The rat epitrochlearis muscle: metabolic characteristics.
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Animals↗
Biomedical subjects
J Henriksson
Publications and source records attributed to J Henriksson.
Chronic stimulation of mammalian muscle: changes in metabolite concentrations in individual fibers.
Single fibers were analyzed from rabbit fast-twitch tibialis anterior muscles freeze-clamped during continuous stimulation at 10 Hz for up to 8 wk. ATP declined after 1 wk to a stable level approximately 30% below controls. Phosphocreatine decreased earlier and to a greater extent (approximately 50%). Glycogen varied considerably among stimulated fibers and decreased on average approximately 75% by 8 wk. Glucose, lactate, citrate, and malate had changed little in the first 30 h and then increased four-, two-, four-, and sevenfold, respectively, over the next 5 wk. Glucose 6-phosphate showed the most unexpected behavior: with an overall upward trend, it descended to extremely low values (10% of control) after approximately 1 wk of stimulation. As long as high- and low-oxidative fibers were present, the former showed slightly higher levels of ATP, lactate, and malate; other metabolites did not differ in a consistent way. These unexpected observations, which differ strikingly from data for acute stimulation, shed light on adaptations that enable a chronically stimulated muscle to sustain a continuous high level of ATP utilization.
Adenine Nucleotides↗
Carbohydrate metabolism in human skeletal muscle during exercise is not regulated by G-1,6-P2.
Glucose 1,6-bisphosphate (G-1,6-P2) is a potent activator of phosphofructokinase (PFK) and an inhibitor of hexokinase in vitro. It has been suggested that increases in G-1,6-P2 are a main means by which PFK can achieve significant catalytic function in vivo despite falling pH and that increases in G-1,6-P2 will inhibit hexokinase in vivo. The purpose of the present study was to determine whether contraction-induced changes in flux through PFK and hexokinase are associated with changes in G-1,6-P2 in skeletal muscle. Ten men performed bicycle exercise for 10 min at 40 and 75% of maximal O2 uptake (VO2max) and to fatigue [4.8 +/- 0.6 (SE) min] at 100% VO2max. Biopsies were obtained from the quadriceps femoris muscle at rest and after each work load and analyzed for G-1,6-P2. G-1,6-P2 averaged 111 +/- 13 mumol/kg dry wt at rest and 121 +/- 16, 123 +/- 15, and 123 +/- 11 mumol/kg dry wt after the low-, moderate-, and high-intensity exercise bouts, respectively (P less than 0.05 for all means vs. rest). Flux through PFK was estimated to increase exponentially as the exercise intensity increased and muscle pH decreased at the higher work loads, whereas flux through hexokinase was estimated to increase during exercise at 40 and 75% VO2max but decrease sharply at 100% VO2max. These data demonstrate that flux through neither PFK nor hexokinase is mediated by changes in G-1,6-P2 in human skeletal muscle during short-term dynamic exercise.
Adult↗
Redox state and lactate accumulation in human skeletal muscle during dynamic exercise.
The relationship between the redox state and lactate accumulation in contracting human skeletal muscle was investigated. Ten men performed bicycle exercise for 10 min at 40 and 75% of maximal oxygen uptake [VO2(max.)], and to fatigue (4.8 +/- 0.6 min; mean +/- S.E.M.) at 100% VO2(max.). Biopsies from the quadriceps femoris muscle were analysed for NADH, high-energy phosphates and glycolytic intermediates. Muscle NADH was 0.20 +/- 0.02 mmol/kg dry wt. of muscle at rest, and decreased to 0.12 +/- 0.01 (P less than 0.01) after exercise at 40% VO2(max.), but no change occurred in the [lactate]/[pyruvate] ratio. These data, together with previous results on isolated cyanide-poisoned soleus muscle, where NADH increased while [lactate]/[pyruvate] ratio was unchanged [Sahlin & Katz (1986) Biochem. J. 239, 245-248], suggest that the observed changes in muscle NADH occurred within the mitochondria. After exercise at 75 and 100% VO2(max.), muscle NADH increased above the value at rest to 0.27 +/- 0.03 (P less than 0.05) and 0.32 +/- 0.04 (P less than 0.001) mmol/kg respectively. Muscle lactate was unchanged after exercise at 40% VO2(max.), but increased substantially at the higher work loads. At 40% VO2(max.), phosphocreatine decreased by 11% compared with the values at rest, and decreased further at the higher work loads. The decrease in phosphocreatine reflects increased ADP and Pi. It is concluded that muscle NADH decreases during low-intensity exercise, but increases above the value at rest during high-intensity exercise. The increase in muscle NADH is consistent with the hypothesis that the accelerated lactate production during submaximal exercise is due to a limited availability of O2 in the contracting muscle. It is suggested that the increases in NADH, ADP and Pi are metabolic adaptations, which primarily serve to activate the aerobic ATP production, and that the increased anaerobic energy production (phosphocreatine breakdown and lactate formation) is a consequence of these changes.
Adenine Nucleotides↗
Reversibility of decreased insulin-stimulated glucose transport capacity in diabetic muscle with in vitro incubation. Insulin is not required.
The mechanisms by which insulin deficiency affects muscle glucose transport were investigated. Epitrochlearis muscles from rats with streptozotocin-induced diabetes and from controls were incubated in vitro for 0.5-14 h. The incubation was shown not to impair muscle energy stores or tissue oxygenation. Diabetes decreased basal 3-O-methylglucose transport by 40% (p less than 0.01), and insulin-stimulated (20 milli-units/ml) glucose transport capacity by 70% (p less than 0.001). In vitro incubation gradually normalized insulin responsiveness (3.77 +/- 0.38 before versus 8.97 +/- 0.65 mumol X ml-1 X h-1 after 12 h of incubation). Basal glucose transport remained significantly reduced. The reversal of the insulin responsiveness did not require the presence of rat serum and, furthermore, took place even in the absence of insulin. In fact, insulin responsiveness was higher after incubation (14 h) with no insulin than with 100 microunits/ml insulin (9.85 +/- 0.59 versus 8.06 +/- 0.59 mumol X ml-1 X h-1, p less than 0.05). Glucose at 30 mM did not affect the normalization of the insulin-stimulated glucose transport capacity, whereas incubation in serum from diabetic rats resulted in a slightly (26%) blunted reversal (7.60 +/- 0.39 versus 8.89 +/- 0.45 mumol X ml-1 X h-1 with diabetic versus control serum for 14 h, p less than 0.05; before incubation the value was 3.87 +/- 0.40). Inhibition of protein synthesis by cycloheximide blocked the normalization by 80%. These results suggest the presence in diabetic serum of some labile factor that might inhibit the glucose transport system. The results indicate that the decreased insulin-stimulated glucose transport capacity, in the insulin-deficient diabetic muscle, is not a direct consequence of the lack of insulin or of high glucose concentrations.
3-O-Methylglucose↗
Enzyme levels of the NADH shuttle systems: measurements in isolated muscle fibres from humans of differing physical activity.
The aim of the present study was to investigate enzyme levels of the malate-aspartate and alpha-glycerophosphate shuttles in type I (slow-twitch) and type II (fast-twitch) fibres of human skeletal muscle. The influence of endurance training on these levels was also elucidated. Biopsy specimens were obtained from the lateral part of the quadriceps femoris muscle of six untrained and six endurance-trained subjects. Type I vs. type II. In both groups the type I fibres exhibited higher levels of the TCA cycle marker enzyme citrate synthase (CS), as well as of the malate-aspartate shuttle enzymes (cytoplasmic and mitochondrial malate dehydrogenase (cMDH, mMDH), and aspartate aminotransferase (cASAT, mASAT]. A more pronounced difference between type I and type II fibres was noted for cMDH (58%) than for mMDH (16%), cASAT (20%), mASAT (18%) and CS (25%). In contrast to these enzymes, the levels of cytoplasmic glycerol-3-phosphate dehydrogenase (cGPDH), the enzyme representative of the alpha-glycerophosphate shuttle, were higher (25%) in the type II fibres. Endurance-trained vs. untrained. In the endurance-trained group, both fibre types were characterized by higher levels of CS (mean for both fibre types: 48%) as well as of mitochondrial malate-aspartate shuttle enzymes (mMDH: 47%, mASAT: 48%) than in the corresponding fibre types in the untrained group, while the differences in the levels of cytoplasmic malate-aspartate shuttle enzymes (cMDH: 13%, cASAT: 16%) were not statistically significant. Nor were the differences in cGPDH levels (8%) between the untrained and endurance-trained groups statistically significant. It is concluded that in human skeletal muscle, malate-aspartate shuttle enzymes are expressed to a higher degree in type I (slow) fibres than in type II (fast) fibres, with cMDH exhibiting the most marked difference. The single fibre analysis indicated that the muscle's activity level might exert a greater influence on the mitochondrial isoenzymes than on the cytoplasmic ones. In contrast to the malate-aspartate shuttle enzymes, the alpha-glycerophosphate shuttle is expressed to a higher degree in type II fibres and its capacity appears to not be influenced by endurance training. The present studies demanded considerable methodological investigations which also are presented in this paper.
Adult↗
Canine diaphragm muscle after 1 yr of continuous electrical stimulation: its potential as a myocardial substitute.
Skeletal muscle has been rendered fatigue resistant by chronic stimulation and therefore has potential as an active substitute for damaged myocardium. It is therefore important to know whether stimulation produces any deleterious effects in the long term. Hemidiaphragm muscles of four dogs were examined after chronic stimulation for 1 yr at either 2 or 4 Hz. The stimulated hemidiaphragms appeared normal on gross inspection and were still contracting vigorously. By histochemical and immunohistochemical criteria, they had acquired a uniformly type I character, in contrast to the mixed fiber type composition of the unstimulated hemidiaphragms. This transformation was also reflected in their complement of myosin isozymes. There was some enzymatic evidence of an associated shift towards aerobic pathways of energy generation. Histological examination revealed no evidence of degenerative changes. Trends, observed in the shorter term (6-8 wk), toward a decrease in fiber area and an increase in connective tissue showed no further progression at 1 yr. Thus hemidiaphragm muscle stimulated at frequencies at or above the normal heart rate does not appear to undergo adverse long-term changes that would constrain its use in a myocardial assist role.
Animals↗
Redox state changes in human skeletal muscle after isometric contraction.
Subjects maintained an isometric contraction of the quadriceps femoris muscle at two-thirds maximal voluntary contraction (m.v.c.) force for 5 s (5.0 +/- 0.3 s; mean +/- S.E. of mean; n = 6) or until fatigue (52 +/- 4 s; n = 13). Muscle biopsies were obtained at rest, immediately after the contractions and also at 1 and 4 min of recovery after contraction to fatigue. In all subjects 5 s isometric contraction resulted in an increase of muscle NADH (0.084 +/- 0.012 at rest to 0.203 +/- 0.041 mmol/kg dry wt.) and a decrease of phosphocreatine (PC; change in concentration = -17.3 +/- 3.8 mmol/kg dry wt.). Glucose-6-phosphate concentration was more than doubled whereas lactate increased in only four of the six subjects. The two subjects who did not show any increase in lactate also had the lowest increase in NADH. At fatigue NADH increased to 0.226 +/- 0.032 mmol/kg dry wt. which was not significantly different from the value after 5 s contraction. Muscle PC was nearly depleted and lactate increased 12-fold above resting levels. The major part (65%) of the NADH increase at fatigue had reverted after 1 min recovery but only a slight further decrease occurred between 1 and 4 min of recovery. In relative terms the time course of the changes in muscle NADH during the first minute of recovery was similar to that of PC resynthesis, suggesting a common regulator such as O2 availability. In contrast to the delayed return of NADH concentration, PC resynthesis continued during the later part of the recovery period and PC concentration was almost fully restored after 4 min of recovery. It is concluded that muscle NADH is already maximally increased in the first seconds of muscle contraction at two-thirds m.v.c. Indirect evidence indicates that this increase reflects a reduction of the mitochondrial NAD-NADH redox couple. The rapid establishment of a reduced mitochondrial redox state at the start of muscle contraction will probably lead to a reduction of the redox state in the cytoplasm also and therefore be important for enhancing lactate formation.
Adult↗
Muscle ammonia metabolism during isometric contraction in humans.
The changes in ammonia (NH3) and amino acid contents in human skeletal muscle during isometric exercise (2/3 maximal voluntary contraction force) to fatigue have been investigated. Biopsies from musculus quadriceps femoris were obtained at rest, fatigue, and 1 and 4 min recovery. Muscle NH3 (n = 9) increased from 1.3 +/- 0.3 (mean +/- SE) mmol/kg dry muscle (dm) at rest to 3.6 +/- 0.6 at fatigue (P less than 0.01) and remained elevated during recovery, whereas the lactate increase after contraction decreased rapidly during recovery. Total adenine nucleotide (TAN) content decreased from 28.7 +/- 0.5 mmol/kg dm at rest to 25.1 +/- 0.6 at fatigue (P less than 0.001). Muscle glutamine did not change after contraction (P greater than 0.05), whereas glutamate decreased (P less than 0.001), and alanine increased (P less than 0.001). In vivo AMP deaminase activity (measured by the rate of TAN decrease) was positively correlated with the percentage of fast-twitch fibers (r = 0.92; P less than 0.001) and the ATP turnover rate (r = 0.75; P less than 0.001) but was not related to the muscle lactate content (r = 0.27; P greater than 0.05). Phosphocreatine decreased to 6.1 +/- 0.7 mmol/kg dm (range = 1-11) after contraction. It is concluded that during exercise activation of AMP deaminase in vivo occurs when a high ATP turnover rate is coupled with a low phosphocreatine level, muscle pH is of minor importance for direct activation of AMP deaminase in vivo, and increases in NH3 do not have an important influence on glycolysis.
AMP Deaminase↗
Chronic stimulation of mammalian muscle: changes in enzymes of six metabolic pathways.
Twenty-one enzymes of different metabolic systems were measured in the rabbit fast-twitch tibialis anterior (TA) muscle after electrical stimulation (10 Hz, 24 h/day) for 1 day to 10 wk. Nine analytical methods are either new, (3-oxoacid CoA-transferase, branched-chain-amino-acid aminotransferase, carnitine acetyltransferase, thiolase), improved (glutamate dehydrogenase, glycogen synthase, adenylic acid deaminase), or specially adapted (hexokinase, phosphoglucomutase). The activities (based on protein) of 12 mitochondrial or partly mitochondrial enzymes were lower in control TA than in control (slow) soleus (30-84% of soleus level). After 2 wk, 11 of these had surpassed the control soleus level. Maximal increases (3- to 14-fold) occurred after 2-5 wk, and thereafter six of the enzymes declined, whereas the other five maintained or increased their levels. Five glycolytic and two high-energy phosphate transfer enzymes, originally much higher in control TA than in control soleus, decreased gradually to levels at 8-10 wk only 27-123% higher than in soleus. Noncollagen protein concentration dropped 46%, explained largely by a sixfold increase in extracellular (chloride) space and a modest increase in collagen. The data constitute strong evidence for coordinate regulation of (mainly cytosolic) enzymes of glycolysis, glycogenolysis, gluconeogenesis, and high-energy phosphate transfer. Changes in the (mainly mitochondrial) enzymes of oxidative metabolism were more divergent, partly because of a hitherto undescribed secondary phase in the metabolic response. This phase may reflect a lower energy consumption in muscles adapted to continuous activity.
Adaptation, Physiological↗
Chronic stimulation of mammalian muscle: enzyme changes in individual fibers.
Single fibers of rabbit fast-twitch tibialis anterior (TA) muscles were analyzed after continuous low-frequency stimulation for up to 8 wk. After 2-5 wk, every fiber showed higher levels of citrate synthase, hexokinase, and 3-oxoacid CoA-transferase than any control fiber; in some cases these levels were 2-10 times higher (well above any found even in the control soleus, a slow-twitch muscle). Average levels of malate dehydrogenase and alanine transaminase also rose dramatically, but peak single fiber levels were not much above the highest in controls. These differential effects confirm at the single fiber level that chronic stimulation can alter mitochondrial composition. Lactate dehydrogenase, fructose-bisphosphatase, and adenylate kinase declined to levels far below those of any control TA fiber, and, in the case of fructose-bisphosphatase, to within the activity range of control soleus fibers. According to their staining reaction for myofibrillar ATPase, TA fibers were initially 23% type IIA, and 74% type IIB, but by 5 wk these had been converted to a mixture of type I, IIA, and IIC fibers. At 5 wk, levels of lactate dehydrogenase, adenylate kinase, and malate dehydrogenase were characteristic of their (new) ATPase type, but 3-oxoacid CoA transferase had increased to levels 6-15 times higher than in control fibers of the same type.
Adaptation, Physiological↗
Muscle ATP turnover rate during isometric contraction in humans.
ATP turnover and glycolytic rates during isometric contraction in humans have been investigated. Subjects contracted the knee extensor muscles at two-thirds maximal voluntary force to fatigue (mean +/- SE, 53 +/- 4 s). Biopsies were obtained before and after exercise and analyzed for high-energy phosphates and glycogenolytic-glycolytic intermediates. Total ATP turnover was 190 +/- 7 mmol/kg dry muscle, whereas the average turnover rate was 3.7 +/- 0.2 mmol . kg dry muscle-1 . S-1. The average ATP turnover rate was positively correlated with the percentage of fast-twitch fibers in the postexercise biopsy (r = 0.71; P less than 0.05) and negatively correlated with contraction duration to fatigue (r = -0.88; P less than 0.05). At fatigue, phosphocreatine ranged from 1 to 11 mmol/kg dry muscle (86-99% depletion of value at rest), whereas lactate ranged from 59 to 101. The mean glycolytic rate was 0.83 +/- 0.05 mmol . kg dry muscle-1 . S-1 and was positively correlated with the rate of glucose 6-phosphate accumulation (r = 0.83; P less than 0.05). It is concluded that a major determinant of the ATP turnover rate is the muscle fiber composition, which is probably explained by a higher turnover rate in fast-twitch fibers; fatigue is more closely related to a low phosphocreatine content than to a high lactate content; and the increase in prephosphofructokinase intermediates is important for stimulating glycolysis during contraction.
Adenosine Triphosphate↗
Skeletal muscle and hormonal adaptation to physical training in the rat: role of the sympatho-adrenal system.
The main purpose of the present study was to test the hypothesis that adrenergic stimulation of muscle fibres during exercise is a major stimulus for the training-induced enhancement of skeletal muscle respiratory capacity. Therefore, Sprague-Dawley rats either underwent bilateral surgical ablation of the adrenal medulla or were sham-operated. Furthermore, unilateral surgical extirpation of the lumbar sympathetic chain was performed. Half of the rats were then trained for 12 weeks by swimming (up to 5.5 h X day-1, 4 days X week-1) and the remaining rats were sedentary controls. In the gastrocnemius muscle, training significantly increased the mitochondrial enzymes citrate synthase, succinate dehydrogenase, cytochrome c oxidase, and 3-hydroxyacyl-CoA dehydrogenase. In sham-operated rats, the increases were 40%, 43%, 66%, and 25%, respectively, in legs with intact sympathetic innervation. The training-induced enzyme adaptation after adrenodemedullation and/or sympathectomy was not significantly lower than these control values. In sham-operated rats, training decreased resting plasma insulin and glucagon levels and increased liver glycogen content. Similar changes were induced by adrenodemedullation, but training did not augment these changes in adrenodemedullated rats. In conclusion, the data suggest that neither adrenomedullary hormones nor local sympathetic nerves are prerequisites for the training-induced increase in muscle mitochondrial enzymes. The training-induced decline in resting plasma insulin and glucagon levels in intact rats may be mediated by adrenomedullary hormones.
3-Hydroxyacyl CoA Dehydrogenases↗
Intracellular pH and electrolytes in human skeletal muscle during adrenaline and insulin infusions.
There is evidence that both beta-adrenergic stimulation and insulin are of importance in controlling intracellular pH. Therefore we have investigated the influence of intravenous infusion of adrenaline or insulin glucose (euglycaemic clamp) on pH and electrolyte composition in resting skeletal muscle (m. quadriceps femoris) and arterial blood in six healthy subjects. A decrease in the arterial potassium concentration was observed during infusion of adrenaline and is in conformity with previous studies. Both adrenaline and insulin infusions resulted in an increased lactate content of muscle and blood, indicating an enhanced glycolysis. The intracellular concentrations of K+, Na+, Mg2+ and H+, however, remained unchanged during the adrenaline infusions as well as during infusions of insulin. It is concluded that increasing the plasma adrenaline and insulin concentrations to levels well above the physiological range (adrenaline) or in the upper physiological range (insulin) does not affect the concentrations of electrolytes and hydrogen ions in resting human muscle to any appreciable extent.
Adult↗
Beta-adrenergic blockade and training in healthy men--effects on central circulation.
The effect of chronic beta-adrenergic blockade on central circulatory adaptations to physical training was investigated. 16 healthy sedentary males (20-31 yrs) trained on cycle ergometers 40 min/day, 4 days a week for 8 weeks at a work load that during the last 5 weeks corresponded to 75% of the pretraining VO2 max. In a single blind way, 8 subjects were during the training period treated with the beta-adrenergic receptor blocker propranolol (160 mg/day), while the remaining 8 received placebo tablets. Pretraining tests were performed before the start of medication and posttraining tests were performed 6 days after the last day of training and medication. The training program resulted in a similar increase (8%) in VO2 max in both groups (p less than 0.01). The resting heart rate (-4 beats/min; p less than 0.05) as well as the exercise heart rate at a moderate work load (120 W: -11 beats/min; p less than 0.01) decreased with training, and no significant difference was seen between the 2 groups. At a high work load (180 W), however, the heart rate decreased significantly more with training in the placebo group as compared with the beta-blockade group (-19 vs. -7 beats/min; p less than 0.05). The oxygen pulse (VO2/HR) increased in both groups at 120 W (+6%; p less than 0.01). At 180 W the oxygen pulse increased only in the placebo group (+8%; p less than 0.05). The estimated stroke volume at 120 and 180 W, as determined by impedance cardiography, did not change significantly with training although there was a tendency towards an increase in the placebo group only. The resting left ventricular wall thickness and diameter, as determined by echocardiography, did not change significantly with training in either group.--In conclusion, the present study indicates that a moderate degree of beta-adrenergic blockade does not prevent or impair the training-induced increase in the maximal oxygen uptake. During submaximal work, however, the circulatory adaptation may be less apparent if training has been performed during partial blockade of the sympatho-adrenal system.
Adaptation, Physiological↗
Skeletal muscle sympathetic activity at rest in trained and untrained subjects.
The effect of physical training on muscle sympathetic activity (MSA) was studied by comparing resting levels of MSA in 8 well-trained racing cyclists and in 8 age-matched untrained subjects (mean age 22 yrs). In addition, MSA was determined for 5 untrained subjects before and after an 8-week training program on cycle ergometers (training group). Recordings were made from the peroneal nerve at the knee with the subject in recumbent position. The well-trained cyclists were characterized by a clearly higher maximal oxygen uptake (VO2 max) and lower heart rate at submaximal exercise (180 W) than their untrained counterparts. These variables were also significantly changed with training in the training group. In contrast, there were no training-related effects on MSA. Thus, MSA expressed as either the number of sympathetic bursts/100 heart beats (+2%, NS) or bursts/min (-10%, NS) did not differ between the well-trained cyclists and the untrained controls. Furthermore, no changes in MSA occurred with training in the training group (bursts/100 heart beats: +8%, NS; bursts/min -2%, NS). Individual variations in MSA were large and independent of training state. It is concluded that differences in physical conditioning do not account for the large inter-individual differences in MSA in resting man.
Adult↗
Enzyme levels in pools of microdissected human muscle fibres of identified type. Adaptive response to exercise.
Enzyme activities were determined in pools of type I (slow twitch) and II A and II B (fast twitch) fibres of the thigh muscle from individuals engaged to a high degree in physical training of an endurance character and from non-endurance-trained controls. The endurance-trained (ET) group had significantly higher activity levels of the mitochondrial enzymes citrate synthase, malate dehydrogenase, and 3-OH-acylCoA dehydrogenase both in type I (2.1X, 1.7X, 1.4X) and in type II A (2.3X, 1.8X, 1.4X) and II B fibres (2.0X, 1.5X, 1.5X) than the non-endurance-trained (NET) group. Of the glycolytic enzymes, phosphofructokinase (PFK) in type I fibres was significantly higher (1.8X) in the ET than in the NET group whereas glyceraldehydephosphate dehydrogenase (GAPDH) in type I fibres was similar in the two groups. In type II fibres both PFK and GAPDH levels tended to be higher in the ET group. Lactate dehydrogenase (LDH) of both fibre types were not different in the two groups. Type I fibres differed significantly from type II fibres for all the six enzymes measured in both groups. However, no significant difference between fibres of types II A and II B was found. The results indicate that fibres of types I, II A and II B in human skeletal muscle all possess great adaptability with regard to their oxidative capacity. Furthermore, the data suggest that extensive endurance training may enhance the glycolytic capacity in both type I and type II fibres although the glycolytic capacity of the muscle as a whole generally is low in endurance trained subjects owing to a predominance of type I fibres. It is concluded that further studies are needed to determine whether there is a metabolic distinction between fibres of types II A and II B.
3-Hydroxyacyl CoA Dehydrogenases↗
Buffer capacity and lactate accumulation in skeletal muscle of trained and untrained men.
Buffer capacity (beta) of skeletal muscle has been determined in trained (n = 7) and in sedentary subjects (n = 8). The trained subjects were active in ball games where a high degree of anaerobic energy utilization is required. Percentage fibre type occurrence in the thigh muscle was not significantly different in the two groups. However, there was a tendency towards a higher proportion of type I (slow-twitch) fibres (61.5 +/- 11.6% vs. 50.2 +/- 12.5%) and a lower proportion of type IIB fibres (2.1 +/- 3.5% vs 14.1 +/- 16.3%) in the trained subjects. The proportion of the cross-sectional area of the muscle biopsies that was made up of type I or type II fibres was not different in the two groups. All subjects performed an isometric contraction of the knee extensors to fatigue at 61% of their maximal voluntary contraction force. Muscle biopsies were taken from the quadriceps femoris muscle at rest and immediately after contraction. The buffer capacity of muscle was calculated from: beta = (Muscle lactate (work)-Muscle lactate (rest)/(Muscle pH (rest)-Muscle pH (work)). A higher buffer capacity (p less than 0.05) was observed in the trained subjects (beta = 194 +/- 30 mmol X pH-1 X kg-1 dry wt.) compared to the sedentary group (beta = 164 +/- 20) (mean +/- SD). An unexpected finding was that muscle lactate after contraction to fatigue was lower (30%, p less than 0.01) and muscle pH was higher (6.80 +/- 0.06 vs. 6.61 +/- 0.12, p less than 0.01) in the trained subjects than in the sedentary controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗