We previously reported unique skin blood flow (SkBF) responses in the face to emotions related to taste. Then we supposed that poor and good motor imaginary reflect to facial SkBF response. We examined whether motor imaginary of volleyball serves are related to facial SkBF responses to underhand- and floater- serve, comparing 1st-person with 3rd-person perspective of the imaginary. The subjective evaluation for the control of motor imagery is high, SkBF in the eyelid showed greater. The results suggests that high controllability of motor imagery related to an increase the SkBF responses in the eyelid. To extract skillful and disadvantaged scenes in sports performance based on facial SkBF responses, we need to examine whether similar SkBF responses can be obtained in other sports events, and the increase response in the nose become conspicuous according to the skill of sports, in future studies.

We reported that the eyelid blood flow increases when one feels tasty, while nose blood flow decreases when one feels not-tasty. We tested the possibility that facial blood flow responses give us objective information regarding to how the person feels the food. Facial skin blood flow was recorded while 89 subjects ate tasty and non-tasty candies without controlling environments. No characteristic response was obtained. Easy detection of one's feeling was impossible without lab environments. Next, to investigate factors inducing characteristic blood flow response to taste, heat and cold stimuli were applied to subjects' face. Blood flow in cheek and forehead changed accordingly to changes in the temperature of the stimuli. Eyelid showed no response in the blood flow to the change in temperature, and nose showed no decrease response to decrease in temperature. The characteristic response in facial blood flow should be dependent on neural factors, not on responsiveness of facial vessels.

To explore the coordinating mechanism of cardiorespiratory system during exercise, the dynamics of main physiological variables in response to sinusoidal-varied work rate exercise using by solely upper (i.e. cranking) or lower (i.e. cycling) limb, and both combined were examined. The responses of the circulation to non-active limb (i.e. brachial artery (BA) during lower limb cycling) and brain (i.e. middle cerebral artery (MCA)) were specially focused. The results summarized that; 1) within the sub-maximal exercise domain, the responses of combined exercise simultaneously using the upper and lower limbs were substantially summed by both responses, and 2) the circulatory responses of BA and MCA were clearly followed as sinusoidal form, but the dynamic characteristics (phase delay and amplitude) in BA were approximately anti-phasic with a relatively large amplitude, whereas those in MCA were very stable with a short delay.

The eyeground is the singe place where we directly observe vessels and arteries, in our body. In this study, we tested a feasibility of a method for easily recording ocular vessels and blood flow and for estimating vascular sclerosis. We found difficulty in the easiest way to record ocular vessels by using smartphones. Then we recorded ocular blood flow by laser speckle flowgraphy, and calculated the half‐value width in a single beat, i.e. BOT. We found a significant effect of ageing on BOT in ocular vessels, and a significant correlation between BOT and IMT, which is the golden-standard method for estimating arteriosclerosis. These results implied that an observation of ocular blood flow can provide us information on vessel sclerosis induced by ageing.

We developed developmental disability check sheet, in order to investigate and then support university freshmen. This check sheet can be useful tool for supporting students’ adaptation not for diagnosing. The answer or request for consultation in their parents can be very important. High score of this check sheet has positive effects on the level of stress and irregular lifestyle, but no direct effects on the failure of earning credits or withdraw from university. However there was a limit to find all students who have developmental disability, because the scores of this check sheet can be also related to the level of anxiety.

We supposed that face and facial color are related to various emotions, since there are many expressions of language using face. Then we tested the hypothesis that facial skin blood flow shows specific response to emotion. Subjects watched videos evoking happiness, sadness, fear, astonishing and fear, then we measured facial skin blood flow. No specific response was obtained in skin blood flow in forehead, nose, cheek and lips. The results may suggested a difficulty judging one's emotion from facial skin blood flow responses as yet. It should be necessary to use stronger stimulus evoking a change in emotion, if we can.

The purpose of this study is to investigate whether it is possible to judge a degree of mood change like depression based on the pattern of physical activity in university students. At first, in order to inquire the availability a device which is popular and relatively cheap, simultaneous measurement during 1 or two days in 6 students was done using two devices of the actigraph and the popular one. There is only low relation between the measurements of the two devices during daytime. Therefore, we think that it is not suitable to use the popular device, in order to measure daytime activity of the students. Consequently we cease the population study of mental state and physical activity measured using the popular device in students.

The short time sleep after the lunch (i.e. nap, 10-20 min shallow sleep) is well known to prevent the declines of work efficiency and arousal level in office workers and drivers. In this study, we examined the effect(s) of short time sleep on the exercise performance and its related basic physiological functions and capacities such as visual acuity, arousal level of the brain, reaction time, nociceptive threshold of the skin, taste sensation, and subjective symptom. The results from the basic and practical experiments indicated that; 1) the nap (less than 20 min with stages 1 and 2) showed some positive effects on information processing system in the brain and visual acuity, and 2) a more long time and deep sleep (i.e. approximately one hour including stages 3 and 4), rather than rest and/or even nap, might have the positive effects on short-term maximal anaerobic power (estimated by the standard test using by the cycle ergometer) and kinetic vision.

The main purpose of this study was to develop the new techniques of work rate forcing for estimating the aerobic working capacity of humans. The proposed techniques are based on ; 1) the sinusoidally fluctuated work rate forcing which simulates the non-steady state physical activities of daily life, and 2) the exponentially incremental work rate forcing, as an alternative way to the conventional ramp-mode exercise test With respect to the sinusoidal exercise, the responses of O2-cascade related variables(i. e. from pulmonary VO2 to O2-utlization in active muscle) and their coordination were examined. Furthermore, the physiological linkage, that is, circulatory adjustments among the O2-cascade related and non-related variables(including the cerebral and non-exercising limb circulations) were explored.

運動選手は風邪を引きやすいと言われるように,いわゆる行動体力の高い運動選手や活動的な学生の上気道感染率は高い.この状況を免疫で説明することは難しい.むしろ,長期的にはトレーニング実施による防衛体力の向上があったとしても,低温環境下での身体運動という環境への暴露の増加が感染リスクを高めていると予想される.運動選手に風邪の罹患が多いことが,トレーニング時の上気道の血流量低下と関連するとの仮説を検証するために,運動時および運動後に上気道部の血流が低下するかどうかについて検討した.
昨年度は,心拍数100～140拍/分相当強度の自転車エルゴメータ運動時には上気道部の血流はほとんど変化しないことを観察したことから,今年度は疲労困憊に至る強度での運動時の上気道部の血流を観察した.健常成人男女11名に,自転車エルゴメータ運動を疲労困憊にいたるまで行わせた.運動前および運動終了5分,10分後の上気道部の血流をレーザースペックルフローグラフィーを用いて,計測した.その結果,上気道部の血流は運動前値と比較して,運動終了後10分後まですることはなかった.このことから,本研究では血流減少と上気道感染との関連は明示されなかった.
補足的ではあるが,舌部では120, 140拍/分強度の運動時に観察されたのと同様に,高強度運動後にも血流低下が観察されたことを追記しておく.
本研究の限界としては,高強度運動時に上気道部の血流を観察することが極めて困難であるため,運動後の観察にとどまる点,また呼吸に伴う気道部温度の影響も微弱ではあるものの観察された.

It has been proposed that salivary alpha-amylase (sAMY) is a useful stress-related biomarker, but further investigation is needed to confirm this assumption. The purpose of our cross-sectional and longitudinal studies was to evaluate whether sAMY activity was really associated with several kinds of experimental and ordinary stress or relaxation among Japanese university students and office workers. The investigated levels of sAMY showed a tendency to increase in response to stress under strict rest condition or when measured frequently. Inter-individual, and possibly intra-individual, differences in the reactivity of sAMY are considered to affect the results. It is suggested that sAMY activity is useful as a stress-related biomarker in the longitudinal, rather than cross-sectional, studies.

運動強度が徐々に漸増し疲労困憊に至るランプ負荷運動を課し,運動に対する中枢の関与を傍証する目的で,運動中は,定期的な時間間隔で痛み閾値を測定する実験をまず実施した。運動中を通して温熱刺激に対する痛み閾値を1分毎に調べた。併せて交感神経出力の指標として瞳孔径も測定した。その結果,安静時に比較して,ランプ負荷運動中,有意な差異を認められなかったが,瞳孔径はAT付近の運動強度を境に増大した。この実験の結果を,研究への協力ならびに助言者として来日いただいた,Dr. B. J. Whipp(英国・Leeds大学)と協議し,運動強度と時間の組み合わせを考慮する必要性,また知覚系の測定も行う必要性が認識されたので,次の実験を計画した。3段階の運動強度(低・中・高強度)での一定負荷運動で,それぞれのエネルギー消費がほぼ等しくなるような運動時間を設定し,運動中と後で,電気刺激に対する知覚ならびに痛みを感じる閾値と脳の情報処理能力(カラーワードコンフリクトテスト:CWCT)を測定し,運動前と比較した。知覚感覚閾値はすべての運動強度で,運動中,有意に低下した。さらに中・高強度運動では,運動直後もその状態が継続した。痛み感覚閾値は,中・高強度運動で同様に,運動中に有意な低下を示し,運動直後も継続した。情報処理能力は必ずしも仮説に反して,CWCTの正答率が運動強度による違い(影響)は特に認められなかった。これらの結果は,運動強度が増大するにつれて,上位脳の活動が運動に占有されてくる度合いが大きくなり,痛みの処理までできなくなるという仮説は支持するものであったが,このことと上位脳の情報処理能力への影響は必ずしも同じように起こるというわけではなく,脳の有する複雑さと,今後のさらなる研究の必要性を示した。

本研究は、唾液の粘度が運動強度に伴って高くなるのか、唾液の粘度には変曲点があるのか、あるとしたらそれは無酸素性作業閾値(AT)と関連するのか、について明らかにすることを目的とした。被験者14名(内女性3名)に3分毎に40W(女性では30W)ずつ負荷が増加する自転車エルゴメータ運動を行わせた。各負荷段階の最後の2分間に唾液を採取し、その粘度を計測した。別の日に、ランプ負荷試験を行わせ、その際のガス分析結果よりATを判定した。スピンドル回転数60rpmで計測した唾液粘度は安静時に3.0±0.2cPだったものが、強度の増加とともに減少を示し、ATよりも56±4W低い強度において2.38±0.1cPの最低値を示した(p<0.05)。AT近辺の強度においても安静値よりも有意に低い2.4cP台を示したが、ATを58±4W超えた時点では3.0±0.2cPを示し、安静値と有意差を示さなかった。最大運動強度時には2.71±0.2cPを示し、安静値と有意差はなかった。唾液粘度は運動強度に対してU字状のカーブを描いたので、全被験者の変曲点を14名の被験者全員に判定させた。ところが、これはガス分析の結果から求めたATと関連しておらず、唾液粘度からATを予想することは難しいことが明らかになった。本研究結果は唾液粘度が運動強度に対してU字状に変化することを示した。また、最大運動時であっても、唾液粘度は安静値と差がないことを示した。交感神経活動が唾液粘度を増加させる、というこれまでの予想は、運動時には適応できないことが示唆された。

有酸素性作業能力(AWC)は,ヒトの日常の身体活動遂行能力である。生理人類学の立場から,それに支える生体内の諸機能やそれら相互の連関といった生理的メカニズムの解明と,その結果に基づいた今日的な諸問題解決を念頭においた新たなAWC評価手法の開発が課題としてあげられる。そこで本企画調査では,関連する海外の専門家を招請して,AWC評価指標の現状を,その生理的メカニズムと実際のAWC評価を目的とした運動負荷試験方法(特に負荷様式)の観点の両者から,次年度の共同研究立案を念頭に議論した。具体的な招請研究者として,7月に運動時循環調節の立場からDr.P.Fadel (USA・Missouri大)と運動時自律神経制御の立場からDr.S.Koba (USA・Pennsylvania大)を,8-9月に運動時骨格筋バイオエナジェテクスの立場からDr.H.Rossiter (UK・Leeds大)を,12月に運動時換気調節の立場からDr.J.Mateika (USA・Wayne State大)と運動負荷試験の数理解析の立場からDr.H.Morton (NZ・Massey大)をそれぞれ招請し,分担研究者や研究協力者を交えて活発な議論を重ねた。その結果,運動負荷試験方法としては,日常での身体活動に重要な動的特性を反映したサイン波状負荷変動の運動負荷試験によるAWC評価法が優れていること,ならびに高齢者や体力の弱い対象者(実際に生理人類学領域の調査研究が必要とされる集団)にとって,ATやVO2maxといったこれまでの調査成果と比較できる静的な指標を捉えるためには,現在のランプ負荷より指数関数型負荷の方が有用であることの2点がコンセンサスとしてえられた。最終的に,本研究を具体的に遂行するにあたり,新たな共同研究者を加え,来年度から2年間に及ぶ科学研究費補助金・基盤研究(B)を申請するに至った。

運動が精神ストレスを軽減させるのに有効であることが知られている.生理的な知見として,運動が血圧を低下させるという報告は多いものの,メカニズムについては明らかではない.今年度は,短期の精神ストレスが起こす高血圧が運動によって軽減されるメカニズムを探るために,精神作業を行った後に運動を行わせ,それによる血圧低減効果が圧反射の機能変化によってもたらされるという仮説を検証した.圧反射は,頸動脈および大動脈弓にある圧受容器に対する動脈圧変化を入力として,延髄内で処理された情報を,自律神経を介して出力する反射系である.したがって,圧反射の短期間の機能変化は延髄の機能変化と捉えられる.【方法】9名の被験者にカラーワードテストを4分間行わせた.CWT試行(対照実験)では,その後8分間の安静を保たせた.一方,CX試行では精神作業の後4分間25Wの自転車運動を行わせた後に,8分間の安静を保たせた.圧反射を評価するため,新たに作成した頸部圧刺激装置によって圧受容器に20mmHgを負荷した.圧受容器周辺の血管は伸展の程度を抑制されるので,実際の血圧よりも低圧を感知し,心拍数が増加する.この心拍数の増加量より圧反射の機能を評価した.【結果と考察】精神作業は心拍数と血圧を増加させた.頸部の加圧に対する心拍数の増加幅は,精神作業によって初期値から増加した.精神作業8分後までの平均血圧の最低値が出現した際の各変量を求めた.CWT試行では平均血圧の最低値と初期値との間に有意差はなかった.一方,CX試行では初期値よりも4±3mmHg有意に減少していた.この際,頸部の加圧による心拍数の増加幅はCWT試行では初期値と有意差がなかった.一方,CX試行では,初期値から有意に減少した.これらの結果から,精神ストレス後における短時間の低強度運動が昇圧を減少させ,その背後には圧反射の機能変容があることが示唆された.

While there are numerous afferent drives to the respiratory center to control exercise ventilation, one of the important drive certainly comes from the exercising skeletal muscles. Stimulation of afferent nerves with endings in hindlimb skeletal muscles is known to have marked reflex effects on the respiratory system of anesthetized animals. The recent animal studies appropriated the neural monitoring system to hemodynamic effect (i.e., a "flow-linked" control) of ventilation. Therefore, to investigated to verify this hypothesis, i.e., whether the mechanosensitive, flow-dependent stimulation in muscle can be linked the ventilatory control in response to exercise in humans, we performed the following experiments, 1; to investigate the effect of occluding of femoral blood flow on the post-exercise ventilatory response of both the sub-and supra-anaerobic threshold (AT) leg cycling, 2; to investigate the effect of static/intermittent compressing stimulus to the lower limb using the anti-shock pant on post-exercise ventilatory response from leg cycling exercise, 3; to investigate the effect of postural change from supine to upright (it means blood retention to the lower limb) just after the cessation of cycling exercise on post-exercise ventilatory response, and 4; to investigate the causal linkage of ventilatory depression and blood flow to the lower limb during cycling exercise just after the 5-minintentional hyperventilation to induce vasoconstriction. As a result, two experiments supported the hypothesis whereas the remaining two did not. Accordingly, further study is clearly needed to deserve these issues.

不活動期間後には,同一運動負荷に対する昇圧応答が減少するが,それを起こすメカニズムは明らかではない.運動時には,運動を開始させる中枢からの情報(セントラルコマンド)と筋からの情報(運動昇圧反射)との2つの神経入力が交感神経性の循環応答を起こす.本研究では,不活動による筋の萎縮によって,活動筋から惹起する運動昇圧反射が減弱し,その結果運動時の昇圧応答が減少する,という仮説を検討した.
ラット(7〜8週齢,オス)の左脚を1週間ギプス固定した.その後,麻酔下にて動静脈および気道にカテーテルを導入し,左右の下腿三頭筋を露出した後,除脳した.筋の機械受容器を刺激して運動昇圧反射を起こすため,30秒間下腿三頭筋を伸張した.ギプス固定した左脚の筋重量は1.0±0.1g(平均±SE)であり,対照の右脚の1.4±0.1gよりも有意に小さい値であった.筋の伸張(229±20g)は,萎縮脚では13±3mmHgの昇圧を起こし,これは対照脚の4±2mmHgよりも有意に大きいものであった。刺激の大きさを下腿三頭筋の重量で除して,相対的に等しい張力に対する応答を比較しても,萎縮脚刺激による応答は,対照脚のそれよりも有意に大きいものであった.このことから,廃用性萎縮が機械受容器を介する運動昇圧反射の大きさを大きくすることが明らかになった.したがって,機械受容器を介した運動昇圧反射は,不活動期間後に見られる昇圧応答の減少を説明できないものと結論された.
また,本研究ではラットの腎臓交感神経活動を記録した.セントラルコマンドおよび昇圧反射を入力した際には,血圧および心拍数の増加と同時に腎臓交感神経活動の増加が見られた.また,これは腎血流の減少を伴っていた.上記ラットでもこれらの計測を試みたが,ギプス固定の影響か,ラットの状態が悪化してしまい,残念ながら良好な記録を得ることが困難であった.

We observed the ventilation during cuff occlusion limiting the flow from and into the active muscle after exercise cessation, as to test the hypothesis that afferent information from muscle metaboreceptors and mechanoreceptors increase ventilation in humans during exercise. The cuff occlusion after the cessation of exercise selectively stimulates metaboreceptors and metaboreceptors in muscles. The results obtained in the first year were that there was no significant difference in ventilation between cuff occlusion and control trials, while the end-tidal CO2 partial pressure, which indicates the arterial CO2 concentration, was lower during cuff occlusion than in control. This implies the possibility that stimulus to the carotid body CO2 sensor decreased by cuff occlusion compromise the increment of afferent information from muscle receptors.
In the next series of experiments, we controlled inspired CO2 partial pressure to oscillate the end-tidal CO2 pressure during cuff occlusion. Six subjects performed 2-min isometric leg extension exercise at 30% of maximal *oluntary contraction. During 3-min cuff occlusion after the cessation of exercise in the experimental trial and corresponding period in the control trial, inspired CO2 was maintained at 0, 3.5 and 5%. The ventilation was plotted against the end-tidal CO2 partial pressure to observe the hyperventilation to a given arterial CO2 concentration by muscle afferent stimulus. The ventilation was higher at 38-42mmHg of end-tidal CO2 partial pressure in five of six subjects, and the increase in ventilation was small, suggesting that the stimulus to metaboreceptors plays a role increasing ventilation during exercise but the amount of this role is limited. We applied change of posture to investigate the mechanoreceptors, but obtained no clear result. The role of mechanoreceptors on ventilation still remains unclear.

Prior heavy exercise which induces lactic acidosis speeds pulmonary oxygen uptake (VO_2) kinetics and reduces its slow component during the following heavy exercise. Two controversial mechanisms are hypothesized to explain this phenomenon : the improved perfusion to exercising limb (i.e. oxygen delivery) or the physiological cause(s) within exercising limb or musculatures (i.e. oxygen utilization). Firstly to clarify the former hypothesis, we investigated the temporal profile between VO_2 and femoral artery blood flow (BFf) during repeated bouts of heavy knee extension exercise. A Doppler ultrasound technique was utilized to measure continuously the BFf. The VO_2 kinetics for the 2nd bout was faster than that for the 1st bout. However, no significant difference was observed for the kinetics of BFf between both bouts. It was concluded that the speeding of VO_2 kinetics during 2nd heavy exercise was not associated with a similar speeding of BFf to the working muscles. Since the thigh muscles involved in leg cycling exercise are complex, especially during heavy exercise, the time- and intensity-dependent differences of muscle use pattern in the thigh may be postulated as one of the factors to explain the phenomenon. As a next step, we, therefore, examined whether the muscle use pattern evaluated by magnetic resonance imaging (MRI) transverse relaxation time (T2 ; i.e. index of muscle activation) in thigh influence the VO_2-kinetics during leg cycle exercise at three exercise intensities (i.e. moderate, heavy, and severe). The T2 in each thigh muscle was evaluated by MRI at rest, 3rd and 6th min of exercise. In heavy and severe exercises, the VO2 slow components were developed and the associated T2 were increases from 3rd to 6th min during exercise in a group of flexor muscles. It seems that the amount of VO2 slow component might be associated with the degree and/or pattern of muscle activation.

The warm-up exercise induces following effects on the main exercise ; Q10 effectdue to increased muscle temperature, facilitation of oxygen unloading in muscle due to the Bohr effect, facilitation of blood flow to the working muscle, and neural adaptation to performing the exercise. We investigated the effect of warm-up exercise on the main heavy exercise, using the estimation of oxygen uptake response.
First, investigating the effect of acidosis on oxygen uptake response, we examined the effect of substituting arm cranking for leg cycling as the warm-up exercise. There was a significant warm-up effect on facilitation of oxygen uptake response during main heavy exercise when we used leg cycling as the warm-up, but no effect when using arm-cranking, suggesting that the facilitation of the oxygen uptake response to heavy exercise is not due to solely the lactic acidosis. Second, investigating the effect of blood flow on the response, we applied facial cold stimulation during main exercise to depress the blood flow to the working muscle, and diathermic warming before main exercise on working muscle as substituting the warm-up exercise to increase the blood flow. Neither the cold stimulation nor the diathermic warming changed the oxygen uptake response during main exercise after the warm-up exercise, suggesting that alternation of blood flow to working muscle can not induce a sufficient effect to facilitate the oxygen uptake response during heavy exercise.

We studied anti-oxidative effects of uric acid on exercise-induced lipid peroxidation. Obese and control high school students were recruited in the first study. The exercise was performed as maximum oxygen consumption test on a cycle ergometer. Thiobarbituric acid reactive substance (TBARS) was assayd in serum before and afer the exercise as an indicator of lipid peroxidation. The exercise induced significant increase in serum TBARS in both groups. There was no significant difference in serum TBARS level between two groups. Obese students had higher uric acid but did not show lower increase in TBARS after the exercise. In the second study road cyclists in high school were recruited as an athlete group. Athlete group showed significantly higher level of plasma uric acid than non-athlete group. TBARS in plasma increased significantly after the cycle ergometer exercise in both groups. However, there was no significant difference in the increase of TBARS between two groups. Athlete group demonstrated higher level of plasma uric acid but did not have lower increase of TBARS after the exercise. We did not obtain the evidence that uric acid prevents from exercise-induced oxidative stress.
Next, we studied anti-oxidative effects of chlorogenic acid on exercise-induced lipid peroxidation in rats. Exercise rats were run on a rodent treadmill. Chlorogenic acid was injected intra-peritoneally 24 and 2 hour before the exercise. The exercise did not increase TBARS significantly in leg muscle, heart, lung and liver. Chlorogenic acid decreased TBARS significantly in four organs. These data indicates anti-oxidative activity of chlorogenic acid. Chlorogenic acid did not influence SOD activity in four organs.

運動開始時に迷走神経活動が循環系を通して酸素摂取量の動態に影響を与えているという仮説をヒトにおいて検証した.まず,顔面冷却刺激が迷走神経活動を増加させる刺激として適当であることを確認するため,男性15名に2分間顔面冷却刺激を暴露した.呼吸数制御下において1拍動毎の心電図R波間隔を記録し,その標準偏差を迷走神経活動の指標とした.顔面冷却によって心拍変動が増加した結果より,顔面冷却が迷走神経活動を増加させることが示された.そこで,運動開始時に迷走神経活動を増加させ,その時の心拍数,心拍出量および酸素摂取量の動態を計測した.男性11名に,3分間無負荷自転車運転の後,換気作業閾値の80%に相当する強度の運動をステップ状に5分間負荷した.顔面冷却を行わないN試行,および運動負荷上昇1分間前から1分後まで顔面冷却を行うS試行を各々4回繰り返し行った.試行中の酸素摂取量を1呼吸毎に,心拍数および心拍量を1拍毎に記録した.データを1秒毎に補間した後、加算平均した.顔面冷却中のデータを除いて変量の動態を1次の指数関数にて近似した.顔面冷却によって心拍数は10±5拍/分減少した.酸素摂取量および心拍量は顔面冷却によって変化しなかった.近似の初期値およびゲインには試行間に有意差はみられなかった.S試行の心拍数,心拍出量および酸素摂取量の遅れ時間(9±20秒,8±9秒,17±5秒)はN試行に比較して有意に遅かった(-7秒±5秒,-3±5秒,13±3秒,p<0.05).迷走神経活動の抑制が遅れると循環系を通して酸素摂取量動態が遅れるという結果から,運動開始時における酸素摂取量の動態に迷走神経活動の速い抑制が関与していることが明らかになった.近赤外線分光法を用いた筋の酸素取り込み動態も測定したが,近似に用いる適当なモデルは得られず,適当なモデルの探索は今後の検討課題である.

The studies using ^<31>P-NMR reported that an inorganic phosphate (Pi) splitted into high and low pH peak during a high intensity exercise. However, it was not clear which factor induces this splitting. We hypothesized that a muscle fiber recruitment pattern explains this splitting. It was essential to improve the resolution time of ^<31>P-NMR to clarify the Pi kinetics. We adjusted the angular and interval of the pulse in ^<31>P-NMR to allow a 5 seconds interval data acquisition. To test the hypothesis, we observed Pi patterns under sufficient and insufficient oxygen conditions, i.e., during active and passive recovery from exercise, and during exercise with and without circulatory occlusion.
High pH Pi disappeared just after the end of calf flexion exercise. Low pH Pi during the active recovery decreased significantly faster than during the passive recovery. This would resulted from insufficient oxygen supply to the fast twitch muscle fiber during the passive recovery. Simultaneously measured near infrared spectroscopy data indicated that more existing blood volume during the active recovery than the passive recovery, revealing more oxygen supplement to muscle during active recoverty. Pi peak splitting was observed during circulatory occlusion on leg by 280 mmHg at lower exercise intensity than non occlusion trial. This means that Pi metabolism covers the energy loss resulted from oxygen deficit. It is suggested that fast twitch muscle fiber recruitment causes the Pi splitting.

The information about the effect of mental activities on detailed cardiovascular responses is limited, though strong and chronic psychological stressors are risk factors of cardiovascular morbidity and mortality in humans. The responses of vascular resistance (VR) during fear-induced stress was studied by measuring the mean arterial pressure (MAP), heart rate (HR), skin blood flow in the index finger and forehead, limb blood flow in the calf and forearm, and blood flow in the renal and superior mesenteric arteries before, during, and after a period of induced fear. After 2 min of rest, baseline data were acquired from eight subjects, after which they watched a 3-min video that was considered to be frightening. Minute-by-minute data were calculated. The MAP was divided by the blood flow to attain the VR. While a clear steady state was not evident in the stress-induced vascular response, stress significantly increased the MAP and HR (e.g., by 10 +/- 3 mm Hg and 8 +/- 3 bpm, respectively, at the 2nd min; mean +/- SEM), and the VR of the forearm and finger skin (e.g., by 80 +/- 26% and 79 +/- 28%, respectively, at the 2nd min). The VR increased slightly in the calf and visceral arteries but not in the forehead throughout the stimulation. The variables returned to baseline levels by the 1st min after cessation of the fearful stimulation. These results suggest that fear-induced stress causes vasoconstriction in the forearm and finger. (C) 2009 Elsevier Inc. All rights reserved.

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.

Someya N, Hayashi N. Chewing and taste increase blood velocity in the celiac but not the superior mesenteric arteries. Am J Physiol Regul Integr Comp Physiol 295: R1921-R1925, 2008. First published October 8, 2008; doi:10.1152/ajpregu.90493.2008.-To investigate the role of chewing and taste in the meal-induced rapid increase in splanchnic blood flow, we compared the blood flow responses in the celiac artery ( CA) and superior mesenteric artery ( SMA) to chewing solid food with a chocolate taste ( FOOD) and paraffin wax without taste ( WAX). After 5 min of baseline measurement, 15 healthy subjects repeated chewing and expectorating the FOOD or WAX every 20 s for 4 min followed by 10 min of recovery measurement. We measured the mean blood velocity ( MBV) in the CA and SMA. The baseline MBVs in the CA and SMA did not differ between the FOOD and WAX trials. The MBV in the CA was lower than baseline at the 1st min of chewing in both trials. It was higher than baseline at the 3rd min of FOOD chewing, whereas it did not increase during and after WAX chewing. The MBV in the CA was higher in the FOOD trial than in the WAX trial at the 3rd min of chewing and thereafter. In contrast, the MBV in the SMA did not change throughout the protocols. These results suggest that the taste of food plays a role in meal-induced hyperemia in the CA but not the SMA.

Blood flow (BF) responses in the celiac artery (CA) and superior mesenteric artery (SMA) during and immediately after a meal are poorly understood. We characterized postprandial BF responses in these arteries in the initial phase of digestion. After a baseline measurement in the overnight fasting state, healthy subjects ingested solid food (300 kcal) and water ad libitum within 5 min (4.6 +/- 0.2 min, means +/- SE), and then rested for 60 min in the postprandial state. Mean blood velocities (MBVs) in CA (n = 7) and SMA (n = 9) and mean arterial pressure (MAP) were measured throughout the procedure. The MAP was divided by the MBV to yield the resistance index (RI). The MBV in CA and SMA started increasing within a minute after beginning the meal. The MBV in CA rapidly reached its peak increase (60 +/- 8% change from baseline) at 5 +/- 1 min after the start of the meal, whereas the MBV in SMA gradually reached its peak increase (134 +/- 14%) at 41 +/- 4 min after the start of the meal, reflecting a decrease in the RI for both CA and SMA. These findings suggested an earlier increase in CA and SMA MBV, implying that the increase of BF in some parts of the small intestine precedes the arrival of chyme.

At rest, respiratory-induced changes in the partial pressure of arterial carbon dioxide (PaCO₂) play a major role in the regulation of cerebral blood flow (CBF). Changes in CBF affect stability of the ventilatory (V_E) responsiveness to CO₂ via alterations in the degree of washout in central chemoreceptor hydrogen [H⁺] . No data, however, is available on the comparison of the CBF and V_E responsiveness to PaCO₂ at rest and during exercise. To describe the CBF and V_E reactivity to PaCO₂, we measured the blood velocity in the middle cerebral artery (MCAV) in six males under various V_E conditions by controlling ventilation for 12 min at rest (V_E = 9 to 38 L/min) and during 40 W ergometer cycling (V_E = 12 to 68 L/min). The MCAV and V_E reactivity to PaCO₂ at rest was similar to that during exercise (-0.9 &plusmn; 0.3 cm/s/mmHg vs. -1.0 &plusmn; 0.5 cm/s/mmHg, respectively, P>0.05; mean &plusmn; SEM). The intercept of MCAV with PaCO₂ tended to be greater during exercise than at rest (83 &plusmn; 11 vs. 66 &plusmn; 9 cm/s when V_E = 0 L/min: P=0.1); this finding indicates that the upward shift of MCAV reactivity to V_E may have a role in washing out CO₂ from the brain, potentially due to the greater amount of CO₂ production during exercise. [J Physiol Sci. 2008;58 Suppl:S182]

We compared responses in heart rate (HR), mean blood pressure (MAP), sweating rate (SR), sweating expulsion (SwE), and skin vascular conductance (VC) to mental task among different ambient temperature (Ta) conditions, i.e., 12, 16, 20, and 24°C. Seven subjects (27±5 yrs, 64±14 kg) underwent a 2-min color word conflict test (CWT) after 2 mins of baseline data acquisition following a 20-min resting period. All subjects wore long sleeve shirts and long pants. The skin blood flow was measured with a laser Doppler probe on the left index finger pulp to calculate skin VC, and the SR and sweating expulsion (SwE) were measured with a ventilated capsule on the left thenar. CWT significantly increased the HR and MAP, while there was no significant effect of Ta on the magnitudes of these responses. CWT significantly decreased the skin VC when the Ta was 24°C, whereas it significantly increased the skin VC when the Ta was 12 or 16°C. CWT significantly increased SR and SwE in all Ta conditions, and the SwE was greater in warmer conditions. These findings suggest that different ambient temperatures induce different responses in finger skin vasculature to mental task, implying the independent response of cutaneous vasomotor tone and sweat glands in glabrous skin to mental task.

Cerebrovascular reactivity to changes in the partial pressure of arterial carbon dioxide (P(a,CO2)) via limiting changes in brain [H(+)] modulates ventilatory control. It remains unclear, however, how exercise-induced alterations in respiratory chemoreflex might influence cerebral blood flow (CBF), in particular the cerebrovascular reactivity to CO(2). The respiratory chemoreflex system controlling ventilation consists of two subsystems: the central controller (controlling element), and peripheral plant (controlled element). In order to examine the effect of exercise-induced alterations in ventilatory chemoreflex on cerebrovascular CO(2) reactivity, these two subsystems of the respiratory chemoreflex system and cerebral CO(2) reactivity were evaluated (n = 7) by the administration of CO(2) as well as by voluntary hypo- and hyperventilation at rest and during steady-state exercise. During exercise, in the central controller, the regression line for the P(a,CO2)-minute ventilation ((V) over dot(E)) relation shifted to higher (V) over dot(E) and P(a,CO2) with no change in gain (P = 0.84). The functional curve of the peripheral plant also reset rightward and upward during exercise. However, from rest to exercise, gain of the peripheral plant decreased, especially during the hypercapnic condition (-4.1 +/- 0.8 to -2.0 +/- 0.2 mmHg l(-1) min(-1), P = 0.01). Therefore, under hypercapnia, total respiratory loop gain was markedly reduced during exercise (-8.0 +/- 2.3 to -3.5 +/- 1.0 U, P = 0.02). In contrast, cerebrovascular CO(2) reactivity at each condition, especially to hypercapnia, was increased during exercise (2.4 +/- 0.2 to 2.8 +/- 0.2% mmHg(-1), P = 0.03). These findings indicate that, despite an attenuated chemoreflex system controlling ventilation, elevations in cerebrovascular reactivity might help maintain CO(2) homeostasis in the brain during exercise.

To investigate the regional hemodynamic responses of abdominal arteries at the onset of exercise and to focus on their transient responses, eight female subjects (21-30 yr) performed ergometer cycling exercise at 40 W for 4 min in a semi-supine position. Mean blood velocities (MBVs) in the right renal (RA), superior mesenteric (SMA), and splenic (SA) arteries were measured by pulsed echo-Doppler ultrasonography, with beat-by-beat measurements of heart rate (HR) and mean arterial pressure (MAP). The vascular resistance index (RI) of each artery was calculated from MBV/MAP. MAP (76 +/- 9 to 83 +/- 8 mmHg at 4 min) and HR (60 +/- 7 to 101 +/- 9 beats/min at 4 min) increased during exercise (P &lt; 0.05). The MBV of RA and SA rapidly decreased after the onset of exercise (30 s; -19 +/- 5% and -19 +/- 12%, respectively), reaching -27 +/- 7% and -27 +/- 15% at the end of exercise (P &lt; 0.05). RI did not change during the initial 30 s of exercise, reflecting a reduction in MAP, and increased toward the end of the exercise (+ 55 +/- 21% and + 59 +/- 39%, respectively). In contrast, both the MBV and RI in the SMA remained constant throughout the exercise. The results indicate that, whereas the responses of renal and splenic vessels changed similarly throughout the protocol, the vascular response of SMA that mainly supplies blood to the intestinal tract was unchanged during exercise. We, therefore, conclude that low-intensity cycling exercise resulted in differential blood flow responses in arteries supplying the abdominal organs.

We investigated the effect of occluding of femoral blood flow on the post-exercise ventilatory response of both the sub- and supra-anaerobic threshold (AT) leg cycling in humans. Seven healthy subjects (aged 21-44 years) volunteered to participate in this study. The protocol consisted of 6 min constant-load upright cycling at either a sub-AT (80% of AT) or supra-AT (midway between AT and VO(2)max) work rate and a subsequent 6 min rest period either with or without femoral blood flow being occluded by a rapid cuff inflation to 250 Torr during the first 2 min of recovery. Blood lactate levels at the cessation of the sub- and supra-AT exercise averaged 1.8 +/- 0.2 and 4.9 +/- 0.4 mequiv. l(-1) (mean S.E.M.), respectively. Compared to spontaneous recovery, the circulatory occlusion significantly reduced ventilation irrespective of the intensity of the preceding exercise. The relative contribution of the ventilatory deficit to the total spontaneous ventilation (defined as the difference between the cumulative ventilation with and without cuff inflation during the first 2 min of recovery) was significantly greater supra-AT (18.0 +/- 3.9%) than sub-AT (9.3 +/- 2.9%, P &lt; 0.05). The subsequent release of occlusion was accompanied by a rapid increase in ventilation that began on the first breath after release. We concluded that the relatively greater speeding of ventilatory decline with occlusion during the first 2 min of recovery from supra-AT exercise argues against a significant role for an intramuscular chemoreflex-induced hyperpnoea. Rather, mechanisms related to the hemodynamic effects of suddenly altered muscle perfusion seem more consistent with this phenomenon. (c) 2006 Elsevier B.V. All rights reserved.

Breathing including abdominal movement could affect the blood velocity (BV) measurement in the visceral arteries. The present study investigated the effect of breathing frequency on the renal artery (RA) and superior mesenteric artery (SMA) BV measurements. We measured mean arterial pressure (MAP), heart rate (HR) and BV in the RA and SMA using the Doppler technique at different respiratory frequencies. Nine subjects performed breath- holding (&lt;40 s), and spontaneous and controlled breathings at a constant rate of 12, 15 and 20 breaths min(-1). The breathing frequency did not significantly affect the BV in either artery. The BVs at these frequencies were not significantly different from those during spontaneous breathing and breath-holding. There were no significant differences in MAP and HR among trials. This result suggests that the effect of breathing frequency adopted in this study could be neglected in the RA and SMA measurements.

Differential sympathetic outflow and vasoconstriction responses at kidney and skeletal muscles during fictive locomotion. Am J Physiol Heart Circ Physiol 290: H861-H868, 2006. First published September 2, 2005; doi:10.1152/ajpheart.00640.2005.-We compared sympathetic and circulatory responses between kidney and skeletal muscles during fictive locomotion evoked by electrical stimulation of the mesencephalic locomotor region (MLR) in decerebrate and paralyzed rats (n = 8). Stimulation of the MLR for 30 s at 40-mu A current intensity significantly increased arterial pressure (+38 +/- 6 mmHg), triceps surae muscle blood flow (+17 +/- 3%), and both renal and lumbar sympathetic nerve activities (RSNA +113 +/- 16%, LSNA +31 +/- 7%). The stimulation also significantly decreased renal cortical blood flow (-18 +/- 6%) and both renal cortical and triceps surae muscle vascular conductances (RCVC +38 +/- 5%, TSMVC -17 +/- 3%). The sympathetic and vascular conductance changes were significantly dependent on current intensity for stimulation at 20, 30, and 40 mu A. The changes in LSNA and TSMVC were significantly less than those in RSNA and RCVC, respectively, at all current intensities. At the early stage of stimulation (0-10 s), decreases in RCVC and TSMVC were significantly correlated with increases in RSNA and LSNA, respectively. These data demonstrate that fictive locomotion induces less vasoconstriction in skeletal muscles than in kidney because of less sympathetic activation. This suggests that a neural mechanism mediated by central command contributes to blood flow distribution by evoking differential sympathetic outflow during exercise.

We investigated the role played by the exercise pressor reflex in sympathetic regulation of the renal circulation in rats. In mid-collicular decerebrate rats, mean arterial pressure (MAP), heart rate (HR), left renal cortical blood flow (RCBF) and left renal sympathetic nerve activity (RSNA) were recorded before and during 30 s of static contraction of the left triceps surae muscles evoked by electrical stimulation of the tibial nerve, which activates both metabo- and mechanosensitive muscle afferents, and during 30 s of passive stretch of the left Achilles tendon, which selectively activates mechanosensitive muscle afferents. Static contraction (n = 17, +344 +/- 34 g developed tension) significantly (P &lt; 0.05) increased MAP (+14 +/- 3 mmHg), HR (+6 +/- 1 beats min(-1)) and RSNA (n = 11, +19 +/- 5%) and significantly decreased renal cortical vascular conductance (RCVC, n = 11, -11 +/- 2%). Passive stretch (n = 20, +378 +/- 11 g) also significantly increased MAP (+11 +/- 2 mmHg), HR (+7 +/- 2 beats min(-1)) and RSNA (n = 15, +14 +/- 4%) and significantly decreased RCVC (n= 11, -12 +/- 3%). RCBF showed no significant changes during static contraction or passive stretch. Renal denervation abolished the decrease in RCVC during contraction (n = 12) or stretch (n = 13). These data indicate that both the exercise pressor reflex and its mechanically sensitive component, the muscle mechanoreflex, induced renal cortical vasoconstriction through sympathetic activation in rats.

This study compared cardiovascular responses to static extension and flexion exercises at four upper and lower limb joints. Eight males performed a 2 min static contraction at 30% of maximal voluntary torque followed immediately by 2 min post-exercise muscle ischaemia (PEMI) using each of four joints: the wrist, elbow, ankle, and knee. In the PEMI, an occlusion cuff placed around the proximal portion of the exercising muscle was inflated to 250 mmHg immediately before the cessation of exercise. Mean arterial pressure (MAP), heart rate (HR), calf blood flow, and calf vascular conductance (CVC) in the non-exercised calf were measured. There was a significant interaction for direction of movement (extension vs. flexion) and limb (upper vs. lower) in HR and CVC during both exercise and PEMI; extension in the wrist and elbow evoked a greater increase in HR and a greater decrease in CVC than flexion, whereas flexion in the ankle and knee elicited a greater increase in HR and a greater decrease in CVC than extension. These results suggest that the cardiovascular responses to extension and flexion differ between arms and legs, partly arising from the activation of the muscle metaboreflex.

We investigated the effect of disuse atrophy on the magnitude of the muscle mechanoreflex. The left leg of eight rats (6-7 wk, male) was put in a plaster cast for 1 wk. The rats were decerebrated at the midcollicular level. We recorded the pressor and cardioaccelerator responses to 30-s stretch of the calcaneal tendon, which selectively stimulated the muscle mechanosensitive receptors in the left atrophied and right control triceps surae muscles. Atrophied muscles showed significantly lower mass control muscles (1.0 +/- 0.1 vs. 1.4 +/- 0.1 g; P &lt; 0.05). At the same stretch tension (229 +/- 20 g), the pressor response to stretch was significantly greater in the atrophied muscles than in the control muscles (13 +/- 3 vs. 4 +/- 2 mmHg, P &lt; 0.05). The cardioaccelerator response was not significantly different (8 +/- 4 vs. 4 +/- 2 beats/min). Comparing responses at the same relative tension (57 +/- 6 vs. 51 +/- 8% of maximal tension), the pressor response was still significantly greater in the atrophied triceps surae than in the control (14 +/- 4 vs. 4 +/- 2 mmHg; P &lt; 0.05). These results suggest that disuse atrophy increases the magnitude of muscle mechanoreflex.

Static exercise has been thought to induce greater pressor response than dynamic exercise, but in contrast it has been recently reported that repetitive muscle contraction recruiting small muscles evokes greater response than sustained contraction. It remained unknown whether sustained contraction induces greater pressor response if large muscles were recruited. Nine subjects performed three types of isometric knee extensions recruiting the large muscle group, i.e., 2-min sustained (20% and 40% maximal voluntary contraction [MVC]) and 4-min repetitive (40% MVC, duty cycle = 1:1 s) muscle contractions. Compared under the equivalent TTI and exercising duration (2 min), the changes in femoral arterial blood flow and VO2 from baseline (DeltaBF, DeltaVO(2)) were significantly less during sustained contraction than during repetitive contraction (sustained vs. repetitive; DeltaBF +92 +/- 195 vs. +1, 174 +/- 269 ml.min(-1), DeltaVO(2): +53 +/- 12 vs. +180 +/- 32 ml.min(-1), mean +/- SE, p &lt; 0.05), although the change in mean arterial pressure (DeltaMAP) was greater during sustained contraction (+24 +/- 3 vs. + 19 +/- 3 mmHg). Compared under the equivalent TTI and peak tension (40% MVC), DeltaBF and DeltaVO(2) were less and DeltaMAP was greater during sustained contraction (DeltaBF: -296 +/- 176 vs. +868 +/- 272 ml.min(-1); DeltaVO(2): +104 +/- 16 vs. + 212 +/- 46 ml.min(-1): DeltaMAP: +37 +/- 8 vs. +20 +/- 4 mmHg). Moreover DeltaMAP during postexercise occlusion of the active limb was significantly greater after sustained contraction than after repetitive contraction (+17.0 +/- 2.8 vs. +9.5 +/- 4.4 mmHg). These results demonstrated that pressor response is greater during sustained than during repetitive contraction.. recruiting a large muscle group. This finding should be mainly due to the greater accumulation of metabolites in active muscles during sustained contraction.

<jats:p> I investigated whether muscular contraction evokes cardiorespiratory increases (exercise pressor reflex) in α-chloralose- and chloral hydrate-anesthetized and precollicular, midcollicular, and postcollicular decerebrated rats. Mean arterial pressure (MAP), heart rate (HR), and minute ventilation (V˙e) were recorded before and during 1-min sciatic nerve stimulation, which induced static contraction of the triceps surae muscles, and during 1-min stretch of the calcaneal tendon, which selectively stimulated mechanosensitive receptors in the muscles. Anesthetized rats showed various patterns of MAP response to both stimuli, i.e., biphasic, depressor, pressor, and no response. Sciatic nerve stimulation to muscle in precollicular decerebrated rats always evoked spontaneous running, so the exercise pressor reflex was not determined from these preparations. None of the postcollicular decerebrated rats showed a MAP response or spontaneous running. Midcollicular decerebrated rats consistently showed biphasic blood pressure response to both stimulations. The increases in MAP, HR, and V˙e were related to the tension developed. The static contractions in midcollicular decerebrated rats (381 ± 65 g developed tension) significantly increased MAP, HR, andV˙e from 103 ± 12 to 119 ± 24 mmHg, from 386 ± 30 to 406 ± 83 beats/min, and from 122 ± 7 to 133 ± 25 ml/min, respectively. After paralysis, sciatic nerve stimulation had no effect on MAP, HR, or V˙e. These results indicate that the midcollicular decerebrated rat can be a model for the study of the exercise pressor reflex. </jats:p>

We investigated the effect of muscle contraction velocity on cardiorespiratory responses during exercise. Eight males (23+/-2 years, 175+/-5cm, 64+/-6kg, mean+/-SD) performed 3-min repetitive one-leg extension exercises at various angular velocities (30, 60, 120, and 240 deg/s) with a controlled relaxation interval, relatively constant (duty cycle=1 : 1, A trial) and absolutely constant (relaxation time=0.75s, B trial) at a total work of 2,100-2,400 J in an isokinetic mode, using a Cybex 11 dynamometer. We measured heart rate (HR), mean blood pressure (MAP), minute ventilation ((V)over dotE), and oxygen uptake ((V)over dotO(2)) during the exercise. The angular velocity significantly affected the increase in HR, MAP, (V)over dotE, and (V)over dotO(2) at the end of exercise from resting in both A and B trials (e.g., MAP: 12+/-2, 10+/-2, 11+/-2, and 18+/-2 mmHg in the A trial). The result suggests that muscle contraction velocity affects cardiorespiratory responses during repetitive isokinetic exercise.

We examined whether lactic acidemia-induced hyperemia at the onset of high-intensity leg exercise contributed to the speeding of pulmonary O-2 uptake ((V) over dot O-2) after prior heavy exercise of the same muscle group or a different muscle group (i.e., arm). Six healthy male subjects performed two protocols that consisted of two consecutive 6-min exercise bouts separated by a 6-min baseline at 0 W: 1) both bouts of heavy (work rate: 50% of lactate threshold to maximal (V) over dot O-2) leg cycling (L1-ex to L2-ex) and 2) heavy arm cranking followed by identical heavy leg cycling bout (A1-ex to A2-ex). Blood lactate concentrations before L1-ex, L2-ex, and A2-ex averaged 1.7 +/- 0.3, 5.6 +/- 0.9, and 6.7 +/- 1.4 meq/l, respectively. An "effective" time constant (tau) of (V) over dot O-2 with the use of the monoexponential model in L2-ex (tau: 36.8 +/- 4.3 s) was significantly faster than that in L1-ex (tau: 52.3 +/- 8.2 s). Warm-up arm cranking did not facilitate the (V) over dot O-2 kinetics for the following A2-ex [tau: 51.7 +/- 9.7 s]. The double-exponential model revealed no significant change of primary tau (phase II) (V) over dot O-2 kinetics. Instead, the speeding seen in the effective tau during L2-ex was mainly due to a reduction of the (V) over do O-2 slow component. Near-infrared spectroscopy indicated that the degree of hyperemia in working leg muscles was significantly higher at the onset of L2-ex than A2-ex. In conclusion, facilitation of (V) over dot O-2 kinetics during heavy exercise preceded by an intense warm-up exercise was caused principally by a reduction in the slow component, and it appears unlikely that this could be ascribed exclusively to systemic lactic acidosis.

To investigate the effect of muscle relaxation time on the cardiorespiratory responses during exercise, seven subjects performed three types of one-leg knee extension exercises, which were 1) 2-min sustained muscle contraction at 20%MVC (maximal voluntary contraction), 2) 2-mm sustained contraction at 40%MVC, and 3) 4-min rhythmic contraction at 40%MVC. Blood flow and oxygen uptake were smaller and blood pressure was larger at sustained contraction than at rhythmic contraction, compared the responses between sustained and rhythmic contraction at either the equivalent tension-time index and exercising time or the equivalent tension-time index and the peak tension. This indicates that muscle relaxation time affects the cardiorespiratory responses during exercise.

In thirteen cats anesthetized with alpha -chloralose, we compared the cardiovascular and ventilatory responses to both static contraction and tendon stretch of a hindlimb muscle group, the triceps surae, with those to contraction and stretch of a forelimb muscle group, the triceps brachii. Static contraction and stretch of both muscle groups increased mean arterial pressure and heart rate, and the responses were directly proportional to the developed tension. The cardiovascular increases, however, were significantly greater (P&lt; 0.05) when the triceps brachii muscles were contracted or stretched than when the triceps surae muscles were contracted or stretched, even when the tension developed by either maneuver was corrected for muscle weight. Likewise, the ventilatory increases were greater when the triceps brachii muscles were stretched than when the triceps surae muscles were stretched. Contraction of either muscle group did not increase ventilation. Our results suggest that in the anesthetized cat the cardiovascular responses to both static contraction and tendon stretch are greater when arising from forelimb muscles than from hindlimb muscles.

We investigated the effect of muscle contraction velocity on cardiorespiratory responses during exercise. Eight subjects performed one-leg extension exercise for three minutes at the contraction velocity of 30-240 degree per second (dps) with a controlled relaxation interval (relativery constant and 0.75 S). Heart Rate, blood pressure and minute ventilation at the end of exercise were higher in 30 and 240 dps trials than in 60 and 120 dps trials. Oxygen uptake and relative intensity had the same trend. It was suggested that the muscle contraction velocity affects the cardiorespiratory responses via energy efficiency.

We investigated the effect of central hypervolaemia during water immersion up to the xiphoid process on the oxygen uptake ((V)over dot O-2) and heart rate (HR) response to arm cranking. Seven men performed a 6-min arm-cranking exercise at an intensity requiring a (V)over dot O-2 at 80% ventilatory threshold both in air [C trial, 29 (SD 9) W] and immersed in water [WI trial, 29 (SD 11) W] after 6 min of sitting. The (V)over dot O-2 (phase 2) and HR responses to exercise were obtained from a mono-exponential fit [f(t) = baseline + gain (1 - e(-(t-TD)/tau))]. The response was evaluated by the mean response time [MRT; sum of time constant (tau) and time delay (TD)]. No significant difference in (V)over dot O-2 and HR gains between the C and WI trials was observed [(V)over dot O-2 0.78 (SD 0.1) vs 0.80 (SD 0.2) l . min(-1). HR 36 (SD 7) vs 37 (SD 8) beats . min(-1), respectively]. Although the HR MRT was not significantly different between the C and WI trials [17 (SD 3), 19 (SD 8) s, respectively), (V)over dot O-2 MRT was greater in the WI trial than in the C trial [40 (SD 6), 45 (SD 6) s, respectively; P &lt; 0.05]. Assuming no difference in (V)over dot O-2 in active muscle between the two trials, these results would indicate that an increased oxygen store and/or an altered response in muscle blood distribution delayed the (V)over dot O-2 response to exercise.

We tested whether the leftward shift of the oxygen dissociation curve of hemoglobin with hyperpnea delays the oxygen uptake ((V) over dotO(2)) response to the onset of exercise. Six male subjects performed cycle ergometer exercise at a work rate corresponding to 80% of the ventilatory threshold (VT) (V)over dotO(2) of each individual after 3 min of 20-W cycling under eupnea [control (Con) trial]. A hyperpnea procedure (minute ventilation = 60 l/min) was undertaken for 2 min before and during 80% VT exercise in hypocapnia (Hypo) and normocapnia (Normo) trials. In the Normo trial, the inspired CO2 fraction was 3% to prevent hypocapnia. The subjects completed two repetitions of each trial. To determine the kinetic variables of (V) over dotO(2) and heart rate (HR) at the onset of exercise, a nonlinear least-squares fitting was applied to the data averaged from two repetitions by a monoexponential model. The end-tidal CO2 partial pressure before the onset of exercise was significantly lower in the Hypo trial than in the Con and Normo trials (22 +/- 1 vs. 38 +/- 3 and 36 +/- 1 mmHg, respectively, P &lt; 0.05). The time constant of (V) over dotO(2) and HR was significantly longer in the Normo trial (28 +/- 7 and 39 +/- 18 s, respectively) than in the Con trial (21 +/- 7, 34 +/- 16 s, respectively, P &lt; 0.05). The (V) over dotO(2) time constant of the Hypo trial (37 +/- 12 s) was significantly longer than that of the Normo trial, although no significant difference in the HR time constant was seen (Hypo, 41 +/- 28 s). These findings suggested that respiratory alkalosis delayed the kinetics of oxygen diffusion in active muscle as a result of the left;ward shift of the oxygen dissociation curve of hemoglobin. This supports an. important role for hemoglobin-O-2 off loading in setting the (V) over barO(2) kinetics at exercise onset.

The effect of delayed vagal activity withdrawal on cardiorespiratory responses at an increase in workload was examined. Eleven volunteers (21 +/- 3 yr, 66 +/- 4 kg) per formed cycle ergometer exercise at a work rate corresponding to 80% of ventilatory threshold after 3 min of unloaded cycling. Facial stimulation was given by applying a vinyl bag filled with cold water (3-5 degrees C) to the face 1 min before to 1 min after the increase in workload (S2 trial) or no stimulation was given (Nr trial). Oxygen uptake (V over dot O-2), heart rate (HR), and cardiac output (Q over dot) were continuously recorded in four transitions for each trial. Data were averaged for each subject and trial. Mean response time (MRT, sum of delay and time constant) was calculated with a monoexponential fitting. Facial stimulation induced acute bradycardia (-10 +/- 5 beats/min in S2 trial). The MRT of HR and Q over dot was significantly longer in the S2 trials (46 +/- 35 and 37 +/- 23 s) than in the Nr trials (26 +/- 18 and 28 +/- 19 s, respectively), but no significant change in V over dot O-2 MRT was shown (36 +/- 7 vs. 38 +/- 12 s). These findings suggest that increased vagal activity delays the central circulatory responses, which does not alter the V over dot O-2 kinetics at the onset of stepwise increase in workload. The maintenance of V over dot O-2 kinetics during acute bradycardia may either reflect the fact that some intramuscular processes (such as oxidative enzyme inertia) limit V over dot O-2 kinetics or alternatively that increased sympathetic vasoconstriction at some remote site defends exercising muscle blood flow.

We examined whether the diving reflex without breath-holding (face immersion alone) increases vagal activity, as determined by heart rate variability. A group of 15 men [mean age 20 (SD 3) stars, height 172 (SD 5) cm, body mass 68 (SD 9) kg] performed 12 trials tit various breathing frequencies (5 10, 15, 20, 30 breaths.min(-1) and uncontrolled breath) with or without face immersion. The R-R intervals of the ECG and gas exchange variables were recorded during the 2 min of each trial. The subjects immersed their faces in 8-10 degrees C water while breathing through a, short snorkel. The subject sat in the same position either with or without face immersion, The mean R-R interval (RRmean), standard deviations (SDRR) and coefficient of variance (CVRR) Of the R-R interval were calculated from the R-R intervals during 30-120 s. The face immersion significantly increased SDRR and CVRR (P &lt;0.05), and increased RRmean (P &lt; 0.05) at 20 breaths min Face immersion itself had no effect on oxygen uptake, tidal volume, end-tidal O-2 and CO2 partial pressures. The diving reflex without breath-holding increased the heart rate variability, indicating that face Immersion alone increases vagal activity.

A study was conducted to investigate the effect of exercise intensity on the recovery of autonomic nervous activity after exercise. Ten subjects performed four kinds of 10–min cycle exercise with target heart rates of 100, 120, 140, and 160beats/min (THR 100, THR 120, THR 140 and THR 160, respectively) following 5 min of exercise to increase the heart rate to the target level. The beat-by-beat variability of the R–R interval was recorded throughout the experiment including the 5-min pre-exercise control period and the 30-min recovery period. Spectral analysis (fast Fourier transform) was applied to every 5-min R-R interval data set before, during (5 —10 min) and after exercise at the target heart rate. The low- (0.05 ∼ 0.15 Hz : P1) and high- (0.15 ∼ 1.0 Hz : Ph) frequency areas were calculated to evaluate sympathetic (SNS) and parasympathetic (PNS) nervous activities as P1/Ph and Ph, respectively. During exercise, SNS of THR 160 was significantly higher, and PNS of THR 140 and THR 160 was significantly lower than the respective pre-exercise values (p&lt
0.05). Although all indicators recovered to, or overshot the pre-exercise values at 20∼30 min after THR 100 and THR 120, heart rate and SNS were still higher and PNS was still lower than the pre-exercise value after THR 160. These results suggest that the recovery of cardiac autonomic nervous activity is slower after high-intensity exercise than after low-intensity exercise, and that the recovery of autonomic nervous activity after acute exercise does not always corrrespond linearly on the exercise intensity. © 1995, The Japanese Society of Physical Fitness and Sports Medicine. All rights reserved.

A study was conducted to investigate the effect of exercise intensity on the recovery of autonomic nervous activity after exercise. Ten subjects performed four kinds of 10–min cycle exercise with target heart rates of 100, 120, 140, and 160beats/min (THR 100, THR 120, THR 140 and THR 160, respectively) following 5 min of exercise to increase the heart rate to the target level. The beat-by-beat variability of the R–R interval was recorded throughout the experiment including the 5-min pre-exercise control period and the 30-min recovery period. Spectral analysis (fast Fourier transform) was applied to every 5-min R-R interval data set before, during (5 —10 min) and after exercise at the target heart rate. The low- (0.05 ∼ 0.15 Hz : P1) and high- (0.15 ∼ 1.0 Hz : Ph) frequency areas were calculated to evaluate sympathetic (SNS) and parasympathetic (PNS) nervous activities as P1/Ph and Ph, respectively. During exercise, SNS of THR 160 was significantly higher, and PNS of THR 140 and THR 160 was significantly lower than the respective pre-exercise values (p&lt
0.05). Although all indicators recovered to, or overshot the pre-exercise values at 20∼30 min after THR 100 and THR 120, heart rate and SNS were still higher and PNS was still lower than the pre-exercise value after THR 160. These results suggest that the recovery of cardiac autonomic nervous activity is slower after high-intensity exercise than after low-intensity exercise, and that the recovery of autonomic nervous activity after acute exercise does not always corrrespond linearly on the exercise intensity. © 1995, The Japanese Society of Physical Fitness and Sports Medicine. All rights reserved.

The purpose of this study was to investigate the recovery kinetics of cardiac autonomic regulation after acute exercises related to exercise intensity. Firstly, eight healthy subjects performed two kinds of constant load exercises at the work rate corresponding to 20 % and 100 % of the individual ventilatory threshold (VT) in addition to the exhaustive incremental exercise using a cycle ergometer. Blood pressure (BP) and oxygen uptake (VO_2) were measured during 9 to 10 min after the exercises as well as the beat-by-beat recording of R-R intervals. Coarse graining spectral analysis (CGSA) was applied to heart rate variability (HRV) data sets of 5 min before exercise, Iast 5 min during exercise, and 8 to 10 min after exercise. The low frequency (O - 0.15 Hz ; LO) and the high frequency (0.15-0.5 Hz : HI) areas under power spectra were calculated for evaluating sympathetic (LO/HI) and vagal (HI) activities. The recovery for 10 min was sufficient to settle both VO_2 and BP even after the exhaustion. Comparing to the pre-exercise value, however, HI was still suppres-sed until 10 min after the 100 % VT exercise (522±300 vs. 122±63 msec^2, p<0.05) while it was recovered at 10 min after the 20 % VT one (353±122 vs. 487±159 msec^2). Secondly, six healthy subjects performed an incremental cycle exercise until exhaustion. The R-R intervals were monitored beat-by-beat during 30 min after exercise. The CGSA was applied to every five min data set of HRV during recovery phase. Comparing to pre-exercise value, the R-R interval was not recovered at 30 min after the exercise (827±44 vs. 597±17 msec). The HI value was still significantly lower (367±154 vs. 24±14 msec^2) and the LO/HI was also higher (3.8±0.9 vs. 16.8±5.1, p<0.05) during 25 to 30 min after the exercise. These results suggest that the recovery of the cardiac autonomic regulation especially after a moderate to high intensity exercise was later than those of the peripheral circulation as well as the oxygen uptake.