Overwork effect on partially denervated rat soleus muscle

The purpose of this study was to assess the effect of overwork induced by synergistic tenotomy on the muscle weight (MW) and isometric tetanic tension (Po) of the partially denervated rat soleus muscle. Forty-nine young adult male Sprague-Dawley rats were divided into six groups (n = 5 to 9): normal control (N), normal synergistically tenotomized (N-ST), L4 denervated control (L4), L4 denervated synergistically tenotomized (L4-ST), L5 denervated control (L5), and L5 denervated synergistically tenotomized (L5-ST). Bilateral L4 or L5 root transections produced partial denervation. To yield soleus muscle overwork the gastrocnemius and plantaris muscles were bilaterally tenotomized in all ST groups at the time of denervation. The soleus MW and Po were examined seven days following denervation and tenotomy. Compared to their respective controls, there was increased MW in the N-ST (43.5%, p less than 0.01) and the L4-ST (38.6% p less than 0.01) groups. The L5-ST group showed no significant change in MW compared to the L5 group. Tetanic tension was increased only in the N-ST group. The L4-ST and L5-ST groups did not show any change in Po compared to their respective controls. Despite marked denervation, the L5 group did not show any atrophy as compared to the N group, suggesting passive stretch of the denervated muscle fibers, hypertrophy of the innervated muscle fibers and peripheral sprouting prevented the loss of MW due to denervation. Overwork in this markedly denervated group could not produce any increase in the MW or Po.(ABSTRACT TRUNCATED AT 250 WORDS)     

Synergistic tenotomy: effect on chronically denervated slow and fast muscles of rat.

A study was conducted with chronically denervated adult female Wistar rats to test the hypothesis that synergistic tenotomy of denervated skeletal muscles does not just retard atrophy but produces an increase in muscle weight. The animals were categorized in three groups-denervated exercised (DE), denervated tenotomized (DT), and denervated-tenotomized-exercised (DTE). Mechanical stretch was induced in the DE group by forcing the animals to stand on their hind legs to reach for food and water. In the DT group, mechanical stretch was induced by tenotomy of two synergists in the gastrocnemius-plantaris-soleus complex of each leg of the rat so that either the soleus or the plantaris was left as the only plantar-flexor of the ankle joint in each leg. Mechanical stretch was induced in the DTE group by forcing the animals to stand after the tenotomy of synergists at eight weeks postdenervation. All animals in the three experimental groups, and in the sedentary control group (D) were sacrificed at nine weeks postdenervation; the soleus and plantaris muscles were removed and evaluated for MW, DW and percent of hydration. The slow muscle (soleus) increased in muscle mass in DT (53%), DE (26%), and DTE (17%). The fast muscle (plantaris) increased in weight in DE (18%) and in DTE (24%), but showed no significant changes in DT. Study results confirm the hypothesis that synergistic tenotomy stimulates an increase in muscle weight rather than merely retarding atrophy, and that this phenomenon can take place in the absence of neuronal influences. It is suggested that the increase in denervated muscle mass stimulated by muscle elongation is not a true work hypertrophy associated with significant changes in protein concentrations but only an adaptation to a new muscle length. The purpose of the adaptational changes is to optimize the overlap of actomyosin bridges in anticipation of forceful muscle contraction.     

Disruption of either the Nfkb1 or the Bcl3 gene inhibits skeletal muscle atrophy

The intracellular signals that mediate skeletal muscle protein loss and functional deficits due to muscular disuse are just beginning to be elucidated. Previously we showed that the activity of an NF-kappaB-dependent reporter gene was markedly increased in unloaded muscles, and p50 and Bcl-3 proteins were implicated in this induction. In the present study, mice with a knockout of the p105/p50 (Nfkb1) gene are shown to be resistant to the decrease in soleus fiber cross-sectional area that results from 10 days of hindlimb unloading. Furthermore, the marked unloading-induced activation of the NF-kappaB reporter gene in soleus muscles from WT mice was completely abolished in soleus muscles from Nfkb1 knockout mice. Knockout of the B cell lymphoma 3 (Bcl3) gene also showed an inhibition of fiber atrophy and an abolition of NF-kappaB reporter activity. With unloading, fast fibers from WT mice atrophied to a greater extent than slow fibers. Resistance to atrophy in both strains of knockout mice was demonstrated clearly in fast fibers, while slow fibers from only the Bcl3(-/-) mice showed atrophy inhibition. The slow-to-fast shift in myosin isoform expression due to unloading was also abolished in both Nfkb1 and Bcl3 knockout mice. Like the soleus muscles, plantaris muscles from Nfkb1(-/-) and Bcl3(-/-) mice also showed inhibition of atrophy with unloading. Thus both the Nfkb1 and the Bcl3 genes are necessary for unloading-induced atrophy and the associated phenotype transition.     

Effect of early low-intensity exercise on rat hind-limb muscles following acute ischemic stroke

This study examined the effects of daily low-intensity exercise following acute stroke on mass, Type I and II fiber cross-sectional area, and myofibrillar protein content of hind-limb muscles in a rat model. Adult male Sprague-Dawley rats were randomly assigned to 1 of 4 groups (n = 7-9 per group): stroke (occlusion of the right middle cerebral artery [RMCA]), control (sham RMCA procedure), exercise, and stroke-exercise. Beginning 48 hours post-stroke induction/sham operation, rats in the exercise group had 6 sessions of exercise in which they ran on a treadmill at grade 10 for 20 min/day at 10 m/min. At 8 days poststroke, all rats were anesthetized and soleus, plantaris, and gastrocnemius muscles were dissected from both the affected and unaffected sides. After 6 sessions of exercise following acute ischemic stroke, the stroke-exercise group showed the following significant (p < .05) increases compared to the stroke-only group: body weight and dietary intake, muscle weight of affected soleus and both affected and unaffected gastrocnemius muscle, Type I fiber cross-sectional area of affected soleus and both affected and unaffected gastrocnemius muscle, Type II fiber cross-sectional area of the unaffected soleus, both affected and unaffected plantaris and gastrocnemius muscle, Type II fiber distribution of affected gastrocnemius muscle, and myofibrillar protein content of both affected and unaffected soleus muscle. Daily low-intensity exercise following acute stroke attenuates hind-limb muscle atrophy in both affected and unaffected sides. The effects of exercise are more pronounced in the soleus and gastrocnemius as compared to the plantaris muscle.     

Overwork-induced axonal hypertrophy in the soleus nerve of the rat

Effect of overwork, induced by synergistic tenotomy (bilateral tenotomy of the gastrocnemius and the plantaris muscles) of the soleus muscle, was evaluated on areas of the large myelinated axons (LMA) (greater than 19.5 micron 2), in the soleus nerve (the tibial nerve branch innervating the soleus muscle) of the rat. Three lots (n = 12-16) of young adult male (body weight of 275 to 325 g), Sprague-Dawley rats were used. One lot of 16 animals was kept as normal, while the other two underwent bilateral L4 or L5 spinal nerve sectioning. Six to seven animals each from the normal, L4-, and L5 neurectomized animals underwent bilateral synergistic tenotomy of the soleus so that the soleus was retained as the sole plantar-flexor of the ankle joint. The remaining animals were kept as normal or neurectomized control groups. Thus, the six groups studied were normal control (n = 9); normal synergistically tenotomized (n = 7); L4 neurectomized control (n = 8); L4 neurectomized and synergistically tenotomized (n = 6); L5 neurectomized control (n = 8); and L5 neurectomized and synergistically tenotomized (n = 7). Seven days after surgery, the soleus muscles were used to evaluate the muscle weights. The soleus nerves were evaluated for the number plus areas of the LMA by computerized planimetric procedures. The data revealed a 13.9% (p less than 0.05) increase in areas of the LMA in the L5 neurectomized control group; whereas the L5 neurectomized and synergistically tenotomized group showed a 39.6% (p less than 0.01) increase in areas of the LMA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Study of skeletal muscle glycogenolysis and glycolysis in chronic steroid myopathy, non-steroid histochemical type-2 fiber atrophy, and denervation

OBJECTIVE: Muscle biopsies from chronic steroid (glucocorticoid) myopathy, non-steroid histochemical type-2 fiber atrophy, and muscle denervation patients were studied to determine if their glycogen contents, or enzymes involved in glycogenolysis and glycolysis might be related to their fiber atrophy. DESIGN AND METHODS: Fast frozen muscle biopsies from the above patients and from patients later judged by histochemistry to be normal were assayed enzymatically for glycogen content, for enzymes involved in glycogenolysis, and for 6 of the enzymes involved in glycolysis. RESULTS AND CONCLUSION: All three groups of patients had glycogen content, but only the chronic steroid myopathy muscle had statistically less glycogen content than did normal human muscle. All 3 groups had statistically low mean values compared to normal muscles for glycogen phosphorylase activity. This suggests that the biosynthesis and phosphorolysis of glycogen are not involved in muscle fiber atrophy, and glucocorticoid administration does not activate muscle glycogen biosynthesis. Histochemical type-2 fiber atrophy muscles were low compared to normal muscles in three glycogenolysis enzyme activities plus four glycolysis enzyme activities. Muscles from denervation patients were low compared to normal muscles in three glycogenolysis enzyme activities plus five glycolysis enzyme activities. This suggests that muscle denervation may lower the rate of glycolysis enough to fail to provide sufficient pyruvate for mitochondrial ATP biosynthesis, resulting in insufficient protein biosynthesis in both fiber types.     

Alterations in skeletal muscle related to impaired physical mobility: An empirical model

The objective of this investigation was to study impaired physical mobility and the resulting skeletal muscle atrophy. An animal model was used to study morphological adaptations of the soleus and plantaris muscles to decreased loading induced by hindlimb suspension of an adult rat for 7, 14, and 28 consecutive days. Alterations in weight, skeletal muscle growth, and changes in fiber type composition were studied in synergistic plantar flexors of the rat hindlimb. Body weight and the soleus muscle mass to body mass ratio demonstrated significant progressive atrophy over th 28-day experimental period with the most significant changes occurring in the first 7 days of hindlimb suspension. Hindlimb suspension produced atrophy of Type I and Type lla muscle fibers as demonstrated by significant decreases in fiber cross-sectional area (γm²). These latter changes account for the loss of contractile force production reported in the rat following hindlimb unloading. When compared to traditional models of hindlimb suspension and immobilization, the ISC model produces a less severe atrophy while maintaining animal mobility and health. We conclude that it is the preferred animal model to address nursing questions of impaired physical mobility. © 1993 John Wiley & Sons, Inc.     

Length and circumference measurements in one-joint and multijoint muscles in rabbits after immobilization

In this article, we compared changes in the length and circumference of the soleus and the plantaris muscles in rabbits. The rabbits were assigned to a nonimmobilized external control group (n = 4), an experimental shortened-position group (n = 10), or an experimental lengthened-position group (n = 9). One hind limb of each animal in the experimental groups was immobilized in a cast for four weeks to put the muscles in either a shortened or lengthened position. The contralateral limb served as an internal control for the animals in the experimental groups. After the immobilization period, the limbs were fixed in situ, the muscles were dissected, and length and circumference measurements were taken. In both experimental conditions, the immobilized soleus muscles were shorter than their contralateral counterparts (p less than .05); the length of the plantaris muscles did not change. The immobilized muscles had decreased circumference values regardless of the immobilization angle. When compared with the control condition, the shortened soleus muscles had a greater decrease in circumference than did the plantaris muscles. More connective tissue was observed in the muscle bellies of the soleus after immobilization than in the plantaris. Similar significant changes (p less than .05) were found in the nonimmobilized limbs of the animals in the experimental groups. Specifically, the soleus muscles demonstrated length and circumference changes, whereas the plantaris muscles showed changes only in circumference. These findings suggest that when a weight-bearing limb is immobilized, adaptations in gross muscle length and circumference are to be expected in the involved and uninvolved limbs. An assessment of similar adaptations in humans should be a part of the evaluation during recovery.     

Recovery of plantaris muscle from impaired physical mobility

The purpose of this investigation was to describe and compare various methods of recovering atrophied fast-twitch skeletal muscle following long-term impaired physical mobility. An animal model was used to study morphological adaptations of atrophied plantaris muscles to the effects of 28 days of hindlimb suspension (HS) followed by either sedentary recovery or run training during a 28-day recovery period. Significant atrophy, demonstrated by decreased mean fiber area (MFA, micron 2), occurred during the 28-day period of HS. However, run training following long-term atrophy induced by HS did not result in the high levels of frank muscle damage and type IIC fibers previously reported in slow-twitch soleus muscle following long-term (28 days) atrophy.     

Carotenoid transporter CD36 expression depends on hypoxia-inducible factor-1α in mouse soleus muscles

Dietary β-carotene induces muscle hypertrophy and prevents muscle atrophy in red slow-twitch soleus muscles, but not in white fast-twitch extensor digitorum longus (EDL) muscles and gastrocnemius muscles. However, it remains unclear why these beneficial effects of β-carotene are elicited in soleus muscles. To address this issue, we focused on carotenoid transporters in skeletal muscles. In mice, Cd36 mRNA levels were higher in red muscle than in white muscle. The siRNA-mediated knockdown of CD36 decreased β-carotene uptake in C2C12 myotubes. In soleus muscles, CD36 knockdown inhibited β-carotene-induced increase in muscle mass. Intravenous injection of the hypoxia marker pimonidazole produced more pimonidazole-bound proteins in soleus muscles than in EDL muscles, and the hypoxia-inducible factor-1 (HIF-1) α protein level was higher in soleus muscles than in EDL muscles. In C2C12 myotubes, hypoxia increased the expression of CD36 and HIF-1α at the protein and mRNA levels, and HIF-1α knockdown reduced hypoxia-induced increase in Cd36 mRNA level. In soleus muscles, HIF-1α knockdown reduced Cd36 mRNA level. These results indicate that CD36 is predominantly involved in β-carotene-induced increase in soleus muscle mass of mice. Furthermore, we demonstrate that CD36 expression depends on HIF-1α in the soleus muscles of mice, even under normal physiological conditions.     

Effect of Extracorporeal Shock Wave Therapy on Denervation Atrophy and Function Caused by Sciatic Nerve Injury

[Purpose] The present study examined the effects of treatment using extracorporeal shock wave therapy (ESWT) on the muscle weight and function of the hind limb in sciatic nerve injury. [Subjects] Forty rats with sciatic nerve crushing injury were randomly divided into two groups: an ESWT group (n=20), and a control group (n=20). [Methods] The ESWT group received extracorporeal shock wave treatment, and the control group did not receive any treatment after injury. Experimental animals were measured for muscle weight on an electronic scale and were tested for function on a sciatic functional index (SFI). [Results] All groups showed significant increases in the weights of the left soleus and gastrocnemius muscles, and decreases in the weights of the right soleus and gastrocnemius muscles (p<0.05). Comparison of SFI scores and muscle weights between the groups showed significant differences in SFI scores, and the right soleus and gastrocnemius muscles (p<0.05) [Conclusion] Exercise programs that use ESWT can be said to be effective at improving the function of the sciatic nerve and preventing the denervation atrophy.Key words: ESWT, Sciatic nerve, Peripheral nerve     

Alterations in skeletal muscle related to short-term impaired physical mobility

The purpose of this investigation was to describe and compare two methods of recovery of atrophied skeletal muscle following short-term impaired physical mobility. An animal model was used to study morphologic adaptations of atrophied soleus and plantaris muscles to the effects of 7 days of hind-limb suspension (HS) followed by either sedentary recovery or run training during a 28-day recovery period. Significant atrophy, demonstrated by decreased mean fiber area (MFA, in square micrometers), occurred during the 7-day period of HS. During recovery, MFA returned to control values 14 days earlier in the sedentary compared with the trained groups. Run training following short-term atrophy induced by HS did not result in the high levels of frank muscle damage and type IIC fibers previously reported following long-term (28-day) atrophy. © 1996 John Wiley & Sons, Inc.     

In vivo time-lapse microscopy reveals no loss of murine myonuclei during weeks of muscle atrophy

Numerous studies have suggested that muscle atrophy is accompanied by apoptotic loss of myonuclei and therefore recovery would require replenishment by muscle stem cells. We used in vivo time-lapse microscopy to observe the loss and replenishment of myonuclei in murine muscle fibers following induced muscle atrophy. To our surprise, imaging of single fibers for up to 28 days did not support the concept of nuclear loss during atrophy. Muscles were inactivated by denervation, nerve impulse block, or mechanical unloading. Nuclei were stained in vivo either acutely by intracellular injection of fluorescent oligonucleotides or in time-lapse studies after transfection with a plasmid encoding GFP with a nuclear localization signal. We observed no loss of myonuclei in fast- or slow-twitch muscle fibers despite a greater than 50% reduction in fiber cross-sectional area. TUNEL labeling of fragmented DNA on histological sections revealed high levels of apoptotic nuclei in inactive muscles. However, when costained for laminin and dystrophin, virtually none of the TUNEL-positive nuclei could be classified as myonuclei; apoptosis was confined to stromal and satellite cells. We conclude that disuse atrophy is not a degenerative process, but is rather a change in the balance between protein synthesis and proteolysis in a permanent cell syncytium.     

Clenbuterol in the prevention of muscle atrophy: a study of hindlimb-unweighted rats.

OBJECTIVE: To determine whether the administration of clenbuterol, a beta2-adrenergic agonist, prevents loss of muscle mass during a period of imposed inactivity. DESIGN: Randomized trial. SETTING: Basic laboratory research. ANIMALS: Thirty Fischer 344 Brown Norway F1 Hybrid rats, 12 and 30 months of age. INTERVENTIONS: The rats were randomly assigned to a control group, or to 1 of 2 experimental groups: hindlimb unweighted for 2 weeks (HU-2), or hindlimb unweighted with daily injections of clenbuterol for 2 weeks (HU-2Cl). MAIN OUTCOME MEASURES: Muscle mass weighed in milligrams and single fiber cross-sectional area histochemically evaluated. RESULTS: In both age groups, the HU-2 animals had greater muscle atrophy (decrease in muscle mass) in the soleus muscle than the extensor digitorum longus (EDL) muscle. In the HU-2Cl groups, the decline in muscle mass of both the soleus and EDL muscles was attenuated by about 4% to 20%. In the HU-2 group, single fiber cross-sectional area decreased for both fiber types (type I, 20%-40%; type II, 37%-50%) in both age groups. Clenbuterol retarded the inactivity-induced decline in single fiber cross-sectional area by 12% to 50%. In the EDL muscles of the HU-2Cl group, we found hypertrophy in both fiber types in the 30-month-old animals and in type I fibers in the 12-month-old animals. CONCLUSIONS: Clenbuterol attenuated the decrease in muscle mass and single fiber cross-sectional area in both age groups. By preventing the loss of muscle mass, clenbuterol administered early in rehabilitation may benefit severely debilitated patients imposed by inactivity. The attenuated muscle atrophy found with clenbuterol in the present study provides cellular evidence for the reported change in muscle strength after its administration after knee surgery. Thus, the administration of clenbuterol may lead to a more rapid rate of rehabilitation.     

Acute effects of ethanol on protein synthesis in different muscles and muscle protein fractions of the rat

1. The effects of a single dose of ethanol (75 mmol/kg body weight) on rates of muscle protein synthesis were examined in young rats. Fractional rates of protein synthesis were measured in the soleus, plantaris, gastrocnemius, diaphragm and stomach by the large 'flooding-dose' technique. 2. After 150 min, the fractional synthesis rates of all muscles were reduced by 15-35%. Skeletal muscles containing a predominance of anaerobic (fast-twitch, type II) fibres showed greater changes when compared with skeletal muscles with a predominance of aerobic (slow-twitch, type I) fibres. 3. Gastrocnemius muscles were separated into sarcoplasmic, stromal and myofibrillar protein fractions. Protein synthesis was reduced similarly in all fractions by ethanol treatment, by approximately 30%. 4. As skeletal muscle mass comprises 40% of body weight, the responses have important physiological implications and may also be responsible for the muscle atrophy observed in alcoholic patients.     

Gonadectomy and reduced physical activity: effects on skeletal muscle

OBJECTIVES: To examine the effects of testosterone (TST) loss on skeletal muscle contractile function and the potential interactive effects of TST loss and physical inactivity. DESIGN: Randomized control trial. ANIMALS: Forty-eight male rats (age, 6mo) were placed into control (Con) or gonadectomized (Orx) groups. INTERVENTION: Two weeks after Orx or sham surgery, half the Con and Orx rats were hind-limb unloaded (HLU) to reduce muscle activity for 2 weeks. Subsequently, in situ contractile function tests were performed on the soleus (SOL), plantaris (PLAN), peroneus longus (PER), and extensor digitorum longus (EDL). These 4 muscles and gastrocnemius (GAST) then were removed, weighed, sectioned, and stained with adenosine triphosphatase for fiber typing and fiber area measures. MAIN OUTCOME MEASURES: Peak tetanic tension (P(0)), time to peak twitch contraction (TPT), half relaxation time (RT(1/2)), muscle mass, fiber area, and specific tension (ratio of P(0)/muscle mass). RESULTS: Body weight and muscle mass were similar in the Con and Orx groups. The ratio of P(0) to muscle mass was significantly (p <.05) reduced with Orx in SOL (20%), PLAN (18%), PER (28%), and EDL (20%). TPT and RT(1/2) were significantly faster after Orx in PLAN, PER, and EDL. HLU significantly reduced muscle mass in SOL, PLAN, and GAST in Orx and intact groups. HLU also caused a significant decline in SOL and PLAN P(0). The loss in P(0) in the Orx-HLU rats was no greater than the decline in P(0) with HLU alone. CONCLUSIONS: Gonadectomy results in a loss of P(0) regardless of muscle fiber type or function, it is likely to speed up TPT and RT(1/2), and it does not exacerbate HLU-related atrophy and P(0) loss. Findings may have implications for men with reduced TST levels, as in aging, for instance.     

Protein adducts in type I and type II fibre predominant muscles of the ethanol-fed rat: preferential localisation in the sarcolemmal and subsarcolemmal region

BACKGROUND: Chronic alcoholic myopathy is characterised by reduced muscle strength and structural changes including a decrease in the diameter of Type II (glycolytic, fast-twitch, anaerobic) fibres. In contrast, the Type I fibres (oxidative, slow-twitch, aerobic) are relatively protected. It is possible that adduct formation with reactive metabolites of ethanol may be a contributory process. MATERIALS AND METHODS: We analysed skeletal muscles from rats fed nutritional-complete liquid diets containing ethanol as 35% of total dietary energy; control rats were fed the same diet in which ethanol was replaced by isocaloric glucose. Reduced-acetaldehyde, unreduced-acetaldehyde, malondialdehyde, malondialdehyde-acetaldehyde and alpha-hydroxyethyl protein-adducts in both soleus and plantaris were analysed by ELISA or immunohistochemistry with comparative studies in liver. RESULTS: After 6 weeks, the weights of the plantaris, but not the soleus, were decreased. ELISA analyses for protein adducts showed increased amounts of unreduced-acetaldehyde adducts in soleus (P < 0.025) and plantaris (P < 0.025). Reduced-acetaldehyde, malondialdehyde, malondialdehyde-acetaldehyde and alpha-hydroxyethyl protein-adducts in both soleus and plantaris muscles from ethanol-fed rats were not significantly different from their pair-fed controls (P > 0.05). In contrast, liver from ethanol-fed rats showed significantly higher levels of unreduced-acetaldehyde (P < 0.025), reduced-acetaldehyde (P < 0.01), malondialdehyde (P < 0.01), malondialdehyde-acetaldehyde (P < 0.025) and alpha-hydroxyethyl radical (P < 0.01) protein adducts compared to pair-fed controls. Immuno-histochemical analysis using an antiserum reacting with both reduced- and unreduced-acetaldehyde adducts showed adducts were increased in soleus (P < 0.05) and plantaris (P < 0.025), confirming ELISA analysis. Adducts were located within the sarcolemmal (i.e. muscle membrane) and subsarcolemmal regions. CONCLUSION: This is the first report of adduct formation in myopathic skeletal muscle due to chronic alcohol ingestion and suggests a role for acetaldehyde in the aetiology of alcoholic myopathy.     

Effect of denervation on the content of cardiac troponin-T and cardiac troponin-I in rat skeletal muscle

Abnormal rhabdomyocyte expression of cardiac troponin-T (cTnT) was thought to interfere with the cTnT assay. cTnT isoforms have been shown to be transiently expressed in skeletal muscle during development and in response to muscle denervation. The effect of denervation and aging on cTnT and cardiac troponin-I (cTnI) content in fast and slow rat skeletal muscles was assessed quantitatively. Sections of the tibial nerve were transected from one hind limb of both young (n=12) and old (n=12) rats. Animals were sacrificed at 1, 2, and 4 weeks after the operation, and the extensor digitorum longus (EDL) and the soleus were removed from both the denervated and the contralateral control limb. There was no significant difference in cTnI content between the fast EDL and slow soleus muscles. The cTnT content was significantly higher in the soleus than the EDL muscle (p<0.001). These data, combined with data on other models in the literature, indicate that re-expression of cTnT and cTnI isoforms in adult skeletal muscle is unlikely and does not interfere with cTnT assays for assessment of cardiac damage.     

Histochemical fiber type alterations secondary to exercise training of reinnervating adult rat muscle

The purpose of this study was to evaluate the effect of exercise training on reinnervating rat muscle histochemistry. Adult female Wistar rats in 5 groups (1 control and 4 experimental) underwent bilateral sciatic nerve crush. The 4 experimental groups were exercised on a motorized treadmill at 35% grade and a speed of 27m/min once (groups J and L) or twice (groups K and M) daily, 5 days/week from the 2nd (groups J and K), and 3rd (groups L and M), to the 6th week after the crush. The exercise sessions lasted 1 hour. The fiber diameter and percent of type I and II fibers (weak and strong myosin ATPase reaction, pH .94) were evaluated in the soleus and superficial and deep regions of the plantaris muscles. Exercise training did not affect the fiber diameters. There was no change in the fiber type distribution in the soleus and superficial region of the plantaris. However, the percent of type II fibers increased significantly (p less than 0.05) in the deep region of the plantaris groups J, K, L and M bu 12%, 7%, 15% and 10%, respectively. This study indicated that exercise did not interfere with reinnervation and that there was an increase in the proportion of fibers with a strong myosin ATPase reaction in the deep region of the plantaris.     

Continuous and pulsed ultrasound do not increase heat shock protein 72 content.

Therapeutic ultrasound (US) is a common treatment used in the rehabilitation of injured muscle. To determine whether therapeutic US could increase the content of heat shock protein (HSP) 72 in skeletal muscle, male Sprague-Dawley rats were anesthetized and the muscles from one hind limb treated with 15 min of US at 1 MHz using either: 1. continuous US at 1.0 W/cm(2), 2. pulsed US at 2.0 W/cm(2) at 50% duty cycle, or 3. pulsed US at 1.0 W/cm(2) at 20% duty cycle. All treatments were applied using a transducer (1.6-cm diameter) on an area of the rat hind limb twice the size of the sound head. At 24 h following treatment, the plantaris, soleus, white and red gastrocnemius muscles were removed and assessed for HSP 72 content by Western blotting. No significant increases in HSP 72 content were detected in any of the muscles examined following any US treatment. These results suggest muscle HSP content is not elevated following a typical therapeutic dose of either continuous or pulsed US in the rat.