Lower citrate synthase activity, mitochondrial complex expression, and fewer oxidative myofibers characterize skeletal muscle from growth restricted fetal sheep

2021 ◽  
Author(s):  
Jane Stremming ◽  
Eileen Chang ◽  
Leslie A Knaub ◽  
Michael L Armstrong ◽  
Peter R Baker ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Metabolism ◽  
Mitochondrial Respiration ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Late Gestation ◽  
Postnatal Life ◽  
Type I ◽  
Mitochondrial Complex ◽  
Fetal Sheep

Skeletal muscle from the late gestation sheep fetus with intrauterine growth restriction (IUGR) has evidence of reduced oxidative metabolism. Using a sheep model of placental insufficiency and IUGR, we tested the hypothesis that by late gestation, IUGR fetal skeletal muscle has reduced capacity for oxidative phosphorylation due to intrinsic deficits in mitochondrial respiration. We measured mitochondrial respiration in permeabilized muscle fibers from biceps femoris (BF) and soleus (SOL) from control and IUGR fetal sheep. Using muscles including BF, SOL, tibialis anterior (TA), and flexor digitorum superficialis (FDS), we measured citrate synthase (CS) activity, mitochondrial complex subunit abundance, fiber type distribution, and gene expression of regulators of mitochondrial biosynthesis. Ex vivo mitochondrial respiration was similar in control and IUGR muscle. However, CS activity was lower in IUGR BF and TA, indicating lower mitochondrial content, and protein expression of individual mitochondrial complex subunits was lower in IUGR TA and BF in a muscle specific pattern. IUGR TA, BF, and FDS also had lower expression of type I oxidative fibers. Fiber type shifts that support glycolytic instead of oxidative metabolism may be advantageous for the IUGR fetus in a hypoxic and nutrient deficient environment, whereas these adaptions may be maladaptive in postnatal life.

scholarly journals Fiber Composition and Oxidative Capacity of Hamster Skeletal Muscle

2002 ◽  
Vol 50 (12) ◽  
pp. 1685-1692 ◽  
Author(s):  
John P. Mattson ◽  
Todd A. Miller ◽  
David C. Poole ◽  
Michael D. Delp
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Rank Order ◽  
Oxidative Capacity ◽  
Type I ◽  
Cross Sectional ◽  
Physiological Investigation ◽  
Combining Data ◽  
Type I Fibers

The hamster is a valuable biological model for physiological investigation. Despite the obvious importance of the integration of cardiorespiratory and muscular system function, little information is available regarding hamster muscle fiber type and oxidative capacity, both of which are key determinants of muscle function. The purpose of this investigation was to measure immunohistochemically the relative composition and size of muscle fibers composed of types I, IIA, IIX, and IIB fibers in hamster skeletal muscle. The oxidative capacity of each muscle was also assessed by measuring citrate synthase activity. Twenty-eight hindlimb, respiratory, and facial muscles or muscle parts from adult (144–147 g bw) male Syrian golden hamsters ( n=3) were dissected bilaterally, weighed, and frozen for immunohistochemical and biochemical analysis. Combining data from all 28 muscles analyzed, type I fibers made up 5% of the muscle mass, type IIA fibers 16%, type IIX fibers 39%, and type IIB fibers 40%. Mean fiber cross-sectional area across muscles was 1665 ± 328 μm2 for type I fibers, 1900 ± 417 μm2 for type IIA fibers, 3230 ± 784 μm2 for type IIX fibers, and 4171 ± 864 μm2 for type IIB fibers. Citrate synthase activity was most closely related to the population of type IIA fibers ( r=0.68, p<0.0001) and was in the rank order of type IIA > I > IIX > IIB. These data demonstrate that hamster skeletal muscle is predominantly composed of type IIB and IIX fibers.

scholarly journals Skeletal muscle of females and males with constitutional thinness: a low intramuscular lipid content and oxidative profile

2020 ◽  
Vol 45 (11) ◽  
pp. 1287-1298 ◽  
Author(s):  
Mélina Bailly ◽  
Natacha Germain ◽  
Léonard Féasson ◽  
Frédéric Costes ◽  
Bruno Estour ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Weight Control ◽  
Glycogen Content ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Muscle Fibers ◽  
Oxidative Capacity ◽  
Normal Weight ◽  
Type I ◽  
Before And After

Constitutional thinness (CT) is a nonpathological state of underweight. The current study aimed to explore skeletal muscle energy storage in individuals with CT and to further characterize muscle phenotype at baseline and in response to overfeeding. Thirty subjects with CT (15 females, 15 males) and 31 normal-weight control subjects (16 females, 15 males) participated in the study. Histological and enzymological analyses were performed on muscle biopsy specimens before and after overfeeding. In the skeletal muscle of CT participants compared with controls, we observed a lower content of intramuscular triglycerides for type I (−17%, p < 0.01) and type IIA (−14%, p < 0.05) muscle fibers, a lower glycogen content for type I (−6%, p < 0.01) and type IIA (−5%, p < 0.05) muscle fibers, a specific fiber-type distribution, a marked muscle hypotrophy (−20%, p < 0.001), a low capillary-to-fiber ratio (−19%, p < 0.001), and low citrate synthase activity (−18%, p < 0.05). In response to overfeeding, CT participants increased their intramuscular triglycerides content in type I (+10%, p < 0.01) and type IIA (+9%, p < 0.01) muscle fibers. CT individuals seem to present an unusual muscle phenotype and different adaptations to overfeeding compared with normal-weight individuals, suggesting a specific energy metabolism and muscle adaptations. ClinicalTrials.gov registration no. NCT02004821. Novelty Low intramuscular triglycerides and glycogen content in skeletal muscle of constitutionally thin individuals. Low oxidative capacity, low capillary supply, and fiber hypotrophy in skeletal muscle of constitutionally thin individuals. Increase in intramuscular triglycerides in constitutional thinness in response to overfeeding.

Skeletal muscle characteristics among distance runners: a 20-yr follow-up study

1995 ◽  
Vol 78 (3) ◽  
pp. 823-829 ◽  
Author(s):  
S. W. Trappe ◽  
D. L. Costill ◽  
W. J. Fink ◽  
D. R. Pearson
Keyword(s):  
Skeletal Muscle ◽  
Succinate Dehydrogenase ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Type I ◽  
Distance Runners ◽  
Type Change ◽  
The Mean ◽  
Type I Fibers

The purpose of this investigation was to examine the histochemical and enzymatic characteristics of skeletal muscle after 20 yr of distance running training. Twenty-eight men were first studied between 1966 and 1974 when they were all highly trained distance runners. On the basis of their training regimens in the interim between testing, subjects were described as highly trained (HI; n = 11), fitness trained (FIT; n = 10), or untrained (UT; n = 7). Gastrocnemius muscle biopsy samples revealed a mean increase (P < 0.05) in the proportion of type I fibers of the FIT and UT groups, whereas the HI group, which was initially characterized by a high percentage (> 70%) of type I fibers, was unchanged. Although the mean fiber type change of the HI group was similar between evaluations, 6 of the 11 subjects did elicit an increase in the percentage of type I fibers. A subgroup of elite distance runners who had continued to train for competition experienced an approximately 25% reduction (P > 0.05) in muscle succinate dehydrogenase activity and decreases (P > 0.05) in types I and II muscle fiber areas. On the average, in 1993 the HI group had higher (P < 0.05) succinate dehydrogenase and citrate synthase activities than the FIT and UT groups, whereas phosphorylase activity did not differ among the three groups. These data suggest that the middle-aged men in this study had a significantly greater proportion of type I muscle fibers than when they were 20 yr younger.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract 16555: Angiotensin II Directly Induces Mitochondrial Dysfunction and Atrophy in the Skeletal Muscle

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tomoyasu Kadoguchi ◽  
Shintaro Kinugawa ◽  
Arata Fukushima ◽  
Takaaki Furihata ◽  
Tadashi Suga ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Angiotensin Ii ◽  
Mitochondrial Dysfunction ◽  
Protein Degradation ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Complex Iii ◽  
Skeletal Muscle Atrophy ◽  
Type I ◽  
Ang Ii

Background: Skeletal muscle abnormalities such as mitochondrial dysfunction, fiber type transition, and atrophy are the main cause of reduced exercise capacity observed in various diseases such as diabetes mellitus and heart failure. Renin-angiotensin system (RAS) was activated in the skeletal muscle in these conditions. We thus hypothesized that angiotensin II (Ang II) could directly induce skeletal muscle abnormalities. Methods and Results: Ang II (1000ng/kg/min, n=8) or vehicle (saline, n=8) was administrated into male C57BL/6J mice (10-12 week of age) via subcutaneously implanted osmotic minipumps for 4 weeks. Ang II significantly decreased body weight (26.6±0.3 vs. 27.6±0.3 g, p<0.05) and hind limb skeletal muscle weight compared with vehicle at 4 weeks (159±2 vs. 166±2 mg, p<0.05). It also decreased myocyte cross-sectional area in the skeletal muscle at 4 weeks (1869±29 vs. 2233±46 μm2, p<0.05). Muscle RING finger-1 and atrogin-1, the markers of protein degradation, were significantly increased in the skeletal muscle tissue from Ang II at 4 weeks by 133% and 102%, respectively (p<0.05). In addition, cleaved caspase-3 and TUNEL positive cells were significantly increased in Ang II at 4 weeks by 2.5 and 1.4-folds, respectively (p<0.05). Citrate synthase (1 week, 121±4 vs. 162±9; 4 weeks, 117±7 vs. 152±4 nmol/min/mg protein), complex I (1 week, 264±27 vs. 396±30; 4 weeks, 281±21 vs. 400±30 nmol/min/mg protein) and complex III (1 week, 321±33 vs. 508±49; 4 weeks, 347±30 vs. 503±43 nmol/min/mg protein) activities were significantly decreased in mitochondria isolated from skeletal muscle from Ang II at 1 and 4 weeks (all p<0.05). NADH staining revealed that type I fiber decreased by 31% and type IIb fiber increased by 38% in Ang II at 1 week. The work (16±1 vs. 27±3 J, p<0.05) and run distance (359±18 vs. 589±59 m, p<0.05) evaluated by treadmill test significantly decreased in Ang II at 4 weeks. An administration of Ang II for 1 week also induced mitochondrial dysfunction, fiber type shift, and protein degradation, but did not skeletal muscle atrophy. Conclusion: Ang II could directly induce the reduction of exercise tolerance in association with the abnormalities in skeletal muscle function and structure.

Diabetic myopathy differs betweenIns2Akita+/−and streptozotocin-induced Type 1 diabetic models

2009 ◽  
Vol 106 (5) ◽  
pp. 1650-1659 ◽  
Author(s):  
Matthew P. Krause ◽  
Michael C. Riddell ◽  
Carly S. Gordon ◽  
S. Abdullah Imam ◽  
Enzo Cafarelli ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Citrate Synthase ◽  
Genetic Model ◽  
Fiber Type ◽  
Type I ◽  
Phenotypic Properties ◽  
Current State ◽  
Type I Fibers

Mechanistic studies examining the effects of Type 1 diabetes mellitus (T1DM) on skeletal muscle have largely relied on streptozotocin-induced diabetic (STZ) rodents. Unfortunately, characterization of diabetic myopathy in this model is confounded by the effects of streptozotocin on skeletal muscle independent of the diabetic phenotype. Here we define adolescent diabetic myopathy in a novel, genetic model of T1DM, Ins2Akita+/−mice, and contrast these findings with STZ mice. Eight weeks of diabetes resulted in significantly reduced gastrocnemius-plantaris-soleus mass (control: 0.16 ± 0.005 g; Ins2Akita+/−: 0.12 ± 0.003 g; STZ: 0.12 ± 0.01g) and IIB/D fiber area in Ins2Akita+/−(1,294 ± 94 μm2) and STZ (1,768 ± 163 μm2) compared with control (2,241 ± 144 μm2). Conversely, STZ type I fibers (1,535 ± 165 μm2) were significantly larger than Ins2Akita+/−(915 ± 76 μm2) but not control (1,152 ± 86 μm2). Intramyocellular lipid increased in STZ (122.9 ± 3.6% of control) but not Ins2Akita+/−likely resultant from depressed citrate synthase (control: 6.2 ± 1.2 μmol·s−1·mg−1; Ins2Akita+/−: 5.2 ± 0.8 μmol·s−1·mg−1; STZ: 2.8 ± 0.5 μmol·s−1·mg−1) and 3-β-hydroxyacyl coenzyme-A dehydrogenase (control: 4.2 ± 0.6 nmol·s−1·mg−1; Ins2Akita+/−: 5.0 ± 0.6 nmol·s−1·mg−1; STZ: 2.7 ± 0.6 nmol·s−1·mg−1) enzyme activity in STZ muscle. In situ muscle stimulation revealed lower absolute peak tetanic force in Ins2Akita+/−(70.2 ± 8.2% of control) while STZ exhibited an insignificant decrease (87.6 ± 7.9% of control). Corrected for muscle mass, no force loss was observed in Ins2Akita+/−, while STZ was significantly elevated vs. control and Ins2Akita+/−. These results demonstrate that atrophy and specific fiber-type loss in Ins2Akita+/−muscle did not affect contractile properties (relative to muscle mass). Furthermore, we demonstrate distinctive contractile, metabolic, and phenotypic properties in STZ vs. Ins2Akita+/−diabetic muscle despite similarity in hyperglycemia/hypoinsulinemia, raising concerns of our current state of knowledge regarding the effects of T1DM on skeletal muscle.

Curcumin induces mitochondrial biogenesis by increasing cAMP levels via PDE4A inhibition in skeletal muscle

2021 ◽  
pp. 1-34
Author(s):  
Hamidie Ronald D Ray ◽  
Tsubasa Shibaguchi ◽  
Tatsuya Yamada ◽  
Rikuhide Koma ◽  
Rie Ishizawa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Respiration ◽  
Citrate Synthase ◽  
Signalling Pathway ◽  
Curcumin Treatment ◽  
Camp Content ◽  
Signalling Molecules ◽  
Camp Levels

Abstract Background: Previous research has suggested that curcumin potentially induces mitochondrial biogenesis in skeletal muscle via increasing cAMP levels. However, the regulatory mechanisms for this phenomenon remain unknown. The purpose of the present study was to clarify the mechanism by which curcumin activates cAMP-related signalling pathways that upregulate mitochondrial biogenesis and respiration in skeletal muscle. Methods: The effect of curcumin treatment (i.p., 100 mg/kg-BW/day for 28 days) on mitochondrial biogenesis was determined in rats. The effects of curcumin and exercise (swimming for 2 h/day for 3 days) on the cAMP signalling pathway were determined in the absence and presence of phosphodiesterase (PDE) or protein kinase A (PKA) inhibitors. Mitochondrial respiration, citrate synthase (CS) activity, cAMP content, and protein expression of cAMP/PKA signalling molecules were analysed. Results: Curcumin administration increased COX-IV protein expression, and CS and complex I activity, consistent with the induction of mitochondrial biogenesis by curcumin. Mitochondrial respiration was not altered by curcumin treatment. Curcumin and PDE inhibition tended to increase cAMP levels with or without exercise. In addition, exercise increased the phosphorylation of PDE4A, whereas curcumin treatment strongly inhibited PDE4A phosphorylation regardless of exercise. Furthermore, curcumin promoted AMPK phosphorylation and PGC-1α deacetylation. Inhibition of PKA abolished the phosphorylation of AMPK. Conclusion: The present results suggest that curcumin increases cAMP levels via inhibition of PDE4A phosphorylation, which induces mitochondrial biogenesis through a cAMP/PKA/AMPK signalling pathway. Our data also suggest the possibility that curcumin utilizes a regulatory mechanism for mitochondrial biogenesis that is distinct from the exercise-induced mechanism in skeletal muscle.

Anemic Hypoxemia Reduces Myoblast Proliferation and Muscle Growth in Late Gestation Fetal Sheep

2021 ◽  
Author(s):  
Paul J. Rozance ◽  
Stephanie R Wesolowski ◽  
Sonnet S. Jonker ◽  
Laura D Brown
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Muscle Growth ◽  
Late Gestation ◽  
Whole Body ◽  
Myoblast Differentiation ◽  
Fetal Sheep ◽  
Body Protein ◽  
Skeletal Muscle Growth ◽  
Myoblast Proliferation

Fetal skeletal muscle growth requires myoblast proliferation, differentiation, and fusion into myofibers in addition to protein accretion for fiber hypertrophy. Oxygen is an important regulator of this process. Therefore, we hypothesized that fetal anemic hypoxemia would inhibit skeletal muscle growth. Studies were performed in late gestation fetal sheep that were bled to anemic, and therefore hypoxemic, conditions beginning at ~125 days of gestation (term = 148 days) for 9 ± 0 days (n=19) and compared to control fetuses (n=16). A metabolic study was performed on gestational day ~134 to measure fetal protein kinetic rates. Myoblast proliferation and myofiber area were determined in biceps femoris (BF), tibialis anterior (TA), and flexor digitorum superficialis (FDS) muscles. mRNA expression of muscle regulatory factors was determined in BF. Fetal arterial hematocrit and oxygen content were 28% and 52% lower, respectively, in anemic fetuses. Fetal weight and whole-body protein synthesis, breakdown, and accretion rates were not different between groups. Hindlimb length, however, was 7% shorter in anemic fetuses. TA and FDS muscles weighed less and FDS myofiber area was smaller in anemic fetuses compared to controls. The percentage of Pax7+ myoblasts that expressed Ki67 was lower in BF and tended to be lower in FDS from anemic fetuses indicating reduced myoblast proliferation. There was less MYOD and MYF6 mRNA expression in anemic vs. control BF consistent with reduced myoblast differentiation. These results indicate that fetal anemic hypoxemia reduced muscle growth. We speculate that fetal muscle growth may be improved by strategies that increase oxygen availability.

Genetic and other determinants of AMP deaminase activity in healthy adult skeletal muscle

1998 ◽  
Vol 85 (4) ◽  
pp. 1273-1278 ◽  
Author(s):  
Barbara Norman ◽  
Donna K. Mahnke-Zizelman ◽  
Amy Vallis ◽  
Richard L. Sabina
Keyword(s):  
Skeletal Muscle ◽  
Enzyme Activity ◽  
Mutant Allele ◽  
Fiber Type ◽  
Type I ◽  
Training Status ◽  
Amp Deaminase ◽  
Normal Allele ◽  
Relative Percentage ◽  
Type I Fibers

AMPD1 genotype, relative fiber type composition, training status, and gender were evaluated as contributing factors to the reported variation in AMP deaminase enzyme activity in healthy skeletal muscle. Multifactorial correlative analyses demonstrate that AMPD1 genotype has the greatest effect on enzyme activity. An AMPD1 mutant allele frequency of 13.7 and a 1.7% incidence of enzyme deficiency was found across 175 healthy subjects. Homozygotes for the AMPD1 normal allele have high enzyme activities, and heterozygotes display intermediate activities. When examined according to genotype, other factors were found to affect variability as follows: AMP deaminase activity in homozygotes for the normal allele exhibits a negative correlation with the relative percentage of type I fibers and training status. Conversely, residual AMP deaminase activity in homozygotes for the mutant allele displays a positive correlation with the relative percentage of type I fibers. Opposing correlations in different homozygous AMPD1 genotypes are likely due to relative fiber-type differences in the expression of AMPD1 and AMPD3 isoforms. Gender also contributes to variation in total skeletal muscle AMP deaminase activity, with normal homozygous and heterozygous women showing only 85–88% of the levels observed in genotype-matched men.

Shortening velocity and ATPase activity of rat skeletal muscle fibers: effects of endurance exercise training

1994 ◽  
Vol 266 (6) ◽  
pp. C1699-C1713 ◽  
Author(s):  
J. M. Schluter ◽  
R. H. Fitts
Keyword(s):  
Atpase Activity ◽  
Endurance Exercise ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Treadmill Running ◽  
Type I ◽  
Marker Enzyme ◽  
Shortening Velocity

Mechanical properties were measured in single skinned fibers from rat hindlimb muscle to test the hypothesis that the fast type IIb fiber exhibits a higher maximal shortening velocity (Vo) than the fast type IIa fiber and that the difference is directly attributable to a higher myofibrillar adenosinetriphosphatase (ATPase) activity in the type IIb fiber. Additional measurements were made to test the hypotheses that regular endurance exercise increases and decreases the Vo of the type I and IIa fiber, respectively, and that the altered Vo is associated with a corresponding change in the fiber ATPase activity. Rats were exercised by 8-12 wk of treadmill running for 2 h/day, 5 day/wk, up a 15% grade at a speed of 27 m/min. Fiber Vo was determined by the slack test, and the ATPase was measured fluorometrically in the same fiber. The myosin isozyme profile of each fiber was subsequently determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The mean +/- SE Vo (7.9 +/- 0.22 fiber lengths/s) of the type IIb fiber was significantly greater than the type IIa fiber (4.4 +/- 0.21 fiber lengths/s), and the higher Vo was associated with a higher ATPase activity (927 +/- 70 vs. 760 +/- 60 microM.min-1.mm-3). The exercise program induced cardiac hypertrophy and an approximately twofold increase in the mitochondrial marker enzyme citrate synthase. Exercise had no effect on fiber diameter or peak tension per cross-sectional area in any fiber type, but, importantly, it significantly increased (23%) both the Vo and the ATPase activity of the slow type I fiber of the soleus.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in skeletal muscle biochemistry and histology relative to fiber type in rats with heart failure

1997 ◽  
Vol 83 (4) ◽  
pp. 1291-1299 ◽  
Author(s):  
Michael D. Delp ◽  
Changping Duan ◽  
John P. Mattson ◽  
Timothy I. Musch
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Enzyme Activities ◽  
Fiber Type ◽  
Left Ventricular ◽  
Type I ◽  
Fiber Composition ◽  
Muscle Biochemistry ◽  
Type I Fibers

Delp, Michael D., Changping Duan, John P. Mattson, and Timothy I. Musch. Changes in skeletal muscle biochemistry and histology relative to fiber type in rats with heart failure. J. Appl. Physiol. 83(4): 1291–1299, 1997.—One of the primary consequences of left ventricular dysfunction (LVD) after myocardial infarction is a decrement in exercise capacity. Several factors have been hypothesized to account for this decrement, including alterations in skeletal muscle metabolism and aerobic capacity. The purpose of this study was to determine whether LVD-induced alterations in skeletal muscle enzyme activities, fiber composition, and fiber size are 1) generalized in muscles or specific to muscles composed primarily of a given fiber type and 2) related to the severity of the LVD. Female Wistar rats were divided into three groups: sham-operated controls ( n = 13) and rats with moderate ( n = 10) and severe ( n = 7) LVD. LVD was surgically induced by ligating the left main coronary artery and resulted in elevations ( P < 0.05) in left ventricular end-diastolic pressure (sham, 5 ± 1 mmHg; moderate LVD, 11 ± 1 mmHg; severe LVD, 25 ± 1 mmHg). Moderate LVD decreased the activities of phosphofructokinase (PFK) and citrate synthase in one muscle composed of type IIB fibers but did not modify fiber composition or size of any muscle studied. However, severe LVD diminished the activity of enzymes involved in terminal and β-oxidation in muscles composed primarily of type I fibers, type IIA fibers, and type IIB fibers. In addition, severe LVD induced a reduction in the activity of PFK in type IIB muscle, a 10% reduction in the percentage of type IID/X fibers, and a corresponding increase in the portion of type IIB fibers. Atrophy of type I fibers, type IIA fibers, and/or type IIB fibers occurred in soleus and plantaris muscles of rats with severe LVD. These data indicate that rats with severe LVD after myocardial infarction exhibit 1) decrements in mitochondrial enzyme activities independent of muscle fiber composition, 2) a reduction in PFK activity in type IIB muscle, 3) transformation of type IID/X to type IIB fibers, and 4) atrophy of type I, IIA, and IIB fibers.

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