Muscle metabolism during intense,heavy-resistance exercise

Summary The objective of this study was to examine the muscle metabolic changes occurring during intense and prolonged, heavy-resistance exercise. Muscle biopsies were obtained from the vastus lateralis of 9 strength trained athletes before and 30 s after an exercise regimen comprising 5 sets each of front squats, back squats, leg presses and knee extensions using barbell or variable resistance machines. Each set was executed until muscle failure, which occurred within 6–12 muscle contractions. The exercise: rest ratio was approximately 12 and the total performance time was 30 min. Concentrations of adenosine triphosphate (ATP), creatine phosphate (CP), creatine, glycogen, glucose, glucose-6-phosphate (G-6-P), -glycerophosphate (-G-P) and lactate were determined on freeze-dried tissue samples using fluorometric assays. Blood samples were analyzed for lactate and glucose. The exercise produced significant reductions in ATP (p<0.01) and CP (p<0.001), while -G-P more than doubled (p<0.05), glucose increased tenfold (p<0.001) and G-6-P fourfold (p<0.001). Muscle lactate concentration at cessation of exercise averaged 17.3 mmol · kg^–1 w.w. Glycogen concentration decreased (p<0.001) from 160 to 118 mmol · kg^–1 w. w. It is concluded that high intensity, heavy resistance exercise is associated with a high rate of energy utilization through phosphagen breakdown and activation of glycogenolysis.     

Brief intense exercise followed by passive recovery modifies the pattern of fuel use in humans during subsequent sustained intermittent exercise

The role of work period duration as the principal factor influencing carbohydrate metabolism during intermittent exercise has been investigated. Fuel oxidation rates and muscle glycogen and free carnitine content were compared between two protocols of sustained intermittent intense exercise with identical treadmill speed and total work duration. In the first experiment subjects (n=6) completed 40 min of intermittent treadmill running involving a work : recovery cycle of 6 : 9 s or 24 : 36 s on separate days. With 24 : 36 s exercise a higher rate of carbohydrate oxidation approached significance (P=0.057), whilst fat oxidation rate was lower (P ≤ 0.01) and plasma lactate concentration higher (P ≤ 0.01). Muscle glycogen was lower post‐exercise with 24 : 36 s (P ≤ 0.05). Muscle free carnitine decreased (P ≤ 0.05), but there was no difference between protocols. In the second experiment a separate group of subjects (n=5) repeated the intermittent exercise protocols with the addition of a 10‐min bout of intense exercise, followed by 43 ± 5 min passive recovery, prior to sustained (40 min) intermittent exercise. For this experiment the difference in fuel use observed previously between 6 : 9 s and 24 : 36 s was abolished. Carbohydrate and fat oxidation, plasma lactate and muscle glycogen levels were similar in 6 : 9 s and 24 : 36 s. When compared with the first experiment, this result was because of reduced carbohydrate oxidation in 24 : 36 s (P ≤ 0.05). There was no difference, and no change, in muscle free carnitine between protocols. A 10‐min bout of intense exercise, followed by 43 ± 5 min of passive recovery, substantially modifies fuel use during subsequent intermittent intense exercise.     

Effect of exercise on hexokinase distribution and mitochondrial respiration in skeletal muscle

Horses were subjected to treadmill running at 65% (submaximal) or 100% (maximal) O_2,max to examine the effects of exercise on subcellular distribution of hexokinase (HK) and on mitochondrial respiration. It is hypothesized that the fraction of HK bound to mitochondria will be reduced due to an elevation of glucose-6-phosphate (G-6-P) concentration in the exercising muscle and that such release of HK from mitochondria will depress oxidative phosphorylation. Changes in muscle G-6-P concentration, pH, subcellular HK distribution, mitochondrial respiration and other metabolites were determined in biopsy samples pre-exercise, immediately post-exercise and during the recovery phase. The fraction of HK associated with mitochondria decreased from 38% to 7% at the end of maximal exercise; exercise at O_2,max also reduced respiratory capacity of muscle homogenates by 20% and was associated with a fivefold increase in muscle [G-6-P], a potent agent known to dissociate HK from mitochondria. The HK distribution returned to normal within 60 min after exercise and the reassociation of the HK with mitochondria parallelled the removal of muscle G-6-P. No changes in muscle HK distribution and respiration were found following the submaximal exercise despite the fact that G-6-P was slightly elevated. Muscle concentrations of adenosine triphosphate, creatine phosphate and glycogen and pH dropped after exercise while lactate concentration increased. The amount of mitochondria-bound HK was also altered in vitro in a preparation of mitochondria isolated from rat skeletal muscle to examine the effect of the bound HK on mitochondrial respiration. The isolated mitochondria were incubated with G-6-P to release the bound HK. G-6-P induced the release of HK from mitochondria and reduced respiration. Mg²⁺ diminished both the G-6-P-induced HK release and the respiratory depression. Our data demonstrate that the fraction of HK associated with mitochondria can be reduced during maximal, but not submaximal, exercise; this reduction of bound HK was probably caused by the large increase in G-6-P concentration and was at least partially responsible for the depressed mitochondrial respiration seen at the end of the maximal exercise.     

Effect of glucose-6-phosphate and pH on glucose transport in skeletal muscle plasma membrane giant vesicles

The effect of glucose-6-phosphate (G-6-P) and pH on glucose transport was studied in skeletal muscle plasma membrane giant vesicles containing GLUT4 but not GLUT1. Vesicles (average diameter 7.6 μm) were obtained by collagenase treatment of muscle. The vesicles were incubated with 10 mmol T^-1 G-6-P and, after 0.5 and 2 h of incubation, the intravesicular G-6-P concentration was 0.93 ± 0.4 mmol 1^-1 and 1.18 ± 0.5 mmol I“¹ (mean ± SE, n = 4), respectively. In order to increase the intravesicular G-6-P concentration, 0.001% saponin was added during incubation, which increased the 2-h intravesicular G-6-P concentration to 4.57±1.0 mmol 1^-1 (n = 4). Initially, vesicles were used for glucose transport studies after 30 min of incubation with 10 mmol 1^-1 of G-6-P. There was no effect of G-6-P on either the affinity constant (K_m) or maximal velocity (V_max) of the glucose transport. Subsequently, vesicles were incubated for 2 h with 10 mmol T^-1 of G-6-P and 0.001 % saponin. Still no effect of G-6-P on glucose transport could be detected. In contrast, the rate of D-glucose transport was affected, when extravesicular pH was varied from 6.0 to 7.8. The maximum glucose transport rate was found at pH 7.2 and was decreased at both higher and lower pH. It is concluded that G-6-P has no effect on GLUT4 intrinsic activity in rat skeletal muscle plasma membrane. In contrast, GLUT4 intrinsic activity is sensitive to changes in pH.     

Skeletal muscle glycolysis during submaximal exercise following acute β-adrenergic blockade in man

The present study describes the influence of β-adrenergic blockade on glycogen utilization and lactate accumulation in skeletal muscle of exercising man. Twelve physically active men were examined during 25 min of continuous cycle exercise equivalent to 65% of their maximal oxygen uptake both with and without oral administration of 80 mg of propranolol (Inderal®). Heart rate, oxygen uptake, rate of perceived exertion (RPE) and blood lactate concentration were measured during exercise. Muscle biopsies were obtained from m. vastus lateralis after 5 and 25 min of exercise, β-adrenergic blockade decreased steady state exercise heart rate by (mean + SD) 35 ± 10 beats min^-1 (P < 0.001) and oxygen uptake from 2.47 to 2.39 1-min^-1 (P < 0.01). Muscle glycogen decreased from the 5th to the 25th min of exercise, and β-blockade had no significant effect on this decrease. In contrast to without drug, β-blockade resulted in a decrease (P < 0.05) in muscle lactate concentration from the 5th (6.9 mmolkg^-1 w./w.) to the 25th min (4.8 mmolkg^-1 w./w.). Similarly blood lactate levels were lower (P < 0.05) with than without β-blockade in the last but not the first 10 min of exercise. The alteration in muscle lactate concentration pattern following β-blockade, may imply that adrenergic effects per se contribute to the stimulation of glycolysis during submaximal exercise, except in its earliest phase. Nevertheless, the effect is not great enough to produce substantial differences in glycogen utilization.     

Non-exercising muscle metabolism during exercise

Glycogen decrements have been observed in non-exercising muscles during exercise. We therefore investigated whether the degraded glycogen was retained within the muscle in the form of glycolytic intermediates, or whether it was effluxed from the non-exercising muscles. For these studies a suspension harness was used to unload the hindlimb muscles at rest and during exercise [McDermott et al. (1987) J Appl Physiol 63:1275–1283]. Concentrations of glycogen and glycolytic intermediates glucose 6-phosphate, fructose 6-phosphate, fructose 1,6-bisphosphate, glycerol 3-phosphate, and lactate) were measured in non-exercising and exercising muscles (soleus, plantaris, red and white gastrocnemius) during a 90-min exercise bout 15 m/min, 8% grade). On-line electromyographic analysis showed that the contractile activity in the non-exercising muscles was markedly lower than in the exercising muscles. Similar decrements in muscle glycogen levels were observed in both the non-exercising and exercising muscles at the end of the 90-min, exercise bout (P<0.05), despite significantly different activity profiles. An increase in tissue lactate concentrations occurred in both non-exercising and exercising muscle (P<0.05), although only slight changes in the glycolytic intermediates occurred. The sum total of all the accumulated glycolytic intermediates and lactate (converted to glucosyl units) in the non-exercising muscles only accounted for a small fraction of the glycogen degraded ( 15%–28%). We conclude that the metabolism of glycogen is enhanced in non-exercising muscle, and that glycogen utilization is uncoupled from the energetic demands of the muscle. Furthermore, the glycogen mobilized in non-exercising muscle is not retained within the muscle in other metabolite pools. We speculate that the carbon units derived from glycogen may be effluxed into the circulation to join the oxidizable/gluconeogenic carbon pool.     

The influence of glucagon on hepatic glycogen mobilization in exercising rats

Summary The significance of glucagon for the alterations in carbohydrate and fat metabolism during swimming has been evaluated. Fed, male rats were used. Blood was drawn by cardiac puncture for glucose analysis and either rabbit-antiglucagonserum (A-rats) or normal rabbitserum (N-rats) injected. Twentynine rats were then forced to swim (S-rats) with a tail weight for 60 min, while 16 rats were resting controls (C-rats). Subsequently blood was drawn and samples of liver and muscle tissue collected. In SN-rats glucagon concentrations increased from 152±18 (S.E.) pg/ml (CN-rats) to 332±61 (P<0.05), while liver glycogen decreased (P<0.001) and blood glucose increased (P<0.05). In SA-rats, however, the changes in liver glycogen and blood glucose were halved indicating that increased glucagon secretion enhances hepatic glycogen depletion during prolonged exercise. NEFA rose in SA-rats (P<0.005) as well as in SN-rats (P<0.05). Glycerol concentrations, however, only increased in SA-rats (P<0.05) indicating a shift towards lipid combustion in antibody treated rats. Muscle glycogen and plasma insulin diminished and blood lactate increased uniformly in exercised rats.     

Splanchnic and renal vasoconstrictor and metabolic responses to neuropeptide Y in resting and exercising man

The local clearance of neuropeptide Y (NPY) and whether NPY influences splanchnic and renal metabolism in man have not been investigated previously. The influence of NPY on splanchnic and renal blood flows at physiologically elevated levels has also not been investigated. The effects of a 40-min constant NPY infusion (3 pmol kg^-1 min^-1) at rest and during 130 min of exercise (50% of Vo_2max) were studied in six healthy subjects and compared with resting and exercising subjects receiving no NPY. Blood samples were drawn from arterial, hepatic and renal vein catheters for the determination of blood flows (indicators: cardiogreen and paraaminohippuric acid [PAH]), NPY, catecholamines, glucose, lactate and glycerol. NPY infusion was accompanied by: (1) significant fractional extraction of NPY-like immunoreactivity (NPY-Li) by splanchnic tissues at rest (58±5%) and during exercise (53±6%), while no arterial–venous differences could be detected across the kidney; (2) a reduction in splanchnic and renal blood flows of up to 18 and 13% respectively (P < 0.01–0.001) at rest without any additional changes during exercise; and (3) metabolic changes as reflected in: (a) a more marked fall in arterial glucose during exercise compared to the reference group (P < 0.05); (b) a 35% lower splanchnic glucose release (P < 0.01) during exercise due to diminished glycogenolysis (P < 0.01); and (c) a lower arterial lactate level (18%P < 0.05) together with unchanged splanchnic lactate uptake during exercise, suggesting reduced lactate production by extrahepatic tissues. The disappearance of plasma NPY-Li after the infusions was biphasic with two similar half-lives at rest (4 and 39 min) and during exercise (3 and 43 min).     

Rapid activation of glycogen synthase and protein phosphatase in human skeletal muscle after isometric contraction requires an intact circulation

The effects of isometric contraction (66% of maximal force) and recovery on glycogen synthase fractional activity (GSF) in human skeletal muscle have been studied. Biopsies were taken from the quadriceps femoris muscle at rest, at fatigue and 5 min postexercise on two occasions: after one of the contractions, the circulation to the thigh was occluded during the 5 min recovery (OCC), and after the other contraction, the circulation was intact (control, CON). During CON, GSF decreased from (mean ± SE) 0.34±0.05 at rest to 0.24±0.02 at fatigue and then increased to 0.74±0.04 at 5 min postexercise; corresponding values for OCC were 0.37±0.04, 0.25±0.04 and 0.48±0.05 (P<0.001 vs. CON for 5 min postexercise only). Compared with the value at fatigue, protein phosphatase activity (PP) increased by 79±16% during CON recovery (P<0.01), whereas no change was observed during OCC recovery. Uridine diphosphate glucose increased by approximately 2.5-fold at fatigue, remained elevated during OCC recovery, but reverted to the preexercise level during CON recovery (P<0.001 vs. OCC recovery). Glucose 6-P increased approximately 5-fold at fatigue and was higher at 5 min postexercise in OCC vs. CON recovery (8.6±1.5 vs. 4.1±0.9 mmol/kg dry wt; P<0.01). It is concluded that the rapid increase in GSF after intense exercise with an intact circulation may be at least partly attributed to an increase in the specific activity of PP. The increase in GSF during recovery in OCC may be at least partly attributed to the high glucose 6-P content in vivo, which enhances the substrate suitability of GS for PP. Thus, separate mechanisms exist for the activation of PP and GS during recovery from intense short term exercise.     

Glycogen and triglyceride utilization in relation to muscle metabolic characteristics in men performing heavy-resistance exercise

Summary Nine bodybuilders performed heavy-resistance exercise activating the quadriceps femoris muscle. Intermittent 30-s exhaustive exercise bouts comprising 6–12 repetitions were interspersed with 60-s periods for 30 min. Venous blood samples were taken repeatedly during and after exercise for analyses of plasma free fatty acid (FFA) and glycerol concentration. Muscle biopsies were obtained from the vastus lateralis muscle before and after exercise and assayed for glycogen, glycerol-3-phosphate, lactate and triglyceride (TG) content. The activities of citrate synthase (CS), lactate dehydrogenase, hexokinase (HK), myokinase, creatine kinase and 3-hydroxyacyl-CoA dehydrogenase (HAD), were analysed. Histochemical staining procedures were used to assess fibre type composition, fibre area and capillary density. TG content before and after exercise averaged (SD) 23.9 (13.3) and 16.7 (6.4) mmol kg^–1 dry wt. The basal triglyceride content varied sixfold among individuals and the higher the levels the greater was the change during exercise. The glycogen content decreased (P<0.001) from 690 (82) to 495 (95) mmol kg^–1 dry wt. and lactate and glycerol-3-phosphate increased (P<0.001) to 79.5 (5.5) and 14.5 (7.3) mmol kg^–1 dry wt., respectively, after exercise. The HK and HAD/CS content respectively correlated with glycogen or TG content at rest and with changes in these metabolites during exercise. FFA and glycerol concentrations increased slightly (P<0.001) during exercise. Lipolysis may, therefore, provide energy during heavy-resistance exercise of relatively short duration. Also, storage and utilization of intramuscular substrates appear to be influenced by the metabolic profile of muscle.     

Effect of beta 1-selective and non-selective beta-blockade on work capacity and muscle metabolism

Six well-trained men were studied while performing a maximal bicycle exercise. The seven experiments included in this study were randomized in a double-blind cross-over fashion. On each occasion the subjects were given either placebo or 40, 80, or 160 mg propranolol (non-selective blockade) or 25,50, or 100 mg atenolol (beta 1-selective blockade). After completion of the study each subject had performed once under each of the seven treatments. Heart rate, maximal oxygen uptake (Vo2max), blood lactate and performance time to exhaustion were measured. A muscle biopsy from vastus lateralis was taken at exhaustion after placebo, 80 mg propranolol and 50 mg atenolol trials, for analysis of ATP, creatine phosphate (CP), glucose-6-phosphate (G-6-P), glucose and lactate. The performance time was reduced (P less than 0.05-0.001) with both blockers compared to placebo. At an equal heart rate reduction, Vo2max was equally reduced by both blockers. Performance time, on the other hand, was reduced to a greater extent (P less than 0.05) with propranolol. ATP and CP levels were decreased (P less than 0.05) by both drugs. G-6-P, however, was lower (P less than 0.05) with propranolol than with either placebo or atenolol. No difference was observed between placebo and atenolol. In conclusion, both beta1-selective and non-selective blockade reduced short-term maximal exercise capacity. The major limiting factor seems to be the reduction in oxygen transport. The finding that at an equivalent reduction in Vo2max propranolol reduced performance time to a greater extent than atenolol suggests that beta 2-blockade may reduce performance by mechanisms additional to those that affect oxygen transport.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of aspirin in modulating myocardial ischemic reperfusion injury

The role of low-dose aspirin (3 mg/kg, i.v.) in attenuating ischemic reperfusion injury was studied in a canine model. Regional ischemia for 40 min was produced by temporary occlusion of the left anterior descending coronary artery and thereafter reperfusion instituted for 3 h. Mean arterial pressure (MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP), positive (+) LV dP/dt _max and negative (–) LV dP/dt _max were monitored alongwith myocardial adenosine triphosphate (ATP), creatine phosphate (CP), glycogen and lactate. Following reperfusion, there was a significant fall in (i) MAP, (ii) (+) LV dP/dt _max and (iii) (–) LV dP/dt _max. LVEDP was corrected after about 2h of reperfusion. Replenishment of only myocardial CP occurred, without any change in ATP and glycogen, although lactate accumulation was corrected.Aspirin administered 15 min before reperfusion (posttreatment) caused normalisation of LVEDP within 15 min and prevented any deterioration in (–) LV dP/dt _max, although it had no effect on MAP and (+) LV dP/dt _max. After 3h of reperfusion (post-treatment), myocardial ATP, CP, glycogen and lactate contents became normal. The number of premature ventricular complexes was significantly reduced after aspirin treatment. The present study indicates that low-dose aspirin post-treatment can ameliorate at least some of the deleterious consequences of reperfusion injury of the myocardium.     

Fuel metabolism during ultra-endurance exercise

 Cyclists either ingested 300 ml 100 g/l U-[¹⁴C] glucose solution every 30 min during 6 h rides at 55% of VO_2max (n=6) or they consumed unlabelled glucose and were infused with U-[¹⁴C] lactate (n=5). Maintenance of euglycaemia limited rises in circulating free fatty acids, noradrenaline and adrenaline concentrations to 0.9±0.1 mM, 27±4 nM and 2.0±0.5 nM, respectively, and sustained the oxidation of glucose and lactate. As muscle glycogen oxidation declined from 100±13 to 71±9 μmol/min/kg in the last 3 h of exercise, glucose and lactate oxidation and interconversion rates remained at approximately 60 and 50 and at about 4 and 5 μmol/min/kg, respectively. Continued high rates of carbohydrate oxidation led to a total oxidation of around 270 g glucose, 130 g plasma lactate and 530 g muscle glycogen. Oxidation of some 530 g of muscle glycogen far exceeded the predicted (about 250 g) initial glycogen content of the active muscles and suggested that there must have been a considerable diffusion of unlabelled lactate from glycogen breakdown in inactive muscle fibres to adjacent active muscle fibres via the interstitial fluid that did not equilibrate with ¹⁴C lactate in the circulation. Received: 19 September 1997 / Received after revision: 15 December 1997 / Accepted: 22 January 1998     

Fuel substrate turnover and oxidation and glycogen sparing with carbohydrate ingestion in non-carbohydrate-loaded cyclists

This study examined the effects of ingesting 500 ml/h of either a 10% carbohydrate (CHO) drink (CI) or placebo (PI) on splanchnic glucose appearance rate (endogenous + exogenous) (R _a), plasma glucose oxidation and muscle glycogen utilisation in 17, non-carbohydrate-loaded, male, endurance-trained cyclists who rode for 180 min at 70% of maximum oxygen uptake. Mean muscle glycogen content at the start of exercise was 130 ± 6 mmol/kg ww; (mean ± SEM). Total CHO oxidation was similar in CI and PI subjects and declined during the trial. R _a increased significantly during the trial (P < 0.05) in both groups. Plasma glucose oxidation also increased significantly during the trial, reaching a plateau in the PI subjects, but was significantly (P < 0.05) higher in CI than PI subjects at the end of exercise [(98 ± 14 vs. 72 ± 10 μmol/min/kg fat-free mass) (FFM) (1.34 ± 0.19 vs. 0.93 ± 0.13 g/min)]. However, mean endogenous R _a was significantly (P < 0.05) lower in the CI than PI subjects throughout exercise (35 ± 7 vs. 54 ± 6 μmol/min/kg FFM), as was the oxidation of endogenous plasma glucose, which remained almost constant in CI subjects, and reached values at the end of exercise of 42 ± 13 and 72 ± 10 μmol/min/kg FFM in the CI and PI groups respectively. Of the 150 g CHO ingested during the trial, 50% was oxidised. Muscle glycogen disappearance was identical during the first 2 h of exercise in both groups and continued at the same rate in PI subjects, however no net muscle glycogen disappearance occurred during the final hour in CI subjects. We conclude that ingestion of 500 ml/h of a 10% CHO solution during prolonged exercise in non carbohydrate loaded subjects has a marked liver glycogen-sparing effect or causes a reduction in gluconeogenesis, or both, maintains plasma glucose concentration and has a muscle glycogen-sparing effect. Received: 25 August 1995/Received after revision: 25 March 1996/Accepted: 29 April 1996     

Training decreases muscle glycogen turnover during exercise

The present study was undertaken to determine the effects of endurance training on glycogen kinetics during exercise. A new model describing glycogen kinetics was applied to quantitate the rates of synthesis and degradation of glycogen. Trained and untrained rats were infused with a 25% glucose solution with 6-³H-glucose and U-¹⁴C-lactate at 1.5 and 0.5?μCi?·?min^?1 (where 1 Ci?=?3.7?×?10¹⁰ Bq), respectively, during rest (30?min) and exercise (60?min). Blood samples were taken at 10-min intervals starting just prior to isotopic infusion, until the cessation of exercise. Tissues harvested after the cessation of exercise were muscle (soleus, deep, and superficial vastus lateralis, gastrocnemius), liver, and heart. Tissue glycogen was quantitated and analyzed for incorporation of ³H and ¹⁴C via liquid scintillation counting. There were no net decreases in muscle glycogen concentration from trained rats, whereas muscle glycogen concentration decreased to as much as 64% (P?P?相似文献   

The effects of diet on muscle pH and metabolism during high intensity exercise

Summary Five healthy male subjects exercised for 3 min at a workload equivalent to 100% on two separate occasions. Each exercise test was performed on an electrically braked cycle ergometer after a four-day period of dietary manipulation. During each of these periods subjects consumed either a low carbohydrate (3±0%, mean ±SD), high fat (73±2%), high protein (24±3%) diet (FP) or a high carbohydrate (82±1%), low fat (8±1%), low protein (10±1%) diet (CHO). The diets were isoenergetic and were assigned in a randomised manner. Muscle biopsy samples (Vastus lateralis) were taken at rest prior to dietary manipulation, immediately prior to exercise and immediately post-exercise for measurement of pH, glycogen, glucose 6-phosphate, fructose 1,6-diphosphate, triose phosphates, lactate and glutamine content. Blood acid-base status and selected metabolites were measured in arterialised venous samples at rest prior to dietary manipulation, immediately prior to exercise and at pre-determined intervals during the post-exercise period. There was no differences between the two treatments in blood acid-base status at rest prior to dietary manipulation; immediately prior to exercise plasma pH (p<0.01), blood (p<0.01), plasma bicarbonate (p<0.001) and blood base-excess (p<0.001) values were all lower on the FP treatment. There were no major differences in blood acid-base variables between the two diets during the post-exercise period. Compared with the CHO diet, the FP diet resulted in plasma alanine (p<0.05), blood lactate (p<0.05), and plasma glutamine (p<0.01) levels being lower immediately prior to exercise; plasma free fatty acids (FFA; p<0.05), glycerol (p<0.01), urea (p<0.001) and blood 3-hydroxybutyrate (3-OHB; p<0.01) levels were all higher. After the FP diet blood alanine, lactate and plasma glutamine levels were lower for the whole or the majority of the post-exercise period, while the concentrations of plasma FFA, glycerol, urea and blood 3-OHB and glucose were higher. There was no difference between the diets in pre-exercise glucose and insulin levels and post-exercise insulin levels. There was no difference in muscle pH between the two diets immediately prior to exercise; the decline in muscle pH was 104% greater during exercise on the FP diet resulting in a significant difference in post-exercise pH (p=0.05). The FP diet resulted in 23% decline in muscle glutamine levels, resulting in lower levels (p<0.05) immediately prior to exercise. Exercise had no influence on muscle glutamine levels after the FP diet but produced a 17% decline on the CHO diet. Muscle glycogen content increased by 23% on the CHO diet, but was unchanged after the FP diet. This resulted in levels being significantly different prior to exercise (p<0.05). The decline in muscle glycogen content during exercise was 50% greater on the CHO diet. There were no differences when comparing the two dietary treatments in any of the pre-exercise glycolytic intermediates measured. Immediately post-exercise glucose 6-phosphate levels were 22% higher and fructose 1,6-diphosphate levels were 130% lower on the FP diet. There were no differences between the two diets in muscle triose phosphate or lactate levels at any point of the study. The present study demonstrates that a FP diet can induce metabolic acidosis and may reduce pre-exercise muscle buffering capacity, which may then influence subsequent exercise performance. However, this appears not to influence the efflux of H⁺ from muscle during and after high intensity exercise.     

Insulin-independent glycogen supercompensation in isolated mouse skeletal muscle: role of phosphorylase inactivation

Glycogen supercompensation (increase in muscle glycogen content above basal) is an established phenomenon induced by unknown mechanisms. It consists of both insulin-dependent and -independent components. Here, we investigate insulin-independent glycogen supercompensation in isolated, intact extensor digitorum longus muscles from mice. Muscles were stimulated electrically, incubated in vitro with 5.5 mM glucose for up to 16 h and then analysed for glycogen, glucose uptake and enzyme activities. Basal glycogen was 84±6 µmol glucosyl units/g dry muscle and was depleted by 80% after 10 min contraction. Glycogen increased after contraction, reaching a peak value of 113±9 µmol glucosyl units/g dry muscle (P<0.05 vs. basal) by 6 h, and returned to basal values by 16 h (84±8). Maximal activities of glycogen synthase, phosphorylase and -glucosidase were not significantly altered by contraction or during the 6-h recovery period. Glycogen synthase fractional activity (0.17/7.2 mM glucose-6-P; inversely related to phosphorylation state of the enzyme) was increased about twofold early after contraction but then decreased and was slightly lower than baseline during the period of supercompensation (4–6 h). Phosphorylase fractional activity (±adenosine monophosphate; directly related to phosphorylation state of the enzyme) decreased to 60% of basal after contraction and decreased further during the initial 4 h of recovery to 40% of basal (P<0.01 vs. basal). After 4 h recovery, glucose uptake was slightly (50%) higher in the stimulated than in the non-stimulated muscle (P<0.01). Thus, insulin-independent glycogen supercompensation involves inactivation of phosphorylase and hence an inhibition of glycogen breakdown.     

Carbohydrate supplementation and alterations in neutrophils, and plasma cortisol and myoglobin concentration after intense exercise

The present study examined the effect of carbohydrate supplementation on changes in neutrophil counts, and the plasma concentrations of cortisol and myoglobin after intense exercise. Eight well-trained male runners ran on a treadmill for 1 h at 85% maximal oxygen uptake on two separate occasions. In a double-blind cross-over design, subjects consumed either 750 ml of a 10% carbohydrate (CHO) drink or a placebo drink on each occasion. The order of the trials was counter-balanced. Blood was drawn immediately before and after exercise, and 1 h after exercise. Immediately after exercise, neutrophil counts (CHO, 49%; placebo, 65%; P<0.05), plasma concentrations of glucose (CHO, 43%; P<0.05), lactate (CHO, 130%; placebo, 130%; P<0.01), cortisol (CHO, 100%; placebo, 161%; P<0.01), myoglobin (CHO, 194%; placebo, 342%; P<0.01) all increased significantly. One hour post-exercise, plasma myoglobin concentration (CHO, 331%; placebo, 482%; P<0.01) and neutrophil count (CHO, 151%; placebo, 230% P<0.01) both increased further above baseline. CHO significantly attenuated plasma myoglobin concentration and the neutrophil count after exercise (P<0.01), but did not affect plasma cortisol concentration. The effects of CHO on plasma myoglobin concentration may be due to alterations in cytokine synthesis, insulin responses or myoglobin clearance rates from the bloodstream during exercise. Plasma cortisol responses to CHO during exercise may depend on the intensity of exercise, or the amount of CHO consumed. Lastly, cortisol appears to play a minor role in the mobilisation of neutrophils after intense exercise.     

Elevated free fatty acid levels inhibit glucose phosphorylation in slow-twitch rat skeletal muscle

The effect of increased free fatty acid concentrations on glucose metabolism in rat skeletal muscle was investigated at several different steps in glucose metabolism including glucose transport, glucose phosphorylation, glucose oxidation and glycogen synthesis. In isolated soleus (slow-twitch) muscles, insulin-stimulated (100 μml^-1) glucose phosphorylation, but not glucose transport, was inhibited by 26 and 22% in the presence of 1.0 and 2.0 mM oleate, respectively (P< 0.01). Regardless of oleate concentration (0.3 or 2.0 mM), insulin-stimulated glucose 6-phosphate levels were elevated to the same extent over the non-insulin-stimulated levels in soleus muscles {P < 0.01). Insulin-stimulated glucose oxidation was inhibited by 44% in soleus muscles exposed to 2.0 mM oleate (P < 0.05), whereas the rate of glucose incorporation into glycogen was not altered. In insulin-stimulated epitrochlearis (fast-twitch) muscles, elevated concentrations of oleate had no effect on the rates of glucose transport or glucose phosphorylation, or on the level of glucose 6-phosphate. These data suggest that increased free fatty acid availability decreases glucose utilization by selectively inhibiting glucose phosphorylation and oxidation in slow-twitch, but not fast-twitch skeletal muscle.     

Local critical power is an index of local endurance

The hypothesis that critical power (CP) is significantly lower than the maximal aerobic power of the knee extensors has been tested in nine endurance-trained subjects, seven gymnasts and seven weight lifters. CP was calculated as being equal to the slope of the linear relationship between exhaustion time and work performed at exhaustion on a knee-extension ergometer. CP was compared with the power output at the end of a progressive knee-extension exercise (P _peak) and the power outputs corresponding to exhaustion times equal to 4 (P _4 min), 6 (P _6 min), 8 (P _8 min) and 10 min (P _10 min), calculated according to the linear relationship between work and exhaustion time. The hypothesis that CP corresponds to a steady state in metabolic and physiological parameters was tested in the gymnasts and the weight lifters by comparing CP with the fatigue thresholds of the integrated electromyogram (iEMG_FT), lactate level (La_FT), oxygen uptake (V˙O_2FT) and heart rate (HR_FT). The results of the present study demonstrate that the value of CP of a local exercise cannot be considered as the equivalent of the maximal aerobic power for general exercises. The values of P _4 min, P _6 min, P _8 min, P _10 min and P _peak were significantly higher than CP, and corresponded to 138, 126, 119, 115 and 151% CP, respectively. The results of the present study indicate that CP can be considered as an index of muscular endurance. Indeed, La_FT, iEMG _FT, V˙O_2FT and HR_FT were not significantly different from CP. All of these fatigue thresholds were significantly correlated with CP (r > 0.92). Moreover, the highest coefficient of correlation (r=0.71; P < 0.01) between the percentage of maximal aerobic power in cycling that corresponds to a blood lactate concentration of 4 mmol · l⁻¹ (OBLA%) and the different local aerobic indices was observed with CP. Received: 22 February 1999 / Accepted: 16 June 1999