scholarly journals Enzymic and metabolic adaptations in the gastrocnemius, plantaris and soleus muscles of hypocaloric rats

1989 ◽  
Vol 261 (1) ◽  
pp. 219-225 ◽  
Author(s):  
M S M Ardawi ◽  
M F Majzoub ◽  
I M Masoud ◽  
E A Newsholme

1. The effect of hypocaloric feeding (25% of normal food intake for 21 days) of rats on the enzymic and metabolic adaptations in the gastrocnemius, plantaris and soleus muscles was studied. 2. In control and hypocaloric rats the muscle relaxation rates at 100 Hz were 35.76 and 11.38% force loss/10 ms respectively. Control rats exhibited enhanced force of muscle contraction as the frequency of stimulation increased from 10 to 100 Hz, with maximum force being at 100 Hz. Hypocaloric rats exhibited a decrease in the increment of force being exerted at high frequencies, with maintenance of force at lower stimulatory frequencies. 3. In muscles of hypocaloric rats, there were significant decreases in the maximal activities of hexokinase (17.6-37.0%), 6-phosphofructokinase (22.7-34.2%), pyruvate kinase (21.2-36.0%), citrate synthase (34.1-41.5%), oxoglutarate dehydrogenase (29.4-52.4%) and 3-hydroxyacyl-CoA dehydrogenase (26.7-32.1%), whereas the activities of glycogen phosphorylase increased (23.8-43.4%) compared with control values. 4. In soleus-muscle strip preparations of hypocaloric rats, there were significant decreases in the rates of lactate production (28.1%) and glucose oxidation (32.6%) compared with control preparations. 5. Mitochondrial preparations from muscles of hypocaloric rats incubated with various substrates exhibited decreased rates of oxygen uptake compared with control preparations. 6. In muscles of hypocaloric rats (gastrocnemius and soleus), there were significant decreases in the concentrations of glycogen (P less than 0.001) and phosphocreatine (P less than 0.001) and increases in those of pyruvate (P less than 0.001), lactate (P less than 0.001) and ADP (P less than 0.001), whereas those of ATP and AMP remained unchanged. 7. Calculated [lactate]/[pyruvate] and [ATP]/[ADP] ratios exhibited significant increases (P less than 0.05) and decreases (P less than 0.05) in muscles of hypocaloric rats respectively. 8. The results are discussed in relation to the genesis of muscle dysfunction caused by malnutrition.

1990 ◽  
Vol 68 (1) ◽  
pp. 193-197 ◽  
Author(s):  
H. Stephen Ewart ◽  
William R. Driedzic

Maximal in vitro activities of hexokinase, phosphofructokinase, pyruvate kinase, lactate dehydrogenase, β-hydroxyacyl-CoA dehydrogenase, citrate synthase, malate dehydrogenase, and cytochrome oxidase were assessed in cod (Gadus morhua) gas gland. The metabolic profile predicts a substantial anaerobic relative to aerobic metabolism. The effect of catecholamines, acetylcholine, and low pH on in vitro rates of lactate production by gas gland was assessed. Adrenaline and acetylcholine both increased the rate of lactate production even under aerobic incubation conditions. However, the rates of lactate production were well below the capacity suggested by the enzyme levels. It is suggested that the tissue has an abundance of enzymes that operate at submaximal rates.


1985 ◽  
Vol 249 (4) ◽  
pp. E360-E365 ◽  
Author(s):  
E. G. Noble ◽  
C. D. Ianuzzo

Muscle homogenates representing slow-twitch oxidative, fast-twitch oxidative-glycolytic, fast-twitch glycolytic, and mixed fiber types were prepared from normal, diabetic, and insulin-treated diabetic rats. Diabetes was induced by injection of 80 mg . kg-1 of streptozotocin. The activities of citrate synthase, succinate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase were employed as markers of oxidative potential, whereas phosphorylase, hexokinase, and phosphofructokinase activities were used as an indication of glycolytic capacity. Diabetes was associated with a general decrement in the activity of oxidative marker enzymes for all fiber types except the fast-twitch glycolytic fiber. In contrast, the fast-twitch glycolytic fibers demonstrated the greatest decline in glycolytic enzymatic activity. Insulin-treated animals, either trained or untrained, exhibited enzyme activities similar to their normal counterparts. Exercise training of diabetic rats mimicked the effect of insulin treatment and caused a near normalization of the activity of the marker enzymes. These findings suggest that the enzymatic potential of all skeletal muscle fiber types of diabetic rats may be normalized by exercise training even in the absence of significant amounts of insulin.


1990 ◽  
Vol 68 (4) ◽  
pp. 1399-1404 ◽  
Author(s):  
K. H. Kline ◽  
P. J. Bechtel

The purpose of this study was to investigate metabolic changes in equine muscle from birth to 1 yr of age. Duplicate biopsies from the middle portion of the gluteus medius were obtained from a depth of 2 cm beneath the superficial fascia at 1 day, 7 days, 1 mo, 3 mo, 6 mo, and 1 yr of age in 11 quarter horses and at 1 day, 3 mo, 6 mo, and 1 yr of age in 5 Standardbreds. Muscle enzyme activities determined were citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, phosphorylase, and lactate dehydrogenase. Percent fast-twitch, fast-twitch high oxidative, and slow-twitch oxidative fiber types were determined using succinate dehydrogenase and myosin adenosinetriphosphatase (pH 9.4) histochemical stains. Histochemically determined muscle fiber-type percents did not change dramatically with increasing age. However, lactate dehydrogenase activity increased threefold in quarter horses and twofold in Standardbreds, and phosphorylase activity increased sixfold in quarter horses and sevenfold in Standardbreds from 1 day to 6 mo of age. Citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities decreased during the first 3 mo of age in quarter horses.


2003 ◽  
Vol 285 (3) ◽  
pp. E481-E489 ◽  
Author(s):  
Bert Binas ◽  
Xiao-Xia Han ◽  
Erdal Erol ◽  
Joost J. F. P. Luiken ◽  
Jan F. C. Glatz ◽  
...  

The low-molecular-mass, cytosolic heart-type fatty acid-binding protein (H-FABP) is thought to be required for shuttling FA through the cytosol. Therefore, we examined the effects of an H-FABP-null mutation on FA and carbohydrate metabolism in isolated soleus muscle at rest and during a period of increased metabolic demand (30-min contraction). There were lower concentrations of creatine phosphate (-41%), ATP (-22%), glycogen (-34%), and lactate (-31%) ( P < 0.05) in H-FABP-null soleus muscles, but no differences in citrate synthase and β-3-hydroxyacyl-CoA dehydrogenase activities or in the intramuscular triacylglycerol (TAG) depots. There was a 43% increase in subsarcolemmal mitochondria in H-FABP-null solei. FA transport was reduced by 30% despite normal content of sarcolemmal long-chain fatty acid transporters fatty acid translocase/CD36 and plasma membrane-associated FABP transport proteins. Compared with wild-type soleus muscles, the H-FABP-null muscles at rest hydrolyzed less TAG (-22%), esterified less TAG (-49%), and oxidized less palmitate (-71%). The H-FABP-null soleus muscles retained a substantial capacity to increase FA metabolism during contraction (TAG esterification by +72%, CO2 production by +120%), although these rates remained lower (TAG esterification -26% and CO2 production -64%) than in contracting wild-type soleus muscles. Glycogen utilization during 30 min of contraction did not differ, whereas glucose oxidation was lower at rest (-24%) and during contraction (-32%) in H-FABP-null solei. Although these studies demonstrate that the absence of H-FABP alters rates of FA metabolism, it is also apparent that glucose oxidation is downregulated. The substantial increase in FA metabolism in contracting H-FABP-null muscle may indicate that other FABPs are also present, a possibility that we were not able to completely eliminate.


2011 ◽  
Vol 301 (4) ◽  
pp. C841-C849 ◽  
Author(s):  
A. Russell Tupling ◽  
Eric Bombardier ◽  
Subash C. Gupta ◽  
Dawar Hussain ◽  
Chris Vigna ◽  
...  

Sarcolipin (SLN) inhibits sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) pumps. To evaluate the physiological significance of SLN in skeletal muscle, we compared muscle contractility and SERCA activity between Sln-null and wild-type mice. SLN protein expression in wild-type mice was abundant in soleus and red gastrocnemius (RG), low in extensor digitorum longus (EDL), and absent from white gastrocnemius (WG). SERCA activity rates were increased in soleus and RG, but not in EDL or WG, from Sln-null muscles, compared with wild type. No differences were seen between wild-type and Sln-null EDL muscles in force-frequency curves or maximum rates of force development (+dF/d t). Maximum relaxation rates (−dF/d t) of EDL were higher in Sln-null than wild type across a range of submaximal stimulation frequencies, but not during a twitch or peak tetanic contraction. For soleus, no differences were seen between wild type and Sln-null in peak tetanic force or +dF/d t; however, force-frequency curves showed that peak force during a twitch and 10-Hz contraction was lower in Sln-null. Changes in the soleus force-frequency curve corresponded with faster rates of force relaxation at nearly all stimulation frequencies in Sln-null compared with wild type. Repeated tetanic stimulation of soleus caused increased (−dF/d t) in wild type, but not in Sln-null. No compensatory responses were detected in analysis of other Ca2+ regulatory proteins using Western blotting and immunohistochemistry or myosin heavy chain expression using immunofluorescence. These results show that 1) SLN regulates Ca2+-ATPase activity thereby regulating contractile kinetics in at least some skeletal muscles, 2) the functional significance of SLN is graded to the endogenous SLN expression level, and 3) SLN inhibitory effects on SERCA function are relieved in response to repeated contractions thus enhancing relaxation rates.


1999 ◽  
Vol 277 (1) ◽  
pp. E39-E48 ◽  
Author(s):  
H. Green ◽  
S. Grant ◽  
E. Bombardier ◽  
D. Ranney

To investigate the hypothesis that training-induced increases in muscle mitochondrial potential are not obligatory to metabolic adaptations observed during submaximal exercise, regardless of peak aerobic power (V˙o 2 peak) of the subjects, a short-term training study was utilized. Two groups of untrained male subjects ( n = 7/group), one with a high (HI) and the other with a low (LO)V˙o 2 peak(means ± SE; 51.4 ± 0.90 vs. 41.0 ± 1.3 ml ⋅ kg−1 ⋅ min−1; P< 0.05), cycled for 2 h/day at 66–69% ofV˙o 2 peak for 6 days. Muscle tissue was extracted from vastus lateralis at 0, 3, and 30 min of standardized cycle exercise before training (0 days) and after 3 and 6 days of training and analyzed for metabolic and enzymatic changes. During exercise after 3 days of training in the combined HI + LO group, higher ( P < 0.05) concentrations (mmol/kg dry wt) of phosphocreatine (40.5 ± 3.4 vs. 52.2 ± 4.2) and lower ( P < 0.05) concentrations of Pi (61.5 ± 4.4 vs. 53.3 ± 4.4), inosine monophosphate (0.520 ± 0.19 vs. 0.151 ± 0.05), and lactate (37.9 ± 5.5 vs. 22.8 ± 4.8) were observed. These changes were also accompanied by reduced levels of calculated free ADP, AMP, and Pi. All adaptations were fully expressed by 3 min of exercise and by 3 days of training and were independent of initialV˙o 2 peak levels. Moreover, maximal activity of citrate synthase, a measure of mitochondrial capacity, was only increased with 6 days of training (5.71 ± 0.29 vs. 7.18 ± 0.37 mol ⋅ kg protein−1 ⋅ h−1; P < 0.05). These results demonstrate that metabolic adaptations to prolonged exercise occur within the first 3 days of training and during the non-steady-state period. Moreover, neither time course nor magnitude of metabolic adaptations appears to depend on increases in mitochondrial potential or on initial aerobic power.


1986 ◽  
Vol 236 (2) ◽  
pp. 469-473 ◽  
Author(s):  
D J Hayes ◽  
R A J Challiss ◽  
G K Radda

A small animal model of arterial insufficiency has been used to investigate enzymic alterations in the gastrocnemius, plantaris and soleus muscles of the hypoperfused limb. At 7 days after induction of arterial insufficiency by unilateral femoral artery ligation, there were significant increases in the maximal activities of hexokinase, phosphorylase and 6-phosphofructokinase, whereas the activities of citrate synthase and 2-oxoglutarate dehydrogenase remained unchanged. Similar increases in hexokinase, phosphorylase and 6-phosphofructokinase were still apparent 8-10 weeks after unilateral artery ligation, although only hexokinase remained significantly higher than contralateral control values. No enhancement of oxidative enzyme activities was observed. The results are discussed in relation to the conflicting findings reported by other groups investigating enzymic adaptations in patients with arterial insufficiency.


2003 ◽  
Vol 88 (11) ◽  
pp. 5444-5451 ◽  
Author(s):  
Clinton R. Bruce ◽  
Mitchell J. Anderson ◽  
Andrew L. Carey ◽  
David G. Newman ◽  
Arend Bonen ◽  
...  

Abstract We determined whole-body insulin sensitivity, long-chain fatty acyl coenzyme A (LCACoA) content, skeletal muscle triglyceride (TGm) concentration, fatty acid transporter protein content, and oxidative enzyme activity in eight patients with type 2 diabetes (TYPE 2); six healthy control subjects matched for age (OLD), body mass index, percentage of body fat, and maximum pulmonary O2 uptake; nine well-trained athletes (TRAINED); and four age-matched controls (YOUNG). Muscle biopsies from the vastus lateralis were taken before and after a 2-h euglycemic-hyperinsulinemic clamp. Oxidative enzyme activities, fatty acid transporters (FAT/CD36 and FABPpm), and TGm were measured from basal muscle samples, and total LCACoA content was determined before and after insulin stimulation. Whole-body insulin-stimulated glucose uptake was lower in TYPE 2 (P &lt; 0.05) than in OLD, YOUNG, and TRAINED. TGm was elevated in TYPE 2 compared with all other groups (P &lt; 0.05). However, both basal and insulin-stimulated skeletal muscle LCACoA content were similar. Basal citrate synthase activity was higher in TRAINED (P &lt; 0.01), whereas β-hydroxyacyl CoA dehydrogenase activity was higher in TRAINED compared with TYPE 2 and OLD. There was a significant relationship between the oxidative capacity of skeletal muscle and insulin sensitivity (citrate synthase, r = 0.71, P &lt; 0.001; β-hydroxyacyl CoA dehydrogenase, r = 0.61, P = 0.001). No differences were found in FAT/CD36 protein content between groups. In contrast, FABPpm protein was lower in OLD compared with TYPE 2 and YOUNG (P &lt; 0.05). In conclusion, despite markedly elevated skeletal muscle TGm in type 2 diabetic patients and strikingly different levels of whole-body glucose disposal, both basal and insulin-stimulated LCACoA content were similar across groups. Furthermore, skeletal muscle oxidative capacity was a better predictor of insulin sensitivity than either TGm concentration or long-chain fatty acyl CoA content.


1999 ◽  
Vol 86 (4) ◽  
pp. 1247-1256 ◽  
Author(s):  
Shane B. Kanatous ◽  
Leonard V. DiMichele ◽  
Daniel F. Cowan ◽  
Randall W. Davis

The objective was to assess the aerobic capacity of skeletal muscles in pinnipeds. Samples of swimming and nonswimming muscles were collected from Steller sea lions ( Eumetopias jubatus, n = 27), Northern fur seals ( Callorhinus ursinus, n = 5), and harbor seals ( Phoca vitulina, n = 37) by using a needle biopsy technique. Samples were either immediately fixed in 2% glutaraldehyde or frozen in liquid nitrogen. The volume density of mitochondria, myoglobin concentration, citrate synthase activity, and β-hydroxyacyl-CoA dehydrogenase was determined for all samples. The swimming muscles of seals had an average total mitochondrial volume density per volume of fiber of 9.7%. The swimming muscles of sea lions and fur seals had average mitochondrial volume densities of 6.2 and 8.8%, respectively. These values were 1.7- to 2.0-fold greater than in the nonswimming muscles. Myoglobin concentration, citrate synthase activity, and β-hydroxyacyl-CoA dehydrogenase were 1.1- to 2.3-fold greater in the swimming vs. nonswimming muscles. The swimming muscles of pinnipeds appear to be adapted for aerobic lipid metabolism under the hypoxic conditions that occur during diving.


1983 ◽  
Vol 244 (3) ◽  
pp. R407-R411
Author(s):  
S. J. Wickler ◽  
B. A. Horwitz

The thermogenic response to catecholamines, i.e., regulatory nonshivering thermogenesis (NST), is significantly reduced in dystrophic hamsters (BIO 14.6) compared with age-matched normals. The possibility that this reduction reflects, in part, lower levels of enzymes in those tissues implicated in NST has been examined by assaying citrate synthase (CS), beta-hydroxyacyl CoA dehydrogenase (HOAD), and phosphofructokinase (PFK), enzymes whose activity reflect the potential flux of substrates through the tricarboxylic acid cycle, beta-oxidation, and glycolysis, respectively. Each enzyme was assayed in brown fat, heart, gastrocnemius, and semitendinosus of 3-mo-old normal (n = 15) and dystrophic (n = 18) hamsters. Brown fat masses from interscapular, cervical, and scapular-axillary regions of dystrophics averaged only 50% those of normals (424 vs. 890 mg). Additionally, markers of aerobic metabolism (CS and HOAD) were significantly reduced in the brown fat from dystrophic animals. (CS activities averaged 59% of normal, whereas HOAD activities averaged 75% of normal). In dystrophic animals CS and HOAD levels were similar to those of normals in cardiac tissue but were significantly elevated in skeletal muscle samples. Tissue PFK activities were reduced only in cardiac tissue of the more affected dystrophics. Thus decreased NST capacity in dystrophic hamsters is accompanied by reduced masses and CS values in brown fat but not by decreases in the aerobic markers in skeletal or cardiac muscle.


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