Biomedical subjects

Masako Endo

Publications and source records attributed to Masako Endo.

11 recordsLinked to original sources

PubMed2006

Volitional hyperventilation during ramp exercise to exhaustion.

The purpose of this study was to determine whether volitional hyperventilation at 20 L x min(-1) above normal exercise values affected exercise duration while performing ramp exercise to exhaustion. Nine healthy subjects performed a ramp exercise test to exhaustion. On a subsequent test they hyperventilated, with the aid of visual and audio feedback, at 20 L x min(-1) greater than their initial test. Ramp exercise time to exhaustion was substantially reduced from 771.6 +/- 85.2 s to 726.6 +/- 86.6 s (p < 0.002) with the additional hyperventilation. Subjects underwent 2 more ramp exercise tests and performed a 5 s maximum voluntary ventilation or a forced vital capacity test at work rates corresponding to rest, below lactate threshold (LT), above LT, immediately after exercise, and 3 min recovery. Generally, the flow rates were not affected by exercise below LT and were enhanced during above-LT exercise, exhaustion, and recovery. This indicated a change in pulmonary function that is dependent on exercise intensity. In spite of this increased ability to generate high flow rates, exercise performance was diminished when respiratory muscle work was increased volitionally by 20 L x min(-1), indicating a strong coupling between respiratory muscle work and fatigue during ramp exercise in normal subjects.

Adult↗

PubMed2005

Kinetics of pulmonary VO2 and femoral artery blood flow and their relationship during repeated bouts of heavy exercise.

The mechanism that alters the pulmonary VO2 response to heavy-intensity exercise following prior heavy exercise has been frequently ascribed to an improvement in pre-exercise blood flow (BF) or O(2) delivery. Interventions to improve O(2) delivery have rarely resulted in a similar enhancement of VO2. However, the actual limb blood flow and VO2 dynamics in the second bout of repeated exercise remain equivocal. Seven healthy female subjects (21-32 years) performed consecutive 6-min (separated by 6 min of 10 W exercise) bilateral knee extension (KE) exercise in a semisupine position at a work rate halfway between the lactate threshold (LT) and VO2peak. Femoral artery blood flow (FBF) was measured by Doppler ultrasound simultaneously with breath-by-breath VO2 each protocol being repeated at least four times for precise kinetic characterization. The effective time-constant (tau') of the VO2 response was reduced following prior exercise (bout 1: 61.0 +/-10.5 vs. bout 2: 51.6+/-9.0 s; mean +/- SD; P<0.05), which was a result of a reduced slow component (bout 1: 16.0+/-8.0 vs. bout 2: 12.5+/-6.7 %; P<0.05) and an unchanged 'primary' tau. FBF was consistently faster than VO2. However, there was no bout-effect on tau' FBF (bout 1: 28.2+/-12.0 vs. bout 2: 34.2+/-8.5 s). The relationship between the exercise-associated VO2 (i.e., deltaVO2) and Delta FBF was similar between bouts, with a tendency (N.S: P>0.05) for deltaVO2/deltaFBF to be increased during the transition to bout 2 rather than decreased, as hypothesized. The return of VO2 kinetics toward first order, therefore, was associated with an 'appropriate', not enhanced, BF to the working muscles. Whether a relative prior-hyperemia in bout 2 enables a more homogeneous intramuscular distribution of BF and/or metabolic response is unclear, however, these data are consistent with events more proximal to the exercise muscle in mediating the VO2 response during repeated heavy-intensity KE exercise.

Adult↗

PubMed2004

Dissociation between the time courses of femoral artery blood flow and pulmonary VO2 during repeated bouts of heavy knee extension exercise in humans.

It has frequently been demonstrated that prior heavy cycling exercise facilitates pulmonary O(2) kinetics at the onset of subsequent heavy exercise. This might be due to improved muscle perfusion via acidosis-induced vasodilating effects. However, it is difficult to measure the blood flow (BF) to the working muscles (via the femoral artery) during cycling exercise. We therefore selected supine knee extension (KE) exercise as an alternative, and investigated whether the faster O(2) kinetics in the 2nd bout was matched by proportionally faster BF kinetics to the exercising muscle. Nine healthy subjects (aged 21-44 years) volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate: 70-75% of peak power) separated by a 6-min baseline rest (EX1 to EX2). During the protocol, a pulsed Doppler ultrasound technique was utilized to continuously measure the BF in the right femoral artery. The protocol was repeated at least 6 times to characterize the precise kinetics. In agreement with previous studies using cycling exercise, the O(2) kinetics in the 2nd bout were facilitated compared with that in the 1st bout [mean +/-s.d. of the 'effective' time constant (tau): EX1, 68.6 +/- 15.9, versus EX2, 58.0 +/- 14.4 s. Phase II-tau: EX1, 48.7 +/- 9.0, versus EX2, 41.2 +/- 13.3 s. Empirical index of the slow component (Delta O(2(6-3))): EX1, 78 +/- 44, versus EX2, 57 +/- 36 ml min(-1) (P < 0.05)]. However, no substantial difference was observed for the facilitation of the femoral artery BF response to the 1st and 2nd exercise bouts [i.e. the 'effective'tau of the femoral artery BF: EX1, 40.8 +/- 16.9, versus EX2, 39.0 +/- 17.1 s (P > 0.05)]. It was concluded that the faster pulmonary O(2) kinetics during heavy KE exercise following prior heavy exercise was not associated with a similar modulation in the BF to the working muscles.

Adult↗

PubMed2004

Pressor response to static and dynamic knee extensions at equivalent workload in humans.

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 VO(2) from baseline (Delta BF, Delta VO(2)) were significantly less during sustained contraction than during repetitive contraction (sustained vs. repetitive; Delta BF: +92 +/- 195 vs. +1,174 +/- 269 ml.min(-1), Delta VO(2): +53 +/- 12 vs. +180 +/- 32 ml.min(-1), mean +/- SE, p < 0.05), although the change in mean arterial pressure (Delta MAP) was greater during sustained contraction (+24 +/- 3 vs. +19 +/- 3 mmHg). Compared under the equivalent TTI and peak tension (40% MVC), Delta BF and Delta VO(2) were less and Delta MAP was greater during sustained contraction (Delta BF: -296 +/- 176 vs. +868 +/- 272 ml.min(-1); Delta VO(2): +104 +/- 16 vs. + 212 +/- 46 ml.min(-1); Delta MAP: +37 +/- 8 vs. +20 +/- 4 mmHg). Moreover Delta MAP 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.

Adult↗

PubMed2003

Effects of priming exercise intensity on the dynamic linearity of the pulmonary VO(2) response during heavy exercise.

Prior heavy-intensity exercise facilitates the pulmonary oxygen uptake ( VO(2)) response during subsequent exercise, such that its kinetics returns towards first-order. To better understand this "priming" phenomenon, we investigated the effect of priming exercise, over a range of intensities, on the VO(2) response to heavy-intensity cycle ergometry at a work rate of Delta50% [halfway between lactate threshold (LT) and VO(2max)]. Eight subjects performed two consecutive 6-min bouts separated by 6 min at 20 W. The first bout was each of: no warm-up control (CON), sub-lactate threshold (LT) at 80% of LT, and three supra-LT conditions (Delta20%, Delta40%, and Delta60%). The VO(2) response during the subsequent bout was evaluated using the "effective" time constant (tau'), and the VO(2) difference between minutes 3 and 6 (Delta VO(2(6-3))). The goodness-of-fit, indicative of "first-order" kinetics, was determined by the residual profile, and the mean square of errors (MSEr). The heart rate and blood lactate concentration ([La]r) just prior to the second bout were also measured. Compared with CON, tau' and Delta VO(2(6-3)) were significantly reduced following all supra-LT priming bouts, while the goodness-of-fit was significantly improved following Delta40% exercise. Delta VO(2(6-3)) and [La]r were negatively correlated ( P<0.05), unlike HR. In conclusion, prior exercise just above, but not below, LT facilitated the VO(2) response in a threshold-like manner. Supra-LT priming exercise influenced the VO(2) response allowing it to return to within as little as 12% from first-order (compared to approximately 50% in CON). The associated increases in circulating lactate and/or related factors seem to be centrally involved in this phenomenon.

Adaptation, Physiological↗

PubMed2003

Chemoreflex drive and the dynamics of ventilation and gas exchange during exercise at hypoxia.

We tested the hypothesis that the promotion of hypoxic ventilatory responsiveness (HVR) and/or hypercapnic ventilatory responsiveness (HCVR) mostly acting on the carotid body with a changing work rate can be attributed to faster hypoxic ventilatory dynamics at the onset of exercise. Eleven subjects performed a cycling exercise with two repetitions of 6 minutes while breathing at FIO(2) = 12%. The tests began with unloaded pedaling, followed by three constant work rates of 40%, 60%, and 80% of the subject's ventilatory threshold at hypoxia. Reference data were obtained at the 80% ventilatory threshold work rate during normoxia. Using three inhaled 100% O(2) breath tests, a comparison of hypoxia and normoxia revealed an augmentation of HVR in hypoxia, which then significantly increased proportionally with the increase in work rate. In contrast, HCVR using three inhaled 10% CO(2) breath tests was unaffected by the difference in work rate at hypoxia but did exceed its level at normoxia. The decrease in the half-time of hypoxic ventilation became significant with an increase in work rates and was significantly lower than at normoxia. Using a multiregression equation, HVR was found to account for 63% of the variance of hypoxic ventilatory dynamics at the onset of exercise and HCVR for 9%. O(2) uptake on-kinetics and off-kinetics under hypoxic conditions were significantly slower than under normoxic conditions, whereas they were not altered by the changing work rates at hypoxia. These results suggest that the faster hypoxic ventilatory dynamics at the onset of exercise can be mostly attributed to the augmentation of HVR with an increase in work rates rather than to HCVR. Otherwise, O(2) uptake dynamics are affected by the lower O(2), not by the changing work rates under hypoxic conditions.

Adult↗

PubMed2003

Facial cooling-induced bradycardia does not slow pulmonary V.O2 kinetics at the onset of high-intensity exercise.

The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (Vo2) by prior heavy-intensity exercise is (are) poorly understood but may be ascribed to either an intramuscular-metabolic or a circulatory modification resulting from "priming" exercise. We investigated the effects of altering the circulatory dynamics by delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the Vo2 kinetics during repeated bouts of heavy-intensity cycling exercise. Five healthy subjects (aged 21-43 yr) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: 50% of the difference between lactate threshold and maximal Vo2) separated by 6-min baseline rest without CFS as a control (N1 and N2). CFS was then applied separately, by gel-filled cold compresses to the face for 2-min spanning the rest-exercise transition, to each of the first bout (CFS1) or second bout (CFS2) of repeated heavy-intensity exercise. In the control protocol, Vo2 responses in N2 showed a facilitated adaptation compared with those in N1, mainly attributable to the reduction of slow component. CFS application successfully slowed and delayed the heart rate (HR) kinetics (P < 0.05) on transition to exercise [HR time constant; N1: 55.6 +/- 16.0 (SD) vs. CFS1: 69.0 +/- 12.8 s and N2: 55.5 +/- 11.8 vs. CFS2: 64.0 +/- 17.5 s]; however, it did not affect the "primary" Vo2 kinetics [Vo2 time constant; N1: 23.7 +/- 7.9 (SD) vs. CFS1: 20.9 +/- 3.8 s, and N2: 23.3 +/- 10.3 vs. CFS2: 17.4 +/- 6.3 s]. In conclusion, increased vagal withdrawal delayed and slowed the circulatory response but did not alter the Vo2 kinetics at the onset of supra-lactate threshold cycling exercise. As the facilitation of Vo2 subsequent to prior heavy leg cycling exercise is not attenuated by slowing the central circulation, it seems unlikely that this facilitation is exclusively determined by a blood flow-related mechanism.

Adult↗

PubMed2003

The curvature constant parameter of the power-duration curve for varied-power exercise.

INTRODUCTION: The tolerable duration (t) for high-intensity cycle ergometry bears a hyperbolic relationship to the power output (P) with an asymptote termed the critical power (CP), and a curvature constant (W') that is numerically equivalent to an amount of work that can be performed above CP. The physiological nature of W' has received little consideration compared with CP, e.g., whether the total amount of work above CP remains constant when the power actually changes during the high-intensity task. PURPOSE: The purpose of this study was to compare W' derived from the standard estimation method, consisting of several different constant-P tests, and the total amount of work above CP during an exhausting exercise bout using a variable-P protocol. METHODS: Eleven healthy male subjects (age: 21-40 yr) volunteered to participate in this study. Each initially performed four-to-six high-intensity square-wave exercise bouts for estimation of CP [mean (SD); 213.3 (22.4) W] and W' [12.68 (3.08) kJ]. The subjects subsequently performed two variable-P tests to the limit of tolerance. During the first part, P was 117% or 134% of CP for a duration that expended approximately half of W'. The work rate was then abruptly increased to 134% (UP protocol) or decreased to 117% (DOWN protocol) of CP for the second part. RESULTS: There were no significant differences between W' [12.68 (3.08) kJ] and the total amount of work above CP during the UP [12.14 (4.18) kJ] and DOWN [12.72 (4.05) kJ] protocols (P > 0.05). CONCLUSION: We conclude that the work equivalent of W' is not affected by power variations during exhausting cycle ergometry, at least in the P range of 100-134% of CP.

Adult↗

PubMed2002

Relationship between the curvature constant parameter of the power-duration curve and muscle cross-sectional area of the thigh for cycle ergometry in humans.

For high-intensity cycle ergometer exercise, the relationship between power output ( P) and its tolerable duration ( t) has been well characterized by the hyperbolic relationship: ( P- theta;(F)). t=W', where theta;(F) has been termed the "critical power" or "fatigue threshold". The curvature constant (W') reflects a constant amount of work which can be performed above theta;(F), and it may be regarded as a muscle energy store. The relationship of this energy store to muscle mass is not known. Therefore, the purpose of this study was to determine the relationships among W', accumulated peak oxygen deficit (accumulated peak O(2)-deficit), and muscle cross-sectional area (CSA) of the thigh for high-intensity cycle ergometry in humans. A group of 17 healthy male subjects (aged 21-41 years) participated in this study. The theta;(F) and W' of the P- t hyperbolic relationship and the accumulated peak O(2)-deficit was calculated by standard procedures. The CSA of muscle, fat and bone in the right thigh were measured using ultrasonography. The mean (SD) of theta;(F), W', accumulated peak O(2)-deficit, and muscle CSA of the thigh were 200.0 (17.8) W, 12.60 (2.94) kJ, 2.29 (0.41) l, and 185.3 (22.6) cm(2), respectively. The muscle CSA of the thigh was positively correlated with W' ( r=0.59, P<0.01) and with accumulated peak O(2)-deficit ( r=0.54, P<0.05). The relationship between W' and accumulated peak O(2)-deficit also showed a positive correlation ( r=0.63, P<0.005). Our results indicated that W' derived from the P- t hyperbolic curve as anaerobic working capacity is related to the CSA of muscle.

Adult↗

PubMed2002

Effects of ischaemia on subsequent exercise-induced oxygen uptake kinetics in healthy adult humans.

Leg muscles were occluded (33 kPa) prior to exercise to determine whether the induced metabolic changes, and reactive hyperaemia upon occlusion release just prior to the exercise, would accelerate the subsequent oxygen consumption (VO2) response. Eight subjects performed double bouts (6 min duration, 6 min rest in-between) of square wave leg cycle ergometry both below and above their lactate threshold (LT). Prior to exercise, large blood pressure cuffs were put around the upper thighs. Occlusion durations were 0 min (control), 5 min and 10 min. Ischaemia was terminated within 5 s prior to exercise onset. Heart rate, VO2, ventilatory rate (V(E)), electromyogram (EMG) and haemoglobin/myoglobin (Hb/Mb) saturation were recorded continuously. Single exponential modelling demonstrated that, compared to control (time constant = 53.9 +/- 13.9 s), ischaemia quickened the VO2 response (P < 0.05) for the first bout of exercise above LT (time constant = 48.3 +/- 14.5 s) but not to any other exercise bout below or above LT. The 3-6 min integrated EMG (iEMG) slope was correlated to the 3-6 min VO2 slope (r = 0.73). Hb/Mb saturation verified the ischaemia but did not show a consistent relation to the VO2 time course. Reactive hyperaemia induced a faster VO2 response for work rates above LT. The effect, while significant, was not large considering the expected favourable metabolic and circulatory changes induced by ischaemia.

Adult↗

PubMed2002

Ventilatory and gas exchange responses under spontaneous and fixed breathing modes during arm exercise.

To evaluate the difference of ventilatory and gas exchange response differences between arm and leg exercise, six healthy young men underwent ramp exercise testing at a rate of 15 W.min-1 on a cycle ergometer separately under either spontaneous (SPNT) or fixed (FIX) breathing modes, respectively. Controlled breathing was defined as a breathing frequency (fb; 30 breaths.min-1) which was neither equal to, nor a multiple of, cranking frequency (50 rev.min-1) to prevent coupling of locomotion and respiratory movement, i.e., so-called locomotor-respiratory coupling (LRC). Breath-by-breath oxygen uptake (VO2), ventilation (VE), CO2 output (VCO2), tidal volume (VT), fb and end-tidal PCO2 (PETCO2) were determined using a computerized metabolic cart. Arm exercise engendered a higher level of VO2 at each work rate than leg exercise under both FIX and SPNT conditions. However, FIX did not notably affect the VO2 response during either arm or leg exercise at each work rate compared to SPNT. During SPNT a significantly higher fb and lower PETCO2 during arm exercise was found compared with leg exercise up to a fb of 30 breaths.min-1 while VE and VT were nearly the same. During fixed breathing when fb was fixed at a higher rate than during SPNT, a significantly lower PETCO2 was observed during both exercise modes. These results suggest that: 1) FIX breathing does not affect the VO2 response during either arm or leg exercise even when non-synchronization between limb locomotion movement and breathing rate was adopted; 2) at a fb of 30 breaths.min-1 FIX breathing induced a hyperventilation resulting in a lower PETCO2 which was not associated with the metabolic rate during either arm or leg exercise, showing that VE during only leg exercise under the FIX condition was significantly higher than under the SPNT condition.

Adult↗