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Effects of training on biochemical and functional properties of rodent neonatal heart
Insights
Neonatal rat endurance training enhanced maximal exercise capacity and heart mass. Despite reduced cardiac ATPase activity, trained rats maintained left ventricular function during exercise, suggesting an energy-saving adaptation.
Area of Science:
- Cardiovascular Physiology
- Exercise Physiology
- Neonatal Adaptation
Background:
- Understanding cardiac adaptations to exercise in early life is crucial for long-term cardiovascular health.
- Neonatal development presents unique physiological challenges and opportunities for adaptation.
Purpose of the Study:
- To investigate the biochemical and functional adaptations of the neonatal rat heart to endurance running.
- To determine if enhanced exercise capacity can be achieved with altered cardiac energy metabolism.
Main Methods:
- Progressive treadmill training of 10-day-old rats until 75 days of age.
- Measurement of heart mass, skeletal muscle citrate synthase activity, and maximal oxygen uptake.
- Assessment of cardiac myosin and myofibril ATPase activity and myosin isozyme profiles.
- In vivo assessment of left ventricular function during submaximal exercise using fluid-filled cannulas.
Main Results:
- Endurance training increased relative heart mass, skeletal muscle citrate synthase activity, and maximal oxygen uptake.
- Cardiac myosin and myofibril ATPase activities were reduced in trained rats.
- A shift in myosin isozyme profile towards the V3 (low ATPase) isozyme was observed in trained hearts.
- Trained rats maintained left ventricular systolic pressure and systemic arterial pressure during submaximal exercise with a lower heart rate.
Conclusions:
- Neonatal endurance training enhances maximal exercise capacity in rats.
- Cardiac adaptations include reduced ATPase activity and a shift towards lower-energy-consuming myosin isozymes.
- These adaptations allow for maintained cardiac performance during exercise while potentially economizing energy expenditure.
Abstract:
This study was undertaken to determine biochemical and functional (in vivo) adaptations of the rodent neonatal heart in response to a training program of endurance running. Ten day-old rats were progressively trained on a treadmill (final intensity, 21 m/min, 30% grade, 1 h/day) until 75 days of age. The training program induced 14, 57, and 24% increases in relative heart mass, skeletal muscle citrate synthase activity, and whole-body maximal O2 uptake, respectively (P less than 0.05). Cardiac myosin (ATPase) and Ca2+-regulated myofibril ATPase were both reduced by approximately 15% in trained vs. sedentary animals (P less than 0.05). In the majority of trained hearts examined, the myosin isozyme profile reflected an estimated 14 +/- 3% shift toward the V3 or low ATPase isozyme. Left ventricular functional indices during submaximal exercise, derived from a fluid-filled indwelling cannula, indicated that the trained animals maintained similar left ventricular (LV) systolic pressure, LV + the time derivative of pressure, and systemic arterial mean blood pressure compared with their sedentary counterparts. These functional parameters were maintained even though the trained animals performed with lower submaximal exercise heart rate. These findings suggest that maximal exercise capacity can be enhanced in neonatal rats even though the biochemical potential for ATP degradation in the cardiac contractile system is lowered. We speculate that the trend to maintain the myosin isozyme pattern further in the direction of the V3 isozyme in the trained neonatal rat heart may reflect a means to economize cross-bridge cycling while maintaining normal levels of ventricle performance at a given submaximal work load.