Hypertrophic stimuli, such as strength training and exercise, induce the up-regulation of heat shock proteins (HSPs), called stress proteins, in skeletal muscles. However, the physiological roles for induction of HSPs in skeletal muscles are still not fully understood. Heat stress also up-regulates the expression of HSPs, which are considered to function as molecular chaperones in eukaryotic cells, via heat shock transcription factor (HSF)-mediated stress response. Intracellular protein synthesis mediated by Akt/p70 S6 kinase (p70S6K) and/or calcineurin signaling pathways might be directly activated by heat stress. The number of muscle satellite cells, which play a key role in postnatal growth and regeneration of skeletal muscle cells, are increased by heat stress. Heat stress facilitates the regenerative process of injured skeletal muscle. Absence of heat shock transcription factor 1 (HSF1) partially depresses the regrowth of unloading-associated muscle atrophy. Therefore, heat stress could in part induce muscle hypertrophy via HSF1-mediated stress response. Heat stress-associated skeletal muscle hypertrophy has been confirmed in experimental animals as well as healthy human subjects. Application of heat stress on skeletal muscle may be a useful tool for gaining muscle mass and force generation not only in healthy subjects but also in patients during rehabilitation. Heat stress could also be a useful countermeasure for prevention of muscle atrophy during bed rest inactivity and/or space flight.

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Previous research has established that both aging and obesity trigger elevation of arterial stiffness and that such elevation is an independent risk factor for cardiovascular morbidity and mortality. Changes in arterial stiffness are known to be caused by alterations in the balance of hormones, inflammatory, nervous system-related, and endothelium-derived vasoactive factors, and levels of oxidative stress - all of which are known to strongly affect vasoconstriction and vasodilation. Lifestyle modifications that promote the restriction of energy intake, maintenance of nutrient balance, and performance of regular aerobic exercise, can decrease arterial stiffness in elderly and obese individuals. In this review, we discuss the lifestyle strategies found effective in decreasing arterial stiffness in elderly and obese individuals via improvement of vasoactive functional factors.

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Appetite has been receiving extensive attention, lately, as a key factor for successful calorie restriction (CR) leading to the prevention of obesity and a slowdown of the aging process. A growing body of evidence has been accumulating, showing that endocrine networks mediate a complex interplay between the central nervous system and numerous organs involved in appetite and energy homeostasis. Gut hormones are known to play important roles in this mechanism. The hormone family is divided into two categories: orexigenic ghrelin and anorexic hormones, such as peptide YY (PYY), and glucagon-like peptide-1 (GLP-1). These endocrine signals interact not only with the hypothalamus, but also with higher neural circuits including the prefrontal cortex and insula, suggesting tight linkages between peripheral and central appetite systems. An increase in physical activity combined with CR are recognized as measures for obesity prevention - sort of like ‘two wheels of one cart’. However, the long-term efficacy of exercise-induced weight loss is generally lower than expected, mainly attributed to a compensatory increase in energy intake (EI) for the energy deficit produced by exercise. Recently, several reports on exercise of various intensities and duration have shown the potent physiological factors contributing to alterations in circulating levels of gut hormones and improved responses of satiety signals following meal intake. These studies prove the presence of ‘crosstalk’ between the ‘two wheels’ mediated by the neuro-endocrine axis. This paper aims to highlight the association of exercise with appetite and EI via the blood kinetics of gut hormones, and discusses future perspectives in this field.

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Exercise promotes protein and amino acid breakdown in skeletal muscle. Proper nutrient intake in relation to exercise is thus important to maintain or build up skeletal muscle. It has been demonstrated that supplementation of branched-chain amino acids (BCAAs) before exercise has beneficial effects on skeletal muscle, such as decreasing exercise-induced muscle damage and soreness. Protein synthesis in skeletal muscle is enhanced after exercise, and proper timing of supplementation of protein and amino acids for effectively stimulating muscle protein synthesis is herein discussed. Treatment of elderly individuals with exercise and nutrient supplementation is also demonstrated to have efficacy against age-related sarcopenia.

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Aerobic and resistance exercises are recommended for elderly people to help maintain their health. Rowing involves almost all of the muscles in the body and may have elements of both aerobic and resistance exercise. Rowing and indoor rowing exercise using ergometers have been widely used among elderly adults and young individuals worldwide. Because rowing is practiced on a seat, less impact is placed upon the knee joints, making it safe for elderly people. It has been reported that elderly male rowers have higher aerobic capacity, greater muscle mass in the thigh and trunk, and a lower risk of atherosclerosis than age-matched sedentary men. In the authors’ recent study, untrained elderly men participated in a 6-month rowing exercise training using a rowing ergometer; and the results indicated that the training increased the participants’ aerobic capacity and muscle size, decreased their visceral fat, and improved their atherogenic index. Rowing exercise training, which offers combined aerobic and resistance training, does not unfavorably affect arterial stiffness or compliance, although resistance training alone induces arterial stiffening. Rowing exercise has both aerobic and resistance exercise health benefits in elderly people.

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Ventilation increases rapidly and significantly in proportion to workload or metabolic rate during dynamic exercise. This increase is called “exercise hyperpnea.” During light to moderate step load exercise, ventilation increases from the first breath and reaches a plateau within 20 s (Phase I), during which metabolites do not reach chemoreceptors; thus Phase I is solely caused by neurogenic drives. It is worthwhile to clarify the aspects of Phase I in order to identify the mechanism of neurally mediated exercise hyperpnea. Until 2000, the mechanisms of exercise hyperpnea during light to moderate step load exercise were assumed to have been derived from two conventional neurogenic drives, “central command,” coming from the motor cortex or the hypothalamus, and “peripheral neural reflex,” originating mainly from the mechanoreceptors in muscles through group III afferents. For about a century there have been a large number of experiments trying to illuminate which mechanism is the cause of exercise hyperpnea. Although central command is thought to be the more likely key source, the consensus is that both central and peripheral neurogenic drives operate ventilation redundantly, building a multiple regulation system during exercise. Recent advantages in technology have enabled us to examine exercise hyperpnea in novel ways. Peripheral neurogenic drive through group III and IV afferents again enters into the limelight by using selective blockers for these afferents without augmenting central command. The vascular distension hypothesis has advocated that a rapid increase in peripheral blood flow is sensed as a plethysmometric change by the mechanoreceptors around the venule near the contracting muscles, stimulating the respiratory center through group IV afferents so as to match ventilation with metabolic rate. On the other hand, “learning” is attracting a growing interest from a central neurogenic point of view. Two types of learning have been proposed: “long term modulation (LTM),” serotonin mediated synaptic adaptation to repeated combined exercise and other stimuli such as an increase in dead space, and “volitional control,” a behavioral and learned response with cognitive function by way of the cerebrum and cerebellum. Nevertheless, these two pathways were derived from, not direct, but circumstantial evidence. The question, “What causes ventilation to increase during exercise?” is not likely to be solved in the near future.

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For many years, lactate was considered as a metabolic waste product, and a cause of fatigue during exercise. However, lactate is now known as a carbohydrate fuel source, shuttled between cells and tissues. The movement of lactate across the plasma membrane is facilitated by a family of monocarboxylate transporters (MCTs). Among 14 identified MCT isoforms, MCT1 and MCT4 are present in the plasma membranes of skeletal muscle and are suggested to be related to exercise performance. Reports have shown that exercise training increases both MCT1 and MCT4 in skeletal muscle. This review will discuss the role of lactate as a fuel and exercise training-induced changes in lactate metabolism. In addition, studies of Thoroughbred horses, as models of elite athletes, are introduced.

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Generally, a single bout of exercise induces a moderate increase in arterial pressure (AP) with marked tachycardia as a result of sympathoexcitation which induces vasoconstriction in the major organs, but not in skeletal muscles, and activates heart function. In this review, the potential brain mechanisms underlying cardiovascular regulation during exercise are introduced, with a focus on the functions of the nucleus of the solitary tract (NTS), which is the central termination site of baroreceptor inputs. During a single bout of exercise, neuronal signals from the central command, mediated by the hypothalamus, as well as those from the muscle receptors, are directly or indirectly projected to the NTS and rostral ventrolateral medulla (RVLM). The signals to the RVLM activate sympathetic premotor neurons that, in turn, induce pressor and tachycardiac responses. However, in the absence of resetting of the baroreceptor reflex to a higher pressure range, sympathoexcitation would be dampened and parasympathetic nerves would be excited by heightened levels of baroreceptor inputs, resulting in the attenuation of continuous increases in AP and heart rate. The GABAergic inter-neurons within the NTS may be involved in baroreceptor reflex resetting by limiting the degree of excitation of barosensitive NTS neurons, and thus are capable of ‘continuous’ increases in sympathetic nerve activity. Among the central command mechanisms, the dorsomedial hypothalamus, hypothalamic paraventricular nucleus, and tuberomammillary nucleus of the posterior hypothalamus may be involved in the GABA-mediated inhibition of NTS functions. Although the recent findings of the central regulatory mechanisms are remarkable, they may provide only a partial explanation of the mechanisms. Since maintaining cardiovascular homeostasis is essential for high exercise performance, further investigations will be required to clarify all aspects of the central regulatory mechanisms underlying cardiovascular responses during exercise.

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Recent developments in neuroscience techniques such as brain imaging, functional brain imaging, and non-invasive brain stimulation, have made it possible to directly study able-bodied humans while engaged in various motor tasks. As a result of these technological advances, the last couple of decades have experienced a significant increase in new findings in the field of motor control and, more specifically, on the control of gait and posture. However, there are still a lot of difficulties and limitations in studying human neural activities during dynamic movements, like walking. In this short review, recent advances in knowledge on human gait and posture will be reviewed.

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In healthy individuals, exercise and nonexercise (i.e. passive body heating) heat stress induces vulnerability in the cardiovascular system, and is apt to cause hypotension during upright posture, resulting in a reduction of orthostatic tolerance. Reduced orthostatic tolerance is linked to multiple physiological mechanisms including 1) a redistribution of blood flow from central parts of the body to skin, 2) an increase in leg venous compliance, 3) altered baroreflex function, 4) an attenuated venoarterial response in the lower extremities, and 5) a decrease in plasma volume. A combination of countermeasures such as cooling of the body, rehydration, and heat acclimation, can improve orthostatic tolerance in a hot environment. The purpose of this review was to summarize findings investigating the causes of and preventive approaches to heat stress-induced orthostatic intolerance.

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In response to increased vascular conductance associated with vasodilation in exercising muscles, many non-exercising organs suppress their blood flow by vasoconstriction, thus helping to maintain blood pressure. This vasoconstriction in non-exercising organs contributes to ensuring a favorable distribution of the blood flow. However, a consequent excessive decrease of blood flow in non-exercising organs should be avoided so that they can maintain appropriate functioning during and/or after exercise. There is now evidence of a decrease in splanchnic blood flow with vasoconstriction during dynamic exercise, which indirectly contributes to an increase in flow in exercising muscles. Hypoperfusion in the splanchnic area, induced by such vasoconstriction, may result in gastrointestinal symptoms. On the other hand, such vasoconstriction is suppressed when exercise is performed after food intake, which may be associated with the maintenance of digestive and absorptive functions in the gastrointestinal tract. In contrast to organs that decrease their blood flow, the choroidal flow, which forms part of the ocular blood flow, increases with exercise intensity, but without vasodilation. The relevance of this phenomenon to visual function and the nature of ocular circulation remain unclear. Competition in blood flow between exercising muscles and non-exercising organs should be examined from the viewpoint of the functions of non-exercising organs and exercising condition, such as the postprandial condition.

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The biomechanical features of skeletal muscles are reviewed, with regard to their form and function and anatomical components (fascicles and tendinous tissues). 1) Studies on fascicle architecture are reviewed, highlighting its importance in the force and velocity potentials of the muscle along with its plasticity and muscle-size dependence. 2) The elastic properties of the muscle-tendon unit are described, pointing out the contribution of tendinous tissues as a spring. Functional consequences of tendon elasticity are summarized with respect to exercise performance under mechanically and neurally controlled joint actions, which lead to energy saving of muscle fibers and enhancing the positive work of the muscle. 3) The task-specificity of the muscle as an actuator or a spring and its position dependence (proximal to distal trend of functional divergence) are mentioned. Literature shows that proximal muscles are architecturally designed for actuation and distal muscles are more suited for a spring function. 4) Unique but strange behavior of tendinous tissues, that is seen in stretch-shortening types of movement, is described, suggesting variable elasticity of tendinous tissues that is modulated by muscle activation. 5) Finally, a need to consider multiple muscle-tendon units as a system is introduced to reasonably understand recent findings that otherwise cannot be accounted for. Collectively, it is suggested that the muscle-tendon unit is not only a simple combination of muscle fiber and tendinous tissues acting as actuator and spring, respectively, but also a unit that acts both anatomically and functionally.

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There is a general consensus that resistance exercise and nutrition (especially amino acids) are the most effective interventions for maintaining skeletal muscle mass. The intracellular signaling pathways through the mammalian target of rapamycin (mTOR), a serine/threonine protein kinase, are the most established mechanism for controlling muscle protein synthesis. Acute bouts of resistance exercise and amino acid ingestion independently activate mTOR and its downstream targets that modulate protein translation initiation and elongation. Although resistance exercise can modulate protein synthesis by endocrine regulation, such as the secretion of hormones and growth factors, one of the most recognized mechanisms for controlling muscle mass by resistance exercise involves mechanical tension. In regard to nutritional regulation, recent research indicates that intracellular amino acid availability, particularly that of leucine, may be a primary regulator of muscle protein synthesis following the ingestion of amino acids. The authors previously reported that leucine catabolism also has a significant impact on amino acid-induced protein synthesis. In contrast to established downstream molecular targets such as p70 S6 kinase (p70S6K) and eukaryotic initiation factor 4E-binding protein (4E-BP1), the upstream mediators, for regulating mTOR and protein synthesis in response to resistance exercise and amino acids, remain to be clarified. In this brief review, current progress regarding the intracellular mechanisms of muscle protein synthesis, in response to resistance exercise and amino acid ingestion, is discussed.

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Indirect calorimetry with a room-size respiratory chamber provides an ideal setting to monitor energy metabolism for a prolonged period. During the last 10 years, experiments with this method have raised interesting observations such as: 1) exercise intensity has no effect on 24 h fat oxidation, 2) exercise has little, if any, effect on 24 h fat oxidation, and 3) exercise before breakfast increases 24 h fat oxidation. To some of the scientific community and general public, the first two statements may be unacceptable. But it can be factually explained that the impact of exercise on energy metabolism is not confined to the period of physical activity itself, and that fat oxidation remains elevated during the post-exercise period. The third observation seems to be insignificant, but contradicts the second one. It is premature to conclude that exercise has no effect on 24 h fat oxidation.

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This review focuses on the effects of exercise on sleep. In its early days, sleep research largely focused on central nervous system (CNS) physiology using standardized tabulations of several sleep-specific landmark electroencephalogram (EEG) waveforms. This method has enabled the observation and inspection of numerous uninterrupted sleep phenomena. Research on the effects of exercise on sleep began, in the 1960’s, with a focus primarily on sleep related EEG changes (CNS sleep). Those early studies only found small effects of exercise on sleep. However, more recent sleep research has explored not only CNS functioning, but somatic physiology as well. Sleep should be affected by daytime exercise, as physical activity alters circadian pacemaker, endocrine, autonomic nervous system (ANS) and other somatic functions. Since endocrinological, metabolic and autonomic changes can be measured during sleep, it should be possible to assess exercise effects on somatic physiology in addition to CNS sleep quality, evaluated by standard polysomnographic (PSG) techniques. Additional measures of somatic physiology have provided enough evidence to conclude that the auto-regulatory, global regulation of sleep is not the exclusive domain of the CNS, but is heavily influenced by inputs from the rest of the body.

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The dose-response association between physical activity (PA) and obesity is well-established; however, the correlates of PA among overweight and obese populations require clarification. Therefore, the purpose of this study was to review the correlates of PA among overweight and obese populations. Literature searches were conducted for English and Japanese-language published articles, between Jan 2000 and Dec 2010, using “PubMed”, “Medline”, “Psycinfo” and the “Japan Medical Abstract Society”. A total of nine eligible articles were included in the analysis: five studies compared the PA correlates between normal-weight and overweight/obese populations; and four studies examined PA correlates in overweight/obese populations. Consistent correlates of PA among overweight and obese populations were age, self-efficacy, social support, perceived good access to facilities, and seeing people being active in the neighborhood. For obesity prevention, particularly in non-Western countries, further research is required with the purpose of developing effective PA interventions among overweight and obese populations. Future studies should examine both perceived and objectively-assessed environmental factors associated with specific PA behavior.

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There is a developing consensus that physical exercise is useful as a preventive strategy for cognitive impairment found in patients with dementia, particularly those affected by Alzheimer’s disease. Many reports state that the exercise-induced improvement of cognitive performance is an enhanced expression of a brain-derived neurotrophic factor and adult neurogenesis in the hippocampus, which is an area of the brain that is important for learning and memory. The process of adult hippocampal neurogenesis consists of the proliferation of neural progenitor cells (NPCs) and neural differentiation and maturation involving the neurite (axons and dendrites) extension of NPCs. Exercise training is well known as a promoter of cell proliferation and survival in the hippocampus; however, little is known about the effects of exercise training on neurite outgrowth in the hippocampus. This review presents the effect of exercise training on neurogenesis and neurite outgrowth in the hippocampus.

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There is limited information about total and regional body composition in children at the organ tissue level. The purpose of this review is to take note of the current body of knowledge regarding body composition research in Japanese children on the basis of recent data centering on fat mass and skeletal muscle (SM) mass. According to the author’s recent findings of fat mass, 1) the value of % fat in overweight boys and girls was over 35% using DXA measurement; 2) about 50% of the difference in whole body fat mass, between overweight and normal weight children, may be attributable to incremental increases in trunk fat mass in both boys and girls; and 3) equations using skinfold calipers and ultrasound seem to be more useful field methods in estimating fat mass specifically for children at the present time. Moreover, the author’s new studies of SM mass indicate that 1) whole body SM mass dramatically increases from prepubertal (9.2 kg for boys, 10.8 kg for girls) to adolescent stages (20.0 kg for boys, 14.6 kg for girls), which is similar to adults (22.3 kg for males, 13.5 kg for females); 2) the increase in SM mass, during each growth stage, seems to be fairly constant on the extremities and trunk area in both boys and girls; and 3) the adult ultrasound-derived prediction equations for SM mass are applicable for adolescents near 14 years of age, but are not valid for prepubertal children. Future research will involve the development of equations for estimating fat mass and SM mass for prepubertal children and adolescents.

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Most animals can adapt physiologically and biochemically when exposed to altered temperatures for prolonged periods. In humans, marked physiological adjustments are apparent following repeated bouts of core temperature elevation, either from exercise, or high ambient environmental temperatures, or both. In this review, the mechanisms for such adjustments, called “heat acclimation”, are discussed. First, the authors focus on thermoregulatory responses in the process of heat acclimation, i.e. how thermoregulation adapts to changes in temperature following repeated exposure to heat and exercise. Once heat acclimation is achieved, skin vasodilation and sweating are initiated at a lower core temperature threshold, and higher sweat rates can be sustained. Second, knowledge regarding the central and peripheral mechanisms for heat acclimation and tolerance is discussed. Recently, two advances - the implication that long-term accommodation to a changing environment involves functional neuronal remodeling associated with transcriptional reprogramming, and the understanding that there is neurogenesis in the hypothalamus - have introduced new concepts to the study of heat acclimation. Although it is still a developing issue, future study will bridge the gap between the classical physiological heat acclimation profile and molecular and cellular mechanisms.

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Matrix-assisted laser desorption/ionization imaging mass spectrometry (MALDI-IMS) is a mass spectrometry-based imaging technique used to visualize the distribution of biomolecules without the need for extraction, purification, separation and labeling of the molecules. This technique can reveal the distribution of hundreds of ion signals in a single measurement, and also helps in understanding metabolite structure, overcoming the inadequate imaging probes for small metabolites. The versatility of MALDI-IMS has opened up new frontiers in several fields, especially in lipidomics. Lipids in skeletal muscle play a fundamental role in both normal muscle metabolism and disease states. Skeletal muscle lipid accumulation is associated with several chronic metabolic disorders, including obesity, insulin resistance, and type 2 diabetes. In this review, we show the applications of MALDI-IMS to mouse skeletal muscle for detecting changes in lipids induced by contraction.

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Fatty acids are derived from the hydrolysis of triacylglycerol (TG) found in white adipose tissue, muscle tissue and circulating lipoproteins. The mobilization of free fatty acids (FFA) from white adipose tissue contributes to about 50% of the FFA utilized during moderate-intensity exercise. The delivery of FFA from white adipose tissue is improved by hormone-stimulated lipolytic events in white adipocytes (WA). Thus, the lipolysis in WA that provides fuel for metabolism has been a highly conserved function throughout the course of evolution. This short review outlines our current understanding of the molecular regulation of TG lipases via the lipolytic cascade in WA, as well as provides an account of our recent findings concerning changes in the lipolytic molecules of WA that result from acute and habitual exercise.

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