Blood-flow restricted training leads to myocelullar macrophage infiltration and upregulation of heat-shock proteins, but no apparent muscle damage

Abstract

Previous studies indicate that low-load muscle contractions performed under local blood-flow restriction (BFR) may initially induce muscle damage and stress. However, whether these factors are evoked with longitudinal BFR training remains unexplored at the myocellular level.

Two distinct study protocols were conducted (3 wk/1 wk). Subjects performed BFR exercise (100 mmHg, 20%-1RM) to concentric failure (BFRE) (3 wk/1 wk), while controls performed work-matched (LLE)(3 wk) or high-load (HLE; 70%-1RM)(1 wk), free-flow exercise. Muscle biopsies (3 wk) were obtained at baseline (Pre), 8 days into the intervention (Mid8) and 3 and 10 days after training cessation (Post3,Post10) to examine macrophage (M1/M2) content as well as heat-shock protein (HSP27/70) and tenascin-C expression. Blood samples (1 wk) were collected before and after (0.1–24 h) the first and last training session to examine markers of muscle damage (CK), oxidative stress (TAC,GSH) and inflammation (MCP1,IL-6,TNFa).

M1-macrophage content increased 108–165% with BFRE and LLE at Post3 (P < 0.05), while M2-macrophages increased (163%) with BFRE only (P < 0.01). Membrane and intracellular HSP27 expression increased 60–132% at Mid8 with BFRE (P < 0.05–0.01). No or only minor changes were observed in circulating markers of muscle damage, oxidative stress and inflammation. The amplitude, timing and localization of the above changes indicate that only limited muscle damage was evoked with BFRE.

This study is the first to show that a period of high-frequency low-load BFR training does not appear to induce general myocellular damage. However, signs of tissue inflammation and focal myocellular membrane stress and/or reorganization were observed, that may be involved in the adaptation processes evoked by BFR muscle exercise.

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