Aging exaggerates blood pressure response to ischemic rhythmic handgrip exercise in humans.

Ischemic skeletal muscle conditions are known to augment exercise-induced increases in blood pressure (BP). Aging is also a factor that enhances the pressor response to exercise. However, the effects of aging on the BP response to ischemic exercise remain unclear. We, therefore, tested the hypothesis that aging enhances the BP response to rhythmic handgrip (RHG) exercise during postexercise muscle ischemia (PEMI). We divided the normotensive participants without cardiovascular diseases into three age groups: young (n = 26; age, 18-28 years), middle-aged (n = 23; age, 35-59 years), and older adults (n = 23; age, 60-80 years). The participants performed RHG exercise with minimal effort for 1 min after rest with and without PEMI, which was induced by inflating a cuff on the upper arm just before the isometric handgrip exercise ended; the intensity was 30% of maximal voluntary contraction force. Under PEMI, the increase in diastolic BP (DBP) from rest to RHG exercise in the older adult group (Δ13 ± 2 mmHg) was significantly higher than that in the young (Δ5 ± 2 mmHg) and middle-aged groups (Δ6 ± 1 mmHg), despite there being no significant difference between the groups in the DBP response from rest to RHG exercise without PEMI. Importantly, based on multiple regression analysis, age remained a significant independent determinant of both the SBP and DBP responses to RHG exercise during PEMI (p < 0.01). These findings indicate that aging enhances the pressor response to ischemic rhythmic exercise.

Inhalation of molecular hydrogen increases breath acetone excretion during submaximal exercise: a randomized, single-blinded, placebo-controlled study.

Aerobic exercise is widely accepted as a beneficial option for reducing fat in humans. Recently, it has been suggested that molecular hydrogen (H2) augments mitochondrial oxidative phosphorylation. Therefore, the hypothesis that inhaling H2 could facilitate lipid metabolism during aerobic exercise was investigated in the current study by measuring the breath acetone levels, which could be used as non-invasive indicators of lipid metabolism. This study aimed to investigate the effect of inhaling H2 on breath acetone output during submaximal exercise using a randomized, single-blinded, placebo-controlled, and cross-over experimental design. After taking a 20-minute baseline measurement, breath acetone levels were measured in ten male subjects who performed a 60% peak oxygen uptake-intensity cycling exercise for 20 minutes while inhaling either 1% H2 or a control gas. In another experiment, six male subjects remained in a sitting position for 45 minutes while inhaling either 1% H2 or a control gas. H2 significantly augmented breath acetone and enhanced oxygen uptake during exercise (P < 0.01). However, it did not significantly change oxidative stress or antioxidant activity responses to exercise, nor did it significantly alter the breath acetone or oxygen uptake during prolonged resting states. These results suggest that inhaling H2 gas promotes an exercise-induced increase in hepatic lipid metabolism. The study was approved by the Ethical Committee of Chubu University, Japan (approved No. 260086-2) on March 29, 2018.

Does degree of alteration in effort sense caused by eccentric exercise significantly affect initial exercise hyperpnea in humans?

Previous research has shown an exaggeration in exercise hyperpnea 2 days after eccentric exercise (ECC). Enhancement in central command has been suggested as one candidate to account for this effect given that ECC-induced neuromuscular dysfunction increases relative exercise intensity, thus resulting in reinforcement of effort sense. The purpose of this study was, therefore, to elucidate whether the degree of alteration in effort sense caused by ECC affects exercise hyperpnea. Ten subjects performed 20-s single-arm extension-flexion exercises with weight strapped to the wrist, and ventilatory response was measured before (Pre) and 2 days after ECC (D2). Relative exercise intensity at Pre was 5 % of maximal voluntary contraction (MVC) of Pre, whereas that at D2 was 9 % MVC of D2 because of decline in muscle strength. Ventilatory responses were significantly exaggerated at D2 with a significant increase in effort sense. Although effort sense was significantly reduced during exercise at D2 when wrist weight was subtracted to match relative exercise intensity at Pre (5 % MVC of D2), ventilatory responses were still significantly higher than those of Pre. After the disappearance of post-ECC muscle damage, subjects performed the same exercise with weight added (9 % MVC of Pre) so that effort was equalized to match that of D2; however, no significant increase in ventilatory response was detected. The fact that the extent of change in effort sense caused by ECC-induced neuromuscular dysfunction did not affect ventilatory response at the onset of exercise after ECC may suggest that the exaggeration of ventilatory response after ECC is caused by mechanisms other than alteration of the central command.

Degree of exercise intensity during continuous chest compression in upper-body-trained individuals.

BACKGROUND: Although chest-compression-only cardiopulmonary resuscitation (CCO-CPR) is recommended for lay bystanders, fatigue is easily produced during CCO-CPR. If CCO-CPR can be performed at a lower intensity of exercise, higher resistance to fatigue is expected. Since chest compression is considered to be a submaximal upper body exercise in a steady rhythm and since the unit of load for chest compression is expressed as work rate, we investigated the possibility that peak work rate of the upper body determines the level of exercise intensity during CCO-CPR. METHODS: Twelve sedentary individuals (group Se), 11 rugby players (group R), and 11 swimmers (group Sw) performed 10-min CCO-CPR, and heart rate (HR) and rating of perceived exertion (RPE) were measured as indices of exercise intensity. Multiple linear regression analysis was carried out to assess potential relationships of upper body weight, peak lumbar extension force, peak work rate, and peak oxygen uptake recorded during arm-crank exercise with HR and RPE during CCO-CPR. RESULTS: Values of peak work rate during arm-crank exercise (Peak WR-AC) in group Se, group R, and group Sw were 108 ± 12, 139 ± 27, and 146 ± 24 watts, respectively. Values of the latter two groups were significantly higher than the value of group Se (group R, P < 0.01; group Sw, P < 0.001). HR during CCO-CPR increased with time, reaching 127.8 ± 17.6, 114.8 ± 16.5, and 118.1 ± 14.2 bpm at the 10th minute in group Se, group R, and group Sw, respectively. On the other hand, RPE during CCO-CPR increased with time, reaching 16.4 ± 1.4, 15.4 ± 1.7, and 13.9 ± 2.2 at the 10th minute in group Se, group R, and group Sw, respectively. Multiple linear regression analysis showed that only peak WR-AC affects both HR and RPE at the 10th minute of CCO-CPR (HR, r = -0.458; P < 0.01; RPE, r = -0.384, P < 0.05). CONCLUSIONS: The degree of exercise intensity during CCO-CPR is lower in individuals who have a higher peak work rate of the upper body.

Higher ventilatory responses during and after passive walking-like leg movement in older individuals.

BACKGROUND: Minute ventilation (V · E) during walking has been shown to be higher in older individuals than in young individuals, but the mechanisms underlying the higher ventilatory response is unclear. Central command and peripheral neural reflex are important neural control mechanisms underlying ventilatory response during exercise. Passive leg movement has been used to exclude the influence of central command due to the lack of voluntary activation of muscles. The aim of the present study was to compare the ventilatory response during and after passive walking-like leg movement (PWM) in young and older individuals. METHODS: Eight young subjects (20 ± 2 years) and seven older subjects (70 ± 1 years) participated in this study. Subjects spent 7 minutes in a quiet standing (QS) position. Thereafter, they performed 14-minute rhythmic PWM at 1 Hz and this was followed by 7 minutes of QS. RESULTS: V · E values during pre-PWM QS were calculated as 1-minute averages using data obtained between 5 and 6 minutes. V · E values at pre-PWM QS in the young and older groups were 8.4 ± 2.1 and 7.5 ± 1.2 l/minute, respectively. V · E values increased significantly at the first minute of PWM to 11.4 ± 2.2 and 10.4 ± 2.5 l/minute in the young and older groups, respectively (P <0.001). In the young group, V · E at the last minute of PWM (9.2 ± 2.0 l/minute) was not significantly different from that at pre-PWM QS due to a decline in V · E, whereas V · E at the last minute of PWM in the older group (9.4 ± 2.2 l/minute) was still significantly higher (P <0.01). On the other hand, V · E at the first minute of post-PWM QS (7.2 ± 1.8 l/minute) was significantly lower than that during pre-PWM QS in the young group (P <0.05) but not in the older group. CONCLUSIONS: Ventilatory response during and after PWM is higher in older individuals than in young individuals. This may be associated with a mechanism(s) other than central command. Our findings may explain part of the higher V · E response while walking in older individuals.

Suppression of cardiocirculatory responses to orthostatic stress by passive walking-like leg movement in healthy young men.

BACKGROUND: Although passive walking-like leg movement in the standing posture (PWM) has been used in the clinical field, the safety of PWM has not been fully determined despite the risks of orthostatic intolerance due to standing posture. The aim of the present study was to examine cardiocirculatory response during PWM in healthy young men. METHODS: The subjects (n = 13) spent 5 min in a sitting position and then 5 min in a quiet standing position to determine baseline levels. Thereafter, they underwent 25-min rhythmic PWM at 1 Hz while standing. In another bout, subjects experienced the same protocol except that they underwent 25-min quiet standing (QS) instead of 25-min PWM. Two subjects dropped out of the 25-min QS due to feeling of discomfort. Thus, data obtained in the remaining eleven subjects are presented. RESULTS: In the PWM trial, systolic arterial blood pressure (SAP) decreased from 112 ± 8 mmHg during the sitting baseline period to 107 ± 8 mmHg during the standing baseline period (p <0.05), while heart rate (HR) increased from 73 ± 9 bpm during the sitting baseline period to 84 ± 10 bpm during the standing baseline period (p <0.001). After the imposition of PWM, SAP increased from 107 ± 8 mmHg in the standing baseline period to 120 ± 6 mmHg (p <0.001), while HR decreased from 84 ± 10 bpm in the standing baseline period to 76 ± 9 bpm (p <0.05). In the QS trial, SAP, which had decreased during the standing baseline period compared to that during the sitting baseline period, remained lowered during the 25-min QS period, while HR, which had increased during the standing baseline period compared to that during the sitting baseline period, remained elevated during the 25-min QS period. In both bouts, HR showed almost mirror-image changes in the high-frequency component of HR variability, suggesting that the changes in HR were due to change in parasympathetic activation. Double product (HR × SAP), as a predictor of myocardial oxygen consumption, during the 25-min QS period tended to increase with time, but double product remained almost constant during the 25-min PWM period. CONCLUSIONS: The results suggest that PWM is effective for suppressing cardiocirculatory responses to orthostatic stress.

Limb oxygenation during the cold pressor test in spinal cord-injured humans.

OBJECTIVE: To investigate changes in tissue oxygenation in the arm and leg during the cold pressor test in humans with spinal cord injury (SCI). METHODS: Subjects with SCI at cervical 6 (n=7) and subjects with SCI at thoracic 5 or thoracic 6 (n=5) experienced 3-min cold water immersion of the foot and subsequent 10-min recovery. Changes in tissue oxygenation and blood pressure were determined. Tissue oxygenation was assessed by hemoglobin/myoglobin concentration (Hb/MbO2) measured using near-infrared spectroscopy. RESULTS: Mean arterial blood pressures increased significantly by 15±9 and 6±6 mmHg during cold water immersion in the cervical and thoracic SCI groups, respectively (P<0.001). Hb/MbO2 in the arm decreased significantly by 23±15 µM cm during cold water immersion only in the cervical SCI group (P<0.001), whereas Hb/MbO2 in the leg decreased significantly by 82±56 µM cm during cold water immersion only in the thoracic SCI group (P<0.001). INTERPRETATION: Afferent activity coming from below the lesion due to cold stimuli would reflexively enhance sympathetic activity in both the arm and leg in individuals with cervical SCI but only in the leg in individuals with thoracic SCI. A decrease in tissue oxygenation might have been caused by sympathetic vasoconstriction. The reduction of tissue oxygenation in the arm was marked in individuals with cervical SCI, suggesting differential control of arm oxygenation and leg oxygenation in the region below SCI.

Hypoventilation during passive leg movement in spinal cord-injured humans.

We examined ventilatory response during passive walking-like exercise in the standing posture in complete spinal cord-injured humans and found that ventilatory equivalent for O(2) uptake, which would be related to the sensation of breathlessness, was lower during passive exercise than during quiet standing.

Unusual blood pressure response during standing therapy in tetraplegic man.

We report a case of an individual with cervical spinal cord injury who showed a unique blood pressure response during passive standing and passive walking-like leg movement, i.e., hypertension with standing and hypotension with leg movement.

Hyperventilation during orthostatic challenge in spinal cord-injured humans.

OBJECTIVE: To determine whether arterial hypotension is related to hyperventilation during standing in individuals with complete spinal cord injury (SCI). METHODS: Sixteen individuals with SCI (thoracic 1 to thoracic level 12, ASIA grade: A) and 18 able-bodied individuals participated in this study. Individuals with SCI were divided into a group with injury level at or above thoracic (T) 7 [higher SCI (HSCI), n = 9] and a group with injury level at or below T10 (lower SCI, n = 7). Subjects carried out 6-min quiet sitting and then 6-min quiet standing using a standing frame. RESULTS: Significant decrease in mean arterial blood pressure (MAP) and significant increase in minute ventilation (V(E)) by postural change from sitting to standing were observed only in HSCI. In HSCI, MAP decreased from 81 +/- 11 to 75 +/- 16 mmHg (P < 0.05), while V(E) increased from 8.4 +/- 1.1 to 9.9 +/- 1.0 l min(-1) (P < 0.01). There was a significant negative correlation between changes in MAP and V(E) in subjects in the HSCI group (r = -0.72, P < 0.05). INTERPRETATION: We concluded that the magnitude of hyperventilation during standing is associated with individual difference in the magnitude of hypotension in individuals with SCI. The mechanism(s) for this relationship remains unresolved, but afferent signals from baroreceptors to the brainstem respiratory center and/or action of pressor substances on the central nervous system might have caused hyperventilation.

Invariable H-reflex and sustained facilitation of stretch reflex with heightened sympathetic outflow.

Stretch reflex shows sustained (3-min) increase with heightened sympathetic outflow [Hjortskov N, Skotte J, Hye-Knudsen C, Fallentin N. Sympathetic outflow enhances the stretch reflex response in the relaxed soleus muscle in humans. J Appl Physiol 2005;98:1366-70], but it is unknown if it accompanies a sustained increase in H-reflex. The purpose of the study was to test if there is a sustained facilitation in the H-reflex in the human soleus muscle during a variety of sustained tasks that are known to elevate sympathetic outflow. Mean arterial blood pressure, heart rate, and H- and stretch reflexes in the relaxed soleus muscle were obtained in healthy young adults who performed mental arithmetic, static handgrip exercise, post-handgrip ischemia, and cold stimulation. Each task lasted 3 min with a 3-min rest in between tasks. Data were analyzed for the initial 30 s and entire 3 min of each task. There was a heightened cardiovascular response in all tasks for both durations of analysis. An increase in H-reflex amplitude was not observed for either the initial or entire duration of the analysis. The tasks increased stretch reflex amplitude for both durations of analysis. Invariable H-reflex and sustained facilitation of stretch reflex with heightened sympathetic outflow would imply sympathetic modulation of muscle spindle sensitivity.

Pressor response to passive walking-like exercise in spinal cord-injured humans.

OBJECTIVE: To examine blood pressure responses during passive walking-like exercise in the standing posture (PWE) in spinal cord-injured (SCI) humans. METHODS: Twelve motor-complete SCI individuals (cervical level 6 to thoracic level 12, ASIA grade: A or B) and twelve able-bodied controls (CON) participated in this study. SCI individuals were divided into a group with injury level at or above thoracic (T) 6 (HSCI, n = 7) and a group with injury level at or below T10 (LSCI, n = 5). Subjects carried out 6-minute quiet standing and then 12-minute PWE at 1 Hz using a gait training apparatus that enables subjects to stand and move their legs passively. RESULTS: Mean arterial blood pressures (MAPs) at standing in HSCI, LSCI and CON were 69 +/- 5, 83 +/- 4 and 93 +/- 2 mmHg, respectively. MAP changed significantly during PWE only in HSCI and CON, increasing to 88 +/- 4 (P < 0.001) and 98 +/- 1 mmHg (P < 0.01), respectively. The former group showed a larger increase in MAP (P < 0.001). INTERPRETATION: Spinal sympathetic reflexes can be induced in a region isolated from the brainstem in response to a stimulus originating below the level of the spinal cord injury, and the magnitude of increase in blood pressure is greater in SCI individuals with lesion level at or above T6 due to loss of supraspinal control of the major sympathetic outflow. This central mechanism may be one of the reasons why greater pressor response to PWE was observed in HSCI.

Metaboreceptor-mediated muscle oxygen saturation during recovery following isometric handgrip exercise.

The aim of the present study was to determine whether oxygen supply to non-exercised muscle during recovery following fatiguing exercise is influenced by accumulated metabolites within exercised muscle. Twelve healthy male subjects performed 2-min isometric handgrip exercise at 40% maximal voluntary contraction with their right hand and the exercise was followed by a 3-min recovery period. Muscle oxygen saturation (SmO(2)) determined by near-infrared spatially resolved spectroscopy was used as an index of oxygen supply to non-exercised muscle and was measured in biceps brachii and tibialis anterior muscles on the left side. Compared to the pre-exercise baseline level, SmO(2) in the biceps brachii muscle (SmO(2BB)) increased significantly from 30 sec to 1 min after the start of exercise, while SmO(2) in the tibialis anterior muscle (SmO(2TA)) remained stable during the initial 1 min of exercise. Both SmO(2BB) and SmO(2TA) began to decrease at about 1 min and continued to decrease thereafter. Due to the initial increase in SmO(2BB), only SmO(2TA) showed a significant decrease during exercise. During recovery, SmO(2BB) did not differ significantly from the pre-exercise baseline level, whereas SmO(2TA) remained significantly lower until about 1.5 min of recovery and then it did not differ significantly from the baseline level. In another bout, subjects performed handgrip exercise of the same intensity, but post-exercise arterial occlusion (PEAO) of the exercised muscle was imposed for 2 min immediately after the end of exercise. During PEAO, SmO(2BB) decreased significantly compared to the baseline level, whereas SmO(2TA) remained significantly lower until the end of PEAO. The significant decrease in SmO(2BB) and the prolongation of decrease in SmO(2TA) by PEAO suggests that the recovery of SmO(2) in the non-exercised arm and leg is mediated by muscle metaboreceptors.

Effects of passive leg movement on the oxygenation level of lower limb muscle in chronic stroke patients.

OBJECTIVE: To evaluate the effects of passive leg movements on the muscle oxygenation level and electromyographic (EMG) activity in the lower limbs in chronic stroke patients. METHODS: With a gait training apparatus, passive movements were imposed on the lower limbs of 15 chronic stroke patients at a frequency of 0.8 Hz for 10 minutes. During the passive leg movements, muscle oxygenation level and muscular EMG activity of the paretic and nonparetic calf muscles were assessed. RESULTS: The passive leg movements caused increases in the EMG activity and muscle oxygenation level in both paretic and nonparetic lower limbs. Although a significant difference was found in the concentration changes of the oxygenated hemoglobin (Oxy-Hb), both paretic and nonparetic sides of the muscle showed enhancement of the tissue oxygenation level (TOI). The degree of the changes of the Oxy-Hb depended on the level of motor recovery after stroke; subjects with good motor recovery showed less difference in the Oxy-Hb level between the paretic and nonparetic sides of the muscle. CONCLUSION: Passive leg movements have the capacity to induce muscular activity and enhance oxygen metabolism, even in the paretic lower limb muscle of chronic stroke patients. This type of exercise might be a useful and efficient method for the prevention of metabolic deterioration in the lower limb paretic muscles of chronic stroke patients.

A 350-S recovery period does not necessarily allow complete recovery of peak power output during repeated cycling sprints.

The aim of this study was to determine whether a 350-s recovery period allows recovery of peak power output (PPO) to its initial value under the condition of a blood lactate (La) concentration higher than 10 mmol.L-1 during repeated cycling sprints (RCS). RCS (10x10-s cycling sprints) were performed under two conditions. Under one condition, the recovery period of RCS was fixed at 35 s (RCS35), and under the other condition, a 350-s recovery period was set before the 5th and 9th sets, and a 35-s recovery period was set before the other sets (RCScomb). In RCScomb, PPO in the 5th set recovered to that in the 1st set, but PPO in the 9th set did not. Under both conditions, blood La concentration progressively increased and reached approximately 14 mmol.L-1 at the end of the RCS. In RCScomb, VO2 immediately before the 5th set was not significantly different from that immediately before the 9th set. Mean power frequency (MPF) values estimated by a surface electromyogram from the vastus lateralis in the 5th and 9th sets were significantly higher in RCScomb than in RCS35. In conclusion, a 350-s recovery period does not allow recovery of PPO to its initial value under the condition of a blood La concentration of 14 mmol.L-1 during RCS.

Effect of blood lactate concentration and the level of oxygen uptake immediately before a cycling sprint on neuromuscular activation during repeated cycling sprints.

The purpose of this study was to determine whether neuromuscular activation is affected by blood lactate concentration (La) and the level of oxygen uptake immediately before a cycling sprint (preVO(2)). The tests consisted of ten repeated cycling sprints for 10 sec with 35-sec (RCS(35)) and 350-sec recovery periods (RCS(350)). Peak power output (PPO) was not significantly changed despite an increase in La concentration up to 12 mmol/L in RCS(350). Mean power frequency (MPF) of the power spectrum calculated from a surface electromyogram on the vastus lateralis showed a significantly higher level in RCS(350). In RCS(35), preVO(2) level and La were higher than those in RCS(350) in the initial stage of the RCS and in the last half of the RCS, respectively. Thus, neuromuscular activation during exercise with maximal effort is affected by blood lactate concentration and the level of oxygen uptake immediately before exercise, suggesting a cyclic system between muscle recruitment pattern and muscle metabolites.

Kinetics of oxygen uptake during arm cranking with the legs inactive or exercising at moderate intensities.

The purpose of this study was to compare the kinetics of oxygen uptake (VO(2)) during arm cranking with the legs inactive or exercising. Each subject (n = 8) performed three exercise protocols: 6-min arm cranking at an intensity of 60% of peak oxygen uptake (VO(2peak), AC(60)) and 6-min combined arm cranking and leg cycling in which AC(60) was added to on-going leg cycling at an intensity of 20% or 40% of VO(2peak) (LC(20) and LC(40): AC(60)LC(20) and AC(60)LC(40), respectively). After the onset of arm cranking, VO(2) tended to increase until the end of arm cranking in all of the three exercise modes. The amplitudes of this increase in VO(2) were 0.98 (0.18), 0.93 (0.16) and 0.84 (0.12) l.min(-1) during AC(60), AC(60)LC(20) and AC(60)LC(40), respectively, and there were significant differences between values for each exercise. The data are presented as means and standard deviations. There were no significant differences in the effective VO(2) time constant, partial O(2) deficit, and the difference between the values of VO(2) measured at 3 and 6 min in the three exercise modes. The present results indicate that the amplitude of the increase in VO(2) is reduced during arm cranking with the legs exercising, that this reduction becomes greater with increases in the intensity of leg cycling, and that the rate of increase in VO(2) is not affected by the additional muscle mass of the legs exercising below moderate intensities. The decrease in the amplitude of increase in VO(2) might be caused by reduction in oxygen supply to the exercising arms due to large muscle mass and/or overlaps of activity of stabilizing muscles during combined arm and leg exercise.

Kinetics of oxygenation in inactive forearm muscle during ramp leg cycling.

This study was carried out to determine whether hemodynamics in inactive forearm muscle during ramp leg cycling is affected from the ventilatory threshold (VT) and respiratory compensation point (RCP), at which the rate of increase in ventilation (VE) against power output begins to increase abruptly. Change in hemodynamics was evaluated by change in oxygenation index (difference between concentrations of oxygenated hemoglobin and deoxygenated hemoglobin, HbD) measured using near-infrared spectrometry (NIRS). Each subject (n=9) performed 4-min constant-work-rate leg cycling and subsequent ramp leg cycling at an increasing rate of 10 watts.min(-1) in power output. The work rates at VT, RCP and peak oxygen uptake (VO(2 peak)) were 107 +/- 11, 172 +/- 21 and 206 +/- 20 watts, respectively. The rates of increase in VE between 10-watt leg cycling, VT, RCP and VO(2 peak) were 0.19 +/- 0.03, 0.44 +/- 0.07 and 1.32 +/- 0.47 l.min(-1).watts(-1), respectively. In one subject, HbD started to decrease during ramp exercise from the VT, and the rate of decrease increased at a high intensity of exercise. In eight subjects, although no decrease in HbD from the VT was observed, HbD showed a sudden drop at a high intensity of exercise. The work rate at which HbD began to decrease at a high intensity of exercise was 174 +/- 23 watts. This work rate was not significantly different from that at the RCP and was significantly correlated with that at the RCP (r=0.72, P<0.05). The results suggest that the abrupt increase in VE from the RCP affects hemodynamics, resulting in a decrease in HbD in inactive forearm muscle.

Relationship in simulation between oxygen deficit and oxygen uptake in decrement-load exercise starting from low exercise intensity.

The purpose of the present study was to determine by simulation whether oxygen deficit kinetics in decrement-load exercise (DLE) starting from a low exercise intensity is related to the oxygen uptake (Vo(2)) kinetics. In this simulation, work rate in DLE was separated into steps that were regarded as constant-load exercises (CLEs). It was assumed that Vo(2) kinetics behaved exponentially at the onset and offset of each CLE, respectively. Vo(2) at the onset of CLEs increases at the same time and becomes a recovery phase step-by-step corresponding to the decrement of work rate. The sum of Vo(2) values at the onset of CLEs at a given time (nt-Vo(2)) corresponds to Vo(2) excluding oxygen debt in DLE. The sum of Vo(2) values at the offset of CLEs at a given time (dt-Vo(2)) corresponds to Vo(2) related to oxygen debt in DLE. The total of net- and dt-Vo(2) values is equivalent to Vo(2) actually observed in DLE (gs-Vo(2)). As the oxygen requirement level is a steady-state value of Vo(2) in CLE, the oxygen deficit level can be obtained by subtracting Vo(2) at the onset of CLE from the steady-state value. The oxygen deficit level at a given time was added in all CLEs. This is oxygen deficit per unit time (df-Vo(2)). Oxygen debt and oxygen deficit were calculated by integrating df-Vo(2) and dt-Vo(2) from the start of exercise to a given time, respectively. Gs-Vo(2) increased, reached a peak, and decreased linearly until the end of the DLE. Oxygen deficit increased rapidly and showed a steady state. Oxygen debt increased linearly after a time lapse. The difference between oxygen deficit and oxygen debt changed like gs-Vo(2) kinetics. Therefore, it is concluded that if we consider the repayment of oxygen debt in the oxygen deficit in DLE, the kinetics of the oxygen deficit becomes similar to gs-Vo(2) kinetics in the simulation.

Approximation equation for oxygen uptake kinetics in decrement-load exercise starting from low exercise intensity.

The purpose of the present study was to determine the degree of fitting an approximation equation for oxygen uptake (Vo(2)) in decrement-load exercise (DLE). Work rate was started from 120 watts and was decreased by a rate of 15 watts per min. The initial work rate of DLE corresponded to 72+/-10% of the work rate at anaerobic threshold determined in incremental-load exercise (ILE). Vo(2) in DLE increased rapidly, reached a peak, and decreased linearly until the end of the exercise. Vo(2) in DLE was higher than that in ILE at the same work rate except in the early periods in ILE and DLE. This difference ranged from 300 to 400 ml/min. This difference is a result of repayment of oxygen debt in DLE and from the oxygen deficit induced by the delay of response of Vo(2) in ILE. As work rate in DLE can be obtained by the difference between work rates in constant-load exercise (CLE) and ILE, we postulated that the approximation equation for Vo(2) kinetics in DLE could be expressed by a combination of approximation equations in CLE and in ILE. When time delay was taken into consideration in this equation, the fitting of data obtained by using the equation was better than that of data obtained by using the equation without a parameter of time delay. The degree of fitting ranged from 94 to 98% (r(2)). Thus, it seems that Vo(2) including oxygen debt in DLE can be approximated by the equation used in this study.