498-P: Resistance Exercise Rapidly Alters Citric Acid Cycle and Amino Acid Metabolism in Skeletal Muscle

Abstract

Muscle glucose metabolism is improved by either aerobic or resistance exercise (RE) training, but the mechanisms leading to improved metabolism for each of these exercise modes are not identical. Much work has been done onimproved oxidative metabolism by aerobic exercise, but far less is known about how RE impacts fuel metabolism. Here, TCA and amino acid metabolites are measured in skeletal muscle after a single bout of RE. Twenty one healthy subjects performed a session of one-legged knee extension RE that consisted of 3 sets of 10 reps at 70% of their 1 rep max. Two muscle biopsies were obtained from the vastus lateralis of each leg. From the RE leg, biopsies were obtained ≤10min post-RE (0hr PEX) and approximately 1hr post-RE (1hr PEX), respectively. From the non-RE leg, biopsies were obtained before and 1hr PEX, respectively. Muscle samples were frozen and stored until mass spectrometry analysis of metabolites was performed. A 2-fold increase in plasma lactate (P<0.05) and a 30-40% increase in muscle glycolytic enzyme activity (P<0.05) at 0hr PEX suggest increased activation of the glycolytic pathway. Also at 0hr PEX, TCA metabolites citrate and isocitrate were increased (P<0.05) compared to the pre-RE biopsy (0.35 and 0.01 mmol/μg, respectively). Further, multiple amino acid metabolites Arg, Asn, Lys, Thr, and Val were increased (P<0.05) in the REmuscle at 0hr PEX. These amino acids can enter the TCA cycle at various steps, indicating increased flux through the TCA cycle immediately after RE. By 1hr PEX, TCA intermediates malate and fumarate were reduced (P<0.05)compared to the non-RE leg (-0.65 and -0.35 mmol/μg, respectively), and multiple amino acid metabolites were also reduced (P<0.05). The decrease in these metabolites at 1hr PEX suggests increased use of metabolites for mitochondrial respiration. These results suggest activation of glycolytic and amino metabolism pathways, contributing to citric acid flux immediately following RE in order to meet energy needs in skeletal muscle. Disclosure M. W. Pataky: None. A. Prabha kumar: None. K. Klaus: None. K. Nair: None. Funding National Institutes of Health (R01AG062859)