The regulation of lipolysis in adipocytes involves coordinated actions of many lipid droplet (LD)-associated proteins such as perilipin, hormone sensitive lipase (HSL), adipose triglyceride lipase (ATGL), and its activator protein, CGI-58. Recently, the author and my colleagues described the cellular origin and physiological significance of micro LDs (mLDs) that emerge in the cytoplasm during active lipolysis, as well as the roles of key liplolytic proteins on mLDs in differentiated 3T3-L1 adipocytes. We suggested that, besides the surface of pre-existing central LDs, LD-associated proteins such as perilipin, CGI-58, HSL, and ATGL are actively involved in lipolysis on mLDs that are formed by FA re-esterification but probably devote to increasing total triacylglycerol (TAG) turnover and thus potentially net FA release. Thus, regulation of mLDs as well as LD-associated proteins may be an attractive therapeutic target against lipid-associated metabolic diseases. Physiological strategies such as exercise training aimed toward fat loss by active lipolysis in adipocytes (i.e. fat mobilization) and fatty acid (FA) oxidation in muscles (i.e. fat utilization) have become of preferred therapeutic agents against metabolic disorders. However, yet remarkably little is known about molecular mechanisms underlying augmented capacity of active lipolysis induced by exercise training, which should be elucidated in the future.

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Many researchers have analyzed dynamic postural control during voluntary arm movements and floor translation, focusing on the anticipatory activation of postural muscles in which the function of frontal lobe is involved. In this review, I address the postural muscle activation preceding arm movements, and consider the effect of arm movement dynamics, behavioral condition, postural set and postural movement pattern. I also address the anticipatory postural control during transient or periodical floor translations, and consider motor preparation, attentional allocation, and the use of event-related brain potentials to investigate frontal lobe activation.

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Thoroughbred racehorses have been selectively bred for racing for centuries. The excellent exercise capacity of Thoroughbreds is thought to depend largely on their extraordinarily high cardiopulmonary function. Their high aerobic capacity (VO_2max) might be amplified by the exercise-induced hypoxemia that they experience even during submaximal exercise. In humans and horses, accumulated O₂ deficit (AOD) has been the primary approach used to assess net anaerobic capacity during exercise. The exercise-induced hypoxemia Thoroughbreds experience allows an alternative approach to measuring net anaerobic energy utilization using plasma lactate accumulation rate (PLAR). Horses increase their aerobic capacity when breathing hyperoxic gas that eliminates exercise-induced hypoxemia, and PLAR decreases stoichiometrically. Relating the decrease in PLAR to the increase in VO_2max yields a quantitative index of how much net aerobic power a horse is utilizing. Comparison in horses of the net anaerobic power estimated by the two methods, AOD and PLAR, shows systematic bias and suggests PLAR may be more accurate.

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Vigorous muscle contraction ultimately results in an inability to produce the desired force, and this is known as muscle fatigue. Commonly, fatigue may persist for prolonged periods of time, in particular, at low activation frequencies. Current efforts to examine the relevant mechanisms involved in muscle fatigue are focused on Ca²⁺-regulation function within the active muscle cell. The sarcoplasmic reticulum (SR) is the major organelle in muscle responsible for regulating cytosolic free Ca²⁺concentration. Numerous studies have demonstrated that SR function, with respect to both Ca²⁺ release and uptake, is impaired after contractile activity that induces fatigue. The mechanisms of disturbances in SR Ca²⁺-cycling that result from fatigue are complex and involve a variety of metabolic and nonmetabolic factors. In this brief review, we will describe the link between altered SR Ca²⁺ kinetics and muscle performance, and the cellular mechanisms for SR Ca²⁺ handling, with attention devoted to both major and minor membrane proteins. Finally, we will discuss possible factors responsible for disturbances in SR Ca²⁺-cycling function.

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Skeletal muscle mass is regulated by a balance of protein synthesis and degradation. The regulation of this protein synthesis/degradation system is linked with muscle activity, and leads to muscle hypertrophy/atrophy. However, recent studies suggested that this system is also linked to the mechanisms underlying muscular dystrophy. In this review, we summarize the recent advances relating to the molecular mechanisms of the protein synthesis/degradation system, and overview the new therapeutic strategy for muscular dystrophy that targets the molecular events that regulate muscle hypertrophy/atrophy.

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There are several pathomechanisms of lower back pain among athletes such as lumbar intervertebral disc degenerations, disc herniations, spondylolysis, zygapophyseal (facet) joint disorders, sacroiliac joint disorders, muscle, fascia and its insertion disorders. In many cases except intervertebral disc herniations, there are less radiological findings so they should be diagnosed using functional classification. In order to decrease the mechanical stress to the pathological portion, it is thought to be important to maintain the proper spinal alignment and the spinal segmental stability. The stabilization exercises which facilitates the deep trunk muscles (transversus abdominis, lumbar multifidus) function and the stretching for the muscles attached to the pelvis are recommended to achieve these tasks.

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We accomplish activities of daily living through a combination of or isolated isometric, shortening (concentric), lengthening (eccentric) contractions regarded as fundamental patterns of muscle activation. It has been widely recognized that a unique neural strategy may control lengthening contractions but it is still unclear if this neural strategy is uniform across muscles. Here we review evidence for task-specific differences in neural control of muscle lengthening and shortening as indexed by surface electromyographic activity, corticospinal excitability, anatomical properties, and motor unit behavior. The emerging hypothesis is that the neural control of task-specificity associated with muscle lengthening and shortening may not be uniform across all healthy human muscles.

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Near-infrared spectroscopy (NIRS) has been a useful method for the detection of changes in in vivo muscle oxygenation and oxidative metabolism in healthy subjects as well as in patients with various diseases. The advantage of using NIRS over other invasive techniques is that the device itself is more portable and the procedure can be performed more simply. So far, commercially available single-distance continuous wave NIRS (NIRS_SDCW) device provide only the relative values of tissue oxygenation mainly due to the unknown path of NIR light through biological tissues. In particular, subcutaneous adipose tissue thickness greatly influences the light pathlength and makes it difficult to quantify tissue oxygenation. Alternatively, the arterial occlusion and sensitivity correction approach using NIRS_SDCW and the pathlength determination using sophisticated time-resolved or phase-modulated spectroscopy could estimate the absolute value of tissue oxygenation. This paper aims at reviewing primarily NIRS_SDCW studies for evaluating skeletal muscle oxygenation and oxidative metabolism, specifically in physiological and medical research area.

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Sarcopenia is a very prevalent age-related decline in skeletal muscle mass and muscle strength, and it has a biologic basis and is a distinct clinical syndrome in elderly people that is associated with high risk for adverse health outcomes. Currently, many parameters can potentially be used to track age-related skeletal muscle decline; among these parameters, biochemical markers for sarcopenia may be particularly useful for developing different aspects of therapeutic intervention. Evidence indicates that extracellular heat shock protein 72 in plasma may be defined, as a potential biomarker of sarcopenia. Extracellular adenosine triphosphate in plasma may trigger the release of heat shock protein 72 during a bout of exercise. Muscle hypertrophy in elderly women was caused by 12-week resistance exercise training, and this hypertrophy induced a reduction in extracellular heat shock protein 72 and pro-inflammatory cytokines and insulin like growth factor-I. The phenomenon in circulating levels of biomarkers may result from the lack of understanding of the mechanisms in exercise or muscle anabolic and catabolic systems, or secreted cell stress proteins are part of an extracellular homeostatic signaling system. Using two or more biomarkers in combination to clearly identify one condition may be one of multiple solutions. Using biomarkers combinatorially may allow clinicians to identify different domains of the sarcopenia syndrome and give them useful insights about the pathophysiological process underlying the phenomenon.

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A growing body of evidence suggests that exposure to hypoxic conditions during rest and exercise may be beneficial for the prevention of metabolic syndrome. Epidemiologic studies indicated that mortality rates from coronary heart disease were lower in populations living at higher altitudes than for those living at lower altitudes. Recent researches demonstrated that exercise training conducted under hypoxic conditions resulted in further reduction of body fat mass, greater improvement of postprandial glycemic control compared with the effects of similar exercise training conducted under normoxic conditions. In particular, the findings strongly suggest that augmented glucose metabolism resulting from exposure to hypoxic conditions is a pronounced advantage. Additionally, moderate hypoxic exposure further improves insulin sensitivity and glycemic regulations when exercise is combined. A further benefic of hypoxic training appears to be a reduction of appetite. Altered regulation of appetite-related hormonal responses might be a key to understanding the mechanisms of weight loss at high altitude stay and/or exercise.

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Appetite and eating behaviour are controlled by a variety of peripheral signals that change in response to food intake and act in the hypothalamus and brainstem. Glucagon-like peptide-1 (GLP-1) is a brain-gut peptide that has a variety of physiological functions and is involved in appetite regulation. Abnormalities in the expression and secretion of GLP-1 have been shown to occur in obesity, diabetes, and hyperlipidemia, and improving these abnormalities has become an important challenge. Exercise has recently been shown to have an influence on GLP-1 concentrations. This short review aims to highlight the association between exercise and the blood kinetics of GLP-1 and discuss the relevance of GLP-1 in the regulation of appetite to prevent obesity.

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The skin functions as a physical barrier to prevent infection and water evaporation within the body. In addition, it regulates the immune system and produces hormones and neurotransmitters. Because these functions are directly related to whole body health, the maintenance of skin health is important. Sunlight is one of the major inducers of skin damage and includes ultraviolet (UV)-A, UVB, and UVC radiation. UV radiation causes skin aging, so-called photoaging, which is characterized by epidermal hyperplasia, degradation of extracellular matrix molecules, and wrinkle formation. Increasing evidence indicates that UV radiation causes dermal photoaging. In particular, UV radiation-induced dermal angiogenesis is a key factor causing dermal photoaging. This review article describes the molecular mechanisms that underlie UV radiation-induced dermal aging.

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Alpha (α)-actinin is an actin-binding protein in mammalian cells. In skeletal muscles, α-actinin is located in the Z-line of sarcomeres, where it creates actin-actin crosslinks. We have recently reported that α-actinin adaptation occurs at the isoform level in rat skeletal muscle under different physiological conditions in an isoform-specific manner. Based on those results, this review briefly summarized the effects of changes in muscle activity on α-actinin expression.

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Macrophage-induced inflammation is an important pathophysiological mechanism of insulin resistance, especially in adipose tissue. It has been demonstrated that exercise has anti-inflammatory effects and enhances insulin sensitivity in skeletal muscles, however, the causal relationship between these two changes is not fully understood. Recently, several reports demonstrated that alternatively-activated, anti-inflammatory macrophages (called M2 macrophages) maintain normal insulin sensitivity in the liver and skeletal muscles. These data suggest that M2 macrophages could be a positive regulator of insulin sensitivity. In this review, we summarize the current understanding of the association of macrophages and insulin sensitivity, and discuss the possible role of M2 macrophages in mediating an exercise-induced increase in insulin sensitivity.

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In recent years, many experiments have investigated the impact of dietary amino acid supplementation on improvements in muscle strength and endurance capacity. However, it is unclear whether this supplementation causes vascular remodelling in skeletal muscle. This review focused on the effects of L-arginine and/or L-ornithine supplementation on capillary growth in cardiac and skeletal muscles. Although the chronic administration of 4% L-arginine did not improve capillarization in rat cardiac and hind-leg muscles, it facilitated exercise-induced capillary growth via vascular endothelial growth factor (VEGF) protein upregulation. In middle-aged rats, moderate intensity endurance training for 6 weeks did not cause capillary growth, whereas training with L-arginine supplementation led to an improvement in capillarization in the hind-leg muscle and left ventricle by promoting VEGF and endothelial nitric oxide synthase (eNOS) protein expression. The administration of L-arginine and L-ornithine for 6 weeks caused a marked increase in capillarization in rat skeletal muscle via the downregulation of endostatin and upregulation of VEGF-R2 protein expression. Moreover, this supplementation facilitated exercise-induced improvements in capillarization in the hind-leg muscles via the downregulation of endostatin and upregulation of VEGF and eNOS protein levels. The evidence presented in this review indicates that L-arginine and/or L-ornithine administration may facilitate capillary growth and endurance exercise capacity. Furthermore, this supplementation may be a useful therapeutic intervention for ischemic-related diseases.

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The purpose of this study was to investigate the influence of cryotherapy on knee joint position sense (JPS) and intraarticular blood flow volume (IBFV) and evaluate their relationships with cooling time as well as with surface temperature and deep temperature. Ten healthy volunteers were examined. This study consisted of a same-subjects repeated-measures design, with the timeframe of cryotherapy application (no therapy [resting control group], 2-min cooling, or 15-min cooling intervention) after exercise being the independent variable, and IBFV, knee JPS, surface temperature, and deep temperature serving as the dependent variables. Dependent variables were examined before 10-min cycle ergometer exercise (baseline), post-exercise, post-cooling, and 15 min later. In the 15-min cooling group, IBFV immediately after cooling and 15 min later were significantly lower than the post-exercise values (P = 0.048 and 0.016, respectively), and knee JPS at 15 min later was significantly lower than the baseline value (P = 0.037). By contrast, the 2-min cooling group showed no significant changes in either knee JPS or IBFV. Although both surface and deep temperatures after cooling were significantly lower than baseline (P = 0.034 and P < 0.001, respectively) in the 2-min cooling group, 15 min later they were significantly higher than post-cooling values (P = 0.023 and 0.023, respectively). These results suggest that 15-min cooling interventions functionally impair the sensitivity of JPS, although cooling is suitable for reduction of IBFV in deep tissue. Cooling interventions lasting less than 2-min did not affect knee JPS; however no reduction of IBFV occurred during this timeframe.

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The Hoffmann (H-) reflex can be depressed when elicited repetitively at a frequency of ~1 Hz. This H-reflex depression is termed homosynaptic depression (HD) and is attributed to impaired neurotransmitter release from the presynaptic Ia terminal. In the present study, we systematically evaluated the extent to which HD in the soleus was modulated by the level of homonymous muscle contraction and the size of the test H-reflex. Changes in HD were also assessed while the target muscle was subjected to fatigue. The participants were 11 healthy male volunteers aged 20−25 years. HD was induced by delivering a percutaneous electrical stimulus at 1 Hz to the right posterior peroneal nerve. HD was proportional to the size of the test reflex size up to 60% of the maximum size of the direct motor response (M_max), at which point values plateaued. HD decreased significantly during voluntary contraction of the homonymous muscle (range, <20% of maximal voluntary contraction [MVC]), irrespective of the degree of contraction. Within 1−5 minutes after completing 4 sets of the MVC for 60 s with ischemic arterial blockade, the degree of HD decreased significantly when the test reflex size was <60% of the M_max. We conclude that test reflex size is a crucial factor when evaluating the nature of HD. Furthermore, HD reduction during voluntary contraction and muscle fatigue may represent an innate mechanism that serves to retain Ia transmission.

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