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Skeletal muscle energy substrates, metabolic products and enzyme activity in infants with symptomatic ventricular
K H Lundell1, B O Eriksson, K G Sabel
1Department of Paediatrics, Central Hospital of Jönköping, Sweden.
Insights
Infants with symptomatic ventricular septal defect (VSD) show reduced ATP and glucose 6-phosphate in skeletal muscle, suggesting low metabolic activity. This may stem from undernourishment or reduced blood flow.
Area of Science:
- Cardiology
- Pediatric Cardiology
- Muscle Physiology
Background:
- Symptomatic ventricular septal defect (VSD) can impact systemic circulation and nutrient delivery.
- Skeletal muscle metabolism in infants with VSD is not well understood.
Purpose of the Study:
- To investigate skeletal muscle energy substrates, metabolic products, and enzyme activity in infants with symptomatic VSD.
- To compare muscle metabolism between infants with VSD and healthy controls.
Main Methods:
- Muscle biopsies were analyzed from 26 infants with symptomatic VSD and 10 healthy infants.
- Measurements included muscle energy substrates, metabolic products, enzyme activity, fibre types, and fibre sizes.
Main Results:
- Infants with VSD had significantly lower ATP and glucose 6-phosphate levels compared to controls.
- Lactate dehydrogenase (LD) activity was lower in the VSD group; other enzyme activities were comparable.
- No correlation was found between muscle substrate levels/enzyme activity and the severity of heart failure within the VSD group.
Conclusions:
- Reduced ATP and glucose 6-phosphate in VSD infants suggest decreased skeletal muscle metabolic activity.
- Low energy levels are likely due to undernourishment and/or reduced blood flow to skeletal muscle.
- The absence of other metabolic discrepancies indicates relatively normal motor activity in these infants.
Abstract:
Muscle biopsy studies were performed on 26 infants with symptomatic ventricular septal defect (VSD) (mean age 4.7 months) and 10 healthy infants (mean age 7.8 months). Analyses were made of muscle energy substrates, metabolic products, muscle enzyme activity, fibre types and fibre sizes. Relatively few differences were noted between the groups. The most important difference was a reduced ATP level in the VSD group. Glucose 6-phosphate concentrations were also lower in the VSD group. These differences could indicate a low metabolic activity in skeletal muscle in infants with heart failure. Most muscle enzyme activity was comparable with the exception of lactate dehydrogenase (LD), which was lower in the VSD group. Within the VSD group, no differences were revealed in muscle substrate concentrations for muscle enzyme activity in terms of the degree of heart failure. We conclude that low energy levels are probably explained by undernourishment and/or reduced blood flow to skeletal muscle and that the lack of other discrepancies in muscle metabolism indicates a desirable relatively normal motor activity in these infants with symptomatic VSD.