Changes In Muscle Weight Research Articles

Analysis of muscle synergy and muscle functional network at different walking speeds based on surface electromyographic signal

An in-depth understanding of the mechanism of lower extremity muscle coordination during walking is the key to improving the efficacy of gait rehabilitation in patients with neuromuscular dysfunction. This paper investigates the effect of changes in walking speed on lower extremity muscle synergy patterns and muscle functional networks. Eight healthy subjects were recruited to perform walking tasks on a treadmill at three different speeds, and the surface electromyographic signals (sEMG) of eight muscles of the right lower limb were collected synchronously. The non-negative matrix factorization (NNMF) method was used to extract muscle synergy patterns, the mutual information (MI) method was used to construct the alpha frequency band (8-13 Hz), beta frequency band (14-30 Hz) and gamma frequency band (31-60 Hz) muscle functional network, and complex network analysis methods were introduced to quantify the differences between different networks. Muscle synergy analysis extracted 5 muscle synergy patterns, and changes in walking speed did not change the number of muscle synergy, but resulted in changes in muscle weights. Muscle network analysis found that at the same speed, high-frequency bands have lower global efficiency and clustering coefficients. As walking speed increased, the strength of connections between local muscles also increased. The results show that there are different muscle synergy patterns and muscle function networks in different walking speeds. This study provides a new perspective for exploring the mechanism of muscle coordination at different walking speeds, and is expected to provide theoretical support for the evaluation of gait function in patients with neuromuscular dysfunction.

The impact of cancer cachexia on gut microbiota composition and short-chain fatty acid metabolism in a murine model

This study investigates the relationship between cancer cachexia and the gut microbiota, focusing on the influence of cancer on microbial composition. Lewis lung cancer cell allografts were used to induce cachexia in mice, and body and muscle weight changes were monitored. Fecal samples were collected for targeted metabolomic analysis for short chain fatty acids and microbiome analysis. The cachexia group exhibited lower alpha diversity and distinct beta diversity in gut microbiota compared to the control group. Differential abundance analysis revealed higher Bifidobacterium and Romboutsia, but lower Streptococcus abundance in the cachexia group. Additionally, lower proportions of acetate and butyrate were observed in the cachexia group. The study observed that a significant impact of cancer cachexia on gut microbiota and their generated metabolites, indicating the host-to-gut microbiota axis.

Impacts of whole-body vibration on denervated skeletal-muscle atrophy in rats.

Whole-body vibration has been considered as a countermeasure against muscle atrophy. However, its effects on muscle atrophy are poorly understood. We evaluated the effects of whole-body vibration on denervated skeletal muscle atrophy. Whole-body vibration was performed on rats from Day 15 to 28 after denervation injury. Motor performance was evaluated using an inclined-plane test. Compound muscle action potentials of the tibial nerve were examined. Muscle wet weight and muscle fiber cross-sectional area were measured. Myosin heavy chain isoforms were analyzed in both muscle homogenates and single myofibers. Whole-body vibration resulted in a significantly decreased inclination angle and muscle weight, but not muscle fiber cross-sectional area of fast-twitch gastrocnemius compared to denervation only. In denervated gastrocnemius, a fast-to-slow shift was observed in myosin heavy chain isoform composition following whole-body vibration. There were no significant changes in muscle weight, muscle fiber cross-sectional area, and myosin heavy chain isoform composition in denervated slow-twitch soleus. These results imply that whole-body vibration does not promote recovery of denervation-induced muscle atrophy.

Distinct Effects of Mesterolone on Oxidative and Glycolytic Fibers of Avian Skeletal Muscle

AimOxidative and glycolytic muscle fibers differ in their responses to physiological stimuli and pathological insults. We examined whether these fibers respond differentially to exogenous anabolic androgenic steroids (AASs) by comparing morphological and histological changes between the oxidative anterior latissimus dorsi (ALD) and glycolytic pectoralis major (PM) fibers in adult avian muscles.MethodsThe AAS mesterolone was selected for this study. Mesterolone is a synthetic steroid that has no estrogenic side effects, low hepatotoxicity, and confers oral activity that allows its oral route of administration. Adult female White Leghorn chickens (Gallus gallus) were randomly divided into five groups: a vehicle control and four mesterolone treatment groups (4, 8, 12, and 16 mg/kg). Mesterolone was administered orally every three days for 4 weeks. Immunocytochemical techniques and morphometric analyses were employed to measure the changes in muscle weight, fiber size, satellite cell (SC) composition, and number of myonuclei.ResultsMesterolone increased both body and muscle weights and induced hypertrophy in glycolytic PM fibers but not in oxidative ALD fibers. Mesterolone induced SC proliferation in both muscles; however, the myonuclear accretion was noticeable only in the PM muscle. In both muscles, the collective changes maintained a constant myonuclear domain size and the changes were dose independent.ConclusionMesterolone induced distinct dose‐independent effects in avian oxidative and glycolytic skeletal muscle fibers; these findings might be clinically valuable in the treatment of age‐related sarcopenia.

Differential response of oxidative and glycolytic skeletal muscle fibers to mesterolone

Oxidative and glycolytic muscle fibers differ in their ultrastructure, metabolism, and responses to physiological stimuli and pathological insults. We examined whether these fibers respond differentially to exogenous anabolic androgenic steroids (AASs) by comparing morphological and histological changes between the oxidative anterior latissimus dorsi (ALD) and glycolytic pectoralis major (PM) fibers in adult avian muscles. Adult female White Leghorn chickens (Gallus gallus) were randomly divided into five groups: a vehicle control and four mesterolone treatment groups (4, 8, 12, and 16 mg/kg). Mesterolone was administered orally every three days for four weeks. Immunocytochemical techniques and morphometric analyses were employed to measure the changes in muscle weight, fiber size, satellite cell (SC) composition, and number of myonuclei. Mesterolone increased both body and muscle weights and induced hypertrophy in glycolytic PM fibers but not in oxidative ALD fibers. Mesterolone induced SC proliferation in both muscles; however, the myonuclear accretion was noticeable only in the PM muscle. In both muscles, the collective changes maintained a constant myonuclear domain size and the changes were dose independent. In conclusion, mesterolone induced distinct dose-independent effects in avian oxidative and glycolytic skeletal muscle fibers; these findings might be clinically valuable in the treatment of age-related sarcopenia.

γ-Oryzanol Improves Exercise Endurance and Muscle Strength by Upregulating PPARδ and ERRγ Activity in Aged Mice.

γ-Oryzanol, a well-known antioxidant, has been used by body builders and athletes to boost strength and increase muscle gain, without major side effects. However, the effect of γ-Oryzanol on sarcopenia and the underlying molecular mechanism is poorly understood. Aged mice fed with the γ-Oryzanol diet do not show significant changes in muscle weight, but show increased running endurance as well as improved grip strength. The expression and activity of PPARδ and ERRγ are increased in skeletal muscle of γ-Oryzanol supplemented mice. γ-Oryzanol upregulates oxidative muscle fibers by MEF2 transcription factor, and PGC-1α and ERRα expressions. Fatty acid oxidation related genes and mitochondria biogenesis are upregulated by γ-Oryzanol. In addition, γ-Oryzanol inhibits TGF-β-Smad-NADPH oxidase 4 pathway and inflammatory cytokines such as TNF-α, IL-1β, IL-6, and p65 NF-κB subunit, which cause skeletal muscle weakness. Collectively, γ-Oryzanol attenuates muscle weakness pathway and increases oxidative capacity by increasing PPARδ and ERRγ activity, which contributes to enhance strength and improve oxidative capacity in muscles, consequently enhancing exercise capacity in aged mice. Particularly, γ-Oryzanol directly binds to PPARδ. These are the first findings showing that γ-Oryzanol enhances skeletal muscle function in aged mice by regulating PPARδ and ERRγ activity without muscle gain.

Differential effects of right and left heart failure on skeletal muscle in rats.

BackgroundExercise intolerance is a cardinal symptom in right (RV) and left ventricular (LV) failure. The underlying skeletal muscle contributes to increased morbidity in patients. Here, we compared skeletal muscle sarcopenia in a novel two‐stage model of RV failure to an established model of LV failure.MethodsPulmonary artery banding (PAB) or aortic banding (AOB) was performed in weanling rats, inducing a transition from compensated cardiac hypertrophy (after 7 weeks) to heart failure (after 22–26 weeks). Cardiac function was characterized by echocardiography. Skeletal muscle catabolic/anabolic balance and energy metabolism were analysed by histological and biochemical methods, real‐time PCR, and western blot.ResultsTwo clearly distinguishable stages of left or right heart disease with a comparable severity were reached. However, skeletal muscle impairment was significantly more pronounced in LV failure. While the compensatory stage resulted only in minor changes, soleus and gastrocnemius muscle of AOB rats at the decompensated stage demonstrated reduced weight and fibre diameter, higher proteasome activity and expression of the muscle‐specific ubiquitin E3 ligases muscle‐specific RING finger 1 and atrogin‐1, increased expression of the atrophy marker myostatin, increased autophagy activation, and impaired mitochondrial function and respiratory chain gene expression. Soleus and gastrocnemius muscle of PAB rats did not show significant changes in muscle weight and proteasome or autophagy activation, but mitochondrial function was mildly impaired as well. The diaphragm did not demonstrate differences in any model or disease stage except for myostatin expression, which was altered at the decompensated stage in both models. Plasma interleukin (IL)‐6 and angiotensin II were strongly increased at the decompensated stage (AOB > > PAB). Soleus and gastrocnemius muscle itself demonstrated an increase in IL‐6 expression independent from blood‐derived cytokines only in AOB animals. In vitro experiments in rat skeletal muscle cells suggested a direct impact of IL‐6 and angiotensin II on distinctive atrophic changes.ConclusionsManifold skeletal muscle alterations are more pronounced in LV failure compared with RV failure despite a similar ventricular impairment. Most of the catabolic changes were observed in soleus or gastrocnemius muscle rather than in the constantly active diaphragm. Mitochondrial dysfunction and up‐regulation of myostatin were identified as the earliest signs of skeletal muscle impairment.

Developing of a Muscle Atrophy Model

Muscle atrophy is one of the most important and frequent problems observed in patients in Intensive Care Units following a surgery, immobilization, extended periods of bed rest as well as in sports medicine. All of these involves loss of muscle mass and decreased muscle strength which increases the risk for future health problems. Immobilization changes the function as well as structure of the peripheral neuromuscular system, and alters both protein degradation and synthesis. Therefore, effective therapeutic strategies to treat muscle wasting induced by immobilization are urgently required but first is necessary to validate and standardize the immobilization technique. In this work we develop a reproducible well‐characterized injury model using a modified Thomas‐ splint validated with mechanical force measurements, histology (H&E and NADH), morphology and ultrasound imaging. Forty young Wistar male rats were divided into two groups: 1) Control‐ no immobilized extremities (CON; n=10) and 2) Unilateral right hindlimb immobilization at 3, 7 or 14 days (Im 3, Im 7, Im 14; n=10 for each group). Results showed a significant increment in body weight for Im 7 and Im 14 compared to CON. Experiments performed in tibialis anterior (TA) of Im muscle showed morphological changes in muscle weight and muscle diameter compared to CON confirmed by Ultrasound imaging. These changes were accompanied with a decrement in peak isometric tetanic force (Po) of immobilized muscles of 20%, 41% and 28% at 3, 7 and 14 days post injury, respectively. Fatigue time for all Im muscles was higher than CON ones (Im 3= 23%, Im 7=33% and Im 14=42%). Metabolic changes using NADH technique denoted an early increase of oxidative fibers and a decrement of glycolytic fibers at 7 days post‐injury compared to CON. In here, we developed, standardized and characterized an immobilization technique that can be used as a first approach to use effective therapeutic strategies to avoid muscle atrophy.Support or Funding InformationSupported partially by UNAM ‐PAPIIT RA207818 and CONACyT AI‐S‐17636 to KPGP.

PO-010 Effects of kickboxing on body composition of adolescents with obesity

Objective In order to find a scientific and effective way to lose weight, the effect of kickboxing exercise was studied by the method of experiment. Through research, it is found that kickboxing can effectively change the body shape and body composition of the human body and achieve a better weight loss effect. This study further enriches and improves the theory of exercise and fitness, which can provide scientific guidance for obese children and adolescents to lose weight and provide a good reference for obesity of other age groups and special populations. 
 Methods In this paper, 20 students of 12~14 years old in the summer class of Wuhan diet training camp were selected as the subjects. Through the test of height and weight, the 20 subjects of drug induced obesity or non secondary obesity were selected by BMI as the main basis, including 8 girls and 12 boys. kickboxing training time is 8 weeks, 3 times a week, each class 60 minutes，from warming up, basically, relax three parts. In order to study the effects of kickboxing on body composition of obese people, skin fold thickness, girth and body fat were monitored and tested. 
 Results After 8 weeks of kickboxing exercise, there was a significant difference in the thickness of the upper arm skin fold of the boys P < 0.05, and the thickness of the skin fold of the lower scapula was P < 0.01, but the changes in the abdomen were not obvious. While the skin thickness of the upper arm and the abdominal skin fold were P < 0.05, and there was no significant difference in the skin fold thickness of the scapula. Male hip circumference P < 0.05 had a very significant change, chest circumference, waist circumference and waist hip ratio P > 0.05 did not change significantly. The waist circumference and waist hip ratio were significantly changed, but there was no significant change in chest circumference and hip circumference. After exercise, the changes in fat content, muscle weight and BMI were the most significant. Girls' weight, fat content, body fat percentage and BMI were the most significant changes, followed by a slight change in muscle weight.
 Conclusions From the qualitative point of view, it can be concluded that the practice of kickboxing exercises can effectively develop flexibility, balance, coordination and so on. It has a significant effect on improving human posture and sports ability. From a quantitative point of view, aerobics can also reduce fat content, increase muscle weight, make the percentage of BMI, body fat change significantly, and have a significant impact on maintaining muscle content and muscle / weight ratio and laying a solid foundation for future exercise. It can be concluded that kickboxing is a suitable exercise for obese people to lose weight.

Immunohistochemical Detection of Motor Endplates in the Long-Term Denervated Muscle.

We have demonstrated that the native motor zone (NMZ) within a muscle is an ideal target for performing nerve-muscle-endplate band grafting (NMEG) to restore motor function of a denervated muscle. This study was designed to determine spatiotemporal alterations of the myofibers, motor endplates (MEPs), and axons in the NMZ of long-term denervated muscles for exploring if NMEG-NMZ technique would have the potential for delayed reinnervation. Sternomastoid (SM) muscles of adult female Sprague-Dawley rats (n = 21) were experimentally denervated and denervation-induced changes in muscle weight, myofiber size, MEPs, and intramuscular nerve axons were evaluated histomorphometrically and immunohistochemically at the end of 3, 6, and 9 months after denervation. The values obtained from the ipsilateral normal side served as control. The denervated SM muscles exhibited a progressive reduction in muscle weight (38%, 31%, and 19% of the control) and fiber diameter (52%, 40%, and 28% of the control) for 3-, 6-, and 9-month denervation, respectively. The denervated MEPs were still detectable even 9 months after denervation. The mean number of the denervated MEPs was 79%, 65%, and 43% of the control in the 3-, 6-, and 9-month denervated SM, respectively. Degenerated axons in the denervated muscles became fragmented. Persistence of MEPs in the long-term denervated SM suggests that some surgeries targeting the MEPs such as NMEG-NMZ technique should be effective for delayed reinnervation. However, more work is needed to develop strategies for preservation of muscle mass and MEPs after denervation.

Increase in carbon dioxide accelerates the performance of endurance exercise in rats.

Endurance exercise generates CO2 via aerobic metabolism; however, its role remains unclear. Exogenous CO2 by transcutaneous delivery promotes muscle fibre-type switching to increase endurance power in skeletal muscles. Here we determined the performance of rats running in activity wheels with/without transcutaneous CO2 exposure to clarify its effect on endurance exercise and recovery from muscle fatigue. Rats were randomised to control, training and CO2 groups. Endurance exercise included activity-wheel running with/without transcutaneous CO2 delivery. Running performance was measured after exercise initiation. We also analysed changes in muscle weight and muscle fibres in the tibialis anterior muscle. Running performance improved over the treatment period in the CO2 group, with a concomitant switch in muscle fibres to slow-type. The mitochondrial DNA content and capillary density in the CO2 group increased. CO2 was beneficial for performance and muscle development during endurance exercise: it may enhance recovery from fatigue and support anabolic metabolism in skeletal muscles.

Transcutaneous carbon dioxide application accelerates muscle injury repair in rat models.

Skeletal muscle injuries are commonly observed in sports and traumatology medicine. Previously, we demonstrated that transcutaneous application of carbon dioxide (CO2) to lower limbs increased the number of muscle mitochondria and promoted muscle endurance. Therefore, we aimed to investigate whether transcutaneous CO2 application could enhance recovery from muscle injury. Tibialis anterior muscle damage was induced in 27 Sprague Dawley rats via intramuscular injection of bupivacaine. After muscle injury, rats were randomly assigned to transcutaneous CO2-treated or -untreated groups. From each group, three rats were sacrificed at weeks one, two, four and six. At each time point, histology and immunofluorescence analyses were performed, and changes in muscle weight, muscle weight/body weight ratio, muscle fibre circumference, gene expression levels and capillary density were measured. Injured muscle fibres were completely repaired at week six in the CO2-treated group but only partially repaired in the untreated group. The repair of basement and plasma membranes did not differ significantly between groups. However, expression levels of genes and proteins related to muscle protein synthesis were significantly higher in the CO2-treated group and significantly more capillaries fourweeks after injury. Transcutaneous CO2 application can accelerate recovery after muscle injury in rats.

Mitochondrial protein synthesis is increased in oxidative skeletal muscles of rats with cardiac cachexia

Since cardiac cachexia could be associated with alterations in muscular mitochondrial metabolism, we hypothesized that the expected alterations in the activities of mitochondrial oxidative enzymes could be associated with changes in mitochondrial protein synthesis in oxidative skeletal muscles. Cardiac cachexia was provoked in male rats by the ligation of the left coronary artery. Six cachectic and 6 control rats were age-paired, and their food intake was observed. The synthesis of mitochondrial proteins was measured by [1-13C]-valine infusion in soleus, tibilais, myocardium, and liver. Muscles (soleus, gastrocnemius, and tibialis anterior), heart, kidneys, liver, and visceral adipose tissue were weighed. Mitochondrial cytochrome c oxydase IV as well as citrate synthase and myosin ATPase activities were measured. As expected, decreased food intake was observed in the cachectic group. Heart, kidney, and liver weights were higher in the cachectic group, while the visceral adipose tissue weight was lower (P < .01). No changes in muscle weights were observed. Soleus mitochondrial proteins fractional synthesis rate was higher in the cachectic group (P = .054). Cytochrome c oxydase IV activity was reduced (P = .009) and increased (P = .038) in the soleus and liver of the cachectic rats, respectively. No change in citrate synthase activity was observed. Myosin ATPase activity was reduced in the gastrocnemius of the cachectic group (P < .01). Mitochondrial protein synthesis is increased in the soleus of rats with cardiac cachexia, suggesting a compensatory mechanism of the impaired oxidative mitochondrial function. Further work should assess whether the mitochondrial protein synthesis is altered in chronic heart failure patients with cardiac cachexia, and whether this is the cause or the consequence of cachexia.

Impact of angiotensin II on skeletal muscle metabolism and function in mice: Contribution of IGF-1, Sirtuin-1 and PGC-1α

Activation of the renin–angiotensin–aldosterone system and increased levels of angiotensin II (Ang-II) occurs in numerous cardiovascular diseases such as chronic heart failure (CHF). Another hallmark in CHF is a reduced exercise tolerance with impaired skeletal muscle function. The aim of this study was to investigate in an animal model the impact of Ang-II on skeletal muscle function and concomitant molecular alterations. Mice were infused with Ang-II for 4 weeks. Subsequently, skeletal muscle function of the soleus muscle was assessed. Expression of selected proteins was quantified by qRT-PCR and Western blot. Infusion of Ang-II resulted in a 33% reduction of contractile force, despite a lack of changes in muscle weight. At the molecular level an increased expression of NAD(P)H oxidase and a reduced expression of Sirt1, PGC-1α and IGF-1 were noticed. No change was evident for the ubiquitin E3-ligases MuRF1 and MafBx and α-sarcomeric actin expression. Cytophotometrical analysis of the soleus muscle revealed a metabolic shift toward a glycolytic profile. This study provides direct evidence of Ang-II-mediated, metabolic deterioration of skeletal muscle function despite preserved muscle mass. One may speculate that the Ang-II-mediated loss of muscle force is due to an activation of NAD(P)H oxidase expression and a subsequent ROS-induced down regulation of IGF-1, PGC-1α and Sirt1.

Leucine contents of isonitrogenous protein sources predict changes in body composition and muscle mass in rats

Increases in intracellular leucine (leu) concentrations stimulate mTOR phosphorylation regulation of skeletal muscle protein synthesis (MPS) and leu content of isonitrogenous complete meals predict MPS potential of individual proteins (J Nutr 139:1103–9, 2009). While the molecular mechanism is established, direct effect of leu on long‐term changes in muscle weight or body composition are unknown. This study evaluated 4 isonitrogenous, isoenergtic diets containing wheat (supplemented with lys), soy, egg, or whey with 6.8, 8.0, 8.8, and 10.9% leu respectively, to determine meal effects of leu on signaling and MPS and long‐term impact on body composition. Male rats (275g) were fed 3 meals/d for 76d consisting of 16/54/30% of energy from protein, carbohydrates and fats. Blood and tissue were taken before or 90min after the breakfast meal at wk 2 and 11. Measurements included muscle weights, body composition by DXA, MPS by D5‐Phe incorporation, and phosphorylation of initiation factors 4E‐BP1 and S6K. Leu content of the meals increased muscle weights and was inversely correlated with bodyfat and these outcomes were associated with greater phosphorylation of 4E‐BP1 and S6K and MPS in animals fed egg and whey. These findings establish that leu content is a crucial factor defining the quality of proteins influencing muscle mass and body composition in adults. Supported by National Dairy Council and Egg Nutrition Center.Grant Funding Source: National Dairy and Egg Nutrition Center

Mitogen‐activated protein kinase‐activated protein kinase 2 (MK2) in skeletal muscle atrophy and hypertrophy

Skeletal muscle is a highly plastic tissue. Overall muscle growth (hypertrophy) or muscle wasting (atrophy) results from alterations in intracellular signaling pathways with important regulatory steps occurring in the nucleus as well as in the cytoplasm. Previous studies have identified components of the Akt/mTor pathway as well as the p38 MAPK pathway as important for skeletal muscle hypertrophy and/or atrophy. The present study tests the hypothesis that MK2, a substrate of p38 which following phosphorylation, can be exported from the nucleus in a complex with p38, may be important for skeletal muscle growth. The expression of MK2 was examined in denervated mouse hind-limb (atrophic) and hemidiaphragm (transiently hypertrophic) muscles. MK2 mRNA expression decreased after denervation in both atrophic (48% of innervated controls, P < 0.001) and hypertrophic muscle (34% of innervated controls, P < 0.01) but MK2 protein expression decreased only in atrophic muscle (32% of innervated controls, P < 0.01). The level of T205 phosphorylated MK2 increased after denervation in both atrophic (fourfold increase, P < 0.01) and hypertrophic muscles (almost sevenfold increase, P < 0.001) whereas the level of T317 phosphorylated MK2 (necessary for nuclear export) increased after denervation in hypertrophic muscle (nearly threefold increase, P < 0.001) but not in atrophic muscle. Logarithmically transformed relative changes in MK2 phosphorylated at T317 correlated well (r(2) = 0.7737) with relative changes in muscle weight. The results suggest a role for MK2 in the regulation of muscle mass, a role which, at least in part, may be related to determining the subcellular localization of p38 in muscle fibers.

Effects of gonadectomy on performance in operant tasks measuring prefrontal cortical function in adult male rats

Previous studies have shown that gonadectomy in adult male rats influences the acquisition and performance of spatial and other working memory tasks that depend in part on the medial prefrontal cortex and its dopamine innervation. Stimulated by previous findings that gonadectomy alters dopamine axon density in not only medial but several other prefrontal fields, the present studies asked whether gonadectomy might also broadly impact dopamine-dependent prefrontal functions, and whether these effects bore any relation to hormone modulation of mesoprefrontal dopamine afferents. Specifically, control, gonadectomized, and gonadectomized rats given estradiol or testosterone propionate were tested on a series of operant tasks that together measured medial prefrontal functions of spatial working memory, impulsivity and extradimensional set shifting and orbital prefrontal functions of reversal learning/perseveration and motivation. Afterwards, animals were sacrificed, their bulbospongiosus muscles were removed and weighed, their brains were processed for immunocytochemistry for the dopamine-synthesizing enzyme tyrosine hydroxylase, and axon densities were measured in orbital and medial prefrontal fields. Statistical evaluations of group effects on behavior and regression analyses comparing individual performance with muscle weights and axon density measures revealed androgen-reversible effects of gonadectomy on acquisition of spatial working memory and extradimensional set shifting that were correlated with bulbospongiosus weight and medial prefrontal dopamine axon density, estrogen-sensitive influences of gonadectomy on motivation and response withholding that were correlated with bulbospongiosus weight but not with dopamine innervation, and still other prefrontal functions, i.e., impulsivity, reversal learning, that were insensitive to gonadectomy and unrelated to gonadectomy-induced changes in muscle weight or prefrontal dopamine innervation.

The Effects of Ad Libitum Feeding and Marked Dietary Restriction on Spontaneous Skeletal Muscle Pathology in Sprague–Dawley Rats

The effects of ad libitum (AL) feeding and marked dietary restriction (DR) on spontaneous age-related skeletal muscle changes in male Sprague-Dawley (SD) rats were evaluated at 1 and 2 years. SD rats were fed Certified UAR A04C Rodent Chow ad libitum (AL), or DR at 50% of AL for (106 weeks). Body weights and organ weights were measured at the 1-year interim and 2-year final necropsies. In addition to the routine histopathologic examination, determination of 5 stereologic parameters was done in the vastus lateralis muscle after histochemistry of ATPase activity at 1 and 2 years. Body and skeletal muscle weights were proportional to the food intake. In AL-fed rats, muscle weights decreased between 1 and 2 years, in correlation with decreased type 2 myofiber numbers. In this group, fibrovascular index markedly increased with aging and muscle degeneration occurred at 2 years. In DR rats, there were no significant changes in muscle weights between 1 and 2 years. No histopathological changes were observed and the fibrovascular index was unchanged. These results demonstrated a protective effect of DR on the age-related skeletal muscle pathology in SD rats.

Stretch-activated ion channels and c-fos expression remain active after repeated eccentric bouts.

This study was undertaken to measure the response of stretch-activated ion channels (SAC) and transcript levels of the oncogene c-fos to separate bouts of eccentric contractions (EC). It was hypothesized that SAC in rat skeletal muscle would contribute to resting membrane potential depolarization after separate repeated bouts of EC. Blockage of SAC during an EC training regime also tested the necessity of SAC for a training response. It was also hypothesized that transcript levels of c-fos would be maximally elevated after the first exposure to EC and diminish with repeated exposures. The results indicate less depolarization after multiple bouts of EC, which could be reversed by blocking the SAC. Transcript levels of c-fos were elevated to a similar degree after either a single or multiple exposures to EC. EC training resulted in significant increases in contractile force and muscle wet and dry weights in nontreated animals. Training in the presence of the SAC-blocker streptomycin produced similar changes in contractile force without changes in muscle weight. SAC and c-fos are activated after several exposures to EC and therefore remain as possible signals in EC training responses.

Body, heart, thyroid gland and skeletal muscle weight changes in rats with altered thyroid status

In the present paper we describe changes of anatomical parameters in inbred Lewis strain rats, namely their body weight, body weight gain per week, absolute and relative heart, thyroid gland and skeletal muscle weights, that are assumed to reflect experimentally altered thyroid status. The hyperthyroid state was induced by DL-thyroxine or Na 3,3',5-triiodo-L-thyronine, while methimazole was employed for inducing hypothyroidism. We have found that when compared to euthyroid rats, hypothyroidism resulted in a significantly lower body weight gain, absolute and relative heart weight and, in contrast, in a significant increase of absolute and relative thyroid gland weight. On the other hand, hyperthyroidism led to a significant increase of absolute and relative heart weight and to a significant reduction of absolute and relative thyroid gland weight. However, the body mass was not significantly altered in hyperthyroidism as compared with euthyroid rats. We conclude that our protocol leads to chronic hyper- or hypothyroidism as demonstrated by body, heart and thyroid gland weight changes. These anatomical data can thus be utilized as supplemental criteria for the assessment of the thyroid state of experimental rats.