Most Japanese people have had their flexibility tested in childhood physical education classes. Recent studies may provide a retrospective answer as to why those measurements may be important. Flexibility is one of the components of physical fitness along with cardiorespiratory fitness and muscular strength. Although flexibility was originally assumed to correlate with other aspects of physical fitness, recent studies demonstrate that a less flexible body indicates arterial stiffening. Arterial stiffness has been identified as an independent risk factor for mortality and cardiovascular disorders. Therefore, there is a possibility that flexibility is a novel fitness indicator related to cardiovascular disease, which can be easily evaluated over all ages and in any area (e.g., medical check-up). Now, flexibility may no longer be simply viewed as important just for optimizing functional movement in daily life and/or reducing the risk of injury. This article reviews the recent findings on the relationship between flexibility and arterial stiffness, emphasizing “flexibility and arterial stiffness”, “genetics and flexibility”, “stretching and arterial stiffness”, and “flexibility and blood pressure”.
The human brain is activated even before a stimulus occurs if a person knows the stimulus will happen within a few seconds. The neural basis for this cognitive function, termed anticipation, is the subject of this review. One method for investigating the brain mechanism of anticipation employs stimulus-preceding negativity (SPN), which is a type of event-related potential (ERP). A critical feature of SPN is that SPN amplitude is greater at the right than at the left hemisphere. This feature suggests that the right hemisphere plays a significant role in the anticipation process. Some neuroimaging studies identified the anterior insula as a physiological source of SPN. The anterior insula is a part of the salience network that detects stimulus salience. Furthermore, recent neuroimaging studies reveal that the right anterior insula is involved in processing the salience outcome, whereas the left anterior insula is related to behavioral adaptation. The SPN study combining functional magnetic resonance imaging (fMRI) and ERP revealed that the right anterior insula showed increased activity preceding a stimulus, while the left anterior insula was not activated. Such studies lead to the hypothesis that saliency of an anticipated stimulus evokes the salience network in advance of a stimulus, and that this network then pre-activates other brain regions in perception of an anticipated stimulus. These processes can be shown as SPN variations in amplitude and cortical distribution. In general, SPN studies suggest that the saliency of an anticipated stimulus is a key factor in evoking anticipatory brain activity.
Originally, in clinical settings, ischemic preconditioning (IPC) has been used to delay cardiac cell injury and protect against myocardial and vascular damage. Furthermore, as this manipulation is relatively easy and noninvasive, previous studies have examined how IPC may have beneficial effects on exercise performance. However, because of various factors, such as different populations, exercise modes and intensities, and IPC protocols, not enough evidence is available to achieve a consensus on the impact of IPC on exercise performance, e.g., time to failure during exercise, time trial performance, and peak power. Existing evidence suggests that IPC seems not to impair exercise performance, though one study found an impairment. However, about half of the previous studies showed beneficial effects of IPC on exercise performance. Similarly, the physiological responses from IPC are varied. It is still possible that various factors, such as exercise mode and intensity, heterogeneous population and IPC protocol may affect exercise performance. Previous studies showed that effective blood flow via an increase in nitric oxide and the improvement of metabolic efficiency might be candidate factors that can explain the effect of IPC on exercise performance, although no direct evidence has been obtained. This review aims to identify potential sources of variation in these effects on exercise performance with IPC.
The mechanism which causes sarcopenia, a loss of muscle mass and strength with aging, remains unclear. Muscle mass is controlled by the net balance between protein synthesis and breakdown; however, net balance differences in the basal state do not contribute to sarcopenia. On the other hand, anabolic resistance, a reduction in muscle protein synthesis in response to protein intake, does seem to be involved in sarcopenia. Muscles which are subject to anabolic resistance do not show incremental blood flow volume during the fed-state. Because the vascular system transports amino acids and other nutrients that are essential for muscle protein synthesis, blood flow volume may be a regulator of anabolic resistance. There is some evidence of a link between blood flow and muscle protein metabolism. In addition, a combination of resistance training and amino acid supplementation promotes a positive net protein balance. Resistance training improves, and detraining reduces blood flow volume; therefore, blood flow volume may be involved as a background mechanism for sarcopenia. Moreover, previous studies have shown that sodium nitroprusside, a vasodilatory nitric oxide donor, enhances muscle protein synthesis. Conversely, angiotensin II, a major vasoconstrictive peptide, induces skeletal muscle protein breakdown. In this review, we discuss a possible role for blood flow in skeletal muscle protein metabolism in elderly adults. The regulation of blood flow may prove to be a beneficial treatment for sarcopenia.
Taurine (2-aminoethanesulfonic acid) is a sulfur-containing β-amino acid present in high concentrations in most tissues, including skeletal muscle, liver, blood, and brain. Taurine has been suggested to have positive effects on some of the physiologic functions considered to be a cause of fatigue during exercise: Ca2+ handling in excitation–contraction coupling, regulation of ion channels, oxidative stress, and the inflammatory response. However, how and where taurine affects these processes have not been elucidated fully. Some in vitro studies have suggested that taurine treatment improves the contractile properties of skeletal muscle. Several studies have suggested that taurine is involved in regulation of energy metabolism. In contrast, whole-body taurine transporter knockout mice exhibit severe intolerance to exercise. Based on these observations, whether taurine treatment may prevent/attenuate fatigue during exercise and then improve exercise performance in humans and experimental animals has been studied. Some recent studies have investigated the effects of taurine administration on post-exercise recovery. Our group investigated the effects of taurine treatment on fatigue induced by endurance exercise. We found that post-exercise taurine administration enhanced the recovery of skeletal muscle glycogen, which is the major determinant for exercise performance. In this review, we introduce studies investigating the effects of taurine administration on exercise-induced fatigue and post-exercise recovery.
Running economy (RE), which is evaluated at an exercise intensity below the lactate threshold (LT), is recognized as the most important physiological variable for estimating running performance. However, middle- and long-distance athletes run above LT intensity during their competitive events. This study elucidates the relation between 1,500-m running performance and physiological variables, including RE measured at intensities below and above the LT. The study included 34 male distance runners (1,500-m velocity: 22.2 ± 0.8 km·h−1, equivalent to race times of 4′03″2 ± 8″5). RE was calculated at four running velocities selected to provide intensities of 90%LT and 95%LT below LT (REbLT) and 105%LT and 110%LT above LT (REaLT). RE was determined from aerobic energy metabolism, calculated from oxygen uptake and the respiratory exchange ratio, combined with anaerobic energy metabolism, calculated from the change in blood lactate concentration. Results show that the 1,500-m velocity was not related to maximal oxygen uptake (VO2max) or LT intensity (r = 0.19 and 0.10, respectively). This velocity correlated with both REaLT and REbLT, with the correlation coefficient being higher for REaLT (r = −0.65 and −0.71 vs −0.56 and −0.58). Furthermore, the coefficient of determination for 1,500-m velocity determined from VO2max, LT intensity and REaLT was higher than that determined from VO2max, LT intensity and REbLT (R2 = 0.603 and 0.640 vs 0.415 and 0.543). These results suggest that RE measured at an intensity above LT intensity may be better than other physiological variables for estimating 1,500-m running performance.
This study protocol introduces the Kasama Study, a mid-sized longitudinal study of health, fitness, and physical activity in older people. The study is a challenging research project that discusses the future of the system for preventive nursing care and for supporting successful aging in Japan. In May 2008, we began the Kasama Study with an exercise program of preventive nursing care for community-dwelling older adults. As of March 2016, we have conducted six study projects: 1) the Kasama health checkup for longevity, 2) an all-round exercise class, 3) the volunteer and the circle, 4) an exercise class for men only, 5) an exercise class for improving cognitive and physical function, and 6) the Kasama Iki-iki checklist survey. We describe each project in detail in the present study protocol.