Exercise with low muscle glycogen augments TCA cycle anaplerosis but impairs oxidative energy provision in humans.
We tested the hypotheses that: (i) exercise with low muscle glycogen would reduce pyruvate flux through the alanine aminotransferase (AAT) reaction and attenuate the increase in tricarboxylic acid (TCA) cycle intermediates, and (ii) attenuation of tricarboxylic acid cycle intermediate (TCAI) pool expansion would limit TCA cycle flux, thereby accelerating phosphocreatine (PCr) degradation. Eight men cycled for 10 min at 70 % of their (VO(2,max) on two occasions: (i) following their normal diet (CON) and (ii) after cycling to exhaustion and consuming a low carbohydrate diet for approximately 2 days (LG). Biopsies (m. vastus lateralis) confirmed that [glycogen] was lower in LG vs. CON at rest (257 +/- 18 vs. 611 +/- 54 mmol (kg dry mass)(-1); P 0.05); however, net glycogenolysis was not different after 1 or 10 min of exercise. PCr degradation from rest to 1 min was approximately 26 % higher in LG vs. CON (38 +/- 4 vs. 28 +/- 4 mmol (kg dry mass)(-1); P< or =0.05). The sum of five measured TCAIs (approximately 90 % of total pool) was not different between trials at rest and after 1 min, but was higher after 10 min in LG vs. CON (5.51 +/- 0.43 vs. 4.45 +/- 0.49 mmol (kg dry mass)(-1); P 0.05). Pyruvate dehydrogenase complex (PDC) activity was lower during exercise in LG vs. CON (2.2 +/- 0.2 vs. 1.4 +/- 0.2 mmol min(-1) (kg wet weight)(-1) after 10 min; P< or =0.05), and acetylcarnitine was approximately threefold less, implying increased pyruvate availability for flux through AAT. Resting muscle [glutamate] was higher in LG vs. CON (16.1 +/- 0.8 vs. 11.8 +/- 0.4 mmol (kg dry mass)(-1); P< or =0.05) and the net decrease in [glutamate] during exercise was approximately 30 % greater in LG vs. CON. These findings suggest that: (i) contrary to our hypotheses, LG increased anaplerosis by decreasing PDC flux and/or increasing the conversion of glutamate carbon to TCAIs, and (ii) accelerating the rate of muscle TCAI expansion did not affect oxidative energy provision during the initial phase of contraction, since changes in [TCAI] were not temporally related to PCr degradation.
Gibala
Martin J
MJ
Copenhagen Muscle Research Centre, Rigshospitalet Section 7652, DK-2200 Copenhagen, Denmark. gibalam@mcmaster.ca
Peirce
Nick
N
Constantin-Teodosiu
Dimitru
D
Greenhaff
Paul L
PL
D000328:Adult; D000409:Alanine / Q000378:metabolism; D000410:Alanine Transaminase / Q000378:metabolism; D002952:Citric Acid Cycle / Q000502:physiology*; D004734:Energy Metabolism; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D018698:Glutamic Acid / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D006801:Humans; D007700:Kinetics; D008168:Lung / Q000502:physiology; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism / Q000502:physiology*; D010101:Oxygen Consumption; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism; D015656:Respiratory Mechanics; D012146:Rest / Q000502:physiology*; D014233:Tricarboxylic Acids / Q000378:metabolism
D011768:Pyruvate Dehydrogenase Complex; D014233:Tricarboxylic Acids; D018698:Glutamic Acid; D006003:Glycogen; D000410:Alanine Transaminase; D000409:Alanine