Tadayoshi Miyamoto

PURPOSE: Acupuncture stimulation is known to act on the autonomic nervous system and elicits depressor and bradycardic effects. However, previous studies on humans did not conduct quantitative analyses on optimal acupuncture conditions such as the stimulation frequency and duration to achieve maximum depressor and bradycardic effects. The aim of the present study was to investigate the effects of varying stimulation frequencies of electroacupuncture on time-dependent changes in blood pressure and heart rate in humans. METHODS: Twelve healthy volunteers participated in the study. An acupuncture needle was inserted at the Ximen acupoint (PC4 according to WHO nomenclature), located at the anterior aspect of the forearm. An electrical stimulation was delivered through the acupuncture needle at an intensity of 1 V, pulse width of 5 ms, and stimulation frequencies of 0.5, 1, 5, and 10 Hz in a random order. The duration of electroacupuncture was 6 min, during which blood pressure and heart rate responses were monitored. RESULTS: Group-averaged data indicated that 1-Hz electroacupuncture decreased blood pressure and heart rate. Blood pressure was significantly decreased from the prestimulation baseline value of 86.6 ± 2.9 to 81.4 ± 2.3 mmHg during 4-6 min of 1-Hz electroacupuncture (mean ± SE, P < 0.01). Heart rate was also significantly decreased (from 66.2 ± 2.0 to 62.7 ± 1.7 beats/min, P < 0.01). CONCLUSIONS: These results provide fundamental evidence that bradycardiac and depressor responses are effectively produced by electrical acupuncture in humans.

<jats:p> The purpose of the present study was to examine whether the response of cerebral blood flow to an acute change in perfusion pressure is modified by an acute increase in central blood volume. Nine young, healthy subjects voluntarily participated in this study. To measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume); and 2) during the recovery phase immediately following release of lower body negative pressure (LBNP; −50 mmHg) that initiated an acute increase in central blood volume. In the thigh-cuff occlusion release protocol, as expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236 ± 0.018 and 0.167 ± 0.025 s<jats:sup>−1</jats:sup>, P = 0.024). Compared with the cuff-occlusion release, the acute increase in central blood volume (relative to the LBNP condition) with LBNP release attenuated dynamic cerebral autoregulation ( P = 0.009). Therefore, the hypercapnia-induced attenuation of dynamic cerebral autoregulation was not observed in the LBNP release protocol ( P = 0.574). These findings suggest that an acute change in systemic blood distribution modifies dynamic cerebral autoregulation during acute hypotension. </jats:p>

OBJECTIVE: The respiratory operating point is determined by the interplay between the controller and plant subsystem elements within the respiratory chemoreflex feedback system. This study aimed to establish the methodological basis for quantitative analysis of the open-loop dynamic properties of the human respiratory control system and to apply the results to explore detailed mechanisms of the regulation of respiration and the possible mechanism of periodic breathing in chronic heart failure. METHODS AND RESULTS: In healthy volunteers, we measured arterial CO2 partial pressure (PaCO2) and minute ventilation [Formula: see text] to estimate the dynamic properties of the controller ( [Formula: see text] relation) and plant ( [Formula: see text] relation). The dynamic properties of the controller and plant approximated first- and second-order exponential models, respectively, and were described using parameters including gain, time constant, and lag time. We then used the open-loop transfer functions to simulate the closed-loop respiratory response to an exogenous disturbance, while manipulating the parameter values to deviate from normal values but within physiological ranges. By increasing both the product of gains of the two subsystem elements (total loop gain) and the lag time, the condition of system oscillation (onset of periodic breathing) was satisfied. CONCLUSION: When abnormality occurs in a part of the respiratory chemoreflex system, instability of the control system is amplified and may result in the manifestation of respiratory abnormalities such as periodic breathing.

The purpose of the present study was to examine whether the response of cerebral blood flow to an acute change in perfusion pressure is modified by an acute increase in central blood volume. Nine young, healthy subjects voluntarily participated in this study. To measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume); and 2) during the recovery phase immediately following release of lower body negative pressure (LBNP; -50 mmHg) that initiated an acute increase in central blood volume. In the thigh-cuff occlusion release protocol, as expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236 ± 0.018 and 0.167 ± 0.025 s(-1), P = 0.024). Compared with the cuff-occlusion release, the acute increase in central blood volume (relative to the LBNP condition) with LBNP release attenuated dynamic cerebral autoregulation (P = 0.009). Therefore, the hypercapnia-induced attenuation of dynamic cerebral autoregulation was not observed in the LBNP release protocol (P = 0.574). These findings suggest that an acute change in systemic blood distribution modifies dynamic cerebral autoregulation during acute hypotension.

The physiological mechanisms underlying the increases observed in glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) plasma levels with exercise currently remain unknown. Previous studies reported that increases in plasma GLP-1 and PYY concentrations were mediated by a neural pathway, regardless of exercise. Therefore, we investigated the neural regulation of GLP-1 and PYY secretion during exercise in rats using a hindlimb muscle contraction model. Hindlimb muscle contraction was induced by electrically stimulating the sciatic nerve for 20 min (5 V, 5 Hz). A fasting arterial blood sample (Baseline) was taken. Rats were subjected to 20 min of hindlimb muscle contraction in vivo, and blood samples were collected at the end of the hindlimb muscle contraction protocol. Although GLP-1 and PYY levels were significantly increased after hindlimb muscle contraction (P < 0.001, respectively), no significant differences were observed in GLP-1 or PYY levels between sham and vagotomy trials. On the other hand, GLP-1 and PYY levels after hindlimb muscle contraction were significantly lower in the sciatic nerve deafferentation trial than in the sham trial (P < 0.01, respectively). These results indicate that the increases observed in GLP-1 and PYY plasma levels with exercise were mediated by the activation of skeletal muscle-derived afferent neurons, and not by mechanisms through the neural pathway of the vagus nerve.

The purpose of this study was to assess blood flow responses to changes in carbon dioxide (CO₂) in the internal carotid artery (ICA), external carotid artery (ECA), and vertebral artery (VA) during normothermic and hyperthermic conditions. Eleven healthy subjects aged 22 ± 2 (SD) yr were exposed to passive whole body heating followed by spontaneous hypocapnic and hypercapnic challenges in normothermic and hyperthermic conditions. Right ICA, ECA, and VA blood flows, as well as left middle cerebral artery (MCA) mean blood velocity ( V_mean), were measured. Esophageal temperature was elevated by 1.53 ± 0.09°C before hypocapnic and hypercapnic challenges during heat stress. Whole body heating increased ECA blood flow and cardiac output by 130 ± 78 and 47 ± 26%, respectively ( P &lt; 0.001), while blood flow (or velocity) in the ICA, MCA, and VA was reduced by 17 ± 14, 24 ± 18, and 12 ± 7%, respectively ( P &lt; 0.001). Regardless of the thermal conditions, ICA and VA blood flows and MCA V_mean were decreased by hypocapnic challenges and increased by hypercapnic challenges. Similar responses in ECA blood flow were observed in hyperthermia but not in normothermia. Heat stress did not alter CO₂ reactivity in the MCA and VA. However, CO₂ reactivity in the ICA was decreased (3.04 ± 1.17 vs. 2.23 ± 1.03%/mmHg; P = 0.039) but that in the ECA was enhanced (0.45 ± 0.47 vs. 0.95 ± 0.61%/mmHg; P = 0.032). These results indicate that hyperthermia is capable of altering dynamic cerebral blood flow regulation.

In normoxic conditions, a reduction in arterial carbon dioxide tension causes cerebral vasoconstriction, thereby reducing cerebral blood flow and modifying dynamic cerebral autoregulation (dCA). It is unclear to what extent these effects are altered by acute hypoxia and the associated hypoxic ventilatory response (respiratory chemoreflex). This study tested the hypothesis that acute hypoxia attenuates arterial CO2 tension-mediated regulation of cerebral blood flow to help maintain cerebral O2 homeostasis. Eight subjects performed three randomly assigned respiratory interventions following a resting baseline period, as follows: (1) normoxia (21% O2); (2) hypoxia (12% O2); and (3) hypoxia with wilful restraint of the respiratory chemoreflex. During each intervention, 0, 2.0, 3.5 or 5.0% CO2 was sequentially added (8 min stages) to inspired gas mixtures to assess changes in steady-state cerebrovascular CO2 reactivity and dCA. During normoxia, the addition of CO2 increased internal carotid artery blood flow and middle cerebral artery mean blood velocity (MCA Vmean), while reducing dCA (change in phase = -0.73 ± 0.22 rad, P = 0.005). During acute hypoxia, internal carotid artery blood flow and MCA Vmean remained unchanged, but cerebrovascular CO2 reactivity (internal carotid artery, P = 0.003; MCA Vmean, P = 0.031) and CO2-mediated effects on dCA (P = 0.008) were attenuated. The effects of hypoxia were not further altered when the respiratory chemoreflex was restrained. These findings support the hypothesis that arterial CO2 tension-mediated effects on the cerebral vasculature are reduced during acute hypoxia. These effects could limit the degree of hypocapnic vasoconstriction and may help to regulate cerebral blood flow and cerebral O2 homeostasis during acute periods of hypoxia.

PURPOSE: The present study investigated the effects of severe-intensity interval training at a frequency of once a week on cardiorespiratory function at rest and during exercise. METHODS: Fourteen young healthy males were randomly assigned to either an interval training group or control group. Cardiorespiratory function was investigated by incremental maximal exercise test and constant work rate submaximal exercise test before and after the intervention period in all subjects. Submaximal exercise test was conducted at two work rates (80% ventilatory threshold (VT) level and 100% VT level plus 50% of the difference between VT and peak oxygen consumption (V˙O2)) for 8 min; the same work rates and duration were used before and after training. Left ventricular adaptations were assessed by echocardiography under supine resting conditions before and after training. In the interval training group, seven subjects performed cycle ergometer training once per week for 3 months. The training consisted of three bouts of exercises to volitional fatigue at 80% maximum work rate. RESULTS: Increased V˙O2max (+13%, P = 0.015), VT (+21%, P = 0.001), and left ventricular posterior wall thickness (+18%, P = 0.002) and reduced minute ventilation (-12%, P = 0.032) and blood lactate concentration (-16%, P = 0.025) during high-intensity exercise were observed after the training program compared with baseline. Although not significant, V˙O2 and cycling economy (V˙O2 per work rate) during high-intensity exercise decreased slightly after training. CONCLUSION: The present results indicate that severe-intensity interval training, even when performed at a low frequency, markedly improves cardiorespiratory function as well as induces cardiac morphological adaptations involving left ventricular hypertrophy and cardiorespiratory metabolic response during submaximal exercise. The present findings may provide new insights for low-frequency, severe-intensity interval training in the field of sports science.

The respiratory operating point (ventilatory or arterial PCO2 response) is determined by the intersection point between the controller and plant subsystem elements within the respiratory control system. However, to what extent changes in central blood volume (CBV) influence these two elements and the corresponding implications for the respiratory operating point remain unclear. To examine this, 17 apparently healthy male participants were exposed to water immersion (WI) or lower body negative pressure (LBNP) challenges to manipulate CBV and determine the corresponding changes. The respiratory controller was characterized by determining the linear relationship between end-tidal PCO2 (PetCO2 ) and minute ventilation (Ve) [Ve = S × (PetCO2 - B)], whereas the plant was determined by the hyperbolic relationship between Ve and PetCO2 (PetCO2 = A/Ve + C). Changes in Ve at the operating point were not observed under either WI or LBNP conditions despite altered PetCO2 (P < 0.01), indicating a moving respiratory operating point. An increase (WI) and a decrease (LBNP) in CBV were shown to reset the controller element (PetCO2 intercept B) rightward and leftward, respectively (P < 0.05), without any change in S, whereas the plant curve remained unaltered at the operating point. Collectively, these findings indicate that modification of the controller element rather than the plant element is the major factor that contributes toward an alteration of the respiratory operating point during CBV shifts.

Appetite and eating behaviour are controlled by a variety of peripheral signals that change in response to food intake and act in the hypothalamus and brainstem. Glucagon-like peptide-1 (GLP-1) is a brain-gut peptide that has a variety of physiological functions and is involved in appetite regulation. Abnormalities in the expression and secretion of GLP-1 have been shown to occur in obesity, diabetes, and hyperlipidemia, and improving these abnormalities has become an important challenge. Exercise has recently been shown to have an influence on GLP-1 concentrations. This short review aims to highlight the association between exercise and the blood kinetics of GLP-1 and discuss the relevance of GLP-1 in the regulation of appetite to prevent obesity.

To investigate the effect of resistance training at lower than the recommended frequency (2–3 times a week) on muscular strength, we recruited 103 college students (67 males 61±8 kg, 36 females 51±4 kg, mean±SD) who had never regularly engaged in resistance training. They performed resistance training in a PE class once a week for seven to ten weeks. We measured one repetition maximum (1 RM) for the bench press and arm curl, and the girth of the thigh and upper arm before and after the training. The training included stretching, three sets of ten repetitions on a bench press, half squat lift, arm curl and three types of training chosen by each subject. The weight load was 10 RM, which was progressively increased; when the subject succeeded in lifting a load ten times at the first set, the load was increased in the following week. After the training period 1RM was increased by more than 10% compared with that before training, for either the bench press or the arm curl, in all subjects. The 1 RM for the bench press significantly increased from 46±9 kg to 54±9 kg in males, and from 22±4 kg to 28±5 kg in females, and that for the arm curl also increased significantly. No significant change was found in the girth of the thigh and upper arm. On the other hand, 49 male students who undertook softball in a PE class did not show any significant change in 1 RM after the eight-week control period, compared to that before the period. These results demonstrate that resistance training at a frequency lower than the recommended one increases muscular strength in college students, possibly through adaptations in the nervous system.