Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Neurology |
| Vol/bind | 72 |
| Udgave nummer | 4 |
| Sider (fra-til) | 317-23 |
| Antal sider | 6 |
| ISSN | 0028-3878 |
| DOI | |
| Status | Udgivet - 2009 |
Bibliografisk note
Keywords: Activities of Daily Living; Bulbo-Spinal Atrophy, X-Linked; Exercise; Exercise Therapy; Female; Humans; Male; Middle Aged; Muscular Atrophy, Spinal; Oxygen ConsumptionAdgang til dokumentet
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Effect of aerobic training in patients with spinal and bulbar muscular atrophy (Kennedy disease). / Preisler, N; Andersen, G; Thøgersen, F; Crone, C; Jeppesen, T D; Wibrand, F; Vissing, J.
I: Neurology, Bind 72, Nr. 4, 2009, s. 317-23.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Effect of aerobic training in patients with spinal and bulbar muscular atrophy (Kennedy disease)
AU - Preisler, N
AU - Andersen, G
AU - Thøgersen, F
AU - Crone, C
AU - Jeppesen, T D
AU - Wibrand, F
AU - Vissing, J
N1 - Keywords: Activities of Daily Living; Bulbo-Spinal Atrophy, X-Linked; Exercise; Exercise Therapy; Female; Humans; Male; Middle Aged; Muscular Atrophy, Spinal; Oxygen Consumption
PY - 2009
Y1 - 2009
N2 - OBJECTIVE: We examined the effect of aerobic exercise in patients with spinal and bulbar muscular atrophy (SBMA). SBMA is caused by a defect androgen receptor. This defect causes motor neuron death, but considering the important function of androgens in muscle, it is possible that muscle damage in SBMA also occurs independently of motor neuron damage. METHODS: Eight patients with SBMA engaged in regular cycling exercise for 12 weeks. Maximum oxygen uptake (Vo(2max)), maximal work capacity (W(max)), muscle morphology, citrate synthase (CS) activity, body composition, EMG, static strength measurements, lung function, plasma proteins, and hormones were evaluated before and after training. Evaluation of improvements in activities of daily living (ADL) was conducted after training. RESULTS: W(max) increased by 18%, and CS activity increased by 35%. There was no significant change in Vo(2max) or any of the other variables examined before and after training, and the patients with SBMA did not feel improvements in ADL. CONCLUSIONS: Frequent, moderate-intensity aerobic conditioning is of little beneficial effect in patients with spinal and bulbar muscular atrophy (SBMA). High levels of plasma creatine kinase and muscle regeneration indicate a primary myopathic affection, which, in parallel with the motor neuron deficiency, may attenuate the response to exercise training in patients with SBMA.
AB - OBJECTIVE: We examined the effect of aerobic exercise in patients with spinal and bulbar muscular atrophy (SBMA). SBMA is caused by a defect androgen receptor. This defect causes motor neuron death, but considering the important function of androgens in muscle, it is possible that muscle damage in SBMA also occurs independently of motor neuron damage. METHODS: Eight patients with SBMA engaged in regular cycling exercise for 12 weeks. Maximum oxygen uptake (Vo(2max)), maximal work capacity (W(max)), muscle morphology, citrate synthase (CS) activity, body composition, EMG, static strength measurements, lung function, plasma proteins, and hormones were evaluated before and after training. Evaluation of improvements in activities of daily living (ADL) was conducted after training. RESULTS: W(max) increased by 18%, and CS activity increased by 35%. There was no significant change in Vo(2max) or any of the other variables examined before and after training, and the patients with SBMA did not feel improvements in ADL. CONCLUSIONS: Frequent, moderate-intensity aerobic conditioning is of little beneficial effect in patients with spinal and bulbar muscular atrophy (SBMA). High levels of plasma creatine kinase and muscle regeneration indicate a primary myopathic affection, which, in parallel with the motor neuron deficiency, may attenuate the response to exercise training in patients with SBMA.
U2 - 10.1212/01.wnl.0000341274.61236.02
DO - 10.1212/01.wnl.0000341274.61236.02
M3 - Journal article
C2 - 19171827
VL - 72
SP - 317
EP - 323
JO - Neurology
JF - Neurology
SN - 0028-3878
IS - 4
ER -