顔面の皮膚血流が，味覚などの情動に伴って変化する．顔面の皮膚血流の反応からスポーツ動作イメージ中の不安場面を抽出することが可能であると予想した．バレーボール選手に1人称および3人称で，アンダーハンドおよびフローターのサーブ動作をイメージさせた際の顔面の皮膚血流を計測した．被験者が動作イメージを鮮明に得られた場合には，瞼部の血流増加反応が大きかった．この反応が他のスポーツの動作でも得られるのか，またスポーツの習熟に応じて増加反応が顕著になるのかについて検討すれば，動作イメージ時の顔面皮膚血流応答の記録から，得手・不得手場面を抽出することが可能になると考えられる．

我々は，おいしいと感じると瞼の血流が増加し，まずいと感じると鼻の血流が低下することを報告した．顔面血流から味覚を容易に判別することが可能かを検討するために，男女89名を対象に，おいしい飴とまずい飴をなめた際の顔面皮膚血流を簡易的に記録した．特異的な変化はなく，いわゆる実験環境以外で味覚を判別するのは困難であった．次に，皮膚血流に部位差が表れる要因を解明するため，顔に温度刺激を与えた．頬，額では，温度変化に伴い血流が変化した一方，瞼では温熱に伴う血流増加はなく，鼻でも冷却に伴う血流減少はなかった．顔面皮膚血流の特異的応答は，血管の拡張・収縮の容易さではなく，神経性因子によるものと示唆された．

上肢・下肢単独運動と，両者を組み合わせた上下肢同時運動を，サイン波・ステップ負荷の２つの運動様式で組み合わせ，呼吸循環系応答を検討した。結果は，最大下の運動である限り，上下肢同時運動の応答は，基本的には，上・下肢の単独運動での応答を加算した関係にあることがわかった。次に，下肢サイン波状運動時の呼吸循環系応答特性を，特に脳と非運動肢への血流調節に注目して検討した。その結果，両血流応答共にサイン波状応答は示すものの，脳血流はほぼ一定に維持されていたのに対して，上肢への血流は大きな振幅を伴う逆位相応答が認められ，筋血流も含め他の部位，臓器への血流配分とは異なる調節を受けていることがわかった。

眼底は，身体内で唯一非侵襲的に直接観察可能な動脈・血管を含んでいる．本研究では，簡便に眼底の血管や血流を記録して，血管の硬化を判定する手法を探索した．スマートフォンを用いる最も簡易な解析は困難であることが分かった．一方，レーザースペックル血流計を用いて眼底血管を撮影し，血流波形を解析したところ，加齢に伴い血流波形が変化することが示された．また，動脈硬化の標準的な指標である頸動脈内膜中膜複合体厚との相関関係も観察された．これらのことから，眼底の血流を記録することによって，加齢に伴う血管の硬化が判定できる可能性が示唆された．

本研究で作成した発達的修学困難チェックシートなどの簡便なチェックシートを、大学入学時に用いることが、発達障害傾向を有する学生への支援の糸口になる可能性が示唆された。特に、保護者の回答や相談希望の有無は、非常に重要であることが分かった。発達的修学困難チェックシートの高得点者では、ストレスを感じやすく不規則な生活になりやすいものの、発達障害傾向は大学での低単位や退学等の問題に直接的には影響していないことが明らかとなった。また、チェックシートの得点には、発達障害傾向だけでなく不安や自信なさが影響している場合や、低得点者でも発達障害を有する場合もあり、質問紙だけでは把握できない部分があることが伺えた。

顔や顔色には様々な情動に関連した変化が予想される．そこで，顔の皮膚血流にも情動に特異的な変化があるという仮説を検証した．幸福，悲しみ，恐怖，驚き，怒りを起こすビデオを視聴した際の顔面皮膚血流を計測したものの，特異的な皮膚血流の変化を示す部位はなかったことから，顔面皮膚血流から情動をとらえることは現段階では困難であることが推察された．今後強い情動を起こすような手段を用いた検討が必要かもしれない．

本研究では，活動のパターンから大学生の気分障害の程度を判定することが可能であるかについて検討することを目的とした．
まず，市販され標準的に利用されている活動量計を研究に利用できるかを検討するために，比較的安価なO社製のデバイスを腰につけ，比較のために高価なA社製のアクチグラフを非利き腕につけた１～２日間にわたる同時計測を，学生6名に実施した．両デバイスの日中のデータの単相関は低かった．このことから，O社のデバイスによって日中の不活動を計測することは困難であると判断した．そこで，当初行うことにしていた比較的安価な活動量計を用いた大規模前向き調査を行うことは中止することとした．

昼食後の眠気による作業効率低下対策として知られている短時間仮眠が，その後の運動パフォーマンスやそれを支える基礎的な生理機能に与える効果について，包括的かつ実践的な検討を行った。結果として，１）昼食後に睡眠ステージ２までの浅い短時間仮眠（napと呼ばれ，10-20分程度）をとると，覚醒したまま安静で過ごすよりも，スポーツ競技時に必要と想定される脳の情報処理能力や視力に正の効果がありそうであること，２）昼食後に睡眠ステージ４まで含む１時間程度のより深い仮眠をとると，安静やnapをとる過ごし方よりも，無酸素性最大発揮パワーに正の効果がありそうであること，の２点が示唆された。

本研究の目的は,ヒトの身体活動を支える有酸素性作業能力評価のための運動テストにおける,新たな負荷方法を検討し,開発することであった。結果として2つの新たな負荷方法が提案された。1)日常の身体活動を模したような,非定常状態の連続であるサイン波状に運動負荷が変動する運動を用いる方法, 2)指数関数的に負荷が漸増する運動を用いる方法,であった。特にサイン波状負荷運動テストについては,基礎的ならびに実用的な視点から詳細な検討を加え,新たな具体的手法が提案された。

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.

唾液αアミラーゼ活性を用いたストレス評価の有用性を明らかにするために、大学生と事務系企業社員を対象として、種々のストレス負荷やリラクセーションの際の変動、入社後の変化や日常の職業性ストレスとの関係、職業生活における長期的な個人内変動などの観点から、唾液αアミラーゼ活性について検討した。厳密な安静や頻回な測定などの条件下では、唾液αアミラーゼ活性とストレスとの関連が認められた。しかし、測定値の個人差が大きく、個人内変動も少なくないことが問題であり、横断的調査よりも縦断的調査のストレス評価指標とする方が妥当と考えられた。

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.

近年,主に動物実験に基づいて,従来は運動時循環系調節でその重要性が指摘される筋内化学受容器に加えて,血管壁への機械的な刺激を介した血液還流状態などの筋内機械受容器情報が,運動時の換気亢進に寄与する可能性が示唆されている。そこで本研究では,この仮説について,ヒト運動時を対象に実験的な証拠を提出することを目的として,以下に述べるような実験を行い,その検証を試みた。1:運動終了直後の回復期に焦点をあて,運動肢に持続的あるいはリズミックな圧迫刺激を与えることで筋機械受容器を刺激し,その時の換気応答を観察した,2:水平位のチルト台上での運動終了時にあわせてすばやく姿勢を立位に変化させることによって下肢の特に静脈系へ血液貯留を起こすプロトコールを行って,その時の換気応答を観察した,3:運動開始前に過換気を行い運動肢内の末梢血管収縮を起こした条件のもとで運動を開始し,その際に観察される換気亢進抑制が,運動肢内の血液環流低下と関連したものか否かを検討した。これら一連の実験結果は,一部のデータは仮説を支持し,一部は逆に支持しないという相反したものであった。本研究の仮説にはさらなる実験的な検討が必要であるが,もしも実証されれば,そのシステム特性への理解が進み,運動時の循環調節の研究者にも大きなインパクトをもつと思われる。さらに,運動に直接かかわっている筋内の血流還流状態の程度や筋収縮の程度を機械的な情報としてモニタし,それと換気亢進が連関しているという考え方は合目的で理解しやすく運動時の生体調節機構解明という身体システム科学の中の1つの研究領域に,新たな展開を促す引き金になると予想される。

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.

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±8kg, 36 females 51±4kg, 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 (1RM) 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, ...

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.

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.

本研究では,運動時の筋弛緩時間の有無が呼吸循環系の応答に与える影響を検討した.7名の健常被験者が3種類の等尺性片脚膝伸展運動((1)筋弛緩時間のない2分間の20%最大随意筋収縮,(2)筋弛緩時間のない2分間の40%最大随意筋収縮,(3)筋弛緩時間がある4分間の40%最大随意筋収縮(1秒収縮1秒弛緩))をそれぞれ行った.運動負荷(力積)と運動時間が同じ場合,また運動負荷と筋力ピーク値が同じ場合の応答を比較した結果,筋弛緩時間がない試行では,筋弛緩時間がある試行よりも,運動時の酸素摂取量,脚への血流は小さく,昇圧応答は大きかった.このことから,筋弛緩時間の有無が運動時の呼吸循環系の応答に影響を与えることが示された.これは,静的・動的運動時の応答の特徴を説明するものである.

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.

呼吸循環系の応答に対する筋収縮速度の影響を検討するため、被験者8名に同一仕事量となるような3分間の片脚伸展運動を行わせた。4種類の脚伸展速度(30〜240度/秒)と、2種類の脚屈曲(筋弛緩)時間を組み合わせて8試行行わせた。その結果、脚屈曲時間の違いに関わらず、脚伸展速度が30、240度/秒の試行での応答が大きかった。最大筋力に対する相対的仕事率は30度/秒の試行で大きく、酸素摂取量は30、240度/秒の試行で大きかった。これらのことから、応答の違いは相対的仕事率の違いに主に起因することが示唆された。また、同じ筋収縮速度でも筋弛緩時間の違いが応答に影響したことから、筋弛緩時間は呼吸循環系に影響を及ぼすことが示唆された。

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.

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.