Populations worldwide are increasingly becoming physically inactive, which is related to somatic and psychological health problems that are prevalent in modern society. Recent epidemiological studies have indicated that the associations between physical inactivity and depression are bidirectional. Numerous animal studies have demonstrated that exercise improves hippocampal function. Because the hippocampus is a pivotal brain region that exerts inhibitory control over stress responses by affecting the hypothalamus-pituitary-adrenal axis, enhanced hippocampal function by exercise can increase stress resilience, which helps prevent stress-related depression. In contrast, physical inactivity is difficult to model in animal studies, and little is known about the effects of physical inactivity on the rodent hippocampus. To fill this gap, we previously developed a mouse model of habituated voluntary wheel running cessation as a reverse intervention to control physical activity. We found that reducing physical activity by cessation of wheel running impairs hippocampal neurogenesis in mice. Thus, this review discusses the relevant literature and provides a hypothesis that physical inactivity can be a potential risk factor for stress-related depression as it increases stress vulnerability by impairing hippocampal function.
The contractile and metabolic properties of skeletal muscle depend on muscle fiber type composition. There are two major fiber types: type 1 fibers (slow-twitch oxidative) and type 2 fibers (fast-twitch glycolytic). Muscle fiber type is a critical physiological property that affects sports performance and metabolic ability. To date, natural food components have not been regarded as regulators of skeletal muscle fiber type. Meanwhile, in the present century, it has been revealed that several nuclear receptors (NRs) and their cofactors affect skeletal muscle fiber type independently from muscular contraction. Interestingly, many compounds from natural food sources have been identified as NR ligands. These facts indicate the possibility of the regulation of muscle fiber type by food components. In this review, we present an overview of the current knowledge of the role of NRs and their cofactors in skeletal muscle fiber type and discuss the perspective of muscle fiber type regulation by food components via NR.
There is no long-term exercise training regimen with high adherence and effectiveness for middle-aged and older people that is broadly available in the field. To solve this problem, we developed an exercise training regimen comprised of interval walking training (IWT) and an IT network system that only requires minimal staff support. We found that adherence to the 22-month IWT program was relatively higher than other previously reported long-term exercise programs requiring more personnel support and that the program was accompanied by greater improvements in lifestyle-related disease risk factors and physical fitness in middle-aged and older people. Moreover, when congenital and acquired factors affecting adherence were assessed, we found that baseline body mass index and gender for all subjects, as well as smoking and vasopressin V1a receptor polymorphisms for men, were independent determinants of adherence to the IWT program. To elucidate the mechanism underlying the effect of V1a receptor polymorphisms on adherence to an exercise program, we assessed whether voluntary locomotion was impaired in mice genetically deficient in V1a receptors (V1a KO). We found that voluntary locomotion in wild-type mice was more probable after cerebral activation, while in V1a KO mice the probability was markedly reduced with no suppression of baroreflex control of heart rate during cerebral activation. Moreover, the findings in V1a KO mice were confirmed after local infusion of a V1a receptor antagonist into the nucleus tractus solitarii of the wild-type mice. Thus, central V1a receptors play an important role in facilitating voluntary exercise and thereby contribute to adherence to the IWT program.
Chronic obstructive pulmonary disease (COPD) is an increasingly important global health problem, including Japan. COPD is associated with an enhanced inflammatory response to irritants in the airways and lungs, in particular cigarette smoke. Cigarette smoke contains gaseous and particulate oxidants, and is considered to be the major etiological factor in the development of COPD. The oxidants in cigarette smoke induce inflammation, and chronic inflammation causes narrowing of the small airways and destruction of the lung parenchyma. Inflammation and oxidative stress are intricately related and seem to play a critical role in the development and/or progression of COPD. There is growing evidence that systemic inflammation exists in patients with stable COPD, leading to extra-pulmonary manifestations including skeletal muscle dysfunction and other comorbidities. Oxidative stress is also observed in skeletal muscle of COPD patients. Therefore, both systemic inflammation and oxidative stress may be associated with skeletal muscle dysfunction in COPD patients, resulting in reduced limb muscle strength and exercise endurance and poor health status and quality of life. Pulmonary rehabilitation is important to improve exercise capacity and health-related quality of life for COPD patients. However, physical exercise, the main component of pulmonary rehabilitation, may increase oxidative stress in the skeletal muscle of such patients. Therefore, rehabilitation programs that not only improve exercise capacity and quality of life, but also reduce exercise-induced oxidative stress should be established in the future.
Sarcopenia from aging, inactivity, weightlessness, disease and malnutrition causes social problems due to associated physical dysfunction, a decrease in QOL, and risk of death. As a means of alleviating sarcopenia, appropriate exercise and nutrition therapy is required. However, nourishment therapy is especially important for a person in a situation where exercise is not feasible for maintaining skeletal muscle mass and muscular strength. Therefore, the authors studied the inhibitory effect of aspartic acid magnesium on disuse muscle atrophy. Herein we have described two of the mechanisms of action of aspartic acid magnesium on disuse muscle atrophy suppression. Initially, inactivity causes a decrease in capillary and oxygen supply, inhibits ATP synthesis, and produces active oxygen. As a result, the proteolysis system is activated and muscle atrophy progresses. We have described the effect of aspartic acid magnesium uptake on this mechanism, and the imbalance of the intracellular mineral with the inactive proteolysis system. The above is the content of this review.
Sports training and competition are significant sources of stress. Elite athletes may be subject to specific exercise-related physical and mental stressors that promote the development of mood, anxiety disorders and depression. Psychological stress has been shown to adversely impact the function of the immune system and compromise host defenses against various infections. Inflammation may also play a role in neuropsychiatric diseases, including major depression. These associations between stress and inflammation are relevant. The current short review discusses psychological stress and the immune system in athletes, providing a comprehensive overview of the effect of the stress response on physical performance.