The respiratory control system is an important chemoreflex-feedback control system that maintains arterial partial pressures of CO2 (PaCO2), O2 and pH remarkably constant via ventilatory regulation. It can be divided into two subsystems: a controller (controlling element) and a plant (controlled element). The respiratory operating point (ventilatory or PaCO2 response) is determined by the interplay between the controller (arterial PCO2 [PaCO2] → minute ventilation [VE] relation) and plant (VE → PaCO2 relation) subsystem elements within the respiratory control system. This review outlines the methodology of converting the closed loop of the respiratory control system to an open loop state, then simplifying the controller and plant subsystems, and identifying the input−output relationship using a systems physiological technique (equilibrium diagram method). Changes in central hemodynamics, exercise stimulus, and regular exercise training modify VE and/or PaCO2 levels at rest and during exercise. These respiratory changes can be quantitatively explained by changes in two subsystem elements on the respiratory equilibrium diagram. Using this analysis technique that allows an integrated and quantitative description of the whole respiratory control system will greatly advance the elucidation of pathological conditions manifesting breathing disorders and respiratory regulation during exercise. By repeating thought experiments utilizing this kind of mathematic model and physiological experiments that provide evidence, deeper understanding will be achieved concerning prediction of the behavior of biological systems beyond the physiological range and understanding of the pathophysiology of diseases that are difficult to study by clinical research.
The cardiovascular response to physical exercise is abnormally exaggerated in hypertension. Since such responses potentially increase the risk for adverse cardiovascular events, it is clinically important to elucidate the cause of this cardiovascular hyper-excitability in this disease. Even if blood pressure is normal at rest, individuals displaying a heightened blood pressure response to exercise are more likely to develop future hypertension. Therefore, early detection of this abnormal circulatory response to physical activity could lead to the early treatment as well as prevention of hypertension. Much evidence suggests that the abnormal exercise pressor reflex (EPR; a reflex originating in exercising skeletal muscle) significantly contributes to the generation of the enhanced circulatory responses in this disease. In addition, it has been demonstrated that the EPR dysfunction is mediated by both mechanically-sensitive fibers associated with the muscle mechanoreflex and chemically-sensitive fibers associated with the muscle metaboreflex. This review focuses on the underlying mechanisms for this overactive EPR function in hypertension. Specifically, updates on our current understanding of the EPR in this disease as well as experimental models used to examine this reflex are presented.
During coordination of the movement of two limbs, the movements often interfere with each other, i.e., interlimb coordination is constrained. Many movement-related parameters such as movement direction, movement frequency, the coupling of limbs, neural network among limbs, and muscle homology are considered constraints of interlimb coordination, and they are roughly consolidated into two constraints, a neuromuscular constraint, and a perceptual-cognitive constraint. Interlimb coordination is considered to be governed by a coalition of neuromuscular and perceptual-cognitive constraints. On the other hand, spontaneous interlimb coordination is considered purely perceptual in nature. In this review, we focused on an influential study on interlimb coordination published in Nature by Mechsner et al. (2001), which supported the latter psychological approach. Thorough verification of the paper with reference to related studies revealed that no studies have yet proposed decisive contrary evidence against the psychological approach. Rather, investigation of interlimb coordination with perceptual-cognitive perspective has uncovered new findings. As a next psychological approach, the proposal of a unified and predictive explanation for movements is required. In addition, neural mechanisms that connect perceptual-cognitive representation to an appropriate motor command, if any, should be addressed.
Although physical activity or exercise has a beneficial effect on brain structure and function, physical activity levels are decreasing due to sedentary lifestyles in contemporary society. For this reason, there has been increasing attention paid to the practical application of mild intensity exercise, which might be more attractive to and applicable for both young and older adults with a sedentary lifestyle. Indeed, long-term mild exercise training in older adults has been shown to prevent atrophy of the prefrontal cortex as well as moderate-intensity exercise intervention. However, it is still unknown whether acute mild exercise has beneficial effects on brain function, particularly executive function, mediated by the prefrontal cortex, and underlying neural substrates. To address this question, we combined an executive-function task that has been confirmed in many neuroimaging studies to target specific neural substrates and fNIRS neuroimaging techniques that allow the monitoring of task-related cortical activation shortly after exercising. We recently demonstrated that even acute mild exercise can improve executive task performance, which was positively correlated with increased arousal level and also evoked task-related cortical activation on the left dorsolateral prefrontal cortex and left frontopolar area. Although the exact neuronal substrate is still intriguing, animal microdialysis studies have demonstrated that mild exercise increased several neurotransmitters such as acetylcholine and dopamine, which could play an important role in the mild-exercise-elicited higher cognitive function.
Cardiovascular and respiratory responses are reflexly augmented during exercise, and the former is known as the exercise pressor reflex. The exercise pressor reflex is thought to be caused by both mechanical and metabolic stimuli to thin-fiber muscle afferents innervating active skeletal muscles. Ischemia induced-acidosis has been reported to augment the exercise pressor reflex. However, protons alone do not excite many thin-fiber afferents. In this short review, we show that protons lower the response threshold and increase the response magnitude to mechanical stimulation of thin-fiber muscle afferents, thus possibly contributing to the exercise pressor reflex. Furthermore, this short review introduces a new sensitizing mechanism by protons (low pH) of thin-fiber muscle afferents via a type of extracellular matrix proteoglycan, versican. The possibility of controlling the augmented reflex during ischemic exercise in people with cardiovascular disease is also discussed.
Skeletal muscle has an important role besides its obvious function in physical movement and locomotion; namely, it maintains whole-body metabolism. Maintaining muscle mass and quality with regular exercise is closely related to quality of life and a healthy life expectancy. However, the ways that exercise, and muscle contraction, in particular, contribute to our health has not been analyzed in detail. Progressive elucidation of the intracellular mechanisms underlying the metabolic changes induced by exercise/contraction and the hormones secreted from skeletal muscle (called myokines) is providing new insights into how exercise affects our health. To research these mechanisms in muscle contraction, various in vivo and in vitro experimental models have been developed. This review article outlines the existing skeletal muscle contraction models in rodents. Each model has its advantages and disadvantages. It is important to keep such features in mind when selecting an appropriate contraction model for the particular experimental purpose.
Skeletal muscle O2 dynamics can be measured during whole body dynamic exercise noninvasively by near-infrared spectroscopy (NIRS), and muscle O2 dynamics can allow us to estimate muscle O2 extraction. Muscle O2 extraction is one of the determinants of peak pulmonary O2 uptake (VO2), and blunted peak VO2 potentially increases cardiovascular-associated morbidity and mortality. However, muscle O2 dynamics and their relation to reduced peak aerobic capacity have not been fully established. This review briefly outlines the relationship between change in muscle O2 dynamics and an improvement of peak VO2. Our findings suggest that aerobic training enhances estimated muscle O2 extraction, and the enhancement is related to an improvement of peak aerobic capacity in elderly subjects, with and without heart disease. The relationship may be potentially affected, however, by some factors such as: the initial level of aerobic capacity and cardiac function (ability of convective O2 supply), and training volume, phase, or type. The number of elderly people who have a low peak aerobic capacity will most likely be increasing in Japan, as a consequence of the aging population and physical inactivity due to advanced technology. Although we recognize several limitations of the NIRS technique and the necessity for further investigation, assessing muscle O2 dynamics is valuable to understand the peripheral impairments and mechanisms of lowered peak VO2.