Since aging is the most important risk factor for dementia, measures to slow the onset of brain aging are an important strategy for preventing dementia. Accumulation of oxidative damage is considered to be a major cause of aging. Catechins in green tea (GTCs) have powerful antioxidative activity. Ingestion of GTCs suppressed oxidative damage, brain atrophy and cognitive decline in aged mice. Age-related cognitive decline was significantly suppressed in mice when middle-aged mice started to drink green tea catechins. Middle-aged people are thus expected to be able to suppress brain aging by ingestion of GTCs. In addition, numerous people are stressed under various conditions. Brain aging was accelerated and lifespan shortened in experimental animals that were chronically and psychosocially stressed. Theanine, an amino acid in green tea, suppressed stress-induced aging. However, the anti-stress effect of theanine is blocked by catechins and caffeine that are main components in green tea. Daily drinking of several cups of green tea is considered to suppress brain aging. In addition, theanine-rich green tea or green tea with a lowered level of caffeine is expected to suppress stress and stress-induced aging.
Low-to-moderate intensity resistance exercise with vascular occlusion induces increased muscle mass and strength, comparable to that after conventional heavy resistance training. Also, participants feel as if they require greater force (effort) to lift a weight when undergoing resistance exercise following vascular occlusion. Vascular occlusion of the proximal upper arm increased perceived magnitude of exerted hand-grip force without causing any accompanying changes either in electromyographic or efferent/afferent activity of the median nerve. There was also no effect on motor evoked potentials in the hand following resting-state transcranial magnetic stimulation (TMS) over the primary motor cortex (M1). Moreover, low-frequency, repetitive transcranial magnetic stimulation (lf-rTMS) over the left primary somatosensory cortex did not significantly affect estimations of right-hand grip force exertion. Thus, the primary factor responsible for the overestimation of force exertion with increased voluntary effort (“sense of effort”) during occlusion was the central signal related to motor command size. Brain imaging studies show that vascular occlusion increases M1 activity during force exertion, which may be related to functions of motor-related cortical areas, e.g., supplementary motor area, as sources of excitatory input to M1. M1 suppression by lf-rTMS during force exertion causes participants’ sense of effort and force perception to increase. This mechanism may also operate during muscular contraction with vascular occlusion. It is easy to imagine perceiving maximal effort when we consciously try to produce maximal force; however, does M1 activity become maximal at that point in time? In this study, the liberation of potential muscular strength, focusing on the motor system state before awareness of motor intention, is looked at.
Neuronal networks in our brain and body are fundamental for sensation, behavior, and all other functions based on neuronal activity. To construct precisely wired networks, the development of neurons is tightly controlled. During development, neurons must alter their shape so as to be able to migrate toward the destination from their origin and to make contact, called a synapse, with a defined target a certain distance away from them. Like the skeleton in our body, neurons have a cytoskeleton to maintain their shape. The cytoskeleton not only supports this shape, but also helps regulate the motility of neurons; and in this regard, the cytoskeleton is comparable to muscle. Therefore, orchestrating the reorganization of the cytoskeleton is of great importance in allowing extensive changes in neuronal morphology during development. In this review, we highlight the crucial roles of the cytoskeleton and associated proteins in each phase of neuronal development, including neurogenesis, neuronal migration, neurite genesis and growth, and synapse formation.
Life in contemporary society is increasingly stressful, and the body is unconsciously exposed to various stressors involving physical, biological, chemical, and social/psychological factors. Exposure to these stressors causes definite biological responses in the body, termed ‘general adaptation syndrome’. Rapid endocrine responses are among the most important reactions following exposure to stressors. These include glucocorticoid and catecholamine secretion into the bloodstream, and are initial biological responses to the stressors. These responses are necessary for the ‘fight-or-flight’ response and must often occur rapidly for the organism to survive. Most biological events, including rapid endocrine responses, also exert effects on circadian rhythms. Indeed, disruption of biological circadian events contributes to numerous diseases, including psychological disorders, immunopathy, serious disorders of the eye, and increases in the incidence of metabolic syndrome components such as obesity, type 2 diabetes, and dyslipidemia. There is increasing evidence that exposure to stressors can affect the amplitude and/or cycle of biological circadian rhythms, and consequently aggravate and/or provoke adverse diseases. In this review, we provide an overview of the relationship between stressors and the stress response, based mainly on results from animal studies. The effects of environmental and social stressors on circadian rhythm are also discussed.
Isoinertial resistance is imposed during natural human dynamics, where muscles contract at varying velocities and joint angles. In many sports, the ability to produce greater force at faster speed is essential for successful outcomes. Hence, power training under isoinertial resistance (e.g., body mass, weights or flywheel, etc.) provides event-specific adaptive stimuli. Conventional power training consists of a combination of strength-oriented (> 70% 1RM) and speed-oriented (< 30% 1RM, e.g., plyometrics) methods, with the aim of being able to overcome variable external loadings across a range of velocities. An alternative maximum power output training (Pmax training, 30-70% 1RM) has been found to elicit equivalent or greater effectiveness compared to the conventional methods. It is, however, difficult to precisely reproduce the prescribed intensities, given several concerns associated with 1RM testing and the variable accuracies of the repetition-intensity or velocity-intensity relationship. No matter what level of resistance is assigned to an exercise, it is far more important to exert as much effort (or fastest concentric speed) as possible per repetition, otherwise, the training effects are reduced. At light intensities, however, a large portion of the concentric phase is spent in deceleration for the subsequent phase transition, which may limit effort. Making projectile motions, therefore, are necessary. The utilization of stretch-shortening cycle effects, with increased power ability, may give a further training edge. Coaches and trainees should be aware that successful movements in power training are defined as greater acceleration, speed and displacement for every repetition, rather than simply neat form or smooth repetitiveness.
The hematopoietic microenvironment composed of stromal cells strictly regulates hematopoietic stem cells and hematopoietic progenitor cells by producing positive- and negative-regulators to supply mature hematopoietic cells to the periphery throughout its entire lifetime. However, hematopoiesis attenuates with aging. Extensive studies have revealed cell-intrinsic deterioration of hematopoietic cells with aging, but the responsibility of the age-associated deterioration of stromal cells has not yet been fully elucidated. Senescence-accelerated mice (SAMP1) exhibited premature senescence-like stromal cell impairment after 30 weeks of age. Thus, this model mouse is a useful tool for clarifying the role of stromal cells during the development of senescence-associated defects in hematopoiesis. It is well known that B lymphopoiesis at steady-state is attenuated with aging, whereas myelopoiesis remains unaffected. At steady-state, SAMP1 mice exhibit simultaneous down-regulation of positive- and negative-regulators of B lymphopoiesis in the bone marrow during premature aging, resulting in suppressive homeostasis in B cell development. While both regulators are down-regulated, the relative cytokine levels are barely maintained at a steady-state. Once SAMP1 mice are in a perturbed condition induced by myeloablation or inflammation, the latent deterioration of stromal cell function becomes apparent in aged mice: they exhibit dysregulation of positive and negative regulators produced by stromal cells, resulting in decreased supportive activity for not only B lymphopoiesis, but also for the hematopoiesis of other lineages, such as myelopoiesis, erythropoiesis and mast cell development. These results suggest that the age-associated deterioration of hematopoiesis may be due not only to hematopoietic cell-intrinsic deterioration, but also to hematopoietic cell-extrinsic deterioration, such as stromal cell deterioration.
Exercise performance cannot be maintained indefinitely, i.e., it deteriorates progressively. Traditionally, deterioration of exercise performance has been attributed to failure of peripheral or central functions of muscle activity. However, muscle rigor (i.e., complete failure of muscle contractile function) never occurs and the muscle force exerted never decreases to zero even with sustained maximal muscle contraction. Furthermore, an increase in central motor output to skeletal limb muscles, and consequently, enhancement of exercise performance, is often observed at the end of a time trial race at which impairment of muscle contractile function is greater. These indicate that only failure of peripheral or central function of muscle activity determines exercise performance. However, recent studies have elucidated that group III/IV muscle afferent inputs to the central nervous system have an important role in the regulation or limitation of exercise performance. This article reviewed two viewpoints regarding contributions of group III/IV muscle afferent feedback to regulation of exercise performance.
Postprandial hyperglycemia is associated with an increase in cardiovascular disease risk. Therefore, it is important to prevent postprandial hyperglycemia. Both daily diet and exercise are important factors to control postprandial hyperglycemia. The short-term intake of a high-fat diet worsens postprandial glucose metabolism. Although a single bout of exercise can improve postprandial glucose metabolism, a single bout of moderate-continuous exercise has less effect on the impact of the short-term intake of a high-fat diet on postprandial glucose metabolism, probably because this type of intake impairs the effect of a single bout of moderate-continuous exercise. Further studies are required to determine the exercise regimen that effectively ameliorates the worsening of postprandial glucose metabolism.
We investigated the relationships between the lower-limb joint kinetic parameters of sprint running and rebound jump during the support phases in 16 male track and field athletes performing sprint running and rebound jump at maximal effort. Sprint running velocity and rebound jump index (i.e., jump height divided by contact time) during rebound jump were calculated. Lower-limb joint kinetic parameters (joint torque and power) during the support phases of these activities were calculated using a force platform and data from a high-speed video camera that recorded movements in the sagittal plane. No significant correlation was observed between sprint velocity and rebound jump index. However, significant correlations were observed between sprint running and rebound jump for mean ankle-joint torque and mean knee-joint torque in the eccentric and concentric phases, as well as for mean negative ankle-joint power and mean negative knee-joint power. These results suggest mechanical similarities in ankle- and knee-joint kinetic parameters, especially in the eccentric phase of sprint running and rebound jump, although such similarities were not observed for sprint velocity and rebound jump index.
Both aerobic exercise and resistance exercise are recommended to enhance health in elderly people. A hybrid training system (HTS), that provides resistance to the motion of a volitionally contracting agonist muscle by electrically stimulating its antagonist, was developed as a resistance exercise technique combining the benefits of electrical stimulation and volitional contractions. We then applied this concept to develop a novel training method using electrically stimulated eccentric contractions during aerobic walking exercise (HTSW). This study was designed to evaluate the effect of the new method on muscle strength and physical function by comparing it to unenhanced walking exercise. 16 subjects (2 male, 14 female; age average, 67.2 ± 2.6) were randomly divided into an HTSW group and a control group (CTR). They trained using either HTSW or unenhanced walking exercise (CTR) for 30 minutes three times a week for 12 weeks. Isokinetic knee extension/flexion torque, muscle volume (MV), a one-leg standing test, a functional reach test, 10-meter maximum gait speed, timed up & go test (TUG), and a 6-minute walking test were measured before and after the training period. We compared the differences between pre-training and post-training using the Wilcoxon signed rank test in each group. In the HTSW group, isokinetic knee extension (12%)/flexion torque (18%), MV (8%), 10-meter maximum gait speed (9%), TUG (26%), and 6-minute walking test (12%) significantly improved after the training period. In the CTR group, isokinetic knee flexion torque (15%), 10-meter maximum gait speed (9%), TUG (22%), and 6-minute walking test (16%) had significantly improved after the training period. HTSW may provide the benefits of both aerobic and resistance exercise.