宮本 忠吉

Since humans are under ceaseless orthostatic stress, the mechanism to maintain arterial pressure (AP) under orthostatic stress against gravitational fluid shift is of great importance. We hypothesized that (1) orthostatic stress resets the arterial baroreflex control of sympathetic nerve activity (SNA) to a higher SNA, and (2) resetting of the arterial baroreflex contributes to preventing postural hypotension. Renal SNA and AP were recorded in eight anaesthetized, vagotomzed and aortic-denervated rabbits. Isolated intracarotid sinus pressure (CSP) was increased stepwise from 40 to 160 mmHg with increments of 20 mmHg (60 s for each CSP level) while the animal was placed supine and at 60 deg upright tilt. Upright tilt shifted the CSP-SNA relationship (the baroreflex neural arc) to a higher SNA, shifted the SNA-AP relationship (the baroreflex peripheral arc) to a lower AP, and consequently moved the operating point to marked high SNA while maintaining AP. A simulation study suggests that resetting in the neural arc would double the orthostatic activation of SNA and increase the operating AP in upright tilt by 10 mmHg, compared with the absence of resetting. In addition, upright tilt did not change the CSP-AP relationship (the baroreflex total arc). A simulation study suggests that although a downward shift of the peripheral arc could shift the total arc downward, resetting in the neural arc would compensate this fall and prevent the total arc from shifting downward to a lower AP. In conclusion, upright tilt increases SNA by resetting the baroreflex neural arc. This resetting may compensate for the reduced pressor responses to SNA in the peripheral cardiovascular system and contribute to preventing postural hypotension.

Background - Despite the accumulated knowledge of human muscle sympathetic nerve activity (SNA) as measured by microneurography, whether muscle SNA parallels renal and cardiac SNAs remains unknown. Method and Results - In experiment 1, muscle ( microneurography, tibial nerve), renal, and cardiac SNAs were recorded in anesthetized rabbits ( n = 6) while arterial pressure was changed by intravenous bolus injections of nitroprusside ( 3 mu g/kg) followed by phenylephrine ( 3 mu g/kg). In experiment 2, the carotid sinus region was vascularly isolated in anesthetized, vagotomized, and aorta-denervated rabbits ( n = 10). The 3 SNAs were recorded while intracarotid sinus pressure was increased stepwise from 40 to 160 mm Hg in 20-mm Hg increments maintained for 60 seconds each. Muscle SNA averaged over 1 minute was well correlated with renal ( r = 0.96 +/- 0.01, mean +/- SE) and cardiac ( r = 0.96 +/- 0.01) SNAs in experiment 1 (baroreflex closed-loop condition) and also with renal ( r = 0.97 +/- 0.01) and cardiac ( r = 0.97 +/- 0.01) SNAs in experiment 2 ( baroreflex open-loop condition). Conclusions - Muscle SNA averaged over 1 minute parallels renal and cardiac SNAs in response to a forced baroreceptor pressure change.

The chemoreflex system controlling ventilation consists of two subsystems, i.e., the central controller ( controlling element), and peripheral plant ( controlled element). We developed an integral framework to quantitatively characterize individual ventilatory regulation by experimental determination of an equilibrium diagram using a modified metabolic hyperbola and the CO2 response curve. In 13 healthy males, the steady-state arterial CO2 pressure (PaCO2) and minute ventilation ((V) over dot(E)) were measured. To characterize the central controller, we changed fraction of inspired CO2 (0, 3.5, 5 and 6% CO2 in 80% oxygen with nitrogen balance) and measured the PaCO2-(V) over dot(E) relation. To characterize the peripheral plant, we altered (V) over dot(E) by hyper- or hypoventilation using a visual feedback method, which made it possible to control both tidal volume and breathing frequency, and measured the (V) over dot(E)-PaCO2 relation. The intersection between the two relationship lines gives the operating point. The relationship between PaCO2 and (V) over dot(E) for the central controller was reasonably linear in each subject (r(2) = 0.808 similar to 0.995). The peripheral plant approximated a modified metabolic hyperbolic curve (r(2) = 0.962 similar to 0.996). The operating points of the system estimated from the two relationship lines were in good agreement with those measured under the closed-loop condition. The gain of the central controller was 1.9 (1.0) l min(-1) mmHg(-1) and that of the peripheral plant was 3.0 (0.5) mmHg l(-1) min(-1). The total loop gain, the product of the two gains, was 5.3 (2.5). We conclude that human ventilatory regulation by the respiratory chemoreflex system can be quantitatively characterized using an equilibrium diagram. This framework should be useful for understanding the mechanisms responsible for abnormal ventilation under various pathophysiological conditions.

Neuronal uptake is the most important mechanism by which norepinephrine ( NE) is removed from the synaptic clefts at sympathetic nerve terminals. We examined the effects of neuronal NE uptake blockade on the dynamic sympathetic regulation of the arterial baroreflex because dynamic characteristics are important for understanding the system behavior in response to exogenous disturbance. We perturbed intracarotid sinus pressure (CSP) according to a binary white noise sequence in anesthetized rabbits, while recording cardiac sympathetic nerve activity (SNA), arterial pressure (AP), and heart rate (HR). Intravenous administration of desipramine ( 1 mg/kg) decreased the normalized gain of the neural arc transfer function from CSP to SNA relative to untreated control (1.03 +/- 0.09 vs. 0.60 +/- 0.08 AU/mmHg, mean +/- SE, P < 0.01) but did not affect that of the peripheral arc transfer function from SNA to AP (1.10 +/- 0.05 vs. 1.08 +/- 0.10 mmHg/AU). The normalized gain of the transfer function from SNA to HR was unaffected (1.01 +/- 0.04 vs. 1.09 +/- 0.12 beats center dot min(-1) center dot AU(-1)). Desipramine decreased the natural frequency of the transfer function from SNA to AP by 28.7 +/- 7.0% (0.046 +/- 0.007 vs. 0.031 +/- 0.002 Hz, P < 0.05) and that of the transfer function from SNA to HR by 64.4 +/- 2.2% (0.071 +/- 0.003 vs. 0.025 +/- 0.002 Hz, P < 0.01). In conclusion, neuronal NE uptake blockade by intravenous desipramine administration reduced the total buffering capacity of the arterial baroreflex mainly through its action on the neural arc. The differential effects of neuronal NE uptake blockade on the dynamic AP and HR responses to SNA may provide clues for understanding the complex pathophysiology of cardiovascular diseases associated with neuronal NE uptake deficiency.

The effects of the muscle mechanoreflex on the arterial baroreflex neural control have not previously been analyzed over the entire operating range of the arterial baroreflex. In anesthetized, vagotomized, and aortic-denervated rabbits (n = 8), we isolated carotid sinuses and changed intracarotid sinus pressure (CSP) from 40 to 160 mmHg in increments of 20 mmHg every minute while recording renal sympathetic nerve activity (SNA) and arterial pressure (AP). Muscle mechanoreflex was induced by passive muscle stretch ( 5 kg of tension) of the hindlimb. Muscle stretch shifted the CSP-SNA relationship ( neural arc) to a higher SNA, whereas it did not affect the SNA-AP relationship ( peripheral arc). SNA was almost doubled [ from 63 +/- 15 to 118 +/- 14 arbitrary units (au), P < 0.05] at the CSP level of 93 +/- 8 mmHg, and AP was increased ∼ 50% by muscle stretch. When the baroreflex negative feedback loop was closed, muscle stretch increased SNA from 63 +/- 15 to 81 +/- 21 au ( P < 0.05) and AP from 93 +/- 8 to 109 +/- 12 mmHg ( P < 0.05). In conclusion, the muscle mechanoreflex resets the neural arc to a higher SNA, which moves the operating point towards a higher SNA and AP under baroreflex closed-loop conditions. Analysis of the baroreflex equilibrium diagram indicated that changes in the neural arc induced by the muscle mechanoreflex might compensate for pressure falls resulting from exercise-induced vasodilatation.

To better understand the pathophysiological significance of high plasma norepinephrine (NE) concentration in regulating heart rate (HR), we examined the interactions between high plasma NE and dynamic vagal control of HR. In anesthetized rabbits with sinoaortic denervation and vagotomy, using a binary white noise sequence (0-10 Hz) for 10 min, we stimulated the right vagus and estimated the transfer function from vagal stimulation to HR response. The transfer function approximated a first-order low-pass filter with pure delay. Infusion of NE (100 mug.kg(-1).h(-1) iv) attenuated the dynamic gain from 6.2 +/- 0.8 to 3.9 +/- 1.2 beats.min(-1).Hz(-1) (n = 7, P < 0.05) without affecting the corner frequency or pure delay. Simultaneous intravenous administration of phentolamine (1 mg.kg(-1).h(-1)) and NE (100 mu g.kg(-1).h(-1)) abolished the inhibitory effect of NE on the dynamic gain (6.3 +/- 0.8 vs. 6.4 +/- 1.3 beats.min(-1).Hz(-1), not significant, n = 7). The inhibitory effect of NE at infusion rates of 10, 50, and 100 mu g.kg(-1).h(-1) on dynamic vagal control of HR was dose-dependent (n = 5). In conclusion, high plasma NE attenuated the dynamic HR response to vagal stimulation, probably via activation of alpha-adrenergic receptors on the preganglionic and/or postganglionic cardiac vagal nerve terminals.

Static characteristics of the baroreflex neural arc from pressure input to sympathetic nerve activity (SNA) show sigmoidal nonlinearity, whereas its dynamic characteristics approximate a derivative filter where the magnitude of SNA response becomes greater as the input frequency increases. To reconcile the static nonlinear and dynamic linear components, we examined the effects of input amplitude on the apparent linear transfer function of the neural arc. In nine anesthetized rabbits, we perturbed isolated carotid sinus pressure by using binary white noise while varying the input amplitude among 5, 10, 20, and 40 mmHg. With increasing input amplitude, the transfer gain at 0.01 Hz decreased from 1.21+/-0.27 to 0.49+/-0.28 arbitrary units/mmHg (P<0.01). Moreover, the slope of the transfer gain between 0.03 and 0.3 Hz decreased from 14.3 +/- 3.7 to 6.5 +/- 2.5 dB/decade (P<0.01). We conclude that the model consisting of a sigmoidal component following rather than preceding a derivative component explains the observed results and thus can be used as a first approximation of the overall neural arc transfer characteristics.

The purpose of this study was to examine the relation ships among muscle oxygenation level measured by a near-infrared spectroscopy (NIRS), blood lactate concentration (La) and substrate utilization during a prolonged 60-min steady-state exercise below the anaerobic threshold (AT). Ten healthy adult subjects (3 males and 7 females) completed an orientation trial, a maximal exercise test, and a submaximal exercise for 60 min. The oxygenated hemoglobin and myoglobin saturation (muscle oxygenation level) measured by NIRS was recorded continuously throughout the tests. The probe was located on the vastus lateralis muscle. At 30 mm after exercise, the calibration of NIRS was performed by the cuff occlusion at 260 mmHg for 10 min. The relative change in muscle oxygenation level was estimated by regarding muscle oxygenation level in the resting condition as 0% and that obtained during thigh occlusion as - 100%. Oxygen consumption (V^^・O_2), carbon dioxide production (V^^・CO_2), minute ventilation (V^^・E), respiratory exchange ratio (RER), heart rate (HR) and La were measured at rest and during exercise. Muscle oxygenation level decreased immediately after the onset of exercise and gradually increased from -24.2±10.8% at 5 min to -3.3± 11.8% at 60 min. From 10 to 60 min, muscle oxygenation level increased by 11.6±3.9% with a significant increase in total hemoglobin. Muscle oxygenation level indicated the balance between oxygen delivery and oxygen utilization. Therefore, the gradual increase in muscle oxygenation level during the prolonged cycle exercise may be affected by more increase in O_2 de livery to exercising muscles than O_2 utilization. From 10 to 60 min, La and RER significantly decreased while the muscle oxygenation level increased. Therefore, Change in muscle oxygenation level between 10 and 60 min was correlated with bothΔLa (r=-0.66, P<0.05) andΔRER (r=-0.71, P<0.05). These results indicated that increase in muscle oxygenation level might facilitate blood lactate disposal and fat oxidation during the prolonged exercise below AT.

Despite the importance of vagal control over the ventricle, little is known regarding vagal efferent conduction and nerve terminal function in the postischemic myocardium. To elucidate postischemic changes in the cardiac vagal efferent neuronal function, we measured myocardial interstitial acetylcholine (ACh) levels by using in vivo cardiac microdialysis and examined the ACh responses to electrical stimulation of the vagi or local administration of ouabain in anesthetized cats. Sixty-minute occlusions of the left anterior descending coronary artery (LAD) followed by 60-min reperfusion abolished electrical stimulation-induced ACh release (20.4 +/- 3.9 vs. 0.9 +/- 0.4 nmol/l; means +/- SE, P &lt; 0.01). In different groups of animals, 60-min LAD occlusion followed by 60-min reperfusion decreased but did not completely abolish ouabain-induced release of ACh (9.2 +/- 1.8 vs. 3.9 +/- 0.7 nmol/l; P &lt; 0.05). These results indicate that function of the vagal efferent axon was completely interrupted, whereas the local ACh release was partially suppressed in the postischemic myocardium. The postischemic disruption of vagal efferent neuronal function might exert deleterious effects on cardiac regulation.

A transfer function from baroreceptor pressure input to sympathetic nerve activity (SNA) shows derivative characteristics in the frequency range below 0.8 Hz in rabbits. These derivative characteristics contribute to a quick and stable arterial pressure (AP) regulation. However, if the derivative characteristics hold up to heart rate frequency, the pulsatile pressure input will yield a markedly augmented SNA signal. Such a signal would saturate the baroreflex signal transduction, thereby disabling the baroreflex regulation of AP. We hypothesized that the transfer gain at heart rate frequency would be much smaller than that predicted from extrapolating the derivative characteristics. In anesthetized rabbits (n = 6), we estimated the neural arc transfer function in the frequency range up to 10 Hz. The transfer gain was lost at a rate of -20 dB/decade when the input frequency exceeded 0.8 Hz. A numerical simulation indicated that the high-cut characteristics above 0.8 Hz were effective to attenuate the pulsatile signal and preserve the open-loop gain when the baroreflex dynamic range was finite.

We examined whether the ACh concentration measured by cardiac microdialysis provided information on left ventricular ACh levels under a variety of vagal stimulatory and modulatory conditions in anesthetized cats. Local administration of KCl (n = 5) and ouabain (n = 7) significantly increased the ACh concentration in the dialysate to 4.3 +/- 0.8 and 7.3 =/- 1.3 nmol/l, respectively, from the baseline value of 0.6 +/- 0.5 nmol/l. Intravenous administration of phenylbiguanide (n = 5) and phenylephrine (n = 6) significantly increased the ACh concentration to 5.4 +/- 0.9 and 6.0 +/- 1.5 nmol/l, respectively, suggesting that the Bezold-Jarisch and arterial baroreceptor reflexes affected myocardial ACh levels. Modulation of vagal nerve terminal function by local administration of tetrodotoxin (n = 6), hemicholinium-3 (n = 6), and vesamicol (n = 5) significantly suppressed the electrical stimulation-induced ACh release from 20.4 +/- 3.9 to 0.6 +/- 0.1, 7.2 +/- 1.9, and 2.7 +/- 0.6 nmol/l, respectively. Increasing the heart rate from 120 to 200 beats/min significantly reduced the myocardial ACh levels during electrical vagal stimulation, suggesting a heart rate-dependent washout of ACh. We conclude that ACh concentration measured by cardiac microdialysis provides information regarding ACh release and disposition under a variety of pathophysiological conditions in vivo.

一過性の中心血液量の増加は運動に対応する心循環系の調節機構に影響を及ぼし,運動負荷(強度レベル×時間)による生理学的ストレスを軽減する可能性が示唆された.それは,高強度運動レベルよりも低強度運動レベルで,顕著であることが示された

<jats:p>We propose a current confinement structure which can be self-formed by thermal annealing of a electrode metal with a self-aligning process. The migrated metal selectively destroys an AlAs/InP tunnel junction to form a high resistance isolation layer. The hole current can be injected through a preserved tunnel junction window. We confirmed its lateral confinement effect from the near-field pattern of fabricated GaInAsP/InP stripe lasers. The proposed current confinement structure is very simple and useful for the lateral injection in semiconductor optical devices including long-wavelength vertical-cavity surface-emitting lasers.</jats:p>

We demonstrate InP-based long-wavelength lasers with an AlAs/InP tunnel junction prepared in the upper cladding of a standard laser structure to convert electron current supplied by the upper n-electrode to hole current. A carbon auto-doped AlAs layer was employed as a heavy p-type layer required for the tunnel junction. The tunnel junction diode showed a small electrical resistance under a reverse-biased condition. In addition, a negative differential resistance characteristic was clearly observed under a forward-biased condition. The introduction of such a tunnel junction can eliminate the p-electrode which normally exhibits a high resistivity in InP-based lasers. In the fabricated lasers with tunnel junctions, it was observed that the tunnel junction can enhance lateral current spreading due to low resistance in the n-layer. The proposed structure for hole sources may be useful for reducing the resistance and homogenizing the carriers in the active region of long-wavelength vertical-cavity surface-emitting lasers (VCSEL).

A study was conducted to establish a method for quantitative evaluation of both the rate and degree of muscle oxygenation during ramp exercise using Near Infrared Spectroscopy (NIRS), and to determine the relationship of the indices to body composition and physical fitness. The subjects were 13 healthy men. After a warm-up period of 3 min at 20-W, the ramp exercise test was conducted. The exercise consisted of an increasing work rate at a slope of 20 W/min on a cycle ergometer performed until volitional fatigue. The NIRS probe used in the cycling exercise was placed on the vastus lateralis muscle. After 30 min of exercise, calibration was performed by cuff occlusion for 10 min with a pressure of 260 mmHg for quantitative determination of the NIRS curve. The oxygenation curve measured by NIRS during the exercise initially exhibited a linear decrease as the work rate increased. This rate of decrease in oxygenation was indicated by the NIRS slope (%/W) obtained from the calibration curve. In later stages of the exercise, the NIRS curve became flattened with increased work rate. The breaking point between the sloping phase and the flat phase was named the "NIRS Threshold 2, NT 2". In addition, the rate of decrease in oxygenation at the end of exercise per maximal NIRS decrease obtained from the calibration curve was indicated as the %NIRS fall. The mean NIRS slope and %NIRS fall were 0.3±0.1%/W (range, 0.13 to 0.50%/W) and 29.9±11.8% (range, 12.0 to 50.0%), respectively. NT 2 was observed in 8 of the 13 subjects. The subjects were divided into two groups (NT 2 (+) and NT 2 (-) ) based on the appearance of NT 2. Both the NIRS slope and %NIRS fall in the NT 2 (+) group were significantly higher than those in the NT 2 (-) group. The NIRS slope was significantly correlated with VO₂/wt at VT (r=0.73, p<0.05) and wattage at VT (r=0.86, p<0.0001) . The %NIRS fall was significantly correlated with VO₂/wt at peak (r=0.80, P<0.001) . The NIRS slope and %NIRS fall were not significantly correlated with body mass index, %fat or thigh circumference.<BR>These findings suggest that the NIRS slope indicates the efficiency of oxygen exchange in muscles activated during incremental exercise, and that the %NIRS fall indicates the ability to utilize Oxy-Hb+Mb against maximal oxygenation capacity in muscles. The NIRS slope and %NIRS fall can therefore be used as indices of muscular limitation during exercise, and as indices of muscular adaptation during exercise.

ランプ負荷運動中における筋内酸素動態に生じる低下反応(NIRS slope)と屈曲点(NT2)を用いて,吸入気ガス濃度(標準ガス,16%O2,40%O2濃度の酸素)の差が酸素動態に及ぼす影響について検討した.活動筋内のNIRS slopeは吸入気ガス濃度の影響を受けないが,酸素交換率の限界(NT2)に達する迄の時間は,低酸素吸入により早められることが明らかになった

健常男性19名を対象に漸増負荷検査を施行した.運動時の換気及びガス交換諸量の変化から無酸素性作業閾値(AT)及び呼吸性代償点(RC)を決定し,RCが検出された群(RC群;12名)と検出されなかった群(Non-RC群;7名)に分けた.同じ換気量(VE)のレベルでの運動中と回復期での一回換気量(VT)の差の平均を示すΔVTは,RC群がNon-RC群よりも高値を示し,RC群では回復期にVTが少なく,呼吸数(f)が多い浅速型の呼吸パターンを呈した.回復期の酸素摂取量(VO2)のfast-コンポーネントでの時定数[τVO2(f)]はRC群がNon-RC群よりも有意に延長したが,VO2のslow-コンポーネントでの時定数には両群間で有意差がなかった.運動終了10分後のVE/VO2の値から安静レベルの値を引いたΔVE/VO2についても,RC群が有意に高値を示した.ΔVTとτVO2(f)及びΔVE/VO2との間にそれぞれ有意な相関が認められた

A study was performed to clarify the effects of endurance training above the anaerobic threshold (AT) on the isocapnic buffering phase during incremental exercise in athletes. Eight middle-distance runners aged 19.6 +/- 1.2 years performed incremental exercise testing with a modified version of Bruce's protocol. After a 6-month high-intensity interval and paced running training at levels above AT, maximal oxygen uptake ((V) over dotO(2)max) (ml . kg(-1) . min(-1)) was significantly increased from 60.1 +/- 5.7 to 64.7 +/- 5.5 (p&lt;0.05). AT (m . lkg(-1) . min(-1)) was slightly but significantly increased from 28.2 +/- 3.5 to 29.6 +/- 4.3 (p &lt;0.05). The respiratory compensation point (RC) (ml . kg(-1) . min(-1)) was markedly increased from 53.0 +/- 8.3 to 57.7 +/- 8.2 (p&lt;0.05). Although neither the slope of the first regression line below AT (S 1) nor that of the second line above AT (S 2) calculated by V-slope analysis was altered, the range of isocapnic buffering (ml . kg(-1) . min(-1)) from AT to RC was significantly extended from 24.8 +/- 5.9 to 28.1 +/- 6.0 after the 6-months of training (p&lt;0.05) In addition, the amount of change in (V) over dot O(2)max after the 6-month of training period (Delta(V) over dotO(2)max) was correlated with a isocapnic buffering (R=0.72, p&lt;0.05). We conclude that the degree of increased respiratory compensation point is larger than that of AT after high-intensity endurance training at levels above AT, and that the range of isocapnic buffering may be an important factor in relation to the increase in the maximal aerobic capacity of athletes.

健常人2例において,Ramp負荷運動中の脂肪酸化量はLT以下の運動中には顕著に増大した.更に1例では,Ramp負荷後の回復期にも安静時より増大することが認められた.但し,回復30分後の脂肪酸化量の増大には,運動中の血清脂質の動態や回復期においてリパーゼ活性に関与するアドレナリン,ノルアドレナリンやインスリンなどのホルモン動態が影響を与えることが推測された

A study was performed to clarify the relationships between oxygen uptake(VO_2)kinetics on recovery from incremental maximal exercise and blood lactate, glucose and alanine metabolism. Eight healthy males aged 21.6±3.3years were studied. The incremental exercise test was performed using a modified version of Bruce's protocol until 30min after exhaustion. The VO_2 responses on recovery were fitted by a two-component exponential model. Blood lactate concentration in the recovery phase was fitted by a bi-exponential time function to assess the velocity constant of the slowly decreasing component(γ2)expressing the rate of blood lactate removal. Both blood lactate and plasma alanine concentration were significantly increased from rest to maximal exercise, and were significantly decreased thereafter, but remained above resting values for 30min after the maximal stage. Blood glucose concentration was significantly decreased following maximal exercise and returned to the pre-exercise value by 30min after the maximal stage. Concentrations of plasma branched-chain amino acids(valine, leucine and isoleucine)were significantly decreased from the maximal stage until 30min after exhaustion. The time constant of the slow component on recovery VO_2[τVO_2(s)] was correlated with neither γ2 nor the degree of change in blood lactate from the maximal stage until 30min after exhaustion(Δlactate). However, τVO_2(s)was significantly correlated with both Δblood glucose and Δalanine. In addition, Δalanine was significantly correlated with Δblood glucose. From these results, we conclude that oxygen uptake kinetics after exhaustive maximal exercise is related to glucose resynthesis through alanine metabolism. as compared with that from lactate metabolism.

ランプ負荷法による自転車運動中において,近赤外分光法により測定された筋肉内酸素濃度の第2屈曲点(NT2)出現の遅延は,トレーニング効果によるものと推察された.このことは,従来よりトレーニング効果の指標として利用されているVO2max, VT, LTに加えNT2が一指標となり得る可能性が示唆された

定常負荷運動後におけるVO2の回復曲線の時定数は,運動能力を表わす指標になり得る可能性が示唆された.一方,VCO2の回復曲線に関しては,負荷量や回復時間を考慮して再検討を行う必要性が示された

健常男性7名(22.1±3.2歳)を対象にTreadmillによるstep運動負荷を施行し,breath-by-breathで求めたVO2の時定数は呼吸数の移動平均数を増すほど延長する傾向にあり,13呼吸以上の移動平均数ではbreath-by-breath値より有意差をもって延長した.更に対象毎に検討すると,2例では5呼吸や9呼吸の移動平均数でも時定数が延長した.これはVO2-kineticsの解析時に呼吸数の移動平均数を増すほど安静時や定常時の値が運動開始直後の値に加味される為に時定数が延長して算出されたと考えられた.又,運動開始前後の呼吸の乱れなども解析値に影響を及ぼす要因の一つとして考えられた

健常人の横隔膜水位では,肺気量の低下及び細気管支での閉塞所見が出現するのに関わらず,運動時の換気反応は良好に保たれ,水圧の換気に対する悪影響はみられなかった.特に,水中運動時では早期にATに至るが,ATを越えて炭酸ガスの排泄量が増した条件下でも換気の効率は良好であった

肥満者の水中歩行時では,浮力による体重減少の影響がより強く現れる為,非肥満者に比べ,陸上での換気循環反応及び自覚症状に及ぼす影響が軽減した

運動開始時のVO2-Kineticsの時定数を規定する要因として,運動筋への酸素輸送能,運動筋での酸素利用能に加え,運動筋からの静脈還流の因子が関与していることが示唆された

肥満者の水中歩行時には,陸上歩行時でみられる体重負荷の影響が浮力により軽減される一方,水中でのVTの早期出現及びrapid shallowな呼吸パターンへの移行が,換気反応の亢進や換気効率の悪化を引き起こし,自覚症状への影響も予想された

肥満者の安静時肺機能では,気道は正常に保たれているが,躯幹上半身の脂肪の為FRC及びTLCが低値を示した.更に運動時では過体重の負荷や,脂肪による胸郭の運動制限により運動中の換気効率が変化したと考えられる.そのためコントロール群よりVTが早期に出現し,VT後呼吸数が増加するのを反映して,呼吸困難感の上昇が認められたものと示唆された

中程度トレーニングの大学女子長距離選手(GR群),高度トレーニングの実業団女子長距離選手(ER群)及び年齢の一致した特別の運動経験を有さない女子大学生(SC群)を対象として,女性長距離選手の左室形態及び左室拡大パターンの特徴を明らかにしようとした. 1)GR群及びER群は,SC群と比較して有意に増大した左室内径,左室壁厚及び左室重量を示した.しかし,選手群の左室形態は,健常人の正常範囲内であった. 2)選手群(GR群,ER群)の左室内径に対する壁厚の比率は,非選手群(SC群)のそれと比較して有意差が認められなかった. 3)ER群の左室形態はGR群より高値を示すが,統計的有意差は選手群間に認められなかった.又,左室内径に対する左室壁厚の比率も同様に選手群間で有意差が認められなかった

1.本研究では, 健常者10名を対象として, 胸郭を水中から出した横隔膜および頸椎の水位で動的及び静的肺機能検査を実施し, 水位差の肺機能に及ぼす影響について検討した.<BR>2.横隔膜の水位では, 機能的残気量, 全肺気量, 肺活量の肺気量分画の軽度の減少と一秒量, V₅₀及びV₂₅の著明な低下が認められた.これは, 水圧による腹壁の圧迫に加え, 胸腔内への血液量の増加による気道狭窄の関与が示唆された.<BR>3.頸椎の水位では, 機能的残気量の著しい低下の出現に加え, 各肺気量分画の減少および一秒量の低下率がさらに増強した.この水位レベルでは, 前述のメカニズムの増強に加え, 水圧による胸壁の圧迫が加わったためと推測された.<BR>4.横隔膜水位から頸椎水位まで水浸レベルを増すと, FRC, VC, TLCの静肺気量位及びFVC, FEV_1・0, V₅₀, V₂₅の低下率が有意に大きくなったが, PF, V₇₅, 及びRVは水浸の程度には影響しなかった.