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A longitudinal study on cardiac effects of deconditioning and physical reconditioning using the anterior cruciate ligament injury as a model.

Steding Ehrenborg, Katarina LU ; Hedén, Bo LU ; Herbertsson, Pär LU and Arheden, Håkan LU (2013) In Clinical Physiology and Functional Imaging 33(6). p.423-430
Abstract
BACKGROUND: Studies of cardiovascular deconditioning are primarily carried out after experimental bed rest. No previous study has followed the cardiovascular effects of decreased and resumed physical activity in athletes after acute physical injury and convalescence. Anterior cruciate ligament (ACL) injury causes a significantly decreased activity level over a long period, making it an ideal model for studying effects of deconditioning and reconditioning. Therefore, the aim of this study was to investigate how cardiac dimensions and maximal exercise capacity change after an ACL-injury. METHOD: Seventeen athletes (5 women) were included. Cardiac magnetic resonance (CMR) was performed within 5 days of the injury (CMR1), before endurance... (More)
BACKGROUND: Studies of cardiovascular deconditioning are primarily carried out after experimental bed rest. No previous study has followed the cardiovascular effects of decreased and resumed physical activity in athletes after acute physical injury and convalescence. Anterior cruciate ligament (ACL) injury causes a significantly decreased activity level over a long period, making it an ideal model for studying effects of deconditioning and reconditioning. Therefore, the aim of this study was to investigate how cardiac dimensions and maximal exercise capacity change after an ACL-injury. METHOD: Seventeen athletes (5 women) were included. Cardiac magnetic resonance (CMR) was performed within 5 days of the injury (CMR1), before endurance training was resumed (CMR2) and 6 months after the second scan (CMR3). Maximal exercise testing was performed on the same day as CMR2 and 3. RESULTS: The deconditioning phase between CMR1 and CMR2 was 59 ± 28 days. Total heart volume (THV) decreased with -3·1 ± 6·7%, P = 0·056. Between CMR2 and 3 (reconditioning), THV increased significantly (2·5 ± 4·6%, P<0·05). Left and right ventricular EDV decreased during deconditioning (-3·0 ± 5·6% and -4·7 ± 6·6%) and increased during reconditioning (1·7 ± 3·9% and 2·6 ± 6·2%) however not statistically significant. Left ventricular mass (LVM) remained unchanged. VO2 peak (mlmin(-1) kg(-1) ) increased significantly during the reconditioning phase (6·1 ± 5·3%, P<0·001). CONCLUSION: Physiological cardiac adaptation to deconditioning and reconditioning caused by severe knee injury with maintained normal daily living during convalescence was smaller than previously shown in bed rest studies. Total heart volume and VO2 peak were significantly affected by reconditioning whilst LVEDV, RVEDV and LVM remained unchanged over the study period. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Clinical Physiology and Functional Imaging
volume
33
issue
6
pages
423 - 430
publisher
John Wiley & Sons Inc.
external identifiers
  • wos:000325145600003
  • pmid:23701425
  • scopus:84884981502
  • pmid:23701425
ISSN
1475-0961
DOI
10.1111/cpf.12048
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Reconstructive Surgery (013240300), Department of Clinical Physiology (Lund) (013013000)
id
ae8e0b10-86b3-4a08-8ca9-30a498418946 (old id 3804227)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/23701425?dopt=Abstract
date added to LUP
2016-04-01 10:28:28
date last changed
2022-04-04 18:25:00
@article{ae8e0b10-86b3-4a08-8ca9-30a498418946,
  abstract     = {{BACKGROUND: Studies of cardiovascular deconditioning are primarily carried out after experimental bed rest. No previous study has followed the cardiovascular effects of decreased and resumed physical activity in athletes after acute physical injury and convalescence. Anterior cruciate ligament (ACL) injury causes a significantly decreased activity level over a long period, making it an ideal model for studying effects of deconditioning and reconditioning. Therefore, the aim of this study was to investigate how cardiac dimensions and maximal exercise capacity change after an ACL-injury. METHOD: Seventeen athletes (5 women) were included. Cardiac magnetic resonance (CMR) was performed within 5 days of the injury (CMR1), before endurance training was resumed (CMR2) and 6 months after the second scan (CMR3). Maximal exercise testing was performed on the same day as CMR2 and 3. RESULTS: The deconditioning phase between CMR1 and CMR2 was 59 ± 28 days. Total heart volume (THV) decreased with -3·1 ± 6·7%, P = 0·056. Between CMR2 and 3 (reconditioning), THV increased significantly (2·5 ± 4·6%, P&lt;0·05). Left and right ventricular EDV decreased during deconditioning (-3·0 ± 5·6% and -4·7 ± 6·6%) and increased during reconditioning (1·7 ± 3·9% and 2·6 ± 6·2%) however not statistically significant. Left ventricular mass (LVM) remained unchanged. VO2 peak (mlmin(-1) kg(-1) ) increased significantly during the reconditioning phase (6·1 ± 5·3%, P&lt;0·001). CONCLUSION: Physiological cardiac adaptation to deconditioning and reconditioning caused by severe knee injury with maintained normal daily living during convalescence was smaller than previously shown in bed rest studies. Total heart volume and VO2 peak were significantly affected by reconditioning whilst LVEDV, RVEDV and LVM remained unchanged over the study period.}},
  author       = {{Steding Ehrenborg, Katarina and Hedén, Bo and Herbertsson, Pär and Arheden, Håkan}},
  issn         = {{1475-0961}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{423--430}},
  publisher    = {{John Wiley & Sons Inc.}},
  series       = {{Clinical Physiology and Functional Imaging}},
  title        = {{A longitudinal study on cardiac effects of deconditioning and physical reconditioning using the anterior cruciate ligament injury as a model.}},
  url          = {{http://dx.doi.org/10.1111/cpf.12048}},
  doi          = {{10.1111/cpf.12048}},
  volume       = {{33}},
  year         = {{2013}},
}