Deleteriuos effects of immobilization
upon rat skeletal muscle: role of creatine supplementation
M.S. Aoki, W.P. Lima, E.H. Miyabara, C.H.A. Gouveia, A.S. Moriscot – Brazil
Clinicial Nutrition, 2004; 23:1176-1183
Summary Aim: The aim of the study was to investigate the impact of creatine feeding (5 g kg1 body weight day1) upon the deleterious adaptations in skeletal muscle induced by immobilization. Methods: Male Wistar rats were submitted to hind limb immobilization together with three dietary manipulations: control, supplemented with creatine for 7 days (along with immobilization) and supplemented with creatine for 14 days (7 days before immobilization and together with immobilization). Muscle weight (wet/dry) was determined in the soleus (SOL) and gastrocnemius (GAS). The analysis of lean mass was performed by DEXA and myosin heavy chain (MHC) distribution by SDSPAGE. Results: After 14 days of creatine loading, immobilized SOL and GAS total creatine content were increased by 25% and 18%, respectively. Regardless of dietary manipulation, the immobilization protocol induced a decrease in the weight of SOL and GAS (Po0.001). However, creatine feeding for 14 days minimized mass loss in the SOL and GAS (Po0.05). Our findings also indicate that creatine supplementation maximizes the expected slow-to-fast MHC shift driven by immobilization (Po0.05). Conclusions: Previous creatine supplementation attenuates muscle wasting induced by immobilization. This effect is associated with the increment of intramuscular creatine content.
CAPON expression in skeletal muscle is regulated by position, repair, NOS activity, and dystrophy
Laurent Ségalat, Karine Grisoni, Jonathan Archer, Cinthya
Vargas, Anne Bertrand and Judy E. Anderson - France and Canada
Experimental Cell
Research, 2005;302(2):170-179
Abstract
In skeletal muscle, the localization of nNOS is destabilized
in the absence of dystrophin, which impacts muscle function and satellite cell activation.
In neurons, the adaptor protein, carboxy-terminal PDZ ligand of nNOS (CAPON),
regulates the distribution of neuronal nitric oxide synthase (nNOS), which
produces the key signaling molecule nitric oxide (NO). While a CAPON-like gene
is known to compensate functionally for a dystrophic phenotype in muscle of Caenorhabditis
elegans, CAPON expression has not been reported for mammalian muscle. Here,
CAPON expression was identified in mouse muscle using Northern and Western
blotting and in situ hybridization in combination with immunostaining for
laminin. CAPON RNA was expressed in developing normal and dystrophic muscles
near fiber junctions with tendons, and levels increased from 1 to 3 weeks. In
regenerating normal muscle and also in dystrophic muscles in the mdx mouse,
CAPON transcripts were prominent in satellite cells and new myotubes. Expression
of CAPON RNA increased in diaphragm muscle of normal and mdx mice after
treatment with L-arginine, the NOS substrate. Both CAPON and utrophin protein
levels increased in dystrophic quadriceps muscle after treatment with the steroid
deflazacort plus L-arginine, known to reduce the dystrophic phenotype. The
identification of CAPON transcripts and protein in mammalian muscle and
responses to L-arginine suggest CAPON may have a functional role in stabilizing
neuronal NOS in skeletal muscle in the cytoskeletal complex associated with
dystrophin/utrophin, with possible applications to therapy for human muscular
dystrophy.
Mivacurium in Children with Duchenne’s
Muscular Dystrophy: A Comparison of Onset and Duration of Neuromuscular Block
with Children without Neuromuscular Diseases
Joachim Schmidt, Tino Munster, Stefanie Wick, Hubert J. Schmitt – Germany
Abstract presented on Annual American Society of Anesthesiologists, October 2004
Introduction: Duchenne’s muscular
dystrophy (DMD), an x-linked recessive disorder, is the most common myopathy
seen in the pediatric population. Children afflicted with this disease may
require anesthesia for muscle biopsy or orthopedic surgery. Of primary concern
in children with this disorder is the choice of the neuromuscular blocking
agent. Pharmacodynamic data of non-depolarising neuromuscular blocking agents
are scarce 1, 2. Succinylcholine is not
recommended due to its adverse side effects. Investigation in DMD children with
advanced disease state showed prolonged recovery after a standard dosage of
rocuronium 2. The aim of this study was to
compare the response to 0,2 mg/kg mivacurium in children with DMD and children without
neuromuscular diseases (control-group).
Discussion: The results of the present
study demonstrate that the recovery of neuromuscular block following a standard
dosage of 0,2 mg/kg mivacurium is significantly prolonged in children with DMD
compared to controls. Our results confirm a retrospective study where an
increased sensitivity to mivacurium in children with DMD was suggested 4. We therefore recommend the monitoring of the
neuromuscular function if mivacurium is used in children with DMD.