Muscle Cell Membrane Research Articles

Low androgen level impairs erectile function of rat by regulating the Ng/CaN/AKT/eNOS pathway in penile corpus cavernosum.

The mechanism by which low androgen status inhibit erectile function has not yet been clearly elucidated. Neurogranin (Ng) is a Ca2+ -sensitive calmodulin binding protein that is expressed in endothelial cells and regulates eNOS function. To investigate whether low androgen status inhibit erectile function by regulating the Ng/CaN/AKT/eNOS pathway in the penile cavernous tissue of rats. Thirty-six 8-week-old male Sprague-Dawley rats were randomly divided into six groups as follows (n=6): 4-week control group (4w-control), 4-week castration group (4w-cast), 4-week castration+testosterone replacement group (4w-cast+T), 8-week control group (8w-control), 8-week castration group (8w-cast), and 8-week castration+testosterone replacement group (8w-cast+T). Four weeks and eight weeks after surgery, the ratio of the maximum intracavernous pressure/mean arterial pressure (ICPmax/MAP) was examined. The level of NO and the expression of Ng, calcineurin (CaN), AKT, p-AKT(S473), eNOS, and p-eNOS(Ser1177) in the penile cavernous tissue of each group were determined. Ng and CaN were mainly expressed in the membrane and cytoplasm of endothelial cells and smooth muscle cells in the penile cavernous tissue of rats. The ICPmax/MAP and the concentration of NO in the cast group were significantly lower than those in the control group and cast+T replacement group (p<0.01). The expression of Ng and the ratios of p-AKT/AKT and p-eNOS/eNOS in the penile cavernous tissue of rats in the cast group were significantly lower than those in the control group and cast+T replacement group (p<0.01). The expression of CaN in the penile cavernous tissue of rats in the cast group was significantly increased compared with that in the control group and the cast+T replacement group (p<0.01). Inhibiting the expression of Ng and subsequently upregulating the expression of CaN in the rat penile cavernous tissue was one of the upstream mechanisms of low androgen status inhibiting erectile function by inhibiting the AKT/eNOS signaling pathway.

Diminished Pulmonary Arterial Smooth Muscle Cell Membrane Cholesterol Unmasks EGFR‐dependent Vasoconstriction

IntroductionChronic hypoxia (CH) leads to increased pulmonary vascular resistance and resultant pulmonary hypertension (PH) in patients with chronic obstructive pulmonary disease, sleep apnea, or in residents at high altitude. Recent studies from our laboratory have demonstrated that CH augments vasoconstrictor reactivity to a variety of stimuli, including pulmonary arterial smooth muscle cell (PASMC) stretch, membrane depolarization, and stimulation of G protein‐coupled receptors. This effect of CH is mediated by a switch in PASMC signaling from Ca2+‐dependent mechanisms towards a novel epidermal growth factor receptor (EGFR)‐NADPH oxidase 2 (NOX2)‐Rho kinase (ROK) Ca2+ sensitization pathway. The overall objective of this study is to understand the mechanism by which CH mediates this switch in signaling. We have recently demonstrated that CH decreases membrane cholesterol, a component of lipid membrane domains that can regulate both EGFR and NOX2 activity in other cell types. Therefore, we hypothesized that this EGFR‐NOX2‐ROK signaling pathway is intact in PASMC from control animals but quiescent due to inhibition by membrane cholesterol.MethodsWe first validated our ability to manipulate membrane cholesterol levels by treating primary cultures of PASMCs from Sprague Dawley rats with either cholesterol (2 mM), epicholesterol (an epimeric form of cholesterol; 2 mM), or MβCD (cholesterol chelator; 10 mM). Membrane cholesterol content was quantified by filipin (50 mg/ml) fluorescence using confocal microscopy. Subsequently, we examined vasoconstrictor responses to increasing concentrations of epidermal growth factor (EGF) (10‐10 – 10‐6 M) in pressurized, endothelium‐disrupted rat pulmonary arteries (~150 mm diameter). The effect of diminished membrane cholesterol on vasomotor responses was tested by substituting native cholesterol with epicholesterol (2 mM), which lacks the ability participate in protein‐sterol interactions while maintaining normal membrane fluidity. Vessels were additionally treated with the selective NOX2 inhibitor gp91ds‐tat (50 mM), the selective Rho kinase inhibitor fasudil (10 mM), or their respective vehicles.ResultsCholesterol supplementation significantly increased PASMC membrane cholesterol as indicated by filipin fluorescence. Conversely, treatment with either MβCD or epicholesterol significantly decreased membrane cholesterol compared to vehicle‐treated cells (Figure 1). In agreement with our hypothesis, epicholesterol‐dependent substitution of cholesterol revealed concentration‐dependent vasoconstriction to EGF in pulmonary arteries (Figure 2A). Treatment with either fasudil (Figure 2A) or gp91ds‐tat (Figure 2B) attenuated this effect.ConclusionsThe EGFR‐NOX2‐RhoA signaling cascade is present in arteries from normoxic animals but is normally inhibited by membrane cholesterol. The results of this study will allow for improved mechanistic analysis of how cholesterol regulates this pathway that is central to enhanced vasoconstrictor reactivity in PH.

Sunitinib inhibits STAT3 phosphorylation in cardiac muscle and prevents cardiomyopathy in the mdx mouse model of Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is a fatal X-linked genetic disorder affecting approximately 1 in 5000 male births worldwide. DMD is caused by mutations in the dystrophin gene. Dystrophin is essential for maintaining muscle cell membrane integrity and stability by linking the cytoskeleton to the extracellular matrix, which protects myofibers from contraction-induced damage. Loss of dystrophin leads to mechanically induced skeletal and cardiac muscle damage. Although the disease is not evident in DMD patients at birth, muscular dystrophy rapidly progresses and results in respiratory and cardiac muscle failure as early as the teenage years. Premature death in DMD patients is due to cardiac arrhythmias and left ventricular dysfunction. Currently, there is no effective treatment for DMD-related cardiac failure. Recently, we have shown that a Food and Drug Administration-approved small molecule, sunitinib, a multi-targeted tyrosine kinase inhibitor can mitigate skeletal muscle disease through an increase in myogenic capacity, cell membrane integrity, and improvement of skeletal muscle function via regulation of STAT3-related signaling pathway. Chronic activation of STAT3 has been shown to promote cardiac hypertrophy and failure. In this study, we examined the effects of long-term sunitinib treatment on cardiac pathology and function. Our results showed sunitinib treatment reduced STAT3 phosphorylation in the heart muscle of mdx mice, improved cardiac electrical function, increased cardiac output and stroke volume, decreased ventricular hypertrophy, reduced cardiomyocytes membrane damage, fibrotic tissue deposition and slightly decreased cardiac inflammation. Together, our studies support the idea that sunitinib could serve as a novel treatment to slow cardiomyopathy progression in DMD. One Sentence Summary In this study, we determined if sunitinib, a Food and Drug Administration-approved drug, could reduce the pathology and improve cardiac function in an animal model for DMD.

Measurements of basal d-glucose transport through GLUT1 across the intact plasma membrane of isolated segments from single fast- and slow-twitch skeletal muscle fibres ofrat.

AimTo develop a method for direct measurement of the fluorescent d‐glucose analogue 2‐NBDG transport across the plasma membrane of single skeletal muscle fibres and derive the theoretical framework for determining the kinetic parameters for d‐glucose transport under basal conditions.MethodsA novel method is described for measuring free 2‐NBDG transport across plasma membrane of single rat muscle fibres at rest. The 2‐NBDG uptake was >90% suppressed by 100 µM cytochalasin B in both fast‐twitch and slow‐twitch fibres, indicating that the 2‐NBDG transport is GLUT‐mediated. Fibres were identified as fast‐twitch or slow‐twitch based on the differential sensitivity of their contractile apparatus to Sr2+.ResultsThe time course of 2‐NBDG uptake in the presence of 50 µM 2‐NBDG follows a one‐phase exponential plateau curve and is faster in fast‐twitch (rate constant 0.053 ± 0.0024 s‐1) than in slow‐twitch fibres (rate constant 0.031 ± 0.0021 s‐1). The rate constants were markedly reduced in the presence of 20 mM d‐glucose to 0.0082 ± 0.0004 s‐1 and 0.0056 ± 0.0002 s‐1 in fast‐twitch and slow‐twitch fibres respectively. 2‐NBDG transport was asymmetric, consistent with GLUT1 being the major functional GLUT isoform transporting 2‐NBDG in muscle fibres at rest. The parameters describing the transport kinetics for both 2‐NBDG and d‐glucose (dissociation constants, Michaelis–Menten constants, maximal rates of uptake and outflow) were calculated from the measurements made with 2‐NBDG.ConclusionFree 2‐NBDG and d‐glucose transport across the plasma membrane of single rat muscle fibres at rest is fast, conclusively showing that the rate‐limiting step in d‐glucose uptake in skeletal muscle is not necessarily the GLUT‐mediated transport of d‐glucose.

Urine proteomics as a non-invasive approach to monitor exertional rhabdomyolysis during military training

Exertional rhabdomyolysis (ERM), a condition often associated with strenuous exercise, a common practice in the military activities, can be defined as the process of injury and rupture of muscle cell membranes, with leakage of its components into the bloodstream. Creatine kinase (CK) has been used for ERM diagnosis, albeit several studies reported the discrepancy between CK levels and clinical signs or symptoms. In this study, we analyzed the biochemical profile of the blood, and the urinary proteome of ten marine soldiers in a special training course. The samples were collected in two periods, M1 and M2, which correspond to the lowest and highest CK levels during training, respectively. Quantitative urinary proteome profile of M1 and M2 showed changes in proteins involved in immune system and cell adhesion-related pathways after strenuous physical exercise. Changes in the abundance of several proteins was observed in individuals carrying genetic polymorphisms related to greater risk for muscle damage. A panel of proteins (CTSH, PIK3IP1, DEFB1, ITGB1, BCAN, and TNFRSF10C) presented high correlation with classical blood biochemical markers of ERM and AGT MET235Thr and ACE I/D polymorphisms. These proteins represent potential urine markers of muscle damage due to intense physical conditions such as military training activities. SignificanceThis study analyzed the blood and urine of a cohort of marine soldiers enrolled in a special training program including missions with low and high exposure to strenuous exercise. The biochemical blood profile, polymorphisms mapping and mass spectrometry-based analyses of the urinary proteome was evaluated in such a controlled samples. A total of 226 urinary proteins associated to immune system, cell adhesion and redox homeostasis were significantly changes during ERM shedding lights on the disease pathogenesis. In particular, a panel of six proteins were associated to classical ERM markers and could be used as early non invasive biomarkers.

Callistephin inhibits amyloid-β protein aggregation and determined cytotoxicity against cerebrovascular smooth muscle cells as an in vitro model of cerebral amyloid angiopathy

It has been indicated that amyloid β (Aβ) plaques can be accumulated within the basement membranes of cerebrovascular smooth muscle cells (CVSMCs) and stimulate the induction of cerebral amyloid angiopathy (CAA). However, the exact mechanism(s) of which small molecules including callistephin mitigate the formation of Aβ aggregation and associated CAA is not well-understood. Therefore, in the present study, Aβ 1–42 samples in the aggregation buffer were co-incubated for 36 h without or with of callistephin and the protein aggregation features along with the associated cytotoxicity against CVSMCs as the core components of cerebral arterial wall were explored by different biochemical and cellular methods. Fluorescence (ThT, Nile red) and CD techniques indicated the inhibition of Aβ 1–42 fibrillization in the presence of callistephin. Cellular assays revealed that cytotoxicity of Aβ 1–42 samples aged in the aggregation buffer with callistephin was much less against CVSMCs than Aβ 1–42 amyloid alone through regulation of membrane leakage and downregulation of TNF-α and IL-6 at protein level. In conclusion, these data may provide useful information about the possible mechanisms by which callistephin can show its protective effect against CAA.

Functional, electrophysiology, and molecular dynamics analysis of quercetin-induced contraction of rat vascular musculature

Quercetin, a flavonoid abundantly present in the Mediterranean diet, is considered a vasodilator despite its recognized capability to stimulate vascular CaV1.2 channel current (ICa1.2). The present study was undertaken to assess its possible vasocontractile activity. Functional and electrophysiology experiments were performed in vitro on rat aorta rings and tail artery myocytes along with an in-depth molecular modelling analysis. The CaV1.2 channel stimulator (S)-(−)-methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl) pyridine-5-carboxylate (Bay K 8644) was used as reference compound. Quercetin and Bay K 8644 caused a significant leftward shift of KCl concentration-response curve. Neither agent affected basal muscle tone, though in rings pre-treated with thapsigargin or 15 mM KCl they caused a strong, concentration-dependent contraction. Both quercetin and Bay K 8644 potentiated the response to Ca2+ in weakly depolarised rings. At high KCl concentrations, however, quercetin caused vasorelaxation. While Bay K 8644 stimulated ICa1.2, this effect being sustained with time, quercetin-induced stimulation was transient, although the molecule in solution underwent only marginal oxidation. Quercetin transient stimulation was not affected by pre-treatment with isoprenaline, sodium nitroprusside, or dephostatin; however, it converted to a sustained one in myocytes pre-incubated with Gö6976. Classical molecular dynamics simulations revealed that quercetin and Bay K 8644 formed hydrogen bonds with target sensing residues of CaV1.2 channel favouring the inactivated conformation. In conclusion, quercetin-induced stimulation of ICa1.2 promoted vasocontraction when Ca2+ buffering function of sarcoplasmic reticulum was impaired and/or smooth muscle cell membrane was moderately depolarised, as it may occur under certain pathological conditions.

CRISPR/Cas9 editing of directly reprogrammed myogenic progenitors restores dystrophin expression in a mouse model of muscular dystrophy.

SummaryGenetic mutations in dystrophin manifest in Duchenne muscular dystrophy (DMD), the most commonly inherited muscle disease. Here, we report on reprogramming of fibroblasts from two DMD mouse models into induced myogenic progenitor cells (iMPCs) by MyoD overexpression in concert with small molecule treatment. DMD iMPCs proliferate extensively, while expressing myogenic stem cell markers including Pax7 and Myf5. Additionally, DMD iMPCs readily give rise to multinucleated myofibers that express mature skeletal muscle markers; however, they lack DYSTROPHIN expression. Utilizing an exon skipping-based approach with CRISPR/Cas9, we report on genetic correction of the dystrophin mutation in DMD iMPCs and restoration of protein expression in vitro. Furthermore, engraftment of corrected DMD iMPCs into the muscles of dystrophic mice restored DYSTROPHIN expression and contributed to the muscle stem cell reservoir. Collectively, our findings report on a novel in vitro cellular model for DMD and utilize it in conjunction with gene editing to restore DYSTROPHIN expression in vivo.

УТОМЛЕНИЕ: ПОНИМАНИЕ ПРОБЛЕМЫ И СИСТЕМНЫЕ МЕХАНИЗМЫ ЕГО РАЗВИТИЯ

The purpose of the research is to determine the modern ideas about fatigue and the physiological mechanisms of its development. Methods and organization of the research: a review of publications using Google Scholar and PubMed databases. Research results and discussion. When analyzing scientific and methodological publications related to the study of fatigue, many problems has been revealed, such as the ambiguity of interpretation of the word "fatigue" often used in sports science and mechanisms of its development that are not fully understood. The exact understanding of each definition will depend both on the semantic groups of the words and on their morphological structure. At the same time, when studying the physiological mechanisms of fatigue, the central and peripheral mechanisms of its development are separated. The first will include processes emanating from the central nervous system, and the second - processes occurring in the peripheral nervous system. The processes of fatigue on the periphery are associated with the depletion of energy resources, an increase in the number of metabolites (hydrogen ions, lactate), with the magnitude and localization of flows through various ion channels, with a change in the electrochemical gradients of Na, K and Cl inside and outside the muscle fiber membrane, with intensity and duration muscle stimulation. At the level of the central nervous system, the processes are associated with limitations in motor control related both to the processes of synaptic transmission of neurotransmitters and psychological factors, which are currently poorly understood, but, nevertheless, show their influence in experimental data. Conclusion: this review article puts forward objective proposals for the exact understanding of each of the above definitions in the Russian-language literature and highlights some of the nuances of understanding in the foreign one. Also, ideas about the physiological mechanisms of central and peripheral fatigue are revealed.

Studies on the identification of frostbitten and frozen meat after defrosting by the spectrophotometric method for determining DNA in muscle tissue extracts

Changes in the state of meat during freezing are determined by the phase transition of water into ice and an increase in the concentration of substances dissolved in the liquid phase. The process of crystal formation leads to a change in the physical characteristics of the meat and may be accompanied by changes in its structural properties. The effect of the proportion of frozen water on the permeability of the membranes of muscle fibers of frostbitten and frozen meat has been established. The ratio of optical densities at wavelengths of 270 nm and 290 nm (R) can be used to judge the thermal state of the meat. It is shown that the value of R after defrosting frozen meat is 2 times higher than for frostbitten meat.

Cocoa flavonoids: a promising ingredient that potentiates vitamin d action in skeletal muscle cells

Rationale: Vitamin D (VitD) effects take place by binding to its receptor (VDR) which is a classical nuclear receptor responsible for genomic effects, but there is also a fraction of the VDR located in the muscle plasma membrane that is responsible for its non-genomic effects. In addition to the established effect of VitD in bone and mineral homeostasis, VitD insufficiency/deficiency is linked to a range of muscle disorders including frailty and muscle loss/dysfunction. Flavonoids decrease insulin resistance and have antioxidant and anti-inflammatory properties by activating Akt signaling pathways. Our study has aimed to evaluate, in VitD deficient conditions, if cocoa flavonoids (CF) are able to mediate the interacction between VitD and skeletal muscle glucose uptake by triggerring the modulation of its genomic and non-genomic signaling pathways. This could be useful in pathological deficient VitD situations, such as diabetes or sarcopenia where muscle function is compromised due to the onset of insulin resistance.

Natural History of a Mouse Model Overexpressing the Dp71 Dystrophin Isoform.

Dystrophin is a 427 kDa protein that stabilizes muscle cell membranes through interactions with the cytoskeleton and various membrane-associated proteins. Loss of dystrophin as in Duchenne muscular dystrophy (DMD) causes progressive skeletal muscle weakness and cardiac dysfunction. Multiple promoters along the dystrophin gene (DMD) give rise to a number of shorter isoforms. Of interest is Dp71, a 71 kDa isoform implicated in DMD pathology by various animal and patient studies. Strong evidence supporting such a role for Dp71, however, is lacking. Here, we use del52;WT mice to understand how Dp71 overexpression affects skeletal and cardiac muscle phenotypes. Apart from the mouse Dmd gene, del52;WT mice are heterozygous for a full-length, exon 52-deleted human DMD transgene expected to only permit Dp71 expression in muscle. Thus, del52;WT mice overexpress Dp71 through both the human and murine dystrophin genes. We observed elevated Dp71 protein in del52;WT mice, significantly higher than wild-type in the heart but not the tibialis anterior. Moreover, del52;WT mice had generally normal skeletal muscle but impaired cardiac function, exhibiting significant systolic dysfunction as early as 3 months. No histological abnormalities were found in the tibialis anterior and heart. Our results suggest that Dp71 overexpression may have more detrimental effects on the heart than on skeletal muscles, providing insight into the role of Dp71 in DMD pathogenesis.

English

Introduction: According to the literature, eccentric exercise has been considered a precursor of neuromuscular changes generated by post-exercise damage, mainly causing an alteration in the muscle cell membrane. Muscle fiber conduction velocity (MFCV) has been one of the physiological variables that have allowed to quantify this alteration. Some investigations have shown a decrease in the MFCV after eccentric exercise protocols; however, few studies have confirmed these findings. This review aimed to describe the recent scientific evidence that reports changes in the MFCV after eccentric exercise protocols. Material and method: From 265 articles, 6 articles were selected from EBSCO and MEDLINE platforms with a temporal filter of 10 years (between 2010 and April 2020), using inclusion/exclusion criteria predetermined. Firstly, the information from eccentric exercise effect on MFCV, and exercise protocols were described. Secondly, the techniques used to record electromyographic signals and some criteria to determine the MFCV were reported. Results: Modifications of MFCV can be observed after eccentric exercise in almost all selected articles. At the same time, a decrease of this variable was observed in four studies, associated with the biceps brachii and two portions of the quadriceps muscles. However, one article describes an increase of the MFCV in the vastus lateralis quadriceps. Conclusion: The articles suggest that eccentric contractions could modify the MFCV behavior of some muscles. However, evidence is still lacking to describe the real cause of these changes.

Insulin, Muscle Glucose Uptake, and Hexokinase: Revisiting the Road Not Taken.

Research conducted over the last 50 yr has provided insight into the mechanisms by which insulin stimulates glucose transport across the skeletal muscle cell membrane Transport alone, however, does not result in net glucose uptake as free glucose equilibrates across the cell membrane and is not metabolized. Glucose uptake requires that glucose is phosphorylated by hexokinases. Phosphorylated glucose cannot leave the cell and is the substrate for metabolism. It is indisputable that glucose phosphorylation is essential for glucose uptake. Major advances have been made in defining the regulation of the insulin-stimulated glucose transporter (GLUT4) in skeletal muscle. By contrast, the insulin-regulated hexokinase (hexokinase II) parallels Robert Frost's "The Road Not Taken." Here the case is made that an understanding of glucose phosphorylation by hexokinase II is necessary to define the regulation of skeletal muscle glucose uptake in health and insulin resistance. Results of studies from different physiological disciplines that have elegantly described how hexokinase II can be regulated are summarized to provide a framework for potential application to skeletal muscle. Mechanisms by which hexokinase II is regulated in skeletal muscle await rigorous examination.

An integrative proteomics metabolomics based strategy reveals the mechanisms involved in wasp sting induced acute kidney injury

The pathophysiological mechanisms involved in wasp-sting-induced acute kidney injury (AKI) remain largely unknown. Here, we combined proteomics and metabolomics to investigate the mechanisms behind multiple wasp sting-induced AKI. Interestingly, we found many differentially abundant proteins in the serum of AKI group compared with that of the non-AKI and control groups, involved in several metabolic pathways and the regulation of cellular processes. In addition, we also detected differentially abundant metabolites in the AKI group; among them many were involved in the glycerophospholipid metabolic pathway (the key pathway in the context of AKI): 50 metabolites, all downregulated in the AKI group. Importantly, the convergent analysis of metabolomics and proteomics data revealed that biomarkers of rhabdomyolysis (CA 3, MYL3, and LDH) and hemolysis (ALT and LDH) were integrated into a regulatory network with phospholipid metabolism products in the AKI group, indicating that wasp sting-induced AKI is secondary to rhabdomyolysis and intravascular hemolysis. Of note, such a phenotype suggests the disruption of the membrane of skeletal muscle cells and red blood cells mediated by the phospholipase A1 (PLA1), PLA2, and mastoparan in the wasp venom, via the disruption of membrane glycerophospholipids. Overall, our results highlight a potential new mechanism behind wasp sting-induced AKI and suggest that PLA inhibitors may be potential agents for the treatment of this condition.

Expression levels of filaggrin-2 in relation to drip loss in pigs.

ObjectiveThe aim of this study was to investigate the expression level of filaggrin-2 (FLG2) in correlation with drip loss.MethodsThe muscle samples were randomly taken from a local meat supplier. Samples were taken from Longissimus lumborum muscles to evaluate the drip loss (n = 100). Five muscles per group (low and high drip loss) were selected to evaluate FLG2 mRNA and protein expression levels.ResultsmRNA of FLG2 gene was not significantly different in pigs with different levels of drip loss (p>0.05). Statistical analysis revealed that FLG2 protein expression levels were significantly different between the drip loss groups. Western blot revealed that the high drip loss group had higher FLG2 protein expression level than the low drip loss group (p<0.001). Moreover, immunohistochemistry revealed the high signal intensity was on the muscle cell membrane and cytoplasm.ConclusionFLG2 protein might play roles in drip loss of pork and will provide the basis for information to improving meat quality traits in pigs.

PHYSIO IN DUCHENNE MUSCULAR DYSTROPHY (DMD)

Duchenne muscular dystrophy is the most common and severe form of muscular dystrophy and is caused by mutations in the dystrophin gene. Dystrophin, together with several other protein components, is part of a complex known as the dystrophin glycoprotein complex (DGC). The DGC plays an essential role in maintaining the structural integrity of the muscle cell membrane by providing a link between the extracellular matrix and the cytoskeleton

194 Avian Breast Muscle Development and Growth: Influence of Temperature on Growth Mediated by Breast Muscle Adult Myoblasts (Satellite Cells)

Abstract Newly hatched poults and chicks have immature thermoregulatory systems and are not able to maintain a constant body temperature when exposed to hot or cold ambient temperatures. During the immediate posthatch period during handling and transport, poults and chicks are commonly exposed to acute thermal conditions. This immediate posthatch period is when satellite cells, adult myoblasts, have their highest period of mitotic activity and are sensitive to extrinsic stimuli including ambient temperature. Variable temperatures can have long-lasting positive or negative effects on skeletal muscle growth. Satellite cells are a self-renewing multipotential stem cell population located between the basement membrane and sarcolemma of muscle fibers. They are responsible for all posthatch growth of muscle through muscle fiber hypertrophy. Results have shown that satellite cells are more sensitive to thermal stress during the period of satellite cell proliferation than during differentiation into multinucleated myotubes, and that pectoralis major muscle satellite cells from growth-selected lines of chickens and turkeys are more sensitive to temperature. Recent findings have shown that the rapamycin, mTOR, signaling pathway which is involved in muscle growth through hypertrophy is differentially affected by thermal stress in a growth-dependent manner. Since satellite cells are a stem cell population, they can also transdifferentiate into other cellular lineages. Anaerobic muscles like the pectoralis major muscle are more prone to converting to an adipogenic lineage compared to aerobic muscles like the biceps femoris. Thus, variable temperatures can impact the intramuscular fat content of the breast muscle. Taken together, changes in ambient temperature alter satellite cell function causing long-term effects on growth, morphological organization, and composition of the pectoralis major, breast, muscle.

The missing 'link'? β-Catenin's role in skeletal muscle glucose uptake during exercise and contraction.

The missing 'link'? β-Catenin's role in skeletal muscle glucose uptake during exercise and contraction.

An Explanation of Subsurface Optical Pathways through Food Myosystems and their Effect on Colorimetry

Light may pass along and across the long axes of muscle fibers in any food myosystem. Thus, incident light may be scattered in several ways before some of it reappears at the surface as diffuse reflectance. Pathways may be short if scattering is strong, or long if scattering is weak. Short pathways minimize selective absorbance by chromophores such as myoglobin, while long pathways maximize selective absorbance. Many food myosystems exhibit a post-mortem decrease in pH caused by anaerobic glycolysis with a series of microstructural changes – glycogen granules between myofibrils are lost, myofibrils shrink laterally as myofilaments move closer together, water moves from within myofibrils to the space between them, muscle fiber membranes leak and lose their electrical capacitance, and myoglobin is flushed into the fluid filled spaces between muscle fibers. These changes increase scattering of light passing across the long axes of muscle fibers. Scattering of light along muscle fibers is caused by sarcomere discs (A-bands). Interference from one or a small number of sarcomere discs may cause iridescence, but in most cases interference from numerous discs causes achromatic diffuse reflectance. Commission International de l’Éclairage (CIE) chromaticity coordinates were calculated for various subsurface optical pathways. Pathways across versus along muscle fibers had a strong effect on CIE y (r = 0.84, P &lt; 0.01) and an even stronger effect on CIE Y% (r = 0.95, P &lt; 0.005).