The mass and structure of bone tissue adapt to the mechanical loads imparted by gravity and movement, and are controlled by the balance between bone formation and bone resorption. The primary adaptations of bone to disuse are demineralization and loss (thinning) of trabecular and cortical bone. Exercise training and electrical muscle stimulation (ES) induce adaptive changes in bone that improve bone strength and inhibit bone loss. ES has been generally applied to patients undergoing physical rehabilitation to maintain and/or recover muscle mass and force-generating capacity in disused muscles. ES-induced muscle contraction of disused muscle can also ameliorate deleterious post-disuse adaptation of bone. The mechanical effects of ES-induced muscle contraction are essential for the maintenance of bone mass and strength, which are achieved through the cooperative functions of osteocytes, osteoblasts, and osteoclasts. The effects of ES, however, are dependent on the stimulation paradigm, including the intensity, frequency, and number of stimuli and the duration of the intervention. This review summarizes the literature on the effects of ES-induced muscle contraction on disuse osteopenia.
Magnetoencephalography is primarily sensitive to current sources tangential to the skull. Therefore, currents generated in area 3b of the primary somatosensory cortex (S1) and area 4 of primary motor cortex (M1) located on the posterior and anterior banks of the central sulcus, respectively, are easily detected. The movement-related cortical magnetic fields (MRCFs) following voluntary movement and the somatosensory magnetic fields (SEFs) generated by peripheral mixed nerve stimulation (e.g., median nerve) have been widely used to investigate the physiology of normal somatosensory cortical processing. Here, we describe the MRCFs produced by two types of movement (experiment 1) and the SEFs elicited by motor point stimulation (experiment 2), passive movement (experiments 3 and 4), and mechanical stimulation (experiments 5, 6, and 7). In addition, we examined the modulation of these fields.
The human circadian system derives from two distinct circadian oscillators that separately regulate circadian rhythms of body temperature and plasma melatonin, and of the sleep-wake cycle. The oscillator for body temperature and melatonin is the central circadian pacemaker, located in the hypothalamic suprachiasmatic nucleus (SCN), and the oscillator for sleep-wake cycle is another oscillator, located in the brain but outside the SCN. Although bright light is a primary zeitgeber for circadian rhythms, non-photic time cues such as a strict sleep schedule and timed physical exercise act as a non-photic zeitgeber for the sleep-wake cycle under dim light conditions, independent on the SCN circadian pacemaker. Recently, timed physical exercise under bright light has been shown to accelerate re-entrainment of circadian rhythms to an advanced sleep schedule. Physical exercise may enhance the phase-shift of circadian rhythm caused by bright light by changing light perception. In the field of sports medicine and exercise science, adjustment of the circadian rhythm is important to enable elite athletes to take a good sleep and enhance exercise performance, especially after inter-continental travel and jet lag.
A healthy elderly person may require nursing care after becoming frail, a condition characterized by slowness, weakness, exhaustion, low activity, and shrinking. Because few cohort studies have examined frailty in detail, the prevalence of frailty among the elderly in Japan is unclear. We examined the prevalence of frailty based on the frailty phenotype established by Fried using a large-scale cohort of randomly selected community-dwelling elderly in Japan. Participants included 871 elderly (446 men and 425 women) aged 65-91 years who participated in the sixth wave examination (July 2008 to July 2010) and seventh wave examination (July 2010 to July 2012) of the National Institute for Longevity Sciences - Longitudinal Study of Aging. The prevalence of shrinking, exhaustion, low activity, slowness, and weakness among the elderly participants was 10.2%, 38.6%, 21.1%, 11.4%, and 15.5%, respectively. The prevalence of frailty characterized by the limitations in 3 or more of these 5 domains was 8.5%. The prevalence of pre-frailty, characterized by limitations in 1 or 2 of 5 domains was 52.2%. Elderly who were diagnosed with frailty and pre-frailty included 3,086,000 people and 17,950,000 people, respectively. These data could contribute to the promotion of prevention and treatment strategies for frailty in Japan.
Duchenne muscular dystrophy (DMD) is a life-limiting X-linked genetic disorder caused by a lack of the membrane-associated protein dystrophin. The absence of dystrophin increases the susceptibility of muscle fibers to damage. Repeated damage results in ineffective muscle repair and the development of pseudo-hypertrophied muscles; these bulky muscles are weak despite their size. The mechanisms underlying the functional impairments in dystrophic muscle have not yet been fully determined. However, several recent studies indicate that elevated intracellular Ca2+ homeostasis is a cause or facilitator of the development of muscle weakness in DMD. This review focuses on abnormalities of Ca2+ homeostasis and the possibilities for treatment by counteracting the Ca2+ dysregulation.
Assessing muscle mechanical properties such as hardness and stiffness has important clinical implications. The use of ultrasound elastography to assess individual muscle hardness or stiffness has been increasing in recent years. Several different ultrasound elastography methods are currently in use, including strain elastography and shear wave elastography, which are capable of capturing the distribution of hardness and stiffness within individual muscles. In the present review, we outline some of the current basic and clinical applications of strain elastography and shear wave elastography, and illustrate how such ultrasound elastography technologies may further advance understanding of individual muscle mechanical properties as well as muscle functions.
We examined the effects of resilience on life stress by measuring subjective and physiological responses. Subjects were 32 college students who reported no remarkable subjective burden at the start of the study (initial period: T1), but some level of stressful burden 3 months later (second period: T2). Resilience levels were evaluated using the Bidimensional Resilience Scale (BRS), which measures innate and acquired resilience. The subjective stress level was assessed with the Stress Response Scale-18 (SRS-18). Saliva was also collected to measure the salivary secretory immunoglobulin A (sIgA) level. BRS was performed at T1, and SRS and saliva collection were administered at both T1 and T2. The subjects were divided into high- and low-resilience groups according to their median scores at T1. Additionally, the high-resilience group was classified as either high-innate resilience (HIR) or high-acquired resilience (HAR), and the low-resilience group as low-innate resilience (LIR) or low-acquired resilience (LAR), respectively, to reveal information in more detail. The depression-anxiety score for the SRS-18 in the low-resilience group was significantly higher than that in the high-resilience group at T2. The sIgA level of the high-resilience group was significantly higher than that of low-resilience group at T2. There were significant negative correlations between innate resilience and depression-anxiety, and total SRS-18 score; and negative correlations among acquired resilience and depression-anxiety, helplessness, total SRS-18 score, and sIgA level, respectively. These results suggested that the stress response in low-innate and acquired resilience differs depending on the length of time elapsed with stress, because low-innate and acquired resilience causes higher susceptibility to “depression-anxiety” as a psychological stress response factor. On the other hand, higher acquired resilience improved immune function in the presence of subjective burden.