Bioelectrical impedance analysis (BIA) involves passing a weak, high-frequency current through the body in order to measure variables such as tissue volume, or the volume of blood, on the basis of electrical resistance. Biometric measurements using BIA date back to the beginning of the 20th century; and since then there have been many technical refinements. BIA is non-invasive, it excels in terms of cost and safety, and it does not require any special measurement skills. It has therefore become an outstanding measurement tool for a range of body composition assessments in areas such as large-scale population studies or sports science. There have already been numerous reports of studies of BIA, and its contribution to sports science is well recognized, so that many researchers have demonstrated an interest in using BIA. However, while BIA is easier to operate than other measurement tools, it requires basic knowledge and precise methodology in order to properly interpret the data. This review summarizes the theory of measuring tissues related to exercise, the method of measuring cardiac output, and the method of estimating skeletal muscle mass. First, while the measurement, by BIA, of cardiac output (CO) at rest yields stable results, previous measurements during dynamic exercise had several limitations. CO measurement during intense exercise has recently become possible as a result of improvements to fast Fourier transform (FFT) and the algorithms. Moreover, the water content and fat mass of the body can now be calculated in terms of electrical models in which resistors and capacitors are arranged in series or in parallel, and cells and tissues have been simplified as far as possible. Finally, new estimation equations using single-frequency BIA and multi-frequency BIA have been developed for measurement of skeletal muscle mass in the limbs, and each are reported to have high reliability and high reproducibility. Development of simple, highly accurate measuring instruments and methods for vital observation, utilizing BIA, and that can contribute to sports science, is expected.
Exercise is widely perceived to be an effective tool for prevention and treatment of type 2 diabetes, since reducing visceral fat accumulation by means of exercise protects against insulin resistance. However, not only reducing visceral fat but other mechanisms contribute to the benefits of exercise. The beneficial effects of exercise for prevention and treatment of type 2 diabetes is also partly due to muscle contraction-induced local adaptations, i.e. an insulin-independent increase in GLUT4-mediated glucose transport, increased insulin action of GLUT4-mediated glucose transport, and increased GLUT4 protein expression in skeletal muscles that actually performed exercise and used glycogen. These local adaptations cause rapid and fully glycogen repletion, leading to post-exercise glycogen supercompensation. This review deals with exercise/muscle contraction-related promotion of GLUT4-mediated glucose transport and GLUT4 protein expression, and especially focuses on the possible mechanisms behind the relationship between increased glucose transport and muscle glycogen repletion during the post-exercise period.
Feedforward control by higher brain centers (central command) plays a role in autonomic regulation of the cardiovascular system during exercise. To reveal central control of cardiac autonomic outflows, a series of experiments have been conducted in our laboratory using conscious or decerebrate animals. Contrary to the traditional concept of vagal withdrawal, central command does not decrease cardiac vagal outflow but allows cardiac sympathetic nerve activity (CSNA) to augment for cardiac acceleration at the onset of exercise. Presumably, central command may also cause an increase in preganglionic adrenal sympathetic nerve activity (AdSNA) at the same time, which in turn releases adrenaline into systemic circulation and contributes to an additional increase in heart rate (HR).
Prevention is the most important measure against osteoporosis, since bone mass, once it is lost, cannot be recovered. Bone mass, in both men and women, reaches a maximum level in the 20s to 30s age range, and maintains this level or slightly increases toward the 40s, and gradually decreases thereafter. In particular, bone mass dramatically decreases in postmenopausal women because of a decrease in serum estrogen level. Bone mass is influenced by genetic and environmental factors such as mechanical loading, nutrition, and lifestyle, besides gender, age, and metabolic factors. Among these factors, mechanical loading, i.e. exercise, and nutrition seem to be important in maintaining bone health, since they are expected to improve with changes in lifestyle. Routine exercise and a diet rich in minerals and vitamins, throughout life, both contribute to maintaining bone health.
The hippocampus is important for learning and memory. It is also one of the few regions in the adult mammalian brain that can generate new neurons (adult hippocampus neurogenesis, AHN). It is suggested that altered hippocampal neurogenesis, by stress or aging, is related to pathophysiology of mood disorders, such as depression. On the other hand, AHN is robustly stimulated by voluntary and treadmill running, and accumulating knowledge indicates that the beneficial effects of exercise on cognition and mental health may be mediated, at least in part, by exercised-induced AHN. Thus, it is important to elucidate the mechanisms underlying exercise-induced AHN. However, the mechanisms and exercise conditions (intensity and frequency etc.) that activate AHN are still undetermined. Since high-intensity exercise elicits a stress response, mild exercise without a stress response may be a useful model for increasing AHN. To address this hypothesis, we used treadmill running, which can be controlled for speed, and developed a mild-intensity treadmill exercise model below the lactate threshold (LT, about 20 m/min) and minimal stress response; the LT is a physiologic index of moderate exercise intensity established in rats, as in humans. Recently, we have demonstrated that mild-intensity exercise enhances hippocampal neuronal activity, neurotrophic factors and neurogenesis. Therefore, a mild exercise model is shown that enhances cognitive functions, and further information, through mechanistic studies with the model, will be of benefit for developing effective exercise programs enhancing cognitive functions in humans, especially in vulnerable people with poor physical fitness.
Recent evidence suggests that the underlying mechanisms involved in beneficial adaptations to aerobic exercise, which promote health and increase endurance capacity, may be due to exercise-induced transient gene responses. In this review, an efficient exercise protocol to promote health and increase endurance capacity is discussed in relation to exercise-induced changes in gene expression. Exercise-induced transient gene responses, which are associated with adaptations to aerobic exercise, have been suggested to be induced by metabolic stress. Exercise to increase aerobic capacity and improve health should aim to increase the expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), which is the key gene to enhance the function of mitochondria. Training at the lactate threshold is suggested to be the threshold intensity for inducing gene expression of PGC-1α. Analysis of training studies assessing the effect on VO2max suggests that individuals with varied baseline VO2max values obtain significant improvement in VO2max at the lactate threshold. High-intensity interval training (HIT), which can induce gene expression of PGC-1α, may be as efficient and effective in increasing aerobic capacity as continuous exercise training, despite a substantial reduction in exercise volume. Exercise at times when muscle glycogen is low could be more effective at improving mitochondrial function. HIT consumes a large amount of muscle glycogen per unit of energy consumption, and studies suggest that longer recovery periods induce glycogen depletion with much lower amounts of exercise compared to continuous exercise. Exercise after HIT-induced glycogen depletion may be a beneficial exercise prescription for endurance capacity and health promotion.
The decline in arterial function with aging is considered to be part of a physiological process reflecting elevated systolic blood pressure. However, the extent and rate of this decline can be manipulated by habitual exercise. In order to prevent and treat cardiovascular diseases (CVD), various types of exercise are recommended. The purpose of this review is to introduce the current findings on the characteristic features of arterial function during acute exercise. Moderate intensity endurance exercise increases the arterial compliance, which has beneficial effects on arterial function. In contrast to endurance exercise, acute middle-high intensity resistance exercise, or acute eccentric exercise, has unfavorable effects on arterial function. Even in endurance exercise, however, a severe intensity of endurance exercise, such as ultra-marathon races decreases arterial compliance and moderate-intensity-arm-cranking increases arterial stiffness. These findings indicate that, in order to establish an optimal exercise prescription for keeping or improving arterial function, various factors, including the exercise mode, exercise intensity or exercise volume should be taken into consideration.
For more than a century, neuroscientists have debated the problem of how self-generated voluntary motor actions are executed without interference from sensory information elicited by the movements. In the 1950's, two theories were proposed: the corollary discharge theory by Sperry1) and the efference copy theory by von Holst and Mittelstaedt2). They are essentially identical in proposing the necessity of specific neuronal mechanisms to suppress undesirable percepts or reflexes, both of which might disturb ongoing movements. However, this raises a simple question as to whether the control system always ignores sensory information whenever the intended movements are in progress. Here, we review recent findings and currently debated problems in corollary discharge theory.
Muscle functional magnetic resonance imaging (mfMRI) is a powerful tool for the visualization of anatomical and functional properties (e.g. levels and patterns of activation) of human skeletal muscles. Fleckenstein et al.1) first reported that working muscles exert acute effects on MRI signals in 1988, and since this time a lot of attempts have been made to assess function and metabolism of activated muscles in healthy and diseased individuals. This review focuses on five aspects of mfMRI; 1) The relation between mfMRI and other functional parameters of working muscles; 2) Muscle activation patterns during single- and multi-joint exercises; 3) The effect of resistance training on mfMRI; 4) The effect of disuse on mfMRI; and 5) The assessment of inhomogenous activation within a single muscle by mfMRI. Finally future application and potential contribution of mfMRI are discussed.
The arterial baroreflex plays an essential role in the short-term regulation of arterial blood pressure, and thus helps ensure that the vital organs are adequately perfused. For standing humans, appropriate arterial baroreflex control of cardiac output and vasomotor tone are particularly important for cerebral blood flow regulation. However, the numerous mechanisms implicated in the regulation of the cerebral vasculature (e.g. cerebral autoregulation, carbon dioxide reactivity) mean that the precise nature of the direct and indirect effects of the arterial baroreflex on cerebral blood flow regulation are highly complex and remain incompletely understood. This review paper provides an update on recent insights into the influence of the arterial baroreflex on cerebral circulation.
In this article, we determine the reference values for sarcopenia, and test the hypothesis that sarcopenia is associated with risk factors for cardiovascular disease. Moreover, we develop prediction models of sarcopenia in Japanese men and women. A total of 1,488 Japanese men and women, aged 18-85 years, participated in this study. Appendicular muscle mass (AMM) was measured by dual-energy X-ray absorptiometry. Reference values for classes 1 and 2 sarcopenia (skeletal muscle index; AMM/height2, kg･m-2) in each sex were defined as values one and two standard deviations below the sex-specific means of reference values obtained in this study from young adults aged 18-40 years. The reference values for classes 1 and 2 sarcopenia were 7.77 kg･m-2 and 6.87 kg･m-2 in men, and 6.12 kg･m-2 and 5.46 kg･m-2 in women, respectively. In subjects with both class 1 and class 2 sarcopenia, body mass index and % body fat were significantly lower than in normal subjects. Despite this, whole blood glycohaemoglobin A1c in men with class 1 sarcopenia was significantly higher than in normal subjects, and brachial-ankle pulse wave velocity in women, with both class 1 and class 2 sarcopenia, was significantly higher than in normal subjects. Stepwise regression analysis indicated that the body mass index (BMI), waist circumference, and age were independently associated with skeletal mass index (SMI) in men; and BMI, handgrip strength, and waist circumference were independently associated with SMI in women. The SMI prediction equations were applied to the validation group, and strong correlations were also observed between DXA (dual-energy x-ray absorptiometry) -measured and predicted SMI in men and women. We concluded that sarcopenia is associated with more glycation of serum proteins in men and with greater arterial stiffness in women. Moreover, the prediction models of SMI using anthropometric measurement are valid for alternative DXA-measured SMI in Japanese adults.
In general, physical activity reduces the risk of cancer and infectious diseases. However, strenuous exercise has been shown to transiently increase the risk of infection, and this is referred to as the “open window.” Indeed, intense exercise reduces the concentrations of several cytokines in plasma in response to pathogens. The mechanisms responsible for this observation may depend on exercise-induced increased stress hormone secretion, especially that of catecholamines. Exercise-induced catecholamines, acting through β-adrenergic receptors, have been found to be responsible for exercise-induced suppression of plasma tumor necrosis factor-alpha (TNF-α) after lipopolysaccharide (LPS) administration. In the signaling mechanisms of cells, there are no changes in the surface expression of Toll-like receptor (TLR) 4. Although there are also no changes in the LPS-induced TNF-α mRNA expression in tissues after exercise, the TNF-α content in the tissues of exercised animals is lower than that in the tissues of non-exercised animals. Therefore, a strenuous exercise-induced reduction in plasma TNF-α concentration, despite pathogen stimulation, depends on the translation of TNF-α in tissues.
In this review, we briefly summarize muscle fiber types and mechanisms that regulate their expression from nutritional stimulus. To begin with, we introduce genes and their location on myosin heavy chains (MyHC). Next, we show three major transcriptional controls for MyHCs as (1) calcium signaling, (2) AMPK signaling, and (3) miRNA/anti-sense RNA regulations. Following this, we summarize possible nutrients that effect muscle fiber type transformation. The possible contributors are caloric restriction, polyphenols, and high-fat and high-protein diets. We think that nutritional intervention will be a useful way to control muscle fiber type switching. This approach could be adopted by athletes as a means to condition their muscles.
Spinal reflexes are known to be strongly modulated in a phase- and task dependent manner during walking in both humans and cats. However it is not clear whether afferent feedback from the leg plays a more important role in regulating this modulation in the leg and arm muscles. This short review mainly describes the recent findings concerning the effect of somatosensory inputs on the excitability of cutaneous reflex and H-reflex pathways during robotic-assisted stepping. The experimental results are discussed with recent advances in the field of human motor control, and the implications of locomotor rehabilitation for individuals with spinal cord injury are discussed as well.
Exercise endurance is reduced by heat. Among several factors that influence exercise performance is central fatigue, which appears to be caused by an increase in brain temperature. During prolonged exercise in heat, the core body temperature rises, and there is a corresponding and proportional increase in minute ventilation. It has been suggested that this hyperthermia-induced hyperventilation is related to central fatigue. Although hyperthermia-induced hyperventilation may have some relationship to heat-dissipating responses, it differs in several ways. For example, hyperthermia-induced hyperventilation causes a reduction in arterial CO2 pressure, which makes it different from thermal panting in animals. In fact, it has been suggested that hyperthermia-induced hyperventilation causes a reduction in cerebral perfusion, which reinforces the increase in brain temperature during exercise. This short review presents an overview of the characteristics of hyperthermia-induced hyperventilation and its effect on central fatigue.
Adult mammalian skeletal muscles possess a stem cell population, called muscle satellite cells. Satellite cells mainly contribute to restoring damaged or diseased muscles. The migration of satellite cells plays an important role in muscle regeneration, and it has been traditionally thought that satellite cell migration is regulated by lamellipodial/filopodial formation. In addition, it has recently been thought that blebbing/amoeboid formation plays an important role in satellite cell migration. On the other hand, the method/mechanism(s) of the migration of satellite cells located within skeletal muscles in vivo has barely been elucidated. However, because, in recent years, in vivo real-time imaging of satellite cell migration in skeletal muscles has been reported, it is expected to markedly expand our understanding of satellite cell migration in vivo. This review will focus on the regulatory mechanism of satellite cell migration in vitro and new insights into in vivo satellite cell mobility using real-time imaging.
The ankle has an important role in stretch shortening cycle (SSC) movement. Thus, it is likely that ankle instability negatively affects the SSC. To investigate the relation between SSC movement and ankle instability. This could contribute to developing a progressive phase of rehabilitation for athletes after ankle sprain, and could also be used as criteria for returning to sport participation. The legs of eight university male football players were categorized as either having ankle instability (AI group) or not having ankle instability (NI group). Ankle instability was defined as functional instability based on the Karlsson score. The rebound drop jump, which is the index of SSC movement, was measured, and the subjects' performances for SSC movement were evaluated. In addition, isokinetic ankle strength, based on the Biodex System Dynamometer to assess the peak torque of the plantar/dorsal muscles of the ankle joint, was recorded. The groups did not differ in regard to flight time. The contact time of the AI group was significantly longer than that of NI group. With regard to isokinetic ankle strength, there was no significant difference in plantar or dorsal flexion between the two groups. This study showed that the contact time of the AI group was longer than that of NI group. In ankles with instability, the function of the stretch reflex may be suppressed, and the efficiency power for exertion during ballistic SSC movement might thus be decreased. These findings suggest that ankle instability relates to SSC movement by prolonging the contact time in the rebound drop jump.
Antioxidants, including garlic, are beneficial to suppress exercise-induced oxidative stress (EIOS), and black garlic (BG) is a recently-developed whole food with strong antioxidant properties. This study investigated the effects of BG supplementation on physiological responses, especially on EIOS and recovery of muscle function. Nineteen untrained males were assigned to either a BG group (n=11, GG) or placebo group (n=8, PG), with a similar age and body mass index, during a 14-day-study. Before and after eccentric exercise of elbow flexors, we measured muscle function, blood and urinary biochemistries concerning muscle injury proteins, inflammatory cells, cytokines, reactive oxygen metabolites (d-ROMs), and antioxidative potential (BAP). Maximal voluntary contraction strength decreased by 35% immediately post-exercise in both groups. Recovery of circumference of biceps brachii in GG was significantly faster than in PG during 3-7 days post-exercise. d-ROMs level was lower in GG than in PG during 1-3 days post-exercise, but no significant difference in BAP was observed between groups. Exercise induced leukocytosis, and monocytes, lymphocytes, and neutrophils all exhibited significant time effects. A significantly greater creatine kinase level was found on day 3 post-exercise in PG than in GG. Lipid peroxide concentration was lower during 3-7 days post-exercise in GG than in PG, and the 8-iso-prostaglandin F2α level was significantly greater in PG than in GG at every post-exercise point. These results suggest that BG supplementation had certain effects on suppression of physiological responses, including EIOS, and might promote the recovery of edema in injured tissue.
The female athlete triad is a syndrome that leads to disordered eating, amenorrhea, and osteoporosis. The pathophysiologic mechanisms that lead to reduced bone mass in female athletes are low energy and functional hypothalamic amenorrhea. The aim of the present study was to establish an animal model of osteoporosis, which is similar to the osteoporosis seen in female athletes. We investigated the effects of long-term energy restriction on bone mineral density (BMD), and the levels of 17β-estradiol (E2) and luteinizing hormone (LH) in voluntary wheel-running female rats. Fourteen female Sprague-Dawley rats (8 weeks old) were randomly categorized into 2 groups: running (RUN) group and sedentary (SED) group. At 18 weeks of age, the rats in the RUN group were further randomly divided into 2 groups: running-ad libitum feeding group (RC group) or running-restricted feeding group (RR group). Twenty-four weeks after the experimental period, the RR group showed significantly lower BMD and plasma LH levels than the RC and SED groups (p < 0.05). Plasma E2 levels in the RR group were significantly lower than that in the SED group (p < 0.05). The present study indicated that long-term energy restriction with voluntary wheel running exhibited low bone mass in female rats with intact ovaries. Furthermore, the distinct endocrine profiles observed in this model suggest that energy restriction with voluntary exercise disturbs the hypothalamic-pituitary-ovarian axis. This may establish a model for the development of osteoporosis in the exercising human female with energy restriction, caused by dysfunction of the reproductive system.
The validity of a new methodological approach, involving the use of exercise endpoints based on fractions of heart rate reserve (HRres), to calculate oxygen uptake efficiency slopes (OUES) was tested. The study involved 48 young, intellectually disabled individuals (age range: 15-17 years) who performed an incremental cycling exercise to exhaustion. Furthermore, regarding the subjects who reached maximum efforts, the relationship between OUES and several exercise performance parameters was assessed. OUES was calculated using 75%, 90%, and 100% of the incremental exercise with data and data corresponding to 60% and 80% of the HRres. Of the 48 participants, 12 subjects did not reach a peak RER of 1.09, and 36 subjects exceeded this value. Significant differences were not detected between the time-based calculations and those obtained using the HRres-based measures of OUES. A Bland-Altman analysis did not reveal a bias that was significantly different from 0 (15.5 and 68.6 for OUES80%HRres-OUES100 and OUES60%HRres-OUES100, respectively), with precisions of 173.2 and 356.0 and 95% confidence limits from -296.8 to +327.8 and from -507.1 to +644.3 for OUES80%HRres-OUES100 and OUES60%HRres-OUES100 comparisons, respectively. High correlations were detected between peak oxygen uptake and OUES60%res and OUES80%HRres, and between VT and OUES60%res and OUES80%HRres. Thus, we found that OUES can be reliably calculated based on HRres endpoints, during incremental cycling exercise, in young individuals with intellectual disabilities. Furthermore, the study confirms the validity of OUES as an indicator of aerobic exercise capability in this population.
Severe diabetes frequently induces skeletal muscle atrophy, and dystrophin disruption has been implicated in the pathogenesis of skeletal muscle atrophy. We hypothesized that the downregulation of dystrophin expression causes diabetic-induced muscle atrophy, and investigated whether dystrophin mRNA and protein levels are altered in the atrophic muscles of diabetic rats. Rats received a single intravenous injection of streptozotocin (STZ) (45 mg/kg body weight). Slow-twitch soleus and fast-twitch extensor digitorum longus muscles were dissected from each rat 4 or 12 weeks after the STZ injection. The STZ group had significantly higher blood glucose levels and lower body weights than the control group. The relative muscle weight per body weight was also lower in the STZ group than in the control group, and these changes accompanied a reduction in glucose transporter 4. The phosphorylation of Akt Ser473 and p70 S6 kinase Thr389 was lower in the soleus and extensor digitorum longus muscles of the diabetic rats than in those of the control rats. In contrast, dystrophin mRNA and protein expression were higher in the muscles of the diabetic rats than in those of the control rats. A histochemical study showed that the localization of dystrophin did not differ between the muscles of the control and diabetic rats. Our data suggest that the downregulation of dystrophin is not a general characteristic associated with skeletal muscle in diabetes.