatory profile (CLIP) [1]

  • We investigated the impact of 3 months of strength training at either high-load (IST) or low-load (SET), compared to a stretching control (CON) intervention on the change in expression of inflammation-related genes in peripheral blood mononuclear cells (PBMC) (Figure 7)

  • This is reflected by the fact that none of the enriched pathways overlapped between both strength training modalities

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Summary

Introduction

Ageing is accompanied by elevated levels of circulating inflammatory biomarkers, described as a chronic low grade inflammatory profile (CLIP) [1]. Circulating IL-6 increases during acute exercise, reaching a maximum near the end of the session and returning to baseline values within 24–48 h [13, 15,16,17,18,19]. This myokine response is different from the cytokine release seen during inflammation. The exercise-induced acute elevation in IL-6 is not preceded by increased TNF-α levels [15] but is immediately followed by significant elevations in IL-1ra and sTNF-R [15] (inhibiting, respectively, IL-1β and TNF-α) and the anti-inflammatory cytokine IL-10, reducing inflammation[15].

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