Abstract
Muscle malonyl-CoA has been postulated to regulate fatty acid metabolism by inhibiting carnitine palmitoyltransferase 1. In nontrained rats, malonyl-CoA decreases in working muscle during exercise. Endurance training is known to increase a muscle's reliance on fatty acids as a substrate. This study was designed to investigate whether the decline in malonyl-CoA with exercise would be greater in trained than in nontrained muscle, thereby allowing increased fatty acid oxidation. After 6-10 wk of endurance training (2 h/day) or treadmill habituation (5-10 min/day), rats were killed at rest or after running up a 15% grade at 21 m/min for 5, 20, or 60 min. Training attenuated the exercise-induced drop in malonyl-CoA and prevented the exercise-induced increase in the constant for citrate activation of acetyl-CoA carboxylase in the red quadriceps muscle of rats run for 20 and 60 min. Hence, contrary to expectations, the decrease in malonyl-CoA was less in trained than in nontrained muscle during a single bout of prolonged submaximal exercise.
Highlights
In light of malonyl-CoA’s proposed importance in regulating muscle fatty acid metabolism, we hypothesized that the reduction in malonyl-CoA might be larger with exercise in trained than in nontrained muscle and that training might attenuate malonyl-CoA’s inhibition of carnitine palmitoyltransferase 1 (CPT 1), thereby allowing increased fatty acid oxidation
This experiment was designed to investigate the malonylCoA response to exercise in endurance-trained rats vs. nontrained rats and to determine whether the kinetic properties of muscle acetyl-CoA carboxylase (ACC) are influenced by the training
If data from a ‘‘trained’’ rat were discarded for this reason, data from the paired nontrained rat killed at the same time point were eliminated
Summary
In light of malonyl-CoA’s proposed importance in regulating muscle fatty acid metabolism, we hypothesized that the reduction in malonyl-CoA might be larger with exercise in trained than in nontrained muscle and that training might attenuate malonyl-CoA’s inhibition of CPT 1, thereby allowing increased fatty acid oxidation. This experiment was designed to investigate the malonylCoA response to exercise in endurance-trained rats vs nontrained rats and to determine whether the kinetic properties of muscle ACC are influenced by the training
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