Muscle fiber regeneration in nerve-intact and free skeletal muscle autografts in cats

1984 ◽  
Vol 246 (1) ◽  
pp. C96-C105 ◽  
Author(s):  
L. C. Maxwell

Extensor digitorum longus (EDL) muscles of adult cats were transplanted as free autografts (FRA) with the nerve severed or as nerve-intact autografts (NIA) with the nerve retained. Histochemical and contractile properties of NIA and FRA were analyzed at selected times from 1 to 14 wk after surgery. Regeneration was qualitatively similar in NIA and FRA. Regenerating fibers were observed in both NIA and FRA within 2 wk. After 14 wk there were fewer type I fibers in both NIA and FRA than in control EDL muscles. Capillarity was greater in NIA than FRA, but both types of autografts had significantly reduced capillarity relative to control muscles. Mean fiber area, muscle mass, and absolute tension development were greater in NIA than FRA but did not reach control muscle values. Muscle mass, mean fiber area, and contractile properties, but not the proportion of type I fibers, develop toward control values more quickly in autografts with the nerve left intact.

1991 ◽  
Vol 260 (2) ◽  
pp. E272-E279 ◽  
Author(s):  
R. M. McAllister ◽  
R. W. Ogilvie ◽  
R. L. Terjung

Functional and metabolic responses of hypothyroid skeletal muscle were evaluated during steady-state isometric contraction conditions, using an isolated perfused rat hindlimb preparation. Treating rats with propylthiouracil (PTU) for 4-5 mo resulted in a 55% decrease (P less than 0.001) in citrate synthase activity in plantaris muscle and phenotypic remodeling of the plantaris, evident by a threefold increase in type I fiber area and a 13% decrease in type II fiber area. Perfusion of PTU (n = 9) and control (n = 9) rat hindlimbs of similar size, with similar inflow (approximately 10 ml/min) and oxygen content (approximately 20 g/100 ml), resulted in similar oxygen deliveries to the contracting muscles (PTU 11.4 +/- 0.58, control 9.54 +/- 0.75 mumol.min-1.g-1; P greater than 0.05). Ten-minute tetanic contraction (100 ms at 100 Hz) periods at 4, 8, 15, 30, and 45 tetani/min were elicited in consecutive ascending order. Oxygen consumption (VO2) was lower in the PTU group at all contraction frequencies (P less than 0.005), with a decrease in peak VO2 of 44% (PTU 3.01 +/- 0.29, control 5.35 +/- 0.42 mumol.min-1.g-1; P less than 0.001). Oxygen extraction by the PTU muscle was only approximately 25% of that delivered. Developed tension was initially less (15%; P less than 0.05) in the PTU group but declined in a similar manner, as a percent of initial, to that of the control group. The slightly lower absolute tension development of the PTU muscle could not account for the large reduction in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)


2009 ◽  
Vol 106 (5) ◽  
pp. 1650-1659 ◽  
Author(s):  
Matthew P. Krause ◽  
Michael C. Riddell ◽  
Carly S. Gordon ◽  
S. Abdullah Imam ◽  
Enzo Cafarelli ◽  
...  

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.


1998 ◽  
Vol 85 (4) ◽  
pp. 1273-1278 ◽  
Author(s):  
Barbara Norman ◽  
Donna K. Mahnke-Zizelman ◽  
Amy Vallis ◽  
Richard L. Sabina

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.


1997 ◽  
Vol 83 (4) ◽  
pp. 1291-1299 ◽  
Author(s):  
Michael D. Delp ◽  
Changping Duan ◽  
John P. Mattson ◽  
Timothy I. Musch

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.


2012 ◽  
Vol 22 (4) ◽  
pp. 292-303 ◽  
Author(s):  
Ildus I. Ahmetov ◽  
Olga L. Vinogradova ◽  
Alun G. Williams

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.


2018 ◽  
Vol 125 (5) ◽  
pp. 1536-1554 ◽  
Author(s):  
Mette Flindt Heisterberg ◽  
Jesper L. Andersen ◽  
Peter Schjerling ◽  
Alberte Lund ◽  
Simone Dalskov ◽  
...  

Our purpose here was to investigate the potential of blocking the angiotensin II type I receptor (AT1R) on the hypertrophy response of elderly human skeletal muscle to 4 mo of heavy-resistance exercise training. Fifty-eight healthy elderly men (+65 yr) were randomized into three groups, consuming either AT1R blocker (losartan, 100 mg/day) or placebo for 4 mo. Two groups performed resistance training (RT) and were treated with either losartan or placebo, and one group did not train but was treated with losartan. Quadriceps muscle biopsies, MR scans, and strength tests were performed at baseline and after 8 and 16 wk. Biopsies were sectioned for immunohistochemistry to determine the number of satellite cells, capillaries, fiber type distribution, and fiber area. Gene expression levels of myostatin, connective tissue, and myogenic signaling pathways were determined by real-time RT-PCR. Four months of heavy-resistance training led in both training groups to expected improvements in quadriceps (∼3–4%) and vastus lateralis (∼5–6%), cross-sectional area, and type II fiber area (∼10–18%), as well as dynamic (∼13%) and isometric (∼19%) quadriceps peak force, but with absolutely no effect of losartan on these outcomes. Furthermore, no changes were seen in satellite cell number with training, and most gene targets failed to show any changes induced by training or losartan treatment. We conclude that there does not appear to be any effect of AT1R blocking in elderly men during 4 mo of resistance training. Therefore, we do not find any support for using AT1R blockers for promoting muscle adaptation to training in humans. NEW & NOTEWORTHY Animal studies have suggested that blocking angiotensin II type I receptor (AT1R) enhances muscle regeneration and prevents disuse atrophy, but studies in humans are limited. Focusing on hypertrophy, satellite cells, and gene expression, we found that AT1R blocking did not result in any greater responses with 4 mo of resistance training. These results do not support previous findings and question the value of blocking AT1R in the context of preserving aging human muscle.


1998 ◽  
Vol 26 (4) ◽  
pp. 598-602 ◽  
Author(s):  
Donald T. Kirkendall ◽  
William E. Garrett

Aging results in a gradual loss of muscle function, and there are predictable age-related alterations in skeletal muscle function. The typical adult will lose muscle mass with age; the loss varies according to sex and the level of muscle activity. At the cellular level, muscles loose both cross-sectional area and fiber numbers, with type II muscle fibers being the most affected by aging. Some denervation of fibers may occur. The combination of these factors leads to an increased percentage of type I fibers in older adults. Metabolically, the glycolytic enzymes seem to be little affected by aging, but the aerobic enzymes appear to decline with age. Aged skeletal muscle produces less force and there is a general “slowing” of the mechanical characteristics of muscle. However, neither reduced muscle demand nor the subsequent loss of function is inevitable with aging. These losses can be minimized or even reversed with training. Endurance training can improve the aerobic capacity of muscle, and resistance training can improve central nervous system recruitment of muscle and increase muscle mass. Therefore, physical activity throughout life is encouraged to prevent much of the age-related impact on skeletal muscle.


1996 ◽  
Vol 270 (1) ◽  
pp. H115-H120 ◽  
Author(s):  
H. N. Sabbah ◽  
H. Shimoyama ◽  
V. G. Sharov ◽  
T. Kono ◽  
R. C. Gupta ◽  
...  

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.


1998 ◽  
Vol 23 (6) ◽  
pp. 594-599 ◽  
Author(s):  
Gary E. Mccall ◽  
William C. Byrnes ◽  
Arthur L. Dickinson ◽  
Steven J. Fleck

This study aimed to determine the skeletal muscle fiber sample size required for a reliable, valid representation of an individual's average fiber area and capillary contacts (CC) per fiber. Biopsies were obtained from the biceps brachii of 11 college-age, recreational resistance-trained men in conjunction with a study investigating how muscle morphology changed after 12 weeks of resistance training. The effect of additional measurements on the rolling cumulative means for fiber area and CC per fiber was evaluated using sequential estimation analysis. Results showed that group cumulative mean and standard deviation had stabilized by 50 fiber measurements per individual for type I and II fibers and CC per fiber. Significant correlations (.96-.99; p < .05) existed between the 50th and 95th/100th cumulative individual means. These results indicate that a typical skeletal muscle needle biopsy would be sufficient to characterize type I and II fiber areas and CC per fiber of an individual in most subject populations, although the required sample size for characterizing fiber subtypes might be different. Key words: muscle biopsy; sequential estimation analysis


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