Mechanical loads on the skeleton imposed by exercise increase bone mass and strength. The sensor in the osteocyte that detects mechanical stress, the mechano-sensor, responds to bone strain caused by mechanical loading. Greater magnitude and rate of strain increases osteogenic response, making high-impact exercise, which imposes large and dynamic strain on the skeleton, an effective mode of exercise. However, the sensitivity of the mechano-sensor (mechano-sensitivity) drops after a large number of repetitions performed within an exercise session, which has diminishing returns. It takes several hours or several days to reestablish mechano-sensitivity after the last loading session. It is important to consider the time to recovery of mechano-sensitivity when determining optimal exercise frequency.
High-intensity interval training (HIIT) consists of repeated short bursts of high-intensity exercise and rest. Here we review recent work focusing on the metabolic adaptations to HIIT, especially in oxidative capacity and substrate availability in skeletal muscle. In this review, HIIT is defined as chronic training, for at least 2 weeks, involving repeated short-duration high-intensity exercise at >85% VO2 max, followed by complete rest or active rest, for any given duration of exercise and rest. First, we describe the effects of HIIT on muscle substrate oxidative metabolism, specifically in terms of mitochondria and substrate transporters. HIIT changes muscle mitochondrial content, function and dynamics. HIIT increases the protein content of transporters of glucose, lactate and fatty acids in skeletal muscle. These adaptations of mitochondria and transporter proteins improve oxidative capacity and substrate availability in skeletal muscle. Second, we introduce a potential mechanism of HIIT-induced adaptations in skeletal muscle, focusing on mitochondrial biogenesis. It is well known that a mechanism of mitochondrial biogenesis involves PGC-1alpha protein and its upstream signaling pathways including Ca2+/calmodulin-dependent protein kinase, AMP-activated protein kinase and mitogen-activated protein kinase p38. Given that mitochondrial biogenesis occurs in an exercise-intensity-dependent manner, mobilization of fast-twitch fibers and lactate accumulation are important. Finally, we discuss the future direction of HIIT research, involving systems biology approaches such as omics technologies and mathematical modeling, which may overcome current limitations and accelerate our understanding of mechanisms of HIIT-induced adaptations.
Cardiometabolic diseases such as type 2 diabetes mellitus, stroke, and coronary heart disease are complex disorders influenced by multiple genetic and environmental factors. Physical activity is one of the most reliable predictors of cardiometabolic diseases among various lifestyle factors. Numerous epidemiological studies have revealed that higher levels of physical activity and cardiorespiratory fitness are strongly associated with a lower incidence of cardiometabolic diseases and all-cause mortality in various populations. On the other hand, genetic factors also contribute to susceptibility to cardiometabolic diseases. Familial and twin studies have demonstrated that the strength of the contribution of genetic factors to cardiometabolic diseases is comparable to that of environmental factors, and a large number of genetic variants associated with cardiometabolic diseases have been identified. Importantly, genetic factors explain the heterogeneity of the effect that regular exercise has on the improvement of cardiometabolic risk, and there is evidence that regular exercise possibly attenuates the genetic predisposition to cardiometabolic diseases. Thus, genetic factors and exercise interact with each other to determine susceptibility to cardiometabolic diseases. This article reviews recent studies exploring genetic factors that determine susceptibility to cardiometabolic diseases, with an emphasis on the studies examining the gene-exercise interactions in cardiometabolic risk.
The present review summarizes current evidence and unresolved issues regarding training-induced changes in the architecture of human skeletal muscles. As architectural parameters, we focused on the fascicle length and pennation angle, which are related to force-generating capability of pennate muscles. Cross-sectional studies in sport athletes suggested changes in both the parameters following chronic sport-specific activities. Longitudinal training intervention experiments indicated direct evidence of the plasticity of the two parameters induced by resistance training, but no consensus has been reached regarding the factors influencing those changes. Considering the importance of fascicle arrangement on muscle function, future studies are required to explain the underpinning mechanisms of the adaptation.
X-ray diffraction analysis is a method to obtain information about periodically repeated structures. When striated muscle is irradiated with X-ray, many of the reflections and the layer lines, which convey information about molecular structures within the muscle fiber, are obtained without chemical modification. Two of the strong equatorial reflections, 1,0 reflection arising from a thick filament array and 1,1 reflection arising from a thick and thin filament array appear on the equator giving information about distance and mass distribution on a radial plane. Thus a 1,1/1,0 intensity ratio is a good index of radial distribution of myosin heads. Meridional reflections and layer lines, such as a myosin reflection of the 14.3 nm repeat and myosin or actin layer lines, give information about longitudinal arrangement of the molecules. Since they are affected by the movement of the myosin heads and the shifting motion of troponin-tropomyosin on the actin filament, they can be used to detect conformational changes of contractile and regulatory systems upon muscle activation. The X-ray diffraction method has been applied to yield fruitful results for many problems such as muscle atrophy by disuse, functional modulation by myosin regulatory light chain phosphorylation, differential characteristics of slow and fast skeletal muscle structure, and pathogenesis of some types of the familial myopathy. The approach using X-ray diffraction analysis will continuously serve as a potent tool for resolving problems in the field of physical fitness and sports medicine.
An increasing number of studies have examined the effects of acute aerobic exercise on executive function (i.e., higher-order cognitive abilities involved in goal-directed behaviors) in healthy children. More recently, studies have begun to extend these empirical findings to children with neurodevelopmental disorders such as attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Here, we review what is known about the effects of acute exercise on executive function in children with and without neurodevelopmental disorders. Overall, moderate acute aerobic exercise can transiently improve executive function in children with and without neurodevelopmental disorders. Further, these effects of acute exercise may differ depending on type of exercise, participant characteristics (e.g., fitness levels, executive function capacity, type of neurodevelopmental disorder), and timing of cognitive task administration (i.e., after versus during exercise). Despite the increasing number of findings, it is still premature to suggest effective exercise types and/or intensity levels to produce improvements in executive function in children. Further studies are needed to address this issue. Finally, future research directions are discussed in more detail.
Sports-associated injuries often involve trauma to soft tissues such as ligaments, tendons, skeletal muscle, and skin. A shortened recovery process for injured tissues is of great interest to athletes, as injury-associated inactivity depresses both sports performance and physical fitness. Recently proposed treatments to accelerate tissue repair include microcurrent electrical neuromuscular stimulation (MENS), low-intensity pulsed ultrasound (LIPUS), hyperbaric oxygen (HBO), and autologous platelet-rich plasma (PRP). Among these treatments, MENS has been applied to alleviate pain and reduce swelling following sports-associated injuries of tendons and ligaments. MENS is reported to stimulate the regeneration of skeletal muscles, a part of the body commonly injured in sports. MENS is expected to soon become a standard therapy for accelerating the repair of injured skeletal muscles and other soft tissues. In this review, we provide an overview of MENS and briefly describe several other proposed treatments for sports-associated injuries.
The technique of vibration-induced illusory movement has been used to study the mechanisms of perception and the brain network responsible for eliciting kinesthesia since it was first reported by Goodwin and colleagues in 1972. Vibration applied to the skin surface over the tendon of limb muscles excites primary afferent spindles, and subjects experience movement sensations as if the vibrated muscle were stretched, despite the limb being immobile. In addition, tendon vibration can induce tonic muscle activities in both the vibrated muscle and its antagonistic muscles. It was formerly believed that these motor responses accompanied the kinesthetic illusion of the vibrated limb. However, if subjects relax their limb completely and focus their attention on the movement sensed during vibration, a movement illusion can be elicited without any motor responses. This review focuses on the relationship between the elicitation of vibration-induced kinesthetic illusions and experimental conditions, and may provide insight into differences among studies of kinesthetic illusion.
Thermoregulation is categorized as either autonomic (i.e., sweating, shivering) or behavioral (i.e., wearing clothes, usage of air conditioner) thermoregulation. Compared to autonomic thermoregulation, the neural pathway of behavioral thermoregulation in cold environments remains unclear. A decrease in ambient temperature is perceived through thermoreceptors for detecting cold, including transient receptor potential (TRP) channels, such as TRPM8 and TRPA1, which are expressed in the sensory nerve endings of the skin. From these receptors, nerves connect to the dorsal root ganglion and dorsal horn in the spinal cord, and arrive at the lateral parabrachial nucleus in the pons, which is the same neural pathway that is used for autonomic thermoregulation. Following this, an unknown neural pathway induces thermoregulatory behavior, such as cold-escape behavior. Both young and climacteric women complain of an unpleasant thermal comfort, which is attributed to “hie-sho” (chill or poor blood circulation). The altered thermal sensation and comfort by an absence or a fluctuation of estrogen (E2) may modulate behavioral thermoregulation in females. This effect is unknown in women. However, in ovariectomized rats, E2 facilitated thermoregulatory behavior in the cold, as evaluated by an operant system and tail-hiding behavior, a possible new behavioral indicator that we reported. E2 decreased neural activity in the insular cortex, as assessed by cFos immunohistochemistry, while tail-hiding behavior increased in colder temperatures. We speculate that the suppression of neural activity in the insular cortex by E2 may be related to behavioral thermoregulation in a cold environment. Therefore, it is necessary to clarify the effects of E2 on TRPM8 and TRPA1 channels, and the neural pathway of behavioral thermoregulation.
Osteoarthritis (OA) is one of the most common age-related degenerative joint disorders. In addition to aging, various life-style-related factors, such as obesity and overuse of joints, have been recognized as major risk factors for OA. It has been revealed that mechanical force acting on articular cartilage induces chondrocytes to produce excess amounts of reactive oxygen species (ROS), which are known to be an OA-related catabolic factor. In addition, it has been reported that mechanical stress-induced ROS directly damage chondrocyte DNA, resulting in the downregulation of cellular activity and induction of apoptosis in osteoarthritic chondrocytes. Notably, molecular events associated with DNA oxidative damage influence the regulation of chondrocyte activity and cellular viability, supporting the notion that mechanical stress-induced oxidization of chondrocyte DNA participates in the pathogenesis of OA. Here, we review accumulating evidence supporting the involvement of mechanical and oxidative stresses in cartilage homeostasis and the pathogenesis of OA.
The purpose of this study was to estimate sex differences in age-related grip strength decline and describe the course of decline in grip strength from age 40 to 89 years by a longitudinal epidemiological study. Participants were randomly selected community-living men (n = 648) and women (n = 598) aged 40 to 79 years at baseline. Grip strength was measured with standard techniques every other year over a 10-year period. The preservation rate of grip strength was calculated as the 10-year follow-up value divided by the baseline value. The relationship between the preservation rates of grip strength and age group (by decade) at baseline by sex was analyzed using Two-Way Analysis of Variance and the Tukey-Kramer method. The trajectories of grip strength over 10 years were plotted for both men and women. The mean grip strength preservation rates of participants in their 40s, 50s, 60s and 70s over 10 years was 0.90, 0.88, 0.84 and 0.79 in men, and 0.89, 0.89, 0.89 and 0.88 in women, respectively. There were significant differences in sex and age group at baseline in the preservation rate of grip strength. Among men, the preservation rate of grip strength for the 70s group was significantly lower than that of younger groups (p < 0.05); however, no significant difference was observed among age groups in women. The trajectories of grip strength decline year by year were steep in men, but even in women. Age-related decline in grip strength markedly increased in older men, but remained constant throughout middle and late adulthood in women.
We investigated the weight transferring aspect of gait pattern during treadmill walking and muscle strength of the knee extensors and flexors following unilateral anterior cruciate ligament (ACL) reconstruction surgery. At 6 and 12 postoperative months, 11 patients (six men, five women) walked on a split-belt treadmill with two embedded force plates at their preferred speeds, 20% slower and 20% faster. Seventeen healthy control subjects (nine men, eight women) were also evaluated. Peak values of three components of ground reaction force (vertical, anteroposterior, and mediolateral) were measured bilaterally, and their variabilities were analyzed by coefficients of variation (CVs). The CVs for the anteroposterior forces differed between the reconstructed and contralateral limbs at 6 postoperative months, and this difference disappeared at 12 months. This was not matched by the time course change of quadriceps strength since quadriceps weakness in the reconstructed limb persisted up to 12 months postoperative. These findings suggest that gait alteration in anteroposterior forces may not be caused by quadriceps weakness alone, and the reconstructed and contralateral limbs may compensate for gait execution over the first year following ACL reconstruction surgery.
No specific hip joint anatomy has been identified as a risk factor for anterior cruciate ligament (ACL) injury in females. This study was conducted to elucidate the correlation of hip rotation with ACL injury incidence in female handball players, and to clarify the association of hip rotation with knee valgus motion, during ACL injury screening tasks, that is a strong predictor of ACL injury. Of 17 female university handball players, the 8 ACL-injured players displayed greater internal and smaller external rotation of the hip than the 9 uninjured players. Logistic regression analyses demonstrated significant association between hip rotation and ACL injury. Hip internal rotation dominance (internal rotation range is greater than external one) was found in 7 out of the 8 ACL-injured females in contrast to 3 out of the 9 uninjured. Knee valgus was induced in 24 and 22 of the 31 healthy female volunteers by vertical jump and single-leg squat tests, respectively. The knee valgus-positive females showed a smaller range of hip external rotation than the negative ones, which was significantly associated with knee valgus during the screening tests. Hip internal rotation dominance was significantly related to knee valgus induced by each screening test. In contrast to the females, male subjects showed lower rates of knee valgus induction by the screening tests, whereas there was no clear association between hip internal rotation dominance and the knee valgus induction. The present findings may indicate the important role of hip rotation measurement in identification of females at risk for ACL injury.