Carbohydrate ingestion prior to exercise augments the exercise-induced activation of the pyruvate dehydrogenase complex in human skeletal muscle

Abstract

During the transition from rest to steady-state exercise, a significant part of the energy necessary to sustain force generation is derived from PCr hydrolysis and glycogenolysis. Classically, the extent of this anaerobic ATP production through substrate level phosphorylation at the onset of exercise has been attributed to a lag in blood flow and oxygen delivery to the contracting muscle (Margaria et al. 1963). More recently, however, it has been demonstrated that the activity of PDC and the availability of acetyl groups to the tricarboxylic acid (TCA) cycle are important determinants of the metabolic responses during the onset of exercise (Timmons et al. 1997(Timmons et al. , 1998. The PDC controls the rate-limiting step in CHO oxidation, the oxidative decarboxylation of pyruvate to acetyl-CoA. The activity of PDC increases during exercise (Constantin-Teodosiu et al. 1992), resulting in an increase in pyruvate flux, the formation of acetyl-CoA and a concomitant increase in CHO oxidation. When the rate of acetyl-CoA formation by the PDC exceeds its rate of oxidation by the TCA cycle, the excess acetyl-CoA is buffered by carnitine, resulting in the formation of acetylcarnitine (Constantin-Teodosiu et al. 1992). However, at the onset of exercise there is a delay in the activation of PDC and provision of acetyl groups to the TCA cycle which seems to be responsible for the increased contribution of substrate level phosphorylation to energy metabolism (Timmons et al. 1997;Howlett et al. 1999). Both hyperglycaemia and hyperinsulinaemia increase the activity of PDC in resting human skeletal muscle (Mandarino et al. 1987(Mandarino et al. , 1993. Therefore, CHO-mediated increases in blood glucose and insulin concentrations may also result in a faster rate of PDC activation, which in turn would increase the provision of substrate (i.e. acetyl groups) for use by the TCA cycle, at the onset of exercise. This could then lead to a faster onset of oxidative ATP production and a reduction in This study examined the effect of pre-exercise carbohydrate (CHO) ingestion on pyruvate dehydrogenase complex (PDC) activation, acetyl group availability and substrate level phosphorylation (glycogenolysis and phosphocreatine (PCr) hydrolysis) in human skeletal muscle during the transition from rest to steady-state exercise. Seven male subjects performed two 10 min treadmill runs at 70% maximum oxygen uptake (ýOµ,max), 1 week apart. Each subject ingested 8 ml (kg body mass (BM))¢ of either a placebo solution (CON trial) or a 5.5% CHO solution (CHO trial) 10 min before each run. Muscle biopsy samples were obtained from the vastus lateralis at rest and immediately after each trial. Muscle PDC activity was higher at the end of exercise in the CHO trial compared with the CON trial (1.78 ± 0.18 and 1.27 ± 0.16 mmol min¢ (kg wet matter (WM))¢, respectively; P < 0.05) and this was accompanied by lower acetylcarnitine (7.1 ± 1.2 and 9.1 ± 1.1 mmol kg¢ (dry matter (DM))¢ in CHO and CON, respectively; P < 0.05) and citrate concentrations (0.73 ± 0....

Elevated Free Fatty Acids Attenuate the Insulin-Induced Suppression of PDK4 Gene Expression in Human Skeletal Muscle: Potential Role of Intramuscular Long-Chain Acyl-Coenzyme A

“…Five-to 10-mg frozen muscle was used to determine the active form of PDC (PDCa) (25). The time delay between sampling and freezing of the sample in liquid nitrogen (on average 10 -12 sec) was unlikely to have resulted in significant changes in PDC activity because the values obtained in the present study were comparable to values previously reported by our laboratory in which samples were snap frozen 2-3 sec after removal from the limb (26,27). LCACs and acetylcarnitine were determined enzymatically using RIAs (28).…”

Combined HIIT and Resistance Training in Very Long-Chain Acyl-CoA Dehydrogenase Deficiency: A Case Report

“…It is known that MCT can circumvent the block in the β-oxidation of long-chain fatty acids in VLCADD and can provide an alternative energy substrate to long-chain triglycerides (LCT) (Shiraev and Barclay, 2012), in addition to decreasing the oxidation of CHO, and reducing the risk of lactic acidosis induced by exercise (Behrend et al, 2012). Moreover, supplementation with CHO increases blood glucose levels and improves performance (Tsintzas et al, 2000). Accordingly, the role of this supplement was to (i) increase the work capacity during the test, (ii) maintain the glycemia level to reduce fat oxidation during recovery, and (iii) provide MCT for oxidation during the hours after assessment, thereby reducing the risk of post-exercise rhabdomyolysis (Diekman et al, 2016).…”

Preexercise Carbohydrate Feeding and High-Intensity Exercise Capacity: Effects of Timing of Intake and Carbohydrate Concentration

“…Pre-exercise elevation of blood glucose and insulin increases glucose uptake and oxidation in 66 contracting skeletal muscle (Febbraio et al, 2000a,b;Tsintzas et al, 2000) through activation of 67 the pyruvate dehydrogenase enzyme complex (PDC). It has also been shown that 68 pharmacological activation of PDC reduces phosphocreatine degradation and muscle lactate 69 accumulation during short intense muscle contraction protocols (Timmons et al, 1998 …”