An experimental model of contusion injury in humans

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dc.citation.issue11
dc.citation.volume17
dc.contributor.authorBarnes M
dc.contributor.authorLomiwes D
dc.contributor.authorParry DAD
dc.contributor.authorStephen M
dc.coverage.spatialUnited States
dc.date.available2022
dc.date.available2022-11-02
dc.date.issued17/11/2022
dc.description.abstractIntroduction 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-E2 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.
dc.description.publication-statusPublished online
dc.format.extente0277765 - ?
dc.identifierhttps://www.ncbi.nlm.nih.gov/pubmed/36395119
dc.identifierPONE-D-22-22230
dc.identifier.citationPLoS One, 2022, 17 (11), pp. e0277765 - ?
dc.identifier.doi10.1371/journal.pone.0277765
dc.identifier.eissn1932-6203
dc.identifier.elements-id458052
dc.identifier.harvestedMassey_Dark
dc.identifier.urihttps://hdl.handle.net/10179/17828
dc.languageeng
dc.publisherPublic Library of Science
dc.relation.isPartOfPLoS One
dc.relation.urihttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0277765
dc.subjectMale
dc.subjectAnimals
dc.subjectHumans
dc.subjectContusions
dc.subjectMuscle, Skeletal
dc.subjectQuadriceps Muscle
dc.subjectCreatine Kinase
dc.subjectPain
dc.subjectModels, Theoretical
dc.titleAn experimental model of contusion injury in humans
dc.typeJournal article
pubs.notesNot known
pubs.organisational-group/Massey University
pubs.organisational-group/Massey University/College of Health
pubs.organisational-group/Massey University/College of Health/School of Sport, Exercise and Nutrition
pubs.organisational-group/Massey University/College of Sciences
pubs.organisational-group/Massey University/College of Sciences/School of Fundamental Sciences
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