Integration/regulation of fuel use during exercise Flashcards
What factors is the balance between carbohydrate and lipid oxidation during exercise dependent on?
Nutritional status/diet, exercise intensity (above or below LT), exercise duration, continuous vs. intermittent exercise, state of training, circulating catecholamines and other hormones, pharmacological interventions.
What does the arterial FFA concentration reflect?
A balance between FFA appearance (from adipose tissue) and FFA disappearance (uptake by active muscle).
How can FFA oxidation rate be estimated?
Using RER or a known infusion rate of labelled FFA (more accurate)
What is the ATP yield from the 16-carbon palmitate?
106 ATP
How can carbohydrate oxidation rate be estimated?
Repeated muscle biopsies for glycogen content.
Describe how the first estimate of carbohydrate oxidation rate was carried out?
Two subjects, sat side by side next to a cycle ergometer and pedalled one crank each until they could no longer. Took biopsied from both legs and compared the glycogen content. Exercised leg had no glycogen, a depleted source or energy and the non-exercised leg was essentially unaltered.
In the days that followed the carbohydrate oxidation rate estimate what happened to the glycogen stores in each leg?
The exercised leg showed an increase far above the resting level.
What is muscle glycogen stores described as after nutritional interventions where classically tested?
Finite and wanes at about 2-3 hours exercise at or close to lactate threshold.
What does altering the lipid intake in the days prior to exercise do?
Has less of an influence on substrate selection.
What may influence lipid and carbohydrate oxidation rates during exercise?
Raising plasma FFA by increasing muscle fat storage.
Give the theories that are suggested to determine the rate of carbohydrate and lipid metabolism?
Glucose fatty acid cycle mediated control of PFK activity via [citrate], Phosphate-mediated regulation of glycogen phosphorylase activity, redox potential ([NADH]/[NAD+]) mediated control or PHD activity, [malonyl-coA] mediated regulation of carnitine acyltranferase 1 activity, carnitine availiability for mitochondrial fatty acyl CoA transport.
Describe glucose fatty acid mediated control of PFK activity via [citrate]?
↑ FFA availability, ↓ carbohydrate metabolism, ↑ acetyl-coA, ↑ citrate, ↑ G6P.
↑ [acetyl-coA] is inhibitory of PDH by activating PDH kinase.
↑ [citrate] once in the cytosol, is inhibitory of PFK.
↑ [G6P] inhibits hexokinase.
↑ FFA availability has been suggested to promote beta-oxidation and carbohydrate oxidation.
Describe phosphate-mediated regulation of glycogen phosphorylase activity?
↑ plasma [FFA] has no major effect on blood [glucose], ↑ in FFA availability ↓ glycogen utilisation by up to 50% during exercise at 80 % VO2max, but no effect on citrate, G6P or PDH activity. ADP and AMP were ↓during the 30 mins of heavy or very-heavy exercise which lessons the activity of GP and slows glycolysis.
Describe the redox potential mediated control of PHD activity?
↓cytosolic of [ADP, AMP, Pi] are seen with↑fat provisions. ↓phosphate feedback to the mitochondrion during exercise implicates a↑NADH- delivery to maintain the same flux for oxidative phosphorylation.↑matrix [NADH] inhibits PDH activation. Experimental support is weak.
Describe [malonyl-coA] mediated regulation of CAT1 activity?
During↑intensity exercise, acidosis inhibits lipoprotein lipase, pyruvate accumulates and the TCA cycle is activates, citrate accumulates and acts as a positive allosteric effector of acetyl CoA carboxylase b that together with malonyl-CoA decarboxylase regulates [malony-CoA]. When flux through glycolysis is↑[malonyl-coA] accumulates and inhibits CPT1 which is required for FFA entry into the mitochondria.
