Regulation of skeletal muscle glycogen phosphorylase and PDH at varying exercise power outputs

Abstract

This study investigated the transformational and posttransformational control of skeletal muscle glycogen phosphorylase and pyruvate dehydrogenase (PDH) at three exercise power outputs [35, 65, and 90% of maximal oxygen uptake (V˙o 2 max)]. Seven untrained subjects cycled at one power output for 10 min on three separate occasions, with muscle biopsies at rest and 1 and 10 min of exercise. Glycogen phosphorylase in the more active ( a) form was not significantly different at any time across power outputs (21.4–29.6%), with the exception of 90%, where it fell significantly to 15.3% at 10 min. PDH transformation increased significantly from rest (average 0.53 mmol ⋅ kg wet muscle−1 ⋅ min−1) to 1 min of exercise as a function of power output (1.60 ± 0.26, 2.77 ± 0.29, and 3.33 ± 0.31 mmol ⋅ kg wet muscle−1 ⋅ min−1at 35, 65, and 90%, respectively) with a further significant increase at 10 min (4.45 ± 0.35) at 90%V˙o 2 max. Muscle lactate, acetyl-CoA, acetylcarnitine, and free ADP, AMP, and Pi were unchanged from rest at 35% V˙o 2 max but rose significantly at 65 and 90%, with accumulations at 90% being significantly higher than 65%. The results of this study indicate that glycogen phosphorylase transformation is independent of increasing power outputs, despite increasing glycogenolytic flux, suggesting that flux through glycogen phosphorylase is matched to the demand for energy by posttransformational factors, such as free Pi and AMP. Conversely, PDH transformation is directly related to the increasing power output and the calculated flux through the enzyme. The rise in PDH transformation is likely due to increased Ca2+concentration and/or increased pyruvate. These results demonstrate that metabolic signals related to contraction and the energy state of the cell are sensitive to the exercise intensity and coordinate the increase in carbohydrate use with increasing power output.

Influence of dietary fatty acid composition and exercise on changes in fat oxidation from a high-fat diet

“…Although the mechanisms of how exercise increases fat oxidation were not examined in this study, other researchers have demonstrated metabolic changes that occur with exercise treatment. Both enzyme levels and gene expression of enzymes that increase fat oxidation in skeletal muscle, such as lipoprotein lipase, triglyceride lipase, CPT-1, mitochondrial number, PDH kinase, fatty acid translocase/CD36, and fatty acid binding protein in the plasma membrane, have all been shown to increase with exercise (7,9,10,20,32).…”

Exercise diminishes the activity of acetyl-CoA carboxylase in human muscle.

“…However, given that during high-intensity exercise malonylCoA concentration and ACC activity are at their nadir, it seems likely that factors other than changes in ACC activity and malonyl-CoA concentration must be involved for the shift in fuel utilization during intense exercise. These factors could include the following: 1) increased activation of glucose transport (30,31) and key enzymes of glycolysis (31), glycogenolysis (31,32), and glucose oxidation (e.g., pyruvate dehydrogenase) (32,33); 2) a reduction in the concentrations of carnitine, CoASH, or palmitoyl-CoA (33,34) and substrates that are necessary for fatty acid oxidation; and 3) inhibition of 3-ketoacyl-CoA thiolase, an enzyme involved in the ␤-oxidation of fatty acids (34). Another factor could be the shift from the use of type 1 to type 2b muscle fibers, which are more glycolytic and have a lower capacity for fatty acid oxidation during very intense exercise.…”

Glucose Turn Point as a Marker of Exercise Intensity in Elite Swimmers

“…The demand of increased intensity may see a proportional reduction in uptake of circulating glucose while the stimulus for glucose perfusion is not diminished (seen by a continual rise in hepatic glucose output). This would be supported by [22], who noted a significant increase in the use of muscle glycogen created by fast oxidative/glycolytic fibre recruitment. The critical switch point between circulating glucose and muscle glycogen use may be the Gt.…”

“…The rise in blood glucose observed with increasing exercise intensity may be the result of the increased percentage of muscle fibres recruited, and or the type of fibers recruited. An increase in the use of oxidative-glycolytic type II a [22] would increase the rate of glycolysis in the working muscle. This may also be linked to an increased rate of glucose oxidation prior to the rise in blood glucose.…”