Leslie Boobis

Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man.

1. The recovery of power output and muscle metabolites was examined following maximal sprint cycling exercise. Fourteen male subjects performed two 30 s cycle ergometer sprints separated by 1.5, 3 and 6 min of recovery, on three separate occasions. On a fourth occasion eight of the subjects performed only one 30 s sprint and muscle biopsies were obtained during recovery. 2. At the end of the 30 s sprint phosphocreatine (PCr) and ATP contents were 19.7 +/‐ 1.2 and 70.5 +/‐ 6.5% of the resting values (rest), respectively, while muscle lactate was 119.0 +/‐ 4.6 mmol (kg dry wt)‐1 and muscle pH was 6.72 +/‐ 0.06. During recovery, PCr increased rapidly to 65.0 +/‐ 2.8% of rest after 1.5 min, but reached only 85.5 +/‐ 3.5% of rest after 6 min of recovery. At the same time ATP and muscle pH remained low (19.5 +/‐ 0.9 mmol (kg dry wt)‐1 and 6.79 +/‐ 0.02, respectively). Modelling of the individual PCr resynthesis using a power function curve gave an average half‐time for PCr resynthesis of 56.6 +/‐ 7.3 s. 3. Recovery of peak power output (PPO), peak pedal speed (maxSp) and mean power during the initial 6 s (MPO6) of sprint 2 did not reach the control values after 6 min of rest, and occurred in parallel with the resynthesis of PCr, despite the low muscle pH. High correlations (r = 0.71‐0.86; P < 0.05) were found between the percentage resynthesis of PCr and the percentage restoration of PPO, maxSp and MPO6 after 1.5 and 3 min of recovery. No relationship was observed between muscle pH recovery and power output restoration during sprint 2 (P > 0.05). 4. These data suggest that PCr resynthesis after 30 s of maximal sprint exercise is slower than previously observed after dynamic exercise of longer duration, and PCr resynthesis is important for the recovery of power during repeated bouts of sprint exercise.

Carbohydrate-electrolyte ingestion during intermittent high-intensity running.

PURPOSE The purpose of this study was to examine the effects of ingesting a carbohydrate-electrolyte beverage or a noncarbohydrate placebo on muscle glycogen utilization during 90 min of intermittent high-intensity running. METHODS Six trained games players (age 24.6 +/- 2.2 yr; height 179.6 +/- 1.9 cm; body mass 74.5 +/- 2.0 kg; VO2max 56.3 +/- 1.3 mL x kg(-1) x min(-1); mean +/- SEM) performed two exercise trials, 7 d apart. The subjects were university soccer, hockey, or rugby players. On each occasion, they completed six 15-min periods of intermittent running, consisting of maximal sprinting, interspersed with less intense periods of running and walking. During each trial, subjects consumed either a 6.9% carbohydrate-electrolyte solution (CHO-E: the CHO trial) or a noncarbohydrate placebo (the CON trial) immediately before exercise (5 mL x kg(-1) BM) and after every 15 min of exercise thereafter (2 mL x kg(-1) BM). Drinks were administered in a double-blind, counter-balanced order, and the total volume of fluid consumed during each trial was 1114 +/- 30 mL. Needle biopsy samples were obtained from the vastus lateralis muscle before and after 90 min of exercise. Venous blood samples were collected from an antecubital vein at rest and every 30 min during exercise. RESULTS Muscle glycogen utilization in mixed muscle samples was lower (P < 0.05) during CHO [192.5 +/- 26.3 mmol glucosyl units (kg x DM(-1))] than CON [245.3 +/- 22.9 mmol glucosyl units (kg x DM(-1))]. Single fiber analysis on the biopsy samples of the subjects during the CON trial showed a greater glycogen utilization in the Type II fibers compared with Type I fibers during this type of exercise [Type I: 182.2 +/- 34.5 vs Type II: 287.4 +/- 41.2 mmol glucosyl units (kg x DM(-1)); P < 0.05). After 30 min of exercise, blood lactate was significantly greater (P < 0.05) and serum insulin concentration lower (P < 0.05) in CON. CONCLUSIONS In summary, when trained games players ingested a carbohydrate-electrolyte beverage, muscle glycogen utilization was reduced by 22% when compared with a control condition.

Carbohydrate ingestion and glycogen utilization in different muscle fibre types in man.

1. The effect of carbohydrate (CHO) ingestion on muscle glycogen utilization during exercise was examined on seven male subjects completing two 60 min treadmill runs at 70% maximum oxygen uptake (VO2,max), 1 week apart. On each occasion the subjects consumed either water or a 5.5% CHO‐electrolyte solution immediately before and during exercise. Muscle samples were obtained from the vastus lateralis by needle biopsy before and immediately after exercise. Venous blood samples were also collected from an ante‐cubital vein at rest and at 10, 20, 40 and 60 min into the run. 2. Higher blood glucose concentrations (P < 0.01) were observed throughout the run during the CHO trial compared with the water trial. Serum insulin concentration was only higher after 20 min of exercise (P < 0.01). 3. A 28% reduction in mixed glycogen utilization was observed as a result of CHO ingestion when compared with water ingestion (108.7 +/‐ 16.3 vs. 150.9 +/‐ 19.9 mmol (kg dry matter)‐1, respectively; P < 0.01). 4. The ingestion of the CHO solution resulted in sparing of glycogen in type I (slow twitch) fibres only (38 +/‐ 7% degradation of glycogen as opposed to 66 +/‐ 3% during the water trial; P = 0.01).

Phosphocreatine degradation in type I and type II muscle fibres during submaximal exercise in man : effect of carbohydrate ingestion

1 The aim of this study was to examine the effect of carbohydrate (CHO) ingestion on changes in ATP and phosphocreatine (PCr) concentrations in different muscle fibre types during prolonged running and relate those changes to the degree of glycogen depletion. 2 Five male subjects performed two runs at 70 % maximum oxygen uptake (V̇O2,max), 1 week apart. Each subject ingested 8 ml (kg body mass (BM))−1 of either a placebo (Con trial) or a 5.5 % CHO solution (CHO trial) immediately before each run and 2 ml (kg BM)−1 every 20 min thereafter. In the Con trial, the subjects ran to exhaustion (97.0 ± 6.7 min). In the CHO trial, the run was terminated at the time coinciding with exhaustion in the Con trial. Muscle samples were obtained from the vastus lateralis before and after each trial. 3 Carbohydrate ingestion did not affect ATP concentrations. However, it attenuated the decline in PCr concentration by 46 % in type I fibres (CHO: 20 ± 8 mmol (kg dry matter (DM))−1; Con: 34 ± 6 mmol (kg DM)−1; P < 0.05) and by 36 % in type II fibres (CHO: 30 ± 5 mmol (kg DM)−1; Con: 48 ± 6 mmol (kg DM)−1; P < 0.05). 4 A 56 % reduction in glycogen utilisation in type I fibres was observed in CHO compared with Con (117 ± 39 vs. 240 ± 32 mmol glucosyl units (kg DM)−1, respectively; P < 0.01), but no difference was observed in type II fibres. 5 It is proposed that CHO ingestion during exhaustive running attenuates the decline in oxidative ATP resynthesis in type I fibres, as indicated by sparing of both PCr and glycogen breakdown. The CHO‐induced sparing of PCr, but not glycogen, in type II fibres may reflect differential recruitment and/or role of PCr between fibre types.

Carbohydrate Ingestion Prior to Exercise Augments the Exercise‐Induced Activation of the Pyruvate Dehydrogenase Complex in Human Skeletal Muscle

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 (V̇O2,max), 1 week apart. Each subject ingested 8 ml (kg body mass (BM))‐1 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‐1 (kg wet matter (WM))‐1, respectively; P 0.05) and this was accompanied by lower acetylcarnitine (7.1 ± 1.2 and 9.1 ± 1.1 mmol kg‐1 (dry matter (DM))‐1 in CHO and CON, respectively; P 0.05) and citrate concentrations (0.73 ± 0.05 and 0.91 ± 0.10 mmol (kg DM)‐1 in CHO and CON, respectively; P 0.05). No difference was observed between trials in the rates of muscle glycogen and PCr breakdown and lactate accumulation. This is the first study to demonstrate that CHO ingestion prior to exercise augments the exercise‐induced activation of muscle PDC and reduces acetylcarnitine accumulation during the transition from rest to steady‐state exercise. However, those changes did not affect the contribution of substrate level phosphorylation to ATP resynthesis.

No acetyl group deficit is evident at the onset of exercise at 90% of maximal oxygen uptake in humans

Abstract The existence of an acetyl group deficit at or above 90% of maximal oxygen uptake ([Vdot]O2max) has proved controversial, with contradictory results likely relating to limitations in previous research. The purpose of the present study was to determine whether the “acetyl group deficit” occurs at the start of exercise at 90%[Vdot]O2max in a well-controlled study. Eight male participants (age: 33.6 ± 2.0 years; [Vdot]O2max: 3.60 ± 0.21 litres · min−1) completed two exercise bouts at 90%[Vdot]O2max for 3 min following either 30 min of saline (control) or dichloroacetate (50 mg · kg−1 body mass) infusion, ending 15 min before exercise. Muscle biopsies were obtained immediately before and after exercise while continuous non-invasive measures of pulmonary oxygen uptake and muscle deoxygenation were made. Muscle pyruvate dehydrogenase activity was significantly higher before exercise following dichloroacetate infusion (control: 2.67 ± 0.98 vs. dichloroacetate: 17.9 ± 1.1 mmol acetyl-CoA · min−1 · mg−1 protein, P = 0.01) and resulted in higher pre- and post-exercise muscle acetylcarnitine (pre-exercise control: 3.3 ± 0.95 vs. pre-exercise dichloroacetate: 8.0 ± 0.88 vs. post-exercise control: 11.9 ± 1.1 vs. post-exercise dichloroacetate: 17.2 ± 1.1 mmol · kg−1 dry muscle, P < 0.05). However, substrate-level phosphorylation (control: 125 ± 20 vs. dichloroacetate: 113 ± 13 mmol adenosine triphosphate · kg−1 dry muscle) and [Vdot]O2 kinetics (control: 19.2 ± 2.2 vs. dichloroacetate: 22.8 ± 2.5 s), were unaltered. Furthermore, dichloroacetate infusion blunted the slow component of [Vdot]O2 and muscle deoxygenation and slowed muscle deoxygenation kinetics, possibly by enhancing oxygen delivery during exercise. These data support the hypothesis that the “acetyl group deficit” does not occur at or above 90%[Vdot]O2max.