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.

scholarly journals Progressive chronic heart failure slows the recovery of microvascular O2 pressures after contractions in the rat spinotrapezius muscle

2010 ◽  
Vol 299 (6) ◽  
pp. H1755-H1761 ◽  
Author(s):  
Steven W. Copp ◽  
Daniel M. Hirai ◽  
Leonardo F. Ferreira ◽  
David C. Poole ◽  
Timothy I. Musch
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Body Weight ◽  
Chronic Heart Failure ◽  
Diastolic Pressure ◽  
Fiber Type ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Type I ◽  
Body Weight Ratio

Chronic heart failure (CHF) induces muscle fiber-type specific alterations in skeletal muscle O2 delivery and utilization during metabolic transitions. As a result, the recovery of microvascular Po2 (PmvO2) is prolonged in slow-twitch skeletal muscle but not fast-twitch skeletal muscle in rats with CHF. We tested the hypothesis that CHF slows PmvO2 recovery in rat skeletal muscle of a mixed fiber-type analogous to human locomotory muscles and that the degree of slowing correlates with central indexes of heart failure. Healthy control [ n = 6, left ventricular end-diastolic pressure (LVEDP): 10 ± 1 mmHg], moderate CHF ( n = 6, LVEDP: 18 ± 2 mmHg), and severe CHF ( n = 4, LVEDP: 34 ± 2 mmHg) female Sprague-Dawley rats had their right spinotrapezius muscles (41% type I, 7% type IIa, and 52% type IIb and d/x) exposed, and PmvO2 was measured via phosphorescence quenching during 180 s of recovery from 180 s of electrically induced twitch contractions (1 Hz, 4–6 V). CHF progressively slowed the mean response time (MRT; the time to reach 63% of the overall dynamic response) of PmvO2 recovery (MRToff; control: 60.2 ± 6.9, moderate CHF: 72.8 ± 6.6, and severe CHF: 109.8 ± 6.6 s, P < 0.05 for all). MRToff correlated positively with central hemodynamic (LVEDP: r = 0.76, P < 0.01) and morphological (right ventricle-to-body weight ratio: r = 0.74, P < 0.01; and lung weight-to-body weight ratio: r = 0.79, P < 0.01) indexes of heart failure. The present investigation suggests that slowed PmvO2 kinetics during recovery in CHF constitutes a mechanistic link between impaired circulatory and metabolic recovery after contractions in CHF.

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.

Gene Polymorphisms and Fiber-Type Composition of Human Skeletal Muscle

2012 ◽  
Vol 22 (4) ◽  
pp. 292-303 ◽  
Author(s):  
Ildus I. Ahmetov ◽  
Olga L. Vinogradova ◽  
Alun G. Williams
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
Human Skeletal Muscle ◽  
Fiber Type ◽  
Vastus Lateralis Muscle ◽  
Type I ◽  
Fiber Types ◽  
Fiber Type Composition ◽  
Type Composition ◽  
Type I Fibers

The ability to perform aerobic or anaerobic exercise varies widely among individuals, partially depending on their muscle-fiber composition. Variability in the proportion of skeletal-muscle fiber types may also explain marked differences in aspects of certain chronic disease states including obesity, insulin resistance, and hypertension. In untrained individuals, the proportion of slow-twitch (Type I) fibers in the vastus lateralis muscle is typically around 50% (range 5–90%), and it is unusual for them to undergo conversion to fast-twitch fibers. It has been suggested that the genetic component for the observed variability in the proportion of Type I fibers in human muscles is on the order of 40–50%, indicating that muscle fiber-type composition is determined by both genotype and environment. This article briefly reviews current progress in the understanding of genetic determinism of fiber-type proportion in human skeletal muscle. Several polymorphisms of genes involved in the calcineurin–NFAT pathway, mitochondrial biogenesis, glucose and lipid metabolism, cytoskeletal function, hypoxia and angiogenesis, and circulatory homeostasis have been associated with fiber-type composition. As muscle is a major contributor to metabolism and physical strength and can readily adapt, it is not surprising that many of these gene variants have been associated with physical performance and athlete status, as well as metabolic and cardiovascular diseases. Genetic variants associated with fiber-type proportions have important implications for our understanding of muscle function in both health and disease.

Effects of ACE inhibition and beta-blockade on skeletal muscle fiber types in dogs with moderate heart failure

1996 ◽  
Vol 270 (1) ◽  
pp. H115-H120 ◽  
Author(s):  
H. N. Sabbah ◽  
H. Shimoyama ◽  
V. G. Sharov ◽  
T. Kono ◽  
R. C. Gupta ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Exercise Intolerance ◽  
Beta Blockade ◽  
Muscle Fiber Types ◽  
Type I ◽  
Fiber Types ◽  
Type Ii ◽  
Early Therapy ◽  
Type I Fibers

The proportion of slow-twitch, fatigue-resistant type 1 skeletal muscle (SM) fibers is often reduced in heart failure (HF), while the proportion of fatigue-sensitive type-II fibers increases. This maladaptation may be partially responsible for the exercise intolerance that characterize HF. In this study, we examined the effects of early monotherapy with the angiotensin-converting enzyme inhibor, enalapril, and the beta-blocker, metoprolol, on SM fiber type composition in 18 dogs with moderate HF produced by intracoronary microembolizations. HF dogs were randomized to 3 mo therapy with enalapril (10 mg twice daily), metoprolol (25 mg twice daily), or no treatment. Triceps muscle biopsies were obtained at baseline, before randomization, and at the end of 30 mo of therapy. Type I and type II SM fibers were differentiated by myofibrillar adenosinetriphosphatase (pH 9.4). In untreated dogs, the proportion of type I fibers was 27 +/- 1% before randomization and decreased to 23 +/- 1% (P < 0.05) at the end of 3 mo of follow up. In dogs treated with enalapril or metoprolol, the proportion of type I fibers was 30 +/- 4 and 28 +/- 2% before randomization and 33 +/- 4 and 33 +/- 1%, respectively, after 3 mo of therapy. In conclusion, in dogs with moderate HF, early therapy with enalapril or metoprolol prevents the progressive decline in the proportion of type I SM fibers.

scholarly journals Altered Skeletal Muscle Fiber Composition and Size Precede Whole-Body Insulin Resistance in Young Men with Low Birth Weight

2007 ◽  
Vol 92 (4) ◽  
pp. 1530-1534 ◽  
Author(s):  
Christine B. Jensen ◽  
Heidi Storgaard ◽  
Sten Madsbad ◽  
Erik A. Richter ◽  
Allan A. Vaag
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Birth Weight ◽  
Capillary Density ◽  
Whole Body ◽  
Type I ◽  
Normal Birth ◽  
Fiber Composition ◽  
Type I Fibers

Abstract Context: Low birth weight (LBW), a surrogate marker of an adverse fetal milieu, is linked to muscle insulin resistance, impaired insulin-stimulated glycolysis, and future risk of type 2 diabetes. Skeletal muscle mass, fiber composition, and capillary density are important determinants of muscle function and metabolism, and alterations have been implicated in the pathogenesis of insulin resistance. Objective: The aim of this study was to investigate whether an adverse fetal environment (LBW) induces permanent changes in skeletal muscle morphology, which may contribute to the dysmetabolic phenotype associated with LBW. Design and Subjects: Vastus lateralis muscle was obtained by percutaneous biopsy from 20 healthy 19-yr-old men with birth weights at 10th percentile or lower for gestational age (LBW) and 20 normal birth weight controls, matched for body fat, physical fitness, and whole-body glucose disposal. Myofibrillar ATPase staining was used to classify muscle fibers as type I, IIa, and IIx (formerly type IIb), and double immunostaining was performed to stain capillaries (LBW, n = 8; normal birth weight, n = 12). Results: LBW was associated with increased proportion of type IIx fibers (+66%; P = 0.03), at the expense of decreased type IIa fibers (−22%; P = 0.003). No significant change was observed in proportion of type I fibers (+16%; P = 0.11). In addition, mean area of type IIa fibers was increased (+29%; P = 0.01) and tended to be increased for type I fibers as well (+17%; P = 0.08). Capillary density was not significantly different between groups. Conclusion: Alterations in fiber composition and size may contribute to development of type 2 diabetes in individuals with LBW.

Genetic effects in human skeletal muscle fiber type distribution and enzyme activities

1986 ◽  
Vol 64 (9) ◽  
pp. 1245-1251 ◽  
Author(s):  
C. Bouchard ◽  
J. A. Simoneau ◽  
G. Lortie ◽  
M. R. Boulay ◽  
M. Marcotte ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
Enzyme Activities ◽  
Fiber Type ◽  
Genetic Effect ◽  
Genetic Effects ◽  
Type I ◽  
Type Distribution ◽  
Fiber Type Distribution ◽  
Mz Twins

The purpose of the study was to estimate the genetic effect for skeletal muscle characteristics using pairs of nontwin brothers (n = 32), dizygotic (DZ) twins (n = 26), and monozygotic (MZ) twins (n = 35). They were submitted to a needle biopsy of the vastus lateralis for the determination of fiber type distribution (I, IIa, IIb) and the following enzymes were assayed for maximal activity: creatine kinase, hexokinase, phosphofructokinase (PFK), lactate dehydrogenase, malate dehydrogenase, 3-hydroxyacyl CoA dehydrogenase, and oxoglutarate dehydrogenase (OGDH). For the percentage of type I fibers, intraclass correlations were 0.33 (p < 0.05), 0.52 (p < 0.01), and 0.55 (p < 0.01) in brothers and DZ and MZ twins, respectively. MZ twins exhibited significant within-pair resemblance for all enzyme activities (0.30 ≤ r ≤ 0.68). In spite of these correlations, genetic analyses performed with the twin data alone indicated that there was no significant genetic effect for muscle fiber type I, IIa, and IIb distribution and fiber areas. Although there were significant correlations in MZ twins for all muscle enzyme activities, the often nonsignificant intraclass coefficients found in brothers and DZ twins suggest that variations in enzyme activities are highly related to common environmental conditions and nongenetic factors. However, genetic factors appear to be involved in the variation of regulatory enzymes of the glycolytic (PFK) and citric acid cycle (OGDH) pathways and in the variation of the oxidative to glycolytic activity ratio (PFK/OGDH ratio). Data show that these genetic effects reach only about 25–50% of the total phenotypic variation when data are adjusted for age and sex differences.

MANIFESTATIONS OF HEART INSUFFICIENCY IN MEN UNDER 60 YEARS OLD WITH MYOCARDIAL INFARCTION COMPLICATED WITH ACUTE KIDNEY DAMAGE

2021 ◽  
pp. 120-127
Author(s):  
Golikov A.V. ◽  
Reiza V.A. ◽  
Tassybayev B.B. ◽  
Gordienko A.V.
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Kidney Injury ◽  
Chronic Heart Failure ◽  
Absolute Risk ◽  
Kidney Injury ◽  
Left Ventricular ◽  
Winter Period ◽  
Study Group ◽  
Type I

Relevance. Acute kidney injury in myocardial infarction worsens its prognosis, including due to the development of chronic heart failure. Moreover, most of the data was obtained for patients over 60 years old. Aim. To evaluate the features of the heart failure manifestations in men under 60 years old with myocardial infarction complicated by acute kidney injury to improve prevention and outcomes. Material and methods. The study included men 19-60 years old with type I myocardial infarction. The patients were divided into two age-comparable groups: I - study group, with acute kidney injury - 25 patients; II - control, without it - 486 patients. A comparative analysis of the heart failure main manifestations frequency in the first 48 hours (1) and at the end of the third week of the disease (2), their dynamics, analysis of their impact on the risk of chronic heart failure development in acute kidney injury (ANOVA) was performed. Results. The study group (4.0%) differed from the control (21.8%) in a lower frequency of acrocyanosis (p = 0.03) and liver enlargement (8.0 and 25.7%; respectively; p = 0.046) at the end of the eighth week diseases. The main risk markers of the chronic heart failure development in study group were: winter period of the year (absolute risk: 94.1%; relative - 3.76; p = 0.0003), respiratory infections 2-3 times a year (absolute risk: 81.8%; p = 0.003), left ventricular myocardial mass index1 ≥ 173.3 g/m2 (absolute risk: 100%; p = 0.008) and mean arterial pressure1 ≥ 120 mm Hg (absolute risk: 100%; relative - 1.88; p = 0.01). Conclusions. Men under 60 years old with acute kidney injury in myocardial infarction are characterized by a higher incidence of chronic heart failure. The listed above values of the different predictors should be used in the formation of the high-risk groups for the chronic heart failure in acute kidney injury development, as well as for prognostic modeling.

Abstract 23: Immunosuppression with FTY720 Reverses Cardiac Dysfunction to Prevent Chronic Heart Failure in Mice that Survive Diet-induced Myocardial Infarction

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Fu Sang Luk ◽  
Roy Y Kim ◽  
Kang Li ◽  
Daniel Ching ◽  
Sunil Joshi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Cardiac Dysfunction ◽  
Coronary Atherosclerosis ◽  
Left Ventricular ◽  
Lv Function ◽  
Chow Diet ◽  
Type I ◽  
Gene Repair

We recently reported that immunosuppression with FTY720 improves cardiac function and extends longevity in the HypoE/SR-BI-/- mouse model of diet-induced coronary atherosclerosis and myocardial infarction (MI). In this study we tested whether FTY720 could also reverse cardiac dysfunction in mice that survive MI and subsequently develop chronic heart failure (CHF). HypoE/SR-BI-/- mice were bred to Mx1-Cre mice and offspring were fed a high fat diet (HFD) for 21 days to provoke hyperlipidemia, coronary atherosclerosis and recurrent MIs. HypoE/SR-BI-/-Mx1-Cre mice were subsequently given oral FTY720 in drinking water or not. Hyperlipidemia was permanently reversed by inducible Cre-mediated gene repair of the HypoE allele (also known as the Apoeh/h allele) that rapidly restores normal apoE expression in all tissues and by switching mice to a normal chow diet. In cohorts of mice that survived this period of HFD, left ventricular (LV) function was monitored using serial echocardiography for up to 15 weeks. In untreated mice, LV performance progressively deteriorated. Although FTY720 treatment did not initially prevent a decline of heart function among HypoE/SR-BI-/-Mx1-Cre mice six weeks after Cre-mediated gene repair, it almost completely restored normal LV function in these mice by 15 weeks after cessation of HFD. Reversal of heart failure did not result from reduced atherosclerosis as the burden of both aortic and coronary atherosclerosis increased to similar levels in both groups of mice. Rather, FTY720 caused systemic immunosuppression as assessed by reduced numbers of circulating T and B lymphocytes. In the heart, FTY720 led to reduced expression of MMP-2 along with the expression of genes involved in Type I innate inflammation that we have recently demonstrated as major contributors to heart failure. Our data demonstrate the benefit of immunosuppression with FTY720 post MI to prevent progressive pathological remodeling of the heart, which leads to CHF.

Muscle fiber type-specific response of Hsp70 expression in human quadriceps following acute isometric exercise

2007 ◽  
Vol 103 (6) ◽  
pp. 2105-2111 ◽  
Author(s):  
A. R. Tupling ◽  
E. Bombardier ◽  
R. D. Stewart ◽  
C. Vigna ◽  
A. E. Aqui
Keyword(s):  
Skeletal Muscle ◽  
Time Course ◽  
Human Skeletal Muscle ◽  
Fiber Type ◽  
Hsp70 Expression ◽  
Type I ◽  
Fiber Types ◽  
Type Ii ◽  
Exercise Induced ◽  
Type I Fibers

To investigate the time course of fiber type-specific heat shock protein 70 (Hsp70) expression in human skeletal muscle after acute exercise, 10 untrained male volunteers performed single-legged isometric knee extensor exercise at 60% of their maximal voluntary contraction (MVC) with a 50% duty cycle (5-s contraction and 5-s relaxation) for 30 min. Muscle biopsies were collected from the vastus lateralis before (Pre) exercise in the rested control leg (C) and immediately after exercise (Post) in the exercised leg (E) only and on recovery days 1 (R1), 2 (R2), 3 (R3), and 6 (R6) from both legs. As demonstrated by Western blot analysis, whole muscle Hsp70 content was unchanged ( P > 0.05) immediately after exercise (Pre vs. Post), was increased ( P < 0.05) by ∼43% at R1, and remained elevated throughout the entire recovery period in E only. Hsp70 expression was also assessed in individual muscle fiber types I, IIA, and IIAX/IIX by immunohistochemistry. There were no fiber type differences ( P > 0.05) in basal Hsp70 expression. Immediately after exercise, Hsp70 expression was increased ( P < 0.05) in type I fibers by ∼87% but was unchanged ( P > 0.05) in type II fibers (Pre vs. Post). At R1 and throughout recovery, Hsp70 content in E was increased above basal levels ( P < 0.05) in all fiber types, but Hsp70 expression was always highest ( P < 0.05) in type I fibers. Hsp70 content in C was not different from Pre at any time throughout recovery. Glycogen depletion was observed at Post in all type II, but not type I, fibers, suggesting that the fiber type differences in exercise-induced Hsp70 expression were not related to glycogen availability. These results demonstrate that the time course of exercise-induced Hsp70 expression in human skeletal muscle is fiber type specific.

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.

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