Metabolic Properties Of Skeletal Muscle Research Articles

Effects Of Low-load, High-repetition Exercise And Sex On Metabolic Properties Of Skeletal Muscle

Effects Of Low-load, High-repetition Exercise And Sex On Metabolic Properties Of Skeletal Muscle

Isolation and Differentiation of Primary Myoblasts from Mouse Skeletal Muscle Explants.

Primary myoblasts are undifferentiated proliferating precursors of skeletal muscle. They can be cultured and studied as muscle precursors or induced to differentiate into later stages of muscle development. The protocol provided here describes a robust method for the isolation and culture of a highly proliferative population of myoblast cells from young adult mouse skeletal muscle explants. These cells are useful for the study of the metabolic properties of skeletal muscle of different mouse models, as well as in other downstream applications such as transfection with exogenous DNA or transduction with viral expression vectors. The level of differentiation and metabolic profile of these cells depends on the length of exposure, and composition of the media used to induce myoblast differentiation. These methods provide a robust system for the study of mouse muscle cell metabolism ex vivo. Importantly, unlike in vivo models, the methods described here provide a cell population that can be expanded and studied with high levels of reproducibility.

Effect of beta2 -adrenergic agonist and resistance training on maximal oxygen uptake and muscle oxidative enzymes in men.

While beta2 -adrenoceptor stimulation has been shown to increase lean mass and to alter metabolic properties of skeletal muscle, adaptations in muscle oxidative enzymes and maximal oxygen uptake ( O2max ) in response to beta2 -adrenergic agonist treatment are inadequately explored in humans, particularly in association with resistance training. Herein, we investigated beta2 -adrenergic-induced changes in O2max , leg and arm composition, and muscle content of oxidative enzymes in response to treatment with the selective beta2 -adrenergic agonist terbutaline with and without concurrent resistance training in young men. Forty-six subjects were randomized to 4weeks of lifestyle maintenance (n=23) or resistance training (n=23). Within the lifestyle maintenance and resistance training group, subjects received daily terbutaline (8×0.5mg) (n=13) or placebo (n=10) treatment. No apparent treatment by training interactions was observed during the study period. Terbutaline increased leg and arm lean mass with the intervention, whereas no treatment differences were observed in absolute O2max and incremental peak power output (iPPO). Treatment main effects were observed for O2 -reserve (P<.05), O2max relative to body mass (P<.05), O2max relative to leg lean mass (P<.01), and iPPO relative to leg lean mass, in which terbutaline had a negative effect compared with placebo. Furthermore, content of electron transport chain complex I-V decreased by 11% (P<.05) for terbutaline compared with placebo. Accordingly, chronic treatment with the selective beta2 -adrenergic agonist terbutaline may negatively affect O2max and iPPO in relative terms, but not in absolute.

Metabolic Changes Associated With Muscle Expression of SOD1G93A.

Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disorder, classified into sporadic or familial forms and characterized by motor neurons death, muscle atrophy, weakness, and paralysis. Among the familial cases of ALS, approximately 20% are caused by dominant mutations in the gene coding for superoxide dismutase (SOD1) protein. Of note, mutant SOD1 toxicity is not necessarily limited to the central nervous system. ALS is indeed a multi-systemic and multifactorial disease that affects whole body physiology and induces severe metabolic changes in several tissues, including skeletal muscle. Nevertheless, whether alterations in the plasticity, heterogeneity, and metabolism of muscle fibers are the result of motor neuron degeneration or alternatively occur independently of it remain to be elucidated. To address this issue, we made use of a mouse model (MLC/SOD1G93A) that overexpresses the SOD1 mutant gene selectively in skeletal muscle. We found an alteration in the metabolic properties of skeletal muscle characterized by alteration in fiber type composition and metabolism. Indeed, we observed an alteration of muscle glucose metabolism associated with the induction of Phosphofructokinases and Pyruvate dehydrogenase kinase 4 expression. The upregulation of Pyruvate dehydrogenase kinase 4 led to the inhibition of Pyruvate conversion into Acetyl-CoA. Moreover, we demonstrated that the MLC/SOD1G93A transgene was associated with an increase of lipid catabolism and with the inhibition of fat deposition inside muscle fibers. All together these data demonstrate that muscle expression of the SOD1G93A gene induces metabolic changes, along with a preferential use of lipid energy fuel by muscle fibers. We provided evidences that muscle metabolic alterations occurred before disease symptoms and independently of motor neuron degeneration, indicating that skeletal muscle is likely an important therapeutic target in ALS.

Skeletal muscle: from birth to old age, routes to mechanical and metabolic failure.

Skeletal muscle (SM) is the most abundant tissue and the largest reservoir of protein in the body. It transports glucose in an insulin dependent manner by the glucose transporter type 4 (GLUT4) and contributes in the maintenance of serum amino acids concentration. By its mass and energetic requirements, it is fundamental for the systemic metabolic balance. In the present work, we present the effect of gestational undernourishment (GU) on the mechanical and metabolic properties of SM at birth and in old age in an animal model. Mechanical studies were performed on isolated muscles, while the GLUT4, amino acid transporters LAT2, SNAT2 and insulin receptors (IR) determination were performed on isolated transverse-tubule membranes (TT). The GU in offspring at birth, results in low muscle mass with increased contraction force and resistance to fatigue. However, in two-years old rats, there was muscle hypotrophy and sarcopenia, the force decreased between 50 and 70% in control rats and rats with GU respectively, accompanied by a lower expression of LAT2, SNAT2 and IR in TT. In conclusion, GU irreversibly affects the SM, an effect that could be similar in humans, which help us to understand the events that associate the GU with the metabolic debacle of SM and the metabolic diseases of human adulthood.

Pregnancy and Smoothelin-like Protein 1 (SMTNL1) Deletion Promote the Switching of Skeletal Muscle to a Glycolytic Phenotype in Human and Mice

Pregnancy promotes physiological adaptations throughout the body, mediated by the female sex hormones progesterone and estrogen. Changes in the metabolic properties of skeletal muscle enable the female body to cope with the physiological challenges of pregnancy and may also be linked to the development of insulin resistance. We conducted global microarray, proteomic, and metabolic analyses to study the role of the progesterone receptor and its transcriptional regulator, smoothelin-like protein 1 (SMTNL1) in the adaptation of skeletal muscle to pregnancy. We demonstrate that pregnancy promotes fiber-type changes from an oxidative to glycolytic isoform in skeletal muscle. This phenomenon is regulated through an interaction between SMTNL1 and progesterone receptor, which alters the expression of contractile and metabolic proteins. smtnl1(-/-) mice are metabolically less efficient and show impaired glucose tolerance. Pregnancy antagonizes these effects by inducing metabolic activity and increasing glucose tolerance. Our results suggest that SMTNL1 has a role in mediating the actions of steroid hormones to promote fiber switching in skeletal muscle during pregnancy. Our findings also bear on the management of gestational diabetes that develops as a complication of pregnancy in ~4% of women.

MicroRNA-23a has minimal effect on endurance exercise-induced adaptation of mouse skeletal muscle.

Skeletal muscles contain several subtypes of myofibers that differ in contractile and metabolic properties. Transcriptional control of fiber-type specification and adaptation has been intensively investigated over the past several decades. Recently, microRNA (miRNA)-mediated posttranscriptional gene regulation has attracted increasing attention. MiR-23a targets key molecules regulating contractile and metabolic properties of skeletal muscle, such as myosin heavy-chains and peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC-1α). In the present study, we analyzed the skeletal muscle phenotype of miR-23a transgenic (miR-23a Tg) mice to explore whether forced expression of miR-23a affects markers of mitochondrial content, muscle fiber composition, and muscle adaptations induced by 4 weeks of voluntary wheel running. When compared with wild-type mice, protein markers of mitochondrial content, including PGC-1α, and cytochrome c oxidase complex IV (COX IV), were significantly decreased in the slow soleus muscle, but not the fast plantaris muscle of miR-23a Tg mice. There was a decrease in type IId/x fibers only in the soleus muscle of the Tg mice. Following 4 weeks of voluntary wheel running, there was no difference in the endurance exercise capacity as well as in several muscle adaptive responses including an increase in muscle mass, capillary density, or the protein content of myosin heavy-chain IIa, PGC-1α, COX IV, and cytochrome c. These results show that miR-23a targets PGC-1α and regulates basal metabolic properties of slow but not fast twitch muscles. Elevated levels of miR-23a did not impact on whole body endurance capacity or exercise-induced muscle adaptations in the fast plantaris muscle.

Nrf2 modulates contractile and metabolic properties of skeletal muscle in streptozotocin-induced diabetic atrophy

The role of Nrf2 in disease prevention and treatment is well documented; however the specific role of Nrf2 in skeletal muscle is not well described. The current study investigated whether Nrf2 plays a protective role in an STZ-induced model of skeletal muscle atrophy.Modulation of Nrf2 through siRNA resulted in a more robust differentiation of C2C12s, whereas increasing Nrf2 with sulforaphane treatment inhibited differentiation. Diabetic muscle atrophy was not dramatically influenced by Nrf2 genotype, since no differences were observed in total atrophy (all fiber types combined) between WT+STZ and KO+STZ animals. Nrf2-KO animals however illustrated alterations in muscle size of Fast, Type II myosin expressing fibers. KO+STZ animals show significant alterations in myosin isoform expression in the GAST. Similarly, KO controls mimic both WT+STZ and KO+STZ muscle alterations in mitochondrial subunit expression. PGC-1α, a well-established player in mitochondrial biogenesis and myosin isoform expression, was decreased in KO control, WT+STZ and KO+STZ SOL muscle. Similarly, PGC-1α protein levels are correlated with Nrf2 levels in C2C12s after modulation by Nrf2 siRNA or sulforaphane treatment.We provide experimental evidence indicating Nrf2 plays a role in myocyte differentiation and governs molecular alterations in contractile and metabolic properties in an STZ-induced model of muscle atrophy.

Increased Fatigue Resistance of Skeletal Muscle with Elevated 2-Deoxy-ATP following Ribonucleotide Reductase Overexpression

Skeletal muscle myosin can use a variety of nucleotides to varying effectiveness as substrates for contraction. We previously demonstrated that complete replacement of ATP with 2 deoxy-ATP (dATP) in activation solutions increases contraction of demembranated rabbit skeletal muscle and that enhanced performance results from increased myosin binding and cycling kinetics, especially during sub-maximal calcium activation. Here we report on a transgenic mouse (Tg-RR) that overexpresses the enzyme, ribonucleotide reductase, which converts ADP to dADP (that is rapidly phosphorylated to dATP). This results in a ∼10x increase in dATP content of skeletal muscle, which still constitutes ≤ 1% of the adenosine triphosphate nucleotide pool. We are examining the contractile and metabolic properties of skeletal muscle in this transgenic model. Preliminary data indicates the phosphocreatine to ATP (PCr:ATP) ratio of Tg-RR mice is significantly elevated relative to wild type (Tg-WT) mice, suggesting the Tg-RR mice may have an energetic advantage due to increased high energy phosphate reserves. Furthermore, the Tg-RR mice ran for a longer period of time at increased speed and for longer distances in a graded exercise test. Direct in situ stimulation of the gastrocnemius muscle indicates improved resistance to fatigue, consistent with both the exercise and the metabolic (PCr:ATP) findings. Interestingly, our preliminary experiments suggest the Tg-RR mice produce significantly less peak force and show signs of atrophy. Ongoing experiments are examining changes in mitochondrial content and function as well as contractile properties of isolated muscles to determine the mechanisms underlying the increased fatigue resistance of the Tg-RR mice. These results suggest a new direction for developing interventions to improve exercise tolerance in human patients. Supported by HL11197 (MR).

The Corepressor NCoR1 Antagonizes PGC-1α and Estrogen-Related Receptor α in the Regulation of Skeletal Muscle Function and Oxidative Metabolism

Skeletal muscle exhibits a high plasticity and accordingly can quickly adapt to different physiological and pathological stimuli by changing its phenotype largely through diverse epigenetic mechanisms. The nuclear receptor corepressor 1 (NCoR1) has the ability to mediate gene repression; however, its role in regulating biological programs in skeletal muscle is still poorly understood. We therefore studied the mechanistic and functional aspects of NCoR1 function in this tissue. NCoR1 muscle-specific knockout mice exhibited a 7.2% higher peak oxygen consumption (VO(2peak)), a 11% reduction in maximal isometric force, and increased ex vivo fatigue resistance during maximal stimulation. Interestingly, global gene expression analysis revealed a high overlap between the effects of NCoR1 deletion and peroxisome proliferator-activated receptor gamma (PPARγ) coactivator 1α (PGC-1α) overexpression on oxidative metabolism in muscle. Importantly, PPARβ/δ and estrogen-related receptor α (ERRα) were identified as common targets of NCoR1 and PGC-1α with opposing effects on the transcriptional activity of these nuclear receptors. In fact, the repressive effect of NCoR1 on oxidative phosphorylation gene expression specifically antagonizes PGC-1α-mediated coactivation of ERRα. We therefore delineated the molecular mechanism by which a transcriptional network controlled by corepressor and coactivator proteins determines the metabolic properties of skeletal muscle, thus representing a potential therapeutic target for metabolic diseases.

Exercise Performance Tests in Mice.

Maximal exercise performance is a multifactorial process in which the cardiovascular component, the innervation of the musculature, and the contractile and metabolic properties of skeletal muscle all play key roles. Here, protocols are provided for assessment of maximal running capacity of mice on a treadmill, with a combination of short high-intensity paradigms primarily intended to test for maximal power and cardiovascular function, and longer low-intensity paradigms to assess endurance and oxidative metabolism in skeletal muscle. The coupling of treadmill running to indirect calorimetry, to correlate performance measurements to maximal oxygen consumption, is also described. Curr. Protoc. Mouse Biol. 1:141-154. © 2011 by John Wiley & Sons, Inc.

Relationship of physical function to vastus lateralis capillary density and metabolic enzyme activity in elderly men and women

There are no data showing whether or not age-related declines in physical function are related to in vitro properties of human skeletal muscle. The purpose of this study was to determine whether physical function is independently associated with histologic and metabolic properties of skeletal muscle in elderly adults. The study was a cross-sectional observational study of 39 sedentary, older (60-85 yrs) men and women. A needle biopsy of the vastus lateralis for assessment of muscle fiber type, fiber area, capillary density and citrate synthase and aldolase activities was performed. Physical function tests included the Short Physical Performance Battery (balance, walking speed, and chair rise time), as well as self-reported disability. Total fiber area (R=-0.41, p=0.02), number of Type II fibers (R=-0.33, p=0.05), and aldolase activity (R=-0.54, p=0.01) were inversely related to age. Persons who reported greater difficulty with daily activities had lower capillary density (R=-0.51, p=0.03) and lower citrate synthase activity (R=-0.66, p=0.03). Walking speed was directly related to fiber area (R=0.40, p=0.02), capillary density (R=0.39, p=0.03), citrate synthase (R=0.45, p=0.03) and aldolase (R=0.55, p<0.01) activities, even after adjustment for age, BMI and disease status. In older adults, skeletal muscle capillary density and metabolic enzymatic activity are independent predictors of lower extremity physical function.

Modulations du génome exprimé dans le muscle squelettique avec l’entraînement physique

Aims Physical exercise leads to changes in contractile and biochemical properties. Muscle characteristics are mainly explained by the presence of several protein families, which exist as different isoforms. Each of these isoforms is encoded by specific genes. The aim of this paper is to present the current knowledge concerning alterations in muscle gene expression in response of physical exercise. In this paper, we stress the knowledge concerning the involvement of intracellular signaling pathways, which ensure the link between the molecular events related to physical exercise and changes in the transcription levels of target genes. Current knowledge Changes in contractile and metabolic properties of skeletal muscle observed during physical training are now well-known. In contrast, the molecular mechanisms at the origin of changes in gene expression remain to be extensively examined. It has been hypothesized that physical exercise leads to elementary signals that are distinctly sensed by skeletal muscle tissue. These signals will recruit specific intracellular pathways and then account for transcriptional adaptations that are seen in skeletal muscle. It has been suggested that transcriptional regulations during physical training result from the influence of many external and internal factors pooled into four categories. Neuronal factors recruit signaling pathways related to transient changes in intracellular calcium, such as calcineurin, calmodulin-dependent protein kinases and PKC pathways. Mechanical factors modulate specific transcriptional changes through mitrogen-activated protein kinase signaling pathways, especially p38 and extracellular signal-regulated kinase-1/2 pathways. Metabolic signals activate the mitochondrial biogenesis through PGC-1α or oxygen-sensitive genes through the hypoxia inducible factor complex. Hormonal signals will not be discussed in the present paper. Futur prospects Future studies are needed to estimate the role played by each of these signaling pathways to explain the phenotypic changes reported in skeletal according to the physical training characteristics. Moreover, the signaling pathways involved to explain muscle adaptation mostly interact; these interactions need to be examined during several forms of physical training.

Consequences of pig domestication for skeletal muscle growth and cellularity

This study was conducted to investigate the impact of domestication of the pig on various cellular properties of skeletal muscle. For this purpose, samples of semitendinosus (ST) , psoas major (PM) , and longissimus (LD) muscles of 24 European wild boars (WB; Sus scrofa scrofa) and of 28 domestic pigs ( Sus scrofa domestica) of German Landrace (DP) were taken at birth, and at 7 and 20 weeks of age and subjected to histological, biochemical, and/or cell culture studies. At birth, DP muscles exhibited lower numbers of myofibers and were less mature, as seen by DNA, RNA, and protein composition and lower proportions of type I fibers. Satellite cell cultures from neonatal ST and LD muscles of WB grew more intensely than that of DP. Additional fiber formation shortly after birth occurred at a higher rate in ST, but not in PM, of DP compared with WB. During postnatal growth, the higher gain in muscle mass of DP resulted mainly from accelerated myofiber hypertrophy and increased protein accretion at the level of transcription. DP muscles exhibited higher proportions of fast-twitch (IIb) and/or white glycolytic fibers than WB. Conclusively, domestication of the pig substantially changed the ontogenic development and the contractile and metabolic properties of skeletal muscle.

Calcineurin Regulates Skeletal Muscle Metabolism via Coordinated Changes in Gene Expression

The metabolic property of skeletal muscle adapts in response to an increased physiological demand by altering substrate utilization and gene expression. The calcium-regulated serine/threonine protein phosphatase calcineurin has been implicated in the transduction of motor neuron signals to alter gene expression programs in skeletal muscle. We utilized transgenic mice that overexpress an activated form of calcineurin in skeletal muscle (MCK-CnA*) to investigate the impact of calcineurin activation on metabolic properties of skeletal muscle. Activation of calcineurin increased glucose incorporation into glycogen and lipid oxidation in skeletal muscle. Activated calcineurin suppressed skeletal muscle glucose oxidation and increased lactate release. The enhancement in lipid oxidation was supported by increased expression of genes for lipid metabolism and mitochondrial oxidative phosphorylation. In a reciprocal fashion, several genes of glycolysis were down-regulated, whereas pyruvate dehydrogenase kinase 4 was markedly induced. This expression pattern was associated with decreased glucose utilization and enhanced glycogen storage. The peroxisome proliferator-activated receptors (PPARs) and PPARgamma coactivator 1alpha (PGC1alpha) are transcription regulators for the expression of metabolic and mitochondrial genes. Consistent with changes in the gene-regulatory program, calcineurin promoted the expression of PPARalpha, PPARdelta, and PPARgamma coactivator 1alpha in skeletal muscle. These results provide evidence that calcineurin-mediated skeletal muscle reprogramming induces the expression of several transcription regulators that coordinate changes in the expression of genes for lipid and glucose metabolism, which in turn alters energy substrate utilization in skeletal muscle.

Remodeling muscles with calcineurin.

Ca(2+) signaling plays a central role in hypertrophic growth of cardiac and skeletal muscle in response to mechanical load and a variety of signals. However, the mechanisms whereby alterations in Ca(2+) in the cytoplasm activate the hypertrophic response and result in longterm changes in muscle gene expression are unclear. The Ca(2+), calmodulin-dependent protein phosphatase calcineurin has been proposed to control cardiac and skeletal muscle hypertrophy by acting as a Ca(2+) sensor that couples prolonged changes in Ca(2+) levels to reprogramming of muscle gene expression. Calcineurin also controls the contractile and metabolic properties of skeletal muscle by activating the slow muscle fiber-specific gene program, which is dependent on Ca(2+) signaling. Transcription factors of the NFAT and MEF2 families serve as endpoints for the signaling pathways whereby calcineurin controls muscle hypertrophy and fiber-type. We consider these findings in the context of a model for Ca(2+)-regulated gene expression in muscle cells and discuss potential implications of these findings for pharmacologic modification of cardiac and skeletal muscle function. BioEssays 22:510-519, 2000.

Physical performance and metabolic recovery among lean, healthy men following a prolonged energy deficit.

Previous studies have demonstrated that full recovery from weight loss may take months or years. The present investigation examined short-term recovery (5 wks "post") of physical performance (muscular strength, muscular power, vertical jump), body composition, metabolic hormones (testosterone, luteinizing hormone, sex hormone binding globulin, insulin-like growth factor-1, triiodothyronine, thyroxine, thyroid binding globulin, and thyroid-stimulating hormone) and metabolic markers (transferrin, ferritin, prealbumin, glycerol, nonesterified fatty acids, high-density lipoproteins, and lactate) in 10 healthy young men after an 8-week Army course with an energy deficit (1000 kcal/d) and loss of body mass (-12%). Subjects ate ad libitum after the course ended ("post"). Body composition was determined by dual-energy X-ray absorptiometry; strength from a simulated power clean, power from body mass and jump height, and metabolic hormones were measured in morning-fasted blood by radioimmunoassay. With the exception of transferrin and glycerol, all study parameters were significantly (p<.05) altered by the training course. At 5 weeks post fat-free mass along with all physical performance measures returned to initial levels; however, fat mass had significantly (p<.05) increased over initial levels. Also, with the exception of lactate, all measured hormones and markers were close to initial levels and within normal ranges. Reported complications during recovery included sleep irregularities, diarrhea, loss of motivation and feelings of fatigue. While the long range effect of this energy deprivation experience is uncertain, these data do suggest that severe weight loss does not result in lasting alterations of the contractile and metabolic properties of skeletal muscle in young, lean, healthy men.

α-CGRP mRNA levels in motoneurons innervating specific rat muscles

Along with acetylcholine, motoneurons express several neuromodulatory peptides. The most extensively studied of these peptides is calcitonin gene-related peptide (CGRP). CGRP modulates the biochemical, physiological and metabolic properties of skeletal muscle primarily through activation of membrane receptors. Virtually all motor pool contain motoneurons that are immunoreactive for CGRP. The purpose of this study was to determine the proportions of motoneurons that express α-CGRP in motor pools innervating muscles with different motor unit compositions. These include the soleus, extensor digitorum longus, tensor fascia latae and the diaphragm muscles as well as the spinal nucleus of the bulbocavernosus. The spinal nucleus of the bulbocavernosus provides innervation to the bulbocavernosus/levator ani muscle complex and the external anal sphincter muscle. The spinal nucleus of the bulbocavernosus contained the greatest proportion of α-CGRP mRNA-positive motoneurons, followed in descending rank order by the tensor fascia latae, the extensor digitorum longus, the soleus and the diaphragm motor pools. In addition, significant differences between motor pools were observed in the mean relative α-CGRP mRNA level among those motoneurons expressing α-CGRP. The highest mean relative α-CGRP mRNA level was observed in soleus and the extensor digitorum longus motor pools; followed in descending rank order by the tensor fascia latae, the diaphragm and the spinal nucleus of the bulbocavernosus. We have previously shown that muscle contractile inactivity increases the number of motoneurons that express α-CGRP and in the relative mRNA levels. The results of the present study suggest that the proportion of motoneurons within a motor pool that express α-CGRP may be closely related to the contractile activity (i.e. activation history) of the target muscle.

Effect of spaceflight on the functional, biochemical, and metabolic properties of skeletal muscle.

This paper summarizes the effects of spaceflight on the functional, morphological, and biochemical properties of human and rodent skeletal muscle. The findings suggest that following as little as 5-6 in space there are deficits in both human and rodent motor capacity, strength, and endurance properties of skeletal muscle. The reduced strength is associated, in part, with a reduction in muscle mass as reflected in smaller cross-sectional areas of both fast- and slow-twitch fibers. Available evidence in animal models suggests that slow-twitch fibers are more sensitive to the atrophying process. Accompanying the atrophy is a transformation of slow to fast protein phenotype involving myosin heavy chain and sarcoplasmic reticulum protein isoforms. These transformations appear to be regulated, in part, by pretranslational processes. Data on the oxidative capacity of rodent skeletal muscle suggest a bias toward preferential utilization of carbohydrate as the primary substrate. These collective findings suggest that skeletal muscles comprised chiefly of slow fibers are highly dependent on gravity for the normal expression of protein mass and slow phenotype. Future studies need to focus on elucidating the mechanisms associated with the atrophy response, as well as identifying suitable exercise and other countermeasures capable of preserving the structural and functional integrity of skeletal muscle.

Fast Twitch Fibres May Predict Anaerobic Performance in Both Females and Males

The aim of the present study was to compare males and females with similar training backgrounds regarding the relationship between anaerobic performance and muscle characteristics and to test whether any of the analysed expressions of muscle characteristics could predict some of the difference in anaerobic performance between sexes. Subjects performed 30 s all-out sprints on a bicycle ergometer (Wingate test) and needle muscle biopsies were taken at rest. Peak and mean power were respectively 44% and 48% higher in males than in females. Activity of total lactate dehydrogenase (LD) was 33% higher and of M subunit of LD 38% higher in males. Anaerobic performance was directly related to the proportion of type II fibres, the relative M subunit activity or the activity of PFK in both males and females and the higher M subunit activity in males could predict some of the sex difference in anaerobic performance. It is suggested that anaerobic performance is directly related to fast contractile or/and anaerobic metabolic properties of skeletal muscle with no sex difference in this relationship. The difference in anaerobic performance between the sexes may partly be related to the sex difference in anaerobic metabolic properties of skeletal muscle.