Shin-ya Ueda

Changes in gut hormone levels and negative energy balance during aerobic exercise in obese young males.

We examined whether changes in gut hormone levels due to a single bout of aerobic exercise differ between obese young males and normal controls, and attempted to determine the involvement of hormonal changes during exercise in the regulation of energy balance (EB) in these obese subjects. Seven obese and seven age-matched subjects of normal weight participated in exercise and rest sessions. Subjects consumed a standardized breakfast that was followed by constant cycling exercise at 50% VO(2max) or rest for 60 min. At lunch, a test meal was presented, and energy intake (EI) and relative energy intake (REI) were calculated. Blood samples were obtained at 30 min intervals during both sessions for measurement of glucose, insulin, glucagon, ghrelin, peptide YY (PYY), and glucagon-like peptide-1 (GLP-1). Plasma levels of PYY and GLP-1 were increased by exercise, whereas plasma ghrelin levels were unaffected by exercise. The areas under the curve (AUC) of the time courses of PYY and GLP-1 levels did not significantly differ between the two groups. In contrast, EI and REI were decreased by exercise in both groups, and energy deficit was significantly larger in obese subjects than in normal controls. The present findings suggest that short-term EB during a single exercise session might be regulated not by increased amounts of these gut hormones per se.

Comparable effects of moderate intensity exercise on changes in anorectic gut hormone levels and energy intake to high intensity exercise

There is growing interest in the effects of exercise on plasma gut hormone levels and subsequent energy intake (EI) but the effects of mode and exercise intensity on anorectic hormone profiles on subsequent EI remain to be elucidated. We aimed to investigate whether circulating peptide YY(3-36) (PYY(3-36)) and glucagon-like peptide-1 (GLP-1 or GCG as listed in the HUGO Database) levels depend on exercise intensity, which could affect subsequent EI. Ten young male subjects (mean+/-s.d., age: 23.4+/-4.3 years, body mass index: 22.5+/-1.0 kg/m(2), and maximum oxygen uptake (VO(2 max)): 45.9+/-8.5 ml/kg per min) received a standardized breakfast, which was followed by constant cycling exercise at 75% VO(2 max) (high intensity session), 50% VO(2 max) (moderate intensity session), or rest (resting session) for 30 min. At lunch, a test meal was presented, and EI was calculated. Blood samples were obtained during three sessions for measurements of glucose, insulin, PYY(3-36), and GLP-1, which includes GLP-1 (7-36) amide and GLP-1 (9-36) amide. Increases in blood PYY(3-36) levels were dependent on the exercise intensity (effect of session: P<0.001 by two-way ANOVA), whereas those in GLP-1 levels were similar between two different exercise sessions. Of note, increase in area under the curve values for GLP-1 levels was negatively correlated with decrease in the EI in each exercise session (high: P<0.001, moderate: P=0.002). The present findings raise the possibility that each gut hormone exhibits its specific blood kinetics in response to two different intensities of exercise stimuli and might play differential roles in regulation of EI after exercise.

Effects of acute hypoxia on cerebrovascular responses to carbon dioxide

What is the central question of this study? In acute hypoxia, the reduction in arterial CO2 tension due to the hypoxic ventilatory response (respiratory chemoreflex) stimulates cerebral vasoconstriction, which opposes the degree of hypoxic cerebral vasodilatation. The aim was to examine this interaction further. Specifically, we questioned whether arterial CO2 tension‐mediated effects on cerebrovascular regulation are attenuated during acute hypoxia. What is the main finding and its importance? Cerebrovascular CO2 reactivity and CO2‐mediated effects on dynamic cerebral autoregulation were attenuated during acute hypoxia. These findings suggest that blunted cerebrovascular responses to CO2 may limit the degree of CO2‐mediated vasoconstriction to help maintain adequate cerebral blood flow for cerebral O2 homeostasis during acute hypoxia.

Effects of exercise training on gut hormone levels after a single bout of exercise in middle-aged Japanese women

The purpose of this study was to investigate the effects of 12 weeks of exercise training on gut hormone levels after a single bout of exercise in middle-aged Japanese women. Twenty healthy middle-aged women were recruited for this study. Several measurements were performed pre and post exercise training, including: body weight and composition, peak oxygen consumption (peak VO2), energy intake after the single bout of exercise, and the release of gut hormones with fasting and after the single bout of exercise. Exercise training resulted in significant increases in acylated ghrelin fasting levels (from 126.6 ± 5.6 to 135.9 ± 5.4 pmol/l, P < 0.01), with no significant changes in GLP-1 (from 0.54 ± 0.04 to 0.55 ± 0.03 pmol/ml) and PYY (from 1.20 ± 0.07 to 1.23 ± 0.06 pmol/ml) fasting levels. GLP-1 levels post exercise training after the single bout of exercise were significantly higher than those pre exercise training (areas under the curve (AUC); from 238.4 ± 65.2 to 286.5 ± 51.2 pmol/ml x 120 min, P < 0.001). There was a tendency for higher AUC for the time courses of PYY post exercise training than for those pre exercise training (AUC; from 519.5 ± 135.5 to 551.4 ± 128.7 pmol/ml x 120 min, P = 0.06). Changes in (delta) GLP-1 AUC were significantly correlated with decreases in body weight (r = −0.743, P < 0.001), body mass index (r = −0.732, P < 0.001), percent body fat (r = −0.731, P < 0.001), and energy intake after a single bout exercise (r = −0.649, P < 0.01) and increases in peak VO2 (r = 0.558, P < 0.05). These results suggest that the ability of exercise training to create a negative energy balance relies not only directly on its impact on energy expenditure, but also indirectly on its potential to modulate energy intake.

The effect of an acute increase in central blood volume on the response of cerebral blood flow to acute hypotension.

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.

Development of an anaesthetized‐rat model of exercise hyperpnoea: an integrative model of respiratory control using an equilibrium diagram

What is the central question of this study? The lack of useful small‐animal models for studying exercise hyperpnoea makes it difficult to investigate the underlying mechanisms of exercise‐induced ventilatory abnormalities in various disease states. What is the main finding and its importance? We developed an anaesthetized‐rat model for studying exercise hyperpnoea, using a respiratory equilibrium diagram for quantitative characterization of the respiratory chemoreflex feedback system. This experimental model will provide an opportunity to clarify the major determinant mechanisms of exercise hyperpnoea, and will be useful for understanding the mechanisms responsible for abnormal ventilatory responses to exercise in disease models.

A novel approach for evaluating the effects of odor stimulation on dynamic cardiorespiratory functions

We aimed to develop a novel method to quantitatively evaluate the effects of odor stimulation on cardiorespiratory functions over time, and to examine the potential usefulness of clinical aromatherapy. Eighteen subjects participated. Nine people were assigned to each of the two resting protocols. Protocol 1: After resting for 2 min in a sitting position breathing room air, the subject inhaled either air or air containing sweet marjoram essential oil from the Douglas bag for 6 min, Protocol 2: After resting for 5 min in a supine position, the subject inhaled the essential oil for 10 min, and then recovered for 10 min breathing room air. All subjects inhaled the essential oil through a face mask attached to one-way valve, and beat-to-beat heart rate (HR) and arterial blood pressure (BP) as well as breath-by-breath respiratory variables were continuously recorded. In both protocols, during fragrance inhalation of the essential oil, time-dependent decrease in mean BP and HR were observed (P<0.05). During post-inhalation recovery, the significant fragrance-induced bradycardic effect lasted at least 5 min (- 3.1 ± 3.9% vs. pre-inhalation baseline value, p<0.05). The mean BP response at the start of odor stimulation was approximated by a first-order exponential model. However, such fragrance-induced changes were not observed in the respiratory variables. We established a novel approach to quantitatively and accurately evaluate the effects of quantitative odor stimulation on dynamic cardiorespiratory functions, and the duration of the effect. This methodological approach may be useful for scientific evaluation of aromatherapy as an approach to integrated medicine, and the mechanisms of action of physiological effects in fragrance compounds.