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

Jakob L Nielsen, Per Aagaard, Tatyana A Prokhorova, Tobias Nygaard, Rune Dueholm Bech, Charlotte Suetta, Ulrik Frandsen

Research output: Contribution to journalJournal articleResearchpeer-review

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. This article is protected by copyright. All rights reserved.

Original languageEnglish
JournalJournal of Physiology
Volume595
Issue number14
Pages (from-to)4857–4873
ISSN0022-3751
DOIs
Publication statusPublished - 2017

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Heat-Shock Proteins
Up-Regulation
Macrophages
Muscles
Tenascin
HSP70 Heat-Shock Proteins
Interleukin-6
Membranes

Keywords

  • Journal Article

Cite this

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title = "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. This article is protected by copyright. All rights reserved.",
keywords = "Journal Article",
author = "Nielsen, {Jakob L} and Per Aagaard and Prokhorova, {Tatyana A} and Tobias Nygaard and Bech, {Rune Dueholm} and Charlotte Suetta and Ulrik Frandsen",
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year = "2017",
doi = "10.1113/JP273907",
language = "English",
volume = "595",
pages = "4857–4873",
journal = "Journal of Physiology",
issn = "0022-3751",
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Blood-flow restricted training leads to myocelullar macrophage infiltration and upregulation of heat-shock proteins, but no apparent muscle damage. / Nielsen, Jakob L; Aagaard, Per; Prokhorova, Tatyana A; Nygaard, Tobias; Bech, Rune Dueholm; Suetta, Charlotte; Frandsen, Ulrik.

In: Journal of Physiology, Vol. 595, No. 14, 2017, p. 4857–4873.

Research output: Contribution to journalJournal articleResearchpeer-review

TY - JOUR

T1 - Blood-flow restricted training leads to myocelullar macrophage infiltration and upregulation of heat-shock proteins, but no apparent muscle damage

AU - Nielsen, Jakob L

AU - Aagaard, Per

AU - Prokhorova, Tatyana A

AU - Nygaard, Tobias

AU - Bech, Rune Dueholm

AU - Suetta, Charlotte

AU - Frandsen, Ulrik

N1 - This article is protected by copyright. All rights reserved.

PY - 2017

Y1 - 2017

N2 - 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. This article is protected by copyright. All rights reserved.

AB - 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. This article is protected by copyright. All rights reserved.

KW - Journal Article

U2 - 10.1113/JP273907

DO - 10.1113/JP273907

M3 - Journal article

C2 - 28481416

VL - 595

SP - 4857

EP - 4873

JO - Journal of Physiology

JF - Journal of Physiology

SN - 0022-3751

IS - 14

ER -