Details
| Original language | English |
|---|---|
| Pages (from-to) | 364-373 |
| Number of pages | 10 |
| Journal | Pediatric Exercise Science |
| Volume | 28 |
| Issue number | 3 |
| Publication status | Published - Aug 2016 |
Abstract
Purpose: Defects in the gene encoding the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) cause CF. Absence of the CFTR may result in skeletal muscle dysfunction. Here, we tested skeletal muscle function in male adolescent patients with CF. Methods: Ten CF and 10 control participants (age: 16.8 ± 0.6 years) performed 7 repetitive sets of maximum voluntary contractions (MVCs) and underwent an isometric fatigue test of the knee extensors. Electromyography (EMG) activity was recorded from the m. vastus lateralis (VL) and m. vastus medialis (VM). Results: In CF, the MVC torque was lower and correlated with the predicted forced expiratory volume in one second (r = .73, p = .012, n = 10). The M-wave in the VL was shorter in CF than in controls (18.6 ± 0.5 vs. 20.3 ± 0.5 ms, p < .028). In the VM, both the M-wave (4.96 ± 0.61 vs. 7.97 ± 0.60 mV, p = .001) and the EMG (0.29 ± 0.04 vs. 0.47 ± 0.04 mV, p = .004) amplitudes were smaller in CF. Conclusion: The differences in the VL and VM EMG signals between the groups indicate that the lower MVC torque in CF did not result from the direct impact of a CFTR defect on the sarcolemmal excitability; the differences more likely resulted from the less developed musculature in the patients with CF.
ASJC Scopus subject areas
- Medicine(all)
- Pediatrics, Perinatology, and Child Health
- Medicine(all)
- Orthopedics and Sports Medicine
- Health Professions(all)
- Physical Therapy, Sports Therapy and Rehabilitation
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In: Pediatric Exercise Science, Vol. 28, No. 3, 08.2016, p. 364-373.
Research output: Contribution to journal › Article › Research › peer review
}
TY - JOUR
T1 - Skeletal muscle function in young patients with cystic fibrosis
AU - Stein, Lothar
AU - Pacht, Constanze
AU - Junge, Sibylle
AU - Kaeding, Tobias S.
AU - Kück, Momme
AU - Maassen, Norbert
AU - Wittke, Torge
AU - Shushakov, Vladimir
N1 - Publisher Copyright: © 2016 Human Kinetics, Inc.
PY - 2016/8
Y1 - 2016/8
N2 - Purpose: Defects in the gene encoding the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) cause CF. Absence of the CFTR may result in skeletal muscle dysfunction. Here, we tested skeletal muscle function in male adolescent patients with CF. Methods: Ten CF and 10 control participants (age: 16.8 ± 0.6 years) performed 7 repetitive sets of maximum voluntary contractions (MVCs) and underwent an isometric fatigue test of the knee extensors. Electromyography (EMG) activity was recorded from the m. vastus lateralis (VL) and m. vastus medialis (VM). Results: In CF, the MVC torque was lower and correlated with the predicted forced expiratory volume in one second (r = .73, p = .012, n = 10). The M-wave in the VL was shorter in CF than in controls (18.6 ± 0.5 vs. 20.3 ± 0.5 ms, p < .028). In the VM, both the M-wave (4.96 ± 0.61 vs. 7.97 ± 0.60 mV, p = .001) and the EMG (0.29 ± 0.04 vs. 0.47 ± 0.04 mV, p = .004) amplitudes were smaller in CF. Conclusion: The differences in the VL and VM EMG signals between the groups indicate that the lower MVC torque in CF did not result from the direct impact of a CFTR defect on the sarcolemmal excitability; the differences more likely resulted from the less developed musculature in the patients with CF.
AB - Purpose: Defects in the gene encoding the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) cause CF. Absence of the CFTR may result in skeletal muscle dysfunction. Here, we tested skeletal muscle function in male adolescent patients with CF. Methods: Ten CF and 10 control participants (age: 16.8 ± 0.6 years) performed 7 repetitive sets of maximum voluntary contractions (MVCs) and underwent an isometric fatigue test of the knee extensors. Electromyography (EMG) activity was recorded from the m. vastus lateralis (VL) and m. vastus medialis (VM). Results: In CF, the MVC torque was lower and correlated with the predicted forced expiratory volume in one second (r = .73, p = .012, n = 10). The M-wave in the VL was shorter in CF than in controls (18.6 ± 0.5 vs. 20.3 ± 0.5 ms, p < .028). In the VM, both the M-wave (4.96 ± 0.61 vs. 7.97 ± 0.60 mV, p = .001) and the EMG (0.29 ± 0.04 vs. 0.47 ± 0.04 mV, p = .004) amplitudes were smaller in CF. Conclusion: The differences in the VL and VM EMG signals between the groups indicate that the lower MVC torque in CF did not result from the direct impact of a CFTR defect on the sarcolemmal excitability; the differences more likely resulted from the less developed musculature in the patients with CF.
UR - http://www.scopus.com/inward/record.url?scp=84979680187&partnerID=8YFLogxK
U2 - 10.1123/pes.2015-0184
DO - 10.1123/pes.2015-0184
M3 - Article
C2 - 27045385
AN - SCOPUS:84979680187
VL - 28
SP - 364
EP - 373
JO - Pediatric Exercise Science
JF - Pediatric Exercise Science
SN - 0899-8493
IS - 3
ER -