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An experimental model of contusion injury in humans

INTRODUCTION: Contusion injuries are common in sport, but our knowledge of the responses to injury primarily come from animal studies and research using eccentric exercise. Therefore, the aim of this study was to develop a model of contusion injury in human participants and, additionally, investigat...

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Autores principales: Barnes, Matthew J., Lomiwes, Dominic, Parry, David A. D., Mackintosh, Stephen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9671306/
https://www.ncbi.nlm.nih.gov/pubmed/36395119
http://dx.doi.org/10.1371/journal.pone.0277765
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author Barnes, Matthew J.
Lomiwes, Dominic
Parry, David A. D.
Mackintosh, Stephen
author_facet Barnes, Matthew J.
Lomiwes, Dominic
Parry, David A. D.
Mackintosh, Stephen
author_sort Barnes, Matthew J.
collection PubMed
description INTRODUCTION: Contusion injuries are common in sport, but our knowledge of the responses to injury primarily come from animal studies and research using eccentric exercise. Therefore, the aim of this study was to develop a model of contusion injury in human participants and, additionally, investigate and compare physiological responses to four impact loads. METHODS: Thirty-two males were exposed to a single impact of either 4.2, 5.2, 6.2 or 7.2kg, dropped from 67 cm, on to the vastus lateralis of one leg. Maximum voluntary and electrically induced quadriceps force, and pressure pain threshold were measured, and blood sampling carried out, prior to and 30min, 24, 48 and 72h post-impact. Magnetic resonance imaging was carried out 24h post-impact to quantify oedema. RESULTS: Despite impact force with 7.2kg (1681.4 ± 235.6 N) not being different to 6.2kg (1690.7 ± 117.6 N), 7.2kg resulted in greater volume of oedema, voluntary force loss, pain and elevations in creatine kinase than the other loads. Although electrically induced force changed over time, post-hoc analysis failed to identify any changes. Interleukin-6 and prostaglandin-E(2) did not change over time for any of the loads. Significant correlations were found between oedema volume, pressure pain threshold and maximum voluntary contraction force. CONCLUSIONS: This is the first experimental study to investigate traumatic loading of skeletal muscle and the subsequent physiological responses associated with contusion injuries in humans. The absence of immediate elevations in creatine kinase and changes in electrically induced force suggest impact, with forces similar to those experienced in contact sport, does not cause significant, direct damage to skeletal muscle. However, the relationship between oedema volume, changes in pressure pain threshold and maximum voluntary contraction force suggests central inhibition plays a role in contusion-related muscle dysfunction.
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spelling pubmed-96713062022-11-18 An experimental model of contusion injury in humans Barnes, Matthew J. Lomiwes, Dominic Parry, David A. D. Mackintosh, Stephen PLoS One Research Article INTRODUCTION: Contusion injuries are common in sport, but our knowledge of the responses to injury primarily come from animal studies and research using eccentric exercise. Therefore, the aim of this study was to develop a model of contusion injury in human participants and, additionally, investigate and compare physiological responses to four impact loads. METHODS: Thirty-two males were exposed to a single impact of either 4.2, 5.2, 6.2 or 7.2kg, dropped from 67 cm, on to the vastus lateralis of one leg. Maximum voluntary and electrically induced quadriceps force, and pressure pain threshold were measured, and blood sampling carried out, prior to and 30min, 24, 48 and 72h post-impact. Magnetic resonance imaging was carried out 24h post-impact to quantify oedema. RESULTS: Despite impact force with 7.2kg (1681.4 ± 235.6 N) not being different to 6.2kg (1690.7 ± 117.6 N), 7.2kg resulted in greater volume of oedema, voluntary force loss, pain and elevations in creatine kinase than the other loads. Although electrically induced force changed over time, post-hoc analysis failed to identify any changes. Interleukin-6 and prostaglandin-E(2) did not change over time for any of the loads. Significant correlations were found between oedema volume, pressure pain threshold and maximum voluntary contraction force. CONCLUSIONS: This is the first experimental study to investigate traumatic loading of skeletal muscle and the subsequent physiological responses associated with contusion injuries in humans. The absence of immediate elevations in creatine kinase and changes in electrically induced force suggest impact, with forces similar to those experienced in contact sport, does not cause significant, direct damage to skeletal muscle. However, the relationship between oedema volume, changes in pressure pain threshold and maximum voluntary contraction force suggests central inhibition plays a role in contusion-related muscle dysfunction. Public Library of Science 2022-11-17 /pmc/articles/PMC9671306/ /pubmed/36395119 http://dx.doi.org/10.1371/journal.pone.0277765 Text en © 2022 Barnes et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Barnes, Matthew J.
Lomiwes, Dominic
Parry, David A. D.
Mackintosh, Stephen
An experimental model of contusion injury in humans
title An experimental model of contusion injury in humans
title_full An experimental model of contusion injury in humans
title_fullStr An experimental model of contusion injury in humans
title_full_unstemmed An experimental model of contusion injury in humans
title_short An experimental model of contusion injury in humans
title_sort experimental model of contusion injury in humans
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9671306/
https://www.ncbi.nlm.nih.gov/pubmed/36395119
http://dx.doi.org/10.1371/journal.pone.0277765
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