Effect of endurance and sprint exercise on the sensitivity of glucose metabolism to insulin in the epitrochlearis muscle of sedentary and trained rats

Summary The effects of two types of acute exercise (1 h treadmill running at 20 m· min^–1, or 6 × 10-s periods at 43 m · min^–1, 0° inclination), as well as two training regimes (endurance and sprint) on the sensitivity of epitrochlearis muscle [fast twitch (FT) fibres] to insulin were measured in vitro in rats. The hormone concentration in the incubation medium producing the half maximal stimulation of lactate (la) production and glycogen synthesis was determined and used as an index of the muscle insulin sensitivity. A single period of moderate endurance as well as the sprint-type exercise increased the sensitivity of la production to insulin although the rate of la production enhanced markedly only after sprint exercise at 10 and 100 U· ml^–1 of insulin. These effects persisted for up to 2 h after the termination of exercise. Both types of exercise significantly decreased the muscle glycogen content, causing a moderate enhancement in the insulin-stimulated rates of glycogen synthesis in vitro for up to 2 h after exercise. However, a significant increase in the sensitivity of this process to insulin was found only in the muscle removed 0.25 h after the sprint effort. Training of the sprint and endurance types increased insulin-stimulated rates of glycolysis 24 h after the last period of exercise. The sensitivity of this process to insulin was also increased at this instant. Both types of training increased the basal and maximal rates of glycogen snythesis, as well as the sensitivity of this process to insulin at the 24^th following the last training session. It was concluded that in the epitrochlearis muscle, containing mainly FT fibres, both moderate and intensive exercise (acute and repeated) were effective in increasing sensitivity of glucose utilization to insulin. Thus, the response in this muscle type to increased physical activity differs from that reported previously in the soleus muscle, representing the slow-twitch, oxidative fibres in which sprint exercise did not produce any changes in the muscle insulin sensitivity.     

Comparative effects of hindlimb suspension and exercise on skeletal muscle myosin isozymes in rats

Summary The purpose of this study was to ascertain the time course of changes, whilst suspending the hindlimb and physical exercise training, of myosin light chain (LC) isoform expression in rat soleus and vastus lateralis muscles. Two groups of six rats were suspended by their tails for 1 or 2 weeks, two other groups of ten rats each were subjected to exercise training on a treadmill for 9 weeks, one to an endurance training programme (1-h running at 20 m · min^–1 5 days · week^–1), and the other to a sprint programme (30-s bouts of running at 60 m · min^–1 with rest periods of 5 min). At the end of these experimental procedures, soleus and vastus lateralis superficialis muscles were removed for myosin LC isoform determination by two-dimensional gel electrophoresis. Hindlimb suspension for 2 weeks significantly increased the proportion of fast myosin LC and decreased slow myosin LC expression in the soleus muscle. The pattern of myosin LC was unchanged in the vastus lateralis muscle. Sprint training or endurance training for 9 weeks increased the percentage of slow myosin LC in vastus lateralis muscle, whereas soleus muscle myosin LC was not modified. These data indicate that hindlimb suspension influences myosin LC expression in postural muscle, whereas physical training acts essentially on phasic muscle. There were no differences in myosin LC observed under the influence of sprint- or endurance-training programme.     

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   

Increase of adiponectin receptor gene expression by physical exercise in soleus muscle of obese Zucker rats

Aerobic exercise, including treadmill running has been widely used to treat insulin resistance and type 2 diabetes. We studied the effects of endurance training on gene expression of adiponectin receptor 1 (AdipoR1) in skeletal muscle of obese Zucker rats: the 8-week moderate exercise program consisted of treadmill running at 20 m/min and 0° gradient for 1 h/day, 7 days/week. After 8 weeks, insulin action on glucose disposal rate was measured by glucose–insulin index, the product of the areas under the curve of glucose and insulin during intraperitoneal glucose tolerance testing. In contrast to results for sedentary obese rats, exercise training decreased plasma levels of insulin and glucose as well as the glucose–insulin index in obese rats, indicating the merit of regular moderate exercise for improvement of insulin sensitivity in this insulin-resistant animal model. Also, diabetes-related reductions in mRNA and protein content of AdipoR1 in soleus muscle were observed in obese rats at baseline; they were markedly reversed after the 8-week exercise program. However, such exercise training did not alter plasma levels of insulin and glucose in lean Zucker rats. Also, AdipoR1 gene expression in soleus muscle was not changed by exercise in lean Zucker rats compared with the sedentary, lean littermates. These results suggest that long-term exercise training may reverse reduced AdipoR1 gene expression in soleus muscle and improve insulin sensitivity in the obese Zucker rats. Thus, an endurance exercise training is probably helpful clinically for obese individuals with insulin resistance.     

Acute and chronic effects of strenuous exercise on glucose metabolism in isolated, incubated soleus muscle of exercise-trained rats

Male and female Wistar rats were exercise-trained for 6 or 11 weeks respectively, to examine the effects of acute exercise or exercise training per se on insulin-stimulated glucose utilization in soleus muscles isolated and incubated in vitro. The maximal activities of hexokinase and 2-oxoglutarate dehydrogenase were significantly elevated (by greater than 50%) in gastrocnemius muscle of exercise-trained male and female rats, indicating an adaptation to the training regime. No significant differences in any of the variables studied were observed between appropriately matched male and female rats. There were no significant differences in the sensitivity or responsiveness of the rates of lactate formation or glycogen synthesis in soleus muscles isolated from exercise-trained and sedentary animals at rest (exercise-trained animals were studied 40 h after the last exercise bout). On the other hand, acute exercise caused significant changes in soleus muscle glucose metabolism. Basal and insulin-stimulated rates of glycogen synthesis were significantly elevated in soleus muscles incubated from both sedentary and exercise-trained rats immediately after an exercise bout. In addition, the responsiveness of glucose utilization to insulin in soleus muscles from exercise-trained rats was significantly increased after acute exercise. The results indicate that significant changes in the control of glucose metabolism by insulin in soleus muscle occur as a result of an acute exercise bout, while no adaptive changes in insulin sensitivity occur in soleus muscle after exercise training.     

Metabolic adaptation to daily exercise of moderate intensity to exhaustion in the rat

Summary The rats were made to run daily to exhaustion, for 28 days at a speed of 1,200 m·h^–1 on a treadmill set at a gradient of + 10°. The training increased the time of running to exhaustion [184 (SD 49) and 308 (SD 28) min on the 1st and 28th day, respectively; P<0.001]. The body mass was reduced by training [257 (SD 21) g before and 221 (SD 20) g after; P<0.001] whereas the food intake increased [9 (SD 1) g·100 g^– body mass before and 14 (SD 2) g after; P0.001]. The heart mass was not affected by training. Training increased the resting glycogen concentration in muscles composed of different fibre types (soleus, white and red vastus muscles) and in the liver, but had no effect on its concentration in the heart and diaphragm. During exercise lasting for 30 min glycogen mobilization in the red vastus and soleus muscles and the liver was more pronounced after than before training. A sparing effect of training on the skeletal muscles and liver glycogen was markedly apparent only after exericse to exhaustion. The trained rats, contrary to the untrained, did not develop hypoglycaemia during exercise to exhaustion. An increase in the plasma free fatty acid concentration during exercise after training was delayed and attenuated compared to that before training. The 24-h excretion of urea after exercise to exhaustion on the 28th day of training was higher than on the 1st day by 39% (P<0.001). It is concluded that metabolic adaptation to training consisting of daily bouts of exercise to exhaustion differs in many aspects from that so far described for other endurance training protocols.     

The effect of high-intensity intermittent swimming on post-exercise glycogen supercompensation in rat skeletal muscle

A single bout of prolonged endurance exercise stimulates glucose transport in skeletal muscles, leading to post-exercise muscle glycogen supercompensation if sufficient carbohydrate is provided after the cessation of exercise. Although we recently found that short-term sprint interval exercise also stimulates muscle glucose transport, the effect of this type of exercise on glycogen supercompensation is uncertain. Therefore, we compared the extent of muscle glycogen accumulation in response to carbohydrate feeding following sprint interval exercise with that following endurance exercise. In this study, 16-h-fasted rats underwent a bout of high-intensity intermittent swimming (HIS) as a model of sprint interval exercise or low-intensity prolonged swimming (LIS) as a model of endurance exercise. During HIS, the rats swam for eight 20-s sessions while burdened with a weight equal to 18% of their body weight. The LIS rats swam with no load for 3 h. The exercised rats were then refed for 4, 8, 12, or 16 h. Glycogen levels were almost depleted in the epitrochlearis muscles of HIS- or LIS-exercised rats immediately after the cessation of exercise. A rapid increase in muscle glycogen levels occurred during 4 h of refeeding, and glycogen levels had peaked at the end of 8 h of refeeding in each group of exercised refed rats. The peak glycogen levels during refeeding were not different between HIS- and LIS-exercised refed rats. Furthermore, although a large accumulation of muscle glycogen in response to carbohydrate refeeding is known to be associated with decreased insulin responsiveness of glucose transport, and despite the fact that muscle glycogen supercompensation was observed in the muscles of our exercised rats at the end of 4 h of refeeding, insulin responsiveness was not decreased in the muscles of either HIS- or LIS-exercised refed rats compared with non-exercised fasted control rats at this time point. These results suggest that sprint interval exercise enhances muscle glycogen supercompensation in response to carbohydrate refeeding as well as prolonged endurance exercise does. Furthermore, in this study, both HIS and LIS exercise prevented insulin resistance of glucose transport in glycogen supercompensated muscle during the early phase of carbohydrate refeeding. This probably led to the enhanced muscle glycogen supercompensation after exercise.     

Effect of exercise training on aortic collagen content in spontaneously hypertensive rats (SHR)

Summary We investigated the effects of exercise training on the amount of aortic collagen and systolic blood pressure in spontaneously hypertensive rats (SHR). Ten-week old SHR were trained either by forced treadmill running (26.8 m·min^–1 h·day^–1, five times a week, 0% incline) or by voluntary running in revolving wheels (7,800 m·day^–1 at peak) for 8 weeks. Succinate dehydrogenase (SDH) activity measured as a marker of an endurance training effect was 13% higher (P<0.01) in the soleus of forced-exercised animals than in that of sedentary ones. (6.56±0.17 mol·g^–1·min^–1; mean ± SEM), whereas SDH activity in that of voluntarily-exercised group was found to be at the same level as in sedentary animals. The systolic blood pressure after training increased by 26.4 in sedentary, 21.1 in voluntarily-exercised, and 33.9 mm Hg in forced-exercised rats, when compared with the value of each group at the beginning of the training programm. A significant difference was observed in the increment of blood pressure only between the voluntarily- and forced-exercised groups (P<0.05). The amount of aortic collagen in voluntarily-trained rats (96.5±2.0 mg·g tissue^–1, 39.8±0.7 mg·100 mg protein^–1) was significantly less than that in forced-trained rats (P<0.05). These results suggest that voluntary, mild exercise training may be more effective in the reduction of collagen accumulation in the aorta associated with the suppression of blood pressure increase than forced, vigorous exercise training in SHR.     

The respiratory system as an exercise limiting factor in normal sedentary subjects

Summary The present study was undertaken to investigate the respiratory system as an exercise limiting factor. Breathing and cycle endurance (i.e. the time until exhaustion at a given performance level) as well as physical working capacity 170 (i.e. the exercise intensity corresponding to a heart rate of 170 beats -min^–1 on a cycle ergometer) were determined in four healthy sedentary subjects. Subsequently, the subjects trained their respiratory system for 4 weeks by breathing daily about 901 · min^–1 for 30 min. Otherwise they continued their sedentary lifestyle. Immediately after the respiratory training and 18 months later, all performance tests carried out at the beginning of the study were repeated. The respiratory training increased breathing endurance from 4.2 (SD 1.9) min to 15.3 (SD 3.8) min. Cycle endurance was improved from 26.8 (SD 5.9) min to 40.2 (SD 9.2) min whereas physical working capacity 170 remained essentially the same. During the endurance cycling test in the respiratory untrained state, the subjects continuously increased their ventilation up to hyperventilation [ventilation at exhaustion = 96.9 (SD 23.6) 1 · min^–1] while after the respiratory training they reached a respiratory steady-state without hyperventilation [ventilation at exhaustion = 63.3 (SD 14.5) 1 · min^–1]. The absence of this marked hyperventilation was the cause of the impressive increase of cycle endurance in normal sedentary subjects after respiratory training. The effects gained by the respiratory training were completely lost after 18 months. Our results indicated that the respiratory system was an exercise limiting factor during an endurance test in normal sedentary subjects.     

The effect of exercise training on glycogen,glycogen synthase and phosphorylase in muscle and liver

Summary It is thought that exercise training in both man and the rat results in a protective effect against the depletion of carbohydrate stores during exercise (glycogen-sparing). However there has been no comprehensive study of the effects of training on glycogen anabolic and catabolic enzymes with liver or muscle. The aim of this study was to examine whether changes in these enzymes occur and whether these changes may provide an explanation for the glycogen-sparing which results from exercise training.Male rats were trained by a treadmill running program at three different workloads. In addition, there were three control groups: free eating (SF), food restricted (SR), and one SF with a single bout of exercise prior to sacrifice.Exercise training was associated with a 60–150% increase in glycogen synthase and phosphorylase and a 50–70% increase in glycogen content in soleus, an intermediate muscle, but not in extensor digitorum longus (EDL), a white muscle nor in liver. The increase in glycogen synthase and phosphorylase in intermediate muscle was proportional to the degree of training and there was a significant correlation between glycogen content, glycogen synthase, and phosphorylase activity in intermediate muscle. Cytochrome c oxidase activity, an indicator of respiratory capacity, increased 50% in gastrocnemius of trained rats and was significantly correlated with glycogen synthase and phosphorylase in soleus.These results indicate a significant effect of exercise training on glycogen anabolic and catabolic enzymes in intermediate muscle, with no significant effects in white muscle or liver. The changes do not provide an explanation for glycogen-sparing, but are consistent with improved capacity of intermediate muscle for rapid glycogen mobilisation and repletion.     

Insulin resistance induced by high-fat feeding is only partially reversed by exercise training

Diets high in saturated fat and simple carbohydrate result in an insulin-resistant state, while training increases insulin sensitivity. Insulin resistance was induced by feeding a high-fat, high-sucrose (HFS) diet to 4-week-old female Sprague-Dawley rats. A control diet (low-fat, complex-carbohydrate) was fed to another group for comparison. During the 4-week dietary treatment, half of each group was trained by treadmill running (2 h day^–1, 6 days week^–1m 30 m min^–1, 0% grade). At the end of this 4-week experimental period, hindquarter perfusions were performed at either basal (0) or maximal (100 nM) insulin concentrations to determine glucose uptake, glycogen synthesis, total glycogen content and the activity of several enzymes. Insulin (100 nM) significantly increased glucose uptake and glycogen synthesis in all four groups (CON-UN, CON-TR, HFS-UN, HFS-TR, where CON, UN and TR refer to control, untrained and trained respectively). HFS feeding significantly decresed (P<0.002) glucose uptake (mol g^–1 h^–1) with maximal insulin stimulation, while training significantly increased uptake (P<0.01) at both insulin concentrations. Glycogen synthesis was also increased by training (P<0.05) at both insulin concentrations, but accounted for only 25–28% of the glucose uptake. Although training improved the insulin resistance caused by the HFS diet, glucose uptake in the HFS-TR group was still significantly lower than the CON-TR group. Changes in glycogen synthesis are not great enough to account for the decrease or increase in glucose uptake found in the HFS-fed or trained animals.     

Lipid metabolism during exercise

Summary Seven physically fit (well-trained, maximal oxygen uptake 69.6±4.4 ml×kg^–1×min^–1) and eight less fit (moderately trained, maximal oxygen uptake 56.1±5.7 ml×kg^–1×min^–1) healthy male subjects were exercised for 4 h by bicycle ergometry against a pedalling resistance calculated to cause oxygen consumption corresponding to approximately 30% of each individual's maximal oxygen uptake value. Respiratory exchange ratio was estimated at 1 h and blood glucose and lactate concentrations and muscle glycogen content at 2 h intervals. Muscle glycogen content decreased markedly during the first 2 h of exercise in the well-trained group but was similar after 4 h exercise in both groups. No major differences were observed between the two subject groups in blood variable concentrations. Calculations based on respiratory exchange ratio showed that the proportion of carbohydrates utilized in the total energy consumption was 14% in the physically fit group and 25% in the less fit group, thus supporting previous observations that more energy is derived by fat oxidation in well-trained than in less-trained individuals during submaximal work at relatively similar oxygen consumption levels.This study was supported by grant no. 9791/79/73 from the Research Council for Physical Education and Sports (Ministry of Education, Finland)It is deeply regretted that our honoured friend and mentor, Professor Esko Karvinen, PhD, MD, died during the preparation of this paper     

Effects of short-term,high intensity (Sprint) training on some contractile and metabolic characteristics of fast and slow muscle of the rat

Summary Effects of a three weeks lasting short-term, high intensity training (sprint training) upon contractile parameters and selected enzyme activities of energy-supplying metabolism in slow soleus and fast rectus femoris muscle were investigated in female rats. Isometric twitch contraction time decreased in the soleus muscle. Maximum tetanic tension was found increased in soleus and rectus femoris muscle. Increases in hexokinase and citrate synthetase activities were induced in both muscles. In soleus muscle there was also an increase of glycogen phosphorylase, triosephosphate dehydrogenase and creatine kinase activities. Increases in the activity of the reference enzyme of fatty acid oxidation as known to be typical for endurance exercise, were neither found in rectus femoris nor in soleus muscle.This study was supported by a grant from Deutscher Sportbund.     

The effects of long-term hyperinsulinaemia on insulin sensitivity in rats

The effects of long-term exposure (7 wk) to hyperinsulinaemia on insulin sensitivity were studied in female rats. The rats were made hyperinsulinaemic by implantation of osmotic minipumps that were changed once a week. Elevated adrenergic activity and secretion of glucocorticoids were controlled by another minipump with propranolol and adrenalectomy with corticosterone substitution, respectively. This resulted in hyperinsulinaemia and moderate hypoglycaemia, the latter probably counteracted by overeating and increased glucagon secretion, as indicated by increased body weight and lower liver glycogen contents, respectively. Euglycaemic, hyperinsulinaemic clamp measurements showed a significantly higher glucose disposal rate (P < 0.05) in the hyperinsulinaemic rats 18.8± 1.1 mg kg^-1 min^-1 compared with the control groups 14.6±0.4 and 15.4±0.9 mg kg^-1 min^-1. Insulin stimulation of 2-deoxyglucose as well as glycogen synthesis was measured in the extensor digitorum longus muscle, the red and white part of the gastrocnemius, the soleus muscle, the liver and in parametrial, retroperitoneal, and inguinal adipose tissue. No differences were found between the groups in the insulin response of the 2-deoxyglucose uptake. Glycogen synthesis was significantly elevated in all muscles in the insulin treated compared with the control rats but no differences were found in the liver. Capillary density was significantly elevated per unit muscle surface area in the soleus and extensor digitorum longus muscles of the insulin-exposed rats. These results suggest that long-term exposure to insulin is followed by increased insulin sensitivity, apparently localized to the insulin regulation of glycogen synthesis in muscles. Muscle capillary density is elevated in parallel.     

Effect of exercise on glycogen metabolism in muscles of triiodothyronine-treated rats

The aim of the present study was to examine the rate of glycogen mobilization during exercise and the rate of the postexercise glycogen replenishment in different muscle types [white (WG), and red (RG) gastrocnemius, soleus (S) and diaphragm (D)] in rats treated with triiodothyronine (T₃, group T). Rats of the control group (C) were treated with saline. The animals were made to run on a treadmill set at 0° gradient and at a speed of 1200 m·h^–1. The time taken to reach exhaustion in group C was 188 (SD 23) min, whereas in group T, it was only 63 (SD 12) min. The content of glycogen in all muscles of the rats from group T at rest and during exercise was significantly lower than in group C at each corresponding time. At exhaustion, the glycogen content was in WG(C) 34.79 (SD 4.65), (T) 20.10 (SD 4.10); in RG(C) 22.82 (SD 4.66), (T) 16.50 (SD 2.00); in S(C) 14.85 (SD 2.48), (T) 11.90 (SD 2.93); in D(C) 18.18 (SD 3.49), (T) 7.54 (SD 3.36) (mol of glucosyl units·g^–1). The amount of glycogen mobilized during exhausting exercise in RG, S and D was similar in both groups whereas in WG it was much higher in rats of group T than in group C. The concentration of glycogen returned to pre-exercise values in each muscle 3 h after exercise. The net amount of glycogen resynthetized during 3 h of recovery depended on the muscle type. It was in WG(C) 3.30, (T) 18.03; in RG(C) 21.34, (T) 25.88, in S(C) 34.00, (T) 17.68, and in D(C) 17.25, (T) 12.22 mol of glucosyl units·g^–1 (each number represents the difference between the means). It concluded that treatment with T₃ markedly affects this exercise-induced metabolism of glycogen in each muscle type.From our study it is suggested that low muscle glycogen content may contribute to a reduction in exercise performance in hyperthyroidism.     

Effect of lowered muscle temperature on the physiological response to exercise in men

Summary The effect of low muscle temperature on the response to dynamic exercise was studied in six healthy men who performed 42 min of exercise on a cycle ergometer at an intensity of 70% of their maximal O₂ uptake. Experiments were performed under control conditions, i.e. from rest at room temperature, and following 45 min standing with legs immersed in a water bath at 12°C. The water bath reduced quadriceps muscle temperature (at 3 cm depth) from 36.4 (SD 0.5)°C to 30.5 (SD 1.7)°C. Following cooling, exercise heart rate was initially lower, the mean difference ranged from 13 (SD 4) beats · min^–1 after 6 min of exercise, to 4 (SD 2) beats · min^–1 after 24 min of exercise. Steady-state oxygen uptake was consistently higher (0.21 · min^–1). However, no difference could be discerned in the kinetics of oxygen uptake at the onset of exercise. During exercise after cooling a significantly higher peak value was found for the blood lactate concentration compared to that under control conditions. The peak values were both reached after approximately 9 min of exercise. After 42 min of exercise the blood lactate concentrations did not differ significantly, indicating a faster rate of removal during exercise after cooling. We interpreted these observations as reflecting a relatively higher level of muscle hypoxia at the onset of exercise as a consequence of a cold-induced vasoconstriction. The elevated steady-state oxygen uptake may in part have been accounted for by the energetic costs of removal of the extra lactate released into the blood consequent upon initial tissue hypoxia.     

Effects of prior heavy exercise,prior sprint exercise and passive warming on oxygen uptake kinetics during heavy exercise in humans

Prior heavy exercise (above the lactate threshold, Th_la) increases the amplitude of the primary oxygen uptake (VO₂) response and reduces the amplitude of the VO₂ slow component during subsequent heavy exercise. The purpose of this study was to determine whether these effects required the prior performance of an identical bout of heavy exercise, or if prior short-duration sprint exercise could cause similar effects. A secondary purpose of this study was to determine the effect of elevating muscle temperature (through passive warming) on VO₂ kinetics during heavy exercise. Nine male subjects performed a 6-min bout of heavy exercise on a cycle ergometer 6 min after: (1) an identical bout of heavy exercise; (2) a 30-s bout of maximal sprint cycling; (3) a 40-min period of leg warming in a hot water bath at 42°C. Prior sprint exercise elevated blood [lactate] prior to the onset of heavy exercise (by ≅5.6 mM) with only a minor increase in muscle temperature (of ≅0.7°C). In contrast, prior warming had no effect on baseline blood lactate concentration, but elevated muscle temperature by ≅2.6°C. Both prior heavy exercise and prior sprint exercise significantly increased the absolute primary VO₂ amplitude (by ≅230 ml·min^–1 and 260 ml·min^–1, respectively) and reduced the amplitude of the VO₂ slow component (by ≅280 ml·min^–1 and 200 ml·min^–1, respectively) during heavy exercise, whereas prior warming had no significant effect on the VO₂ response. We conclude that the VO₂ response to heavy exercise can be markedly altered by both sustained heavy-intensity submaximal exercise and by short-duration sprint exercise that induces a residual acidosis. In contrast, passive warming elevated muscle temperature but had no effect on the VO₂ response. Electronic Publication     

Different metabolic responses to exercise training programmes in single rat muscle fibres

Summary The aim of this report is to elucidate the effects of exercise training on metabolic properties of different muscle fibre types of the rat hindlimb. Single muscle fibres were dissected from soleus (SOL) or extensor digitorum longus (EDL) muscles of Wistar strain male rats trained on a treadmill for 16 weeks. Each fibre was typed histochemically (SO, slow-twitch oxidative; FOG, fast-twitch oxidative glycolytic; FG, fast-twitch glycolytic). Then glycolytic and oxidative enzymes (CK, LDH, PFK, PK, SDH, and MDH) activities were measured biochemically. Slow,-type fibres (SO) were hypertrophied following endurance training and fast-twitch fibres (FOG and FG) were hypertrophied following sprint training. In EDL muscles the distribution of the slow-type fibres was reduced following the sprint training. The activity of glycolytic enzymes increased significantly in the fast-type fibres (FOG and FG) following sprint training, while oxidative enzymes activities increased in both fast (FOG and FG) and slow (SO) muscle fibres following the endurance training. Neither glycolytic nor oxidative enzymes' activities always increased equally in all types of fibre following exercise training. Consequently, the metabolic profiles in each type of single muscle fibre were affected differently by different intensities of exercise training. These results suggest that the functional (enzymes activity) and structural (muscle fibre hypertrophy) changes of skeletal muscle fibre following exercise training appeared gradually, and would be controlled by different factors.     

Dynamics of metabolic responses to prolonged elevation of circulating adrenaline in resting and exercising rats

The purpose of this study was to follow the time course of metabolic responses to hyperadrenalinemia sustained up to 3 days. Hyperadrenalinemia was produced in rats by s.c. implantation of tablets releasing adrenaline (A) at a constant rate (1.6 g x min^–1). After 6, 12, 24 and 72 h of hyperadrenalinemia and 3 days after the tablet removal rats were sacrificed and liver, 3 types of muscles and blood samples were taken. Each time 14 rats were used: 7 of them were sedentary and 7 performed treadmill endurance exercise before decapitation. Sham operated animals served as controls. In preliminary experiments working ability was examined in 10 hyperadrenalinemic and 10 control rats. Duration of exercise until exhaustion was reduced in hyperadrenalinemic rats on the average by 40%. In sedentary rats, hyperglycemia, marked depletion of liver glycogen (by approx. 80%) and muscle glycogen (by 60–80%) as well as an elevation (2–4 times) of muscle lactate (LA) were found only during the first day after A-tablet implantation. At the end of the experiment these values approached the control ones. Muscle contents of ATP and creatine phosphate (CrP) were decreased by approx. 20% and 30–60%, respectively. Plasma FFA were markedly enhanced, varying in the time-course of the experiment from 0.8 to 1.4 mmol×1^–1. Post-exercise values for blood glucose, liver and muscle glycogen were always lower in hyperadrenalinemic rats than in controls sacrificed after timematched exercise (30 min). Circulating FFA decreased during excercise at all time points following A-tablet implantation, but they were still above the post-exercise levels in sham-operated rats. The response of muscle adenine nucleotides to exercise was not uniform, and changes in their values in the time-course of hyperadrenalinemia paralelled those in circulating FFA.It is concluded that during sustained hyperadrenalinemia some metabolic effects of adrenaline in sedentary animals are only transient, but impaired exercise tolerance persists for the whole time, being caused, at least in part, by early exhaustion of liver and muscle glycogen.This work was supported by the Polish Programme for Basic Research 06.-02.III.     

Calcineurin is not involved in some mitochondrial enzyme adaptations to endurance exercise training in rat skeletal muscle

The purpose of this study was to test the hypothesis that calcineurin, a calcium-dependent protein phosphatase recently implicated in the signaling of skeletal muscle hypertrophy and fiber type conversion, is required to induce some mitochondrial enzyme adaptations to endurance exercise training in skeletal muscle. Three- to four-week-old male Sprague-Dawley rats with an initial body weight ranging from 45 to 55 g were used in this study. The rats were randomly assigned to groups injected with either a specific calcineurin inhibitor, cyclosporin A (CsA), (group CI) or vehicle (group VI). CsA was subcutaneously injected into the rats at a rate of 50 mg·kg^–1 body weight per day for 10 days. The CI and VI groups were further assigned to sedentary (SED) or exercise training (EX) groups. In the EX group, the rats were trained for 10 days (90 min·day^–1, 14–20 m·min^–1, 10% grade). The citrate synthase (CS) activities in the soleus and plantaris muscles of the EX group rats were significantly higher than those of the SED group rats (p<0.001). Furthermore, 3--hydroxyacyl-CoA dehydrogenase (3-HAD) activities in the soleus and plantaris muscles were significantly higher in the EX group rats than in the SED group rats (p<0.001). However, there were no significant differences in CS and 3-HAD activities between the VI and CI groups. The interactions between CsA injection and exercise training were not statistically significant in any of the parameters. These results may suggest that calcineurin is not involved in some mitochondrial enzyme adaptations to endurance exercise training.S. Terada and H. Nakagawa contributed equally to this work.