Neuromuscular electrical stimulation improves GLUT-4 and morphological characteristics of skeletal muscle in rats with heart failure.
OBJECTIVE
Changes in skeletal muscle morphology and metabolism are associated with limited functional capacity in heart failure, which can be attenuated by neuromuscular electrical stimulation (ES). The purpose of the present study was to analyse the effects of ES upon GLUT-4 protein content, fibre structure and vessel density of the skeletal muscle in a rat model of HF subsequent to myocardial infarction.


METHODS
Forty-four male Wistar rats were assigned to one of four groups: sham (S), sham submitted to ES (S+ES), heart failure (HF) and heart failure submitted to ES (HF+ES). The rats in the ES groups were submitted to ES of the left leg during 20 days (2.5 kHz, once a day, 30 min, duty cycle 50%- 15 s contraction/15 s rest). After this period, the left tibialis anterior muscle was collected from all the rats for analysis.


RESULTS
HF+ES rats showed lower values of lung congestion when compared with HF rats (P = 0.0001). Although muscle weight was lower in HF rats than in the S group, thus indicating hypotrophy, 20 days of ES led to their recovery (P < 0.0001). In both groups submitted to ES, there was an increase in muscle vessel density (P < 0.04). Additionally, heart failure determined a 49% reduction in GLUT-4 protein content (P < 0.03), which was recovered by ES (P < 0.01).


CONCLUSIONS
In heart failure, ES improves morphological changes and raises GLUT-4 content in skeletal muscle.
de Leon
E B
EB
Laboratório de Fisiologia, UFCSPA, Rio Grande do Sul, Brazil.
Bortoluzzi
A
A
Rucatti
A
A
Nunes
R B
RB
Saur
L
L
Rodrigues
M
M
Oliveira
U
U
Alves-Wagner
A B
AB
Xavier
L L
LL
Machado
U F
UF
Schaan
B D
BD
Dall'Ago
P
P
D000818:Animals; D004599:Electric Stimulation Therapy; D051275:Glucose Transporter Type 4 / Q000378:metabolism*; D006333:Heart Failure / Q000150:complications* / Q000503:physiopathology; D006439:Hemodynamics; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D009135:Muscular Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D009203:Myocardial Infarction / Q000150:complications; D051381:Rats; D017208:Rats, Wistar
D051275:Glucose Transporter Type 4; C495694:Slc2a4 protein, rat