Effects of heat exposure in the absence of hyperthermia on power output during repeated cycling sprints.

The aim of this study was to investigate the effects of heat exposure in the absence of hyperthermia on power output during repeated cycling sprints. Seven males performed four 10-s cycling sprints interspersed by 30 s of active recovery on a cycle ergometer in hot-dry and thermoneutral environments. Changes in rectal temperature were similar under the two ambient conditions. The mean 2-s power output over the 1st-4th sprints was significantly lower under the hot-dry condition than under the thermoneutral condition. The amplitude of the electromyogram was lower under the hot-dry condition than under the thermoneutral condition during the early phase (0-3 s) of each cycling sprint. No significant difference was observed for blood lactate concentration between the two ambient conditions. Power output at the onset of a cycling sprint during repeated cycling sprints is decreased due to heat exposure in the absence of hyperthermia.

Associations of time to return to performance following acute posterior thigh injuries with running biomechanics, hamstring function, and structure in collegiate sprinters: A prospective cohort design.

BACKGROUND: The time to return to sport from acute hamstring strain injuries is associated with several functional and structural impairments. However, not all previous studies assessed the preinjury level before acute hamstring strain injuries directly. The purpose of this study was to examine the associations of the time to return to performance following acute hamstring strain injuries with deficits in running biomechanics, hamstring function and structure in collegiate sprinters by a prospective study. METHODS: Using a prospective cohort design, 72 participants were recruited from a collegiate track and field team. At the preinjury assessment, a 60-m running-specific test, passive straight leg raise test and isometric knee flexion strength test were assessed at the beginning of the competitive season for three consecutive years (2017-2019). Afterwards, postinjury examinations were performed only in sprinters with acute hamstring strain injuries. FINDINGS: Twelve sprinters strained their hamstring muscle (incidence rate of hamstring strain injuries: 16.7%); the majority (n = 10) were classified as grades 0-2. The running speed deficit of the running-specific test was associated with the time to return to performance as well as the passive straight leg raise test deficit. In the running-specific test, lower-limb kinetic deficits were more strongly associated with the time to return to performance compared to lower-limb kinematic deficits. INTERPRETATION: A running-specific test may be considered one of the most convenient and valid tests for assessing rehabilitation progress after acute hamstring strain injuries.

Effects of resistive load on performance and surface EMG activity during repeated cycling sprints on a non-isokinetic cycle ergometer.

OBJECTIVES: To determine the effects of resistive load on performance and surface electromyogram (SEMG) activity during repeated cycling sprints (RCS) on a non-isokinetic cycle ergometer. METHODS: Participants performed two RCS tests (ten 10-second cycling sprints) interspersed with both 30- and 360-second recovery periods under light (RCS(L)) and heavy load conditions (RCS(H)) in a random counterbalanced order. Recovery periods of 360 seconds were set before the fifth and ninth sprints. RESULTS: In the 9th and 10th sprints, the values of peak power output divided by body mass were significantly higher in RCS(H) than in RCS(L). Changes in blood lactate concentration were not different between the two conditions. In RCS(L), the root mean square calculated from the SEMG was significantly lower in the ninth sprint than in the first sprint, but there were no differences between the root mean square in the first sprint and that in the ninth sprint in RCS(H). CONCLUSIONS: During RCS on a non-isokinetic cycle ergometer, performance and SEMG activity are influenced by resistive load. It is thought that regulation of skeletal muscle recruitment by the central nervous system is associated with fatigue during RCS with a light resistive load.

Effects of sodium bicarbonate ingestion on hyperventilation and recovery of blood pH after a short-term intense exercise.

To determine the relationship between hyperventilation and recovery of blood pH during recovery from a heavy exercise, short-term intense exercise (STIE) tests were performed after human subjects ingested 0.3 g.kg(-1) body mass of either NaHCO3 (Alk) or CaCO3 (Pla). Ventilation (VE)-CO2 output (VCO2) slopes during recovery following STIE were significantly lower in Alk than in Pla, indicating that hyperventilation is attenuated under the alkalotic condition. However, this reduction of the slope was the result of unchanged VE and a small increase in VCO2. A significant correlation between VE and blood pH was found during recovery in both conditions. While there was no difference between the VE-pH slopes in the two conditions, VE at the same pH was higher in Alk than in Pla. Furthermore, the values of pH during recovery in both conditions increased toward the preexercise levels of each condition. Thus, although VE-VCO2 slope was decreased under the alkalotic condition, this could not be explained by the ventilatory depression attributed to increase in blood pH. We speculate that hyperventilation after the end of STIE is determined by the VE-pH relationship that was set before STIE or the intensity of the exercise performed.

Relationship between hyperventilation and excessive CO2 output during recovery from repeated cycling sprints.

The purpose of the present study was to examine whether excessive CO2 output (VCO2excess) is dominantly attributable to hyperventilation during the period of recovery from repeated cycling sprints. A series of four 10-sec cycling sprints with 30-sec passive recovery periods was performed two times. The first series and second series of cycle sprints (SCS) were followed by 360-sec passive recovery periods (first recovery and second recovery). Increases in blood lactate (DeltaLa) were 11.17+/-2.57 mM from rest to 5.5 min during first recovery and 2.07+/-1.23 mM from the start of the second SCS to 5.5 min during second recovery. CO2 output (VCO2) was significantly higher than O2 uptake (VO2) during both recovery periods. This difference was defined as VCO2excess. VCO2excess was significantly higher during first recovery than during second recovery. VCO2excess was added from rest to the end of first recovery and from the start of the second SCS to the end of second recovery (CO2excess). DeltaLa was significantly related to CO2excess (r=0.845). However, ventilation during first recovery was the same as that during second recovery. End-tidal CO2 pressure (PETCO2) significantly decreased from the resting level during the recovery periods, indicating hyperventilation. PETCO2 during first recovery was significantly higher than that during second recovery. It is concluded that VCO2excess is not simply determined by ventilation during recovery from repeated cycle sprints.

Comparison of oxygen uptake at the onset of decrement-load and constant-load exercise.

The purpose of the present study was to examine whether the level of oxygen uptake (V(.)(O2) at the onset of decrement-load exercise (DLE) is lower than that at the onset of constant-load exercise (CLE), since power output, which is the target of V(.)(O2) response, is decreased in DLE. CLE and DLE were performed under the conditions of moderate and heavy exercise intensities. Before and after these main exercises, previous exercise and post exercise were performed at 20 watts. DEL was started at the same power output as that for CLE and power output was decreased at a rate of 15 watts per min. V(.)(O2) in moderate CLE increased at a fast rate and showed a steady state, while V(.)(O2) in moderate DLE increased and decreased linearly. V(.)(O2) at the increasing phase in DLE was at the same level as that in moderate CLE. V(.)(O2) immediately after moderate DLE was higher than that in the previous exercise by 98+/-77.5 ml/min. V(.)(O2) in heavy CLE increased rapidly at first and then slowly increased, while V(.)(O2) in heavy DLE increased rapidly, showing a temporal convexity change, and decreased linearly. V(.)(O2) at the increasing phase of heavy DLE was the same level as that in heavy CLE. V(.)(O2) immediately after heavy DLE was significantly higher than that in the previous exercise by 156+/-131.8 ml/min. Thus, despite the different modes of exercise, V(.)(O2) at the increasing phase in DLE was at the same level as that in CLE due to the effect of the oxygen debt expressed by the higher level of V(.)(O2) at the end of DLE than that in the previous exercise.

Relationship between oxygenation in inactive biceps brachii muscle and hyperventilation during leg cycling.

Inactive forearm muscle oxygenation has been reported to begin decreasing from the respiratory compensation point (RCP) during ramp leg cycling. From the RCP, hyperventilation occurs with a decrease in arterial CO2 pressure (PaCO2). The aim of this study was to determine which of these two factors, hyperventilation or decrease in PaCO2, is related to a decrease in inactive biceps brachii muscle oxygenation during leg cycling. Each subject (n = 7) performed a 6-min two-step leg cycling. The exercise intensity in the first step (3 min) was halfway between the ventilatory threshold and RCP (170+/-21 watts), while that in the second step (3 min) was halfway between the RCP and peak oxygen uptake (240+/-28 watts). The amount of hyperventilation and PaCO2 were calculated from gas parameters. The average cross correlation function in seven subjects between inactive muscle oxygenation and amount of hyperventilation showed a negative peak at the time shift of zero (r = -0.72, p<0.001), while that between inactive muscle oxygenation and calculated PaCO2 showed no peak near the time shift of zero. Thus, we concluded that decrease in oxygenation in inactive arm muscle is closely coupled with increase in the amount of hyperventilation.

Effects of rate of decrease in power output in decrement-load exercise on oxygen uptake.

The purpose of this study was to examine how oxygen uptake (Vo2) in decrement-load exercise (DLE) is affected by changing rate of decrease in power output. DLE was performed at three different rates of decrease in power output (10, 20 and 30 watts.min(-1): DLE10, DLE20 and DLE30, respectively) from power output corresponding to 90 % of peak Vo2. Vo2 exponentially increased and then decreased, and the rate of its decrease was reduced at low power output. The values of Vo2 in the three DLE tests were not different for the first 2 min despite the difference in power output. The relationship between Vo2 and power output below 50 watts was obtained as a slope to estimate excessive Vo2 (ex-Vo2) above 50 watts. The slopes were 10.0+/-0.9 for DLE10, 9.9+/-0.7 for DLE20 and 10.2+/-1.0 ml.min(-1).watt(-1) for DLE30. The difference between Vo2 estimated from the slope and measured Vo2 was defined as ex-Vo2. The peak value of ex-Vo2 for DLE10 (189+/-116 ml.min(-1)) was significantly greater than those for DLE20 and for DLE30 (93+/-97 and 88+/-34 ml.min(-1)). The difference between Vo2 in DLE and that in incremental-load exercise (ILE) below 50 watts (DeltaVo2) was greater in DLE30 and smallest in DLE10. There were significant differences in DeltaVo2 among the three DLE tests. The values of DeltaVo2 at 30 watts were 283+/-152 for DLE10, 413+/-136 for DLE20 and 483+/-187 ml.min(-1) for DLE30. Thus, a faster rate of decrease in power output resulted in no change of Vo2 at the onset of DLE, smaller ex-Vo2 and greater DeltaVo2. These results suggest that Vo2 is disposed in parallel in each motor unit released from power output or recruited in DLE.

Excessive oxygen uptake during exercise and recovery in heavy exercise.

The aim of this study was to determine whether excessive oxygen uptake (Vo2) occurs not only during exercise but also during recovery after heavy exercise. After previous exercise at zero watts for 4 min, the main exercise was performed for 10 min. Then recovery exercise at zero watts was performed for 10 min. The main exercises were moderate and heavy exercises at exercise intensities of 40 % and 70 % of peak Vo2, respectively. Vo2 kinetics above zero watts was obtained by subtracting Vo2 at zero watts of previous exercise (DeltaVo2). Delta Vo2 in moderate exercise was multiplied by the ratio of power output performed in moderate and heavy exercises so as to estimate the Delta Vo2 applicable to heavy exercise. The difference between Delta Vo2 in heavy exercise and Delta Vo2 estimated from the value of moderate exercise was obtained. The obtained Vo2 was defined as excessive Vo2. The time constant of excessive Vo2 during exercise (1.88+/-0.70 min) was significantly shorter than that during recovery (9.61+/-6.92 min). Thus, there was excessive Vo2 during recovery from heavy exercise, suggesting that O2/ATP ratio becomes high after a time delay in heavy exercise and the high ratio continues until recovery.

Computed tomography in a verified case of tuberculous meningitis.

In a verified case of tuberculous meningitis, postcontrast computed tomograms demonstrated enhancement of the area corresponding to the cistern surrounding the brainstem. This enhancement disappeared after successful drug treatment of the meningitis.

[A case of eclampsia with intraventricular hemorrhage].

Our case is a 31-year-old primipara who had undergone a cesarean section for multiple pregnancy and was referred to our clinic because of attack of eclampsia. On admission, her consciousness level was lethargic. Computed tomography on admission showed high density area indicating right paraventricular hemorrhage with ventricular perforation, and low density areas in bilateral basal ganglia. Examination of the cerebral angiogram done six days after onset of symptoms revealed multisegmental vasospasm in Willis' circle mainly. An emergent ventricular drainage was performed. Two weeks later, repeat angiogram revealed that spasm had almost disappeared. Repeat CT scan three months after the onset showed small low density area in the right caudate nucleus and disappearance of the low density areas in bilateral basal ganglia. Her clinical course was uneventful and she was discharged without neurological deficit at about three weeks after the onset. In spite of absence of subarachnoid clot on CT scan, remarkable multisegmental spasm was found on cerebral angiogram. We suspected that eclampsia may have been responsible for the spasm in this case. Bleeding was believed to have originated in the superolateral angle of the lateral ventricle. It was supposed that infarcted hemorrhage or bleeding from small artery due to changes in arterial or venous pressure might have occurred and penetrated into the lateral ventricle.

[Sustained-release pellet of vasodilators--basic experiment].

We examined the efficacy of slow-release, and prolonged diffusion silicone pellets mixed with papaverine hydrochloride in the treatment of cerebral vasospasms following subarachnoid hemorrhage. In addition the diffusion of the other vasodilating agents (diltiazem and nicardipine) into the saline solution using the same silicone materials was also investigated. Papaverine hydrochloride was either packed in silicone tubes (packed type) or polymerized with silicone elastomer, Silastic MDX-4-4210 (solid type). The solid type pellet is cylindrical-(diameter 3 mm, length 30 mm) and contains 40 w/v% of pure powder of papaverine. The amount of the delivered drug was measured for 5 weeks at 37 degrees C and at room temperature. The diffusion rate of the solid type pellet was about 5 times higher than that of the packed one. The diffusion rates of both types of pellets were about 10 times higher at 37 degrees C than at room temperature. The cummulative amount of the delivered drug from the solid type pellet was 37.1% of the initial packed volume at 37 degrees C in the first 3 weeks. The diffusion of diltiazem and nicardipine which were polymerized 30 w/v% in silicone elastomer was observed for 3 weeks at 37 degrees C only in solid type pellet form. The diffusion rate was measured under the condition of either continuous shaking or standing. The results showed the same diffusion rates for diltiazem and nicardipine, with no difference in diffusion rate between the "shaking" and "standing" groups. The diffusion rate showed inverse exponential curves, and was 5-20 X 10(-5)/day/mm2 of initial volume until 5 days.(ABSTRACT TRUNCATED AT 250 WORDS)

[Evaluation of the role of brain scintigraphy in pineal tumors (author's transl)].

From January, 1969 to December, 1975, 1700 patients underwent sequential brain scintigraphy with Tc-99-m-pertechnetate. All the scintigrams were obtained on a scintillation camera with high-resolution collimator in our clinic. Intracranial tumors were confirmed in 449 cases and 21 cases out of those were pineal tumors which were diagnosed by clinical symptoms, air study, angiography and Conray-or Myodil-ventriculography. In these pineal tumors, 14 (67%) out of the 21 cases had positive scan on scintigrams. All of our cases of teratoma (one case) and teratocarcinoma (two cases) showed clear abnormal uptake, though it had been reported that they do not tend to have positive results on scintigrams. We also performed scintigraphy on 11 cases out of the 21, both before and after 60Co radiation therapy. In the cases which showed either same grade or more increased abnormal uptake on scintigrams after radiation therapy, compared with that before radiation therapy, compared with that before radiation, their prognoses were poor. On the other hand, those cases which showed decreased abnormal uptake after radiation, have had a healthy daily activities. From these experiences, it may be concluded that brain scintigraphy is clinically valuable not only for making the diagnosis, but for evaluating the effect of radiation therapy and the prognosis in the cases of pineal tumor.

[Effect of various kinds of glucocorticoids on experimental brain edema (author's transl)].

Although the effectiveness of glucocorticoids for the treatment of cerebral edema has been widely accepted in neurosurgical practice, but its mechanism is still obscure. Also the dose equivalent of various kinds of glucocorticoid preparation is still uncertain. Only the dose equivalent determined by the test examining an antiinflammatory effect on a growth of glanulation, has been applied for the treatment of brain edema. The authors attempted to establish the dose equivalent of each kinds of glucocorticoid for the treatment of cerebral edema. Cold induced cerebral edema was produced by touching a metal probe at the temperature of -90 degrees C for 3 minutes on the right parietal cortex of rat brain. Hydrocortisone (16 mg/kg), prednisolone (3.2 mg/kg), methylprednisolone (3.2 mg/kg), dexamethasone (0.8 mg/kg) and betamethasone (0.8 mg/kg) were administered at the time of 3 hours prior or after the cold injury. The animals were sacrificed 24 hours after injury and the grade of brain edema was determined by the changes of water content in the brain tissue. For this purpose, the authors developed a new method of measuring water content in the brain tissue using tritiated water and a liquid scintillation counter. In the group of animals which were treated with prednisolone, dexamethasone or betamethasone, the water content was significantly decreased compared to the value of non-treated animals. But in the animals treated with hydrocortisone or methylprednisolone, no significant changes of the water content was observed. But in the animals treated with double doses of hydrocortisone (32 mg/kg) or methylprednisolone (6.4 mg/kg), cerebral edema was improved significantly. From these results the authors concluded that the dose equivalent of each kinds of glucocorticoid for the treatment of the brain edema was as follows: hydrocortisone: prednisolone: methylprednisolone: dexamethasone: betamethasone = 40 : 4 : 8 : 1 : 1.

Response of end tidal CO2 pressure to impulse exercise.

The purpose of the present study was to examine how end tidal CO(2) pressure (PETCO(2)) is controlled in impulse exercise. After pre-exercise at 25 watts for 5 min, impulse exercise for 10 sec with 200 watts followed by post exercise at 25 watts was performed. Ventilation (VE) significantly increased until the end of impulse exercise and significantly re-increased after a sudden decrease. Heart rate (HR) significantly increased until the end of impulse exercise and then decreased to the pre-exercise level. PETCO(2) remained constant during impulse exercise. PETCO(2) significantly increased momentarily after impulse exercise and then significantly decreased to the pre-exercise level. PETCO(2) showed oscillation. The average peak frequency of power spectral density in PETCO(2) appeared at 0.0078 Hz. Cross correlations were obtained after impulse exercise. The peak cross correlations between VE and PETCO(2), HR and PETCO(2), and VE and HR were 0.834 with a time delay of -7 sec, 0.813 with a time delay of 7 sec and 0.701 with a time delay of -15 sec, respectively. We demonstrated that PETCO(2) homeodynamics was interactively maintained by PETCO(2) itself, CO(2) transportation (product of cardiac output and mixed venous CO(2) content) into the lungs by heart pumping and CO(2) elimination by ventilation, and it oscillates as a result of their interactions.

Effect of work intensity on time delay in mediation of ventilation by arterial carbon dioxide during recovery from impulse exercise.

Time delay in the mediation of ventilation (V(.)E) by arterial CO(2) pressure (PaCO(2)) was studied during recovery from short impulse-like exercises with different work loads of recovery. Subjects performed two tests including 10-s impulse like exercise with work load of 200 watts and 15-min recovery with 25 watts in test one and 50 watts in test two. V(.)E, end tidal CO(2) pressure (PETCO(2)) and heart rate (HR) were measured continuously during rest, warming up, exercise and recovery. PaCO(2) was estimated from PETCO(2) and tidal volume (V(T)). Results showed that predicted arterial CO(2) pressure (PaCO(2 pre)) increased during recovery in both tests. In both tests, V(.)E increased and peaked at the end of exercise. V(.)E decreased in the first few seconds of recovery but started to increase again. The highest correlation coefficient between PaCO(2 pre) and V(.)E was obtained in the time delay of 7 s (r=0.854) in test one and in time delays of 6 s (r=0.451) and 31 s (r=0.567) in test two. HR was significantly higher in test two than in test one. These results indicate that PaCO(2 pre) drives V(.)E with a time delay and that higher work intensity induces a shorter time delay.

Oscillation in O2 uptake in impulse exercise.

The purpose of the present study was to examine 1) whether O(2) uptake (VO(2)) oscillates during light exercise and 2) whether the oscillation is enhanced after impulse exercise. After resting for 1 min on a bicycle seat, subjects performed 5-min pre-exercise with 25 watts work load, 10-s impulse exercise with 200 watts work load and 15-min post exercise with 25 watts work load at 80 rpm. VO(2) during pre-exercise significantly increased during impulse exercise and suddenly decreased and re-increased until 23 s after impulse exercise. In the cross correlation between heart rate (HR) and VO(2) after impulse exercise, VO(2) strongly correlated to HR with a time delay of -4 s. Peak of power spectral density (PSD) in HR appeared at 0.0039 Hz and peak of PSD in VO(2) appeared at 0.019 Hz. The peak of the cross power spectrum between VO(2) and HR appeared at 0.0078 Hz. The results suggested that there is an oscillation in O(2) uptake during light exercise that is associated with the oscillation in O(2) consumption in active muscle. The oscillation is enhanced not only by change in O(2) consumption but also by O(2) content transported from active muscle to the lungs.

Effects of deception for intensity on surface electromyogram (SEMG) activity and blood lactate concentration during intermittent cycling followed by exhaustive cycling.

The purpose of the present study was to determine the effects of deception for exercise intensity on surface electromyogram (SEMG) activity and blood lactate concentration during intermittent cycling exercise (ICE) tests. Sixteen healthy male were randomly assigned to two groups who completed two ICE [three 4-min cycling at 80% peak power output (PPO) with 3-min passive recovery periods followed by exhaustive cycling] tests (ICE-1 and ICE-2). The experimental group (ICED) was deceived of the actual cycling intensity, while the control group (ICEC) was informed of the actual protocol in ICE-2. In ICE-1, both groups were informed of the actual protocol. In ICE-2, root mean square (RMS) calculated from SEMG during submaximal cycling was significantly higher in the ICEC than in the ICED and blood lactate concentration ([La-]) was significantly higher in the ICEC than in the ICED. In particular, the difference in RMS between the groups was also observed during the first 4-min cycling, in which there was no difference in [La-] between the groups. These results suggest that the CNS modulates skeletal muscle recruitment due to the prior deception for exercise intensity.

Comparison of oscillation of oxygenation in skeletal muscle between early and late phases in prolonged exercise.

The aim of the present study was to compare the oscillations of oxygenation in skeletal muscle between early and late phases in prolonged exercise. During prolonged exercise at 60 % of peak oxygen uptake (V(.)o(2)) for 60 min and at rest, oxygenated hemoglobin/myoglobin (Hb/MbO(2)) and total Hb/Mb (THb/Mb) were determined by near-infrared spectroscopy in the vastus lateralis. Power spectra density (PSD) for the difference between Hb/MbO(2) and THb/Mb (-HHb/MbO(2): deoxygenation) was obtained by fast Fourier transform at rest, in the early phase (1-6 min) and in the late phase (55-60 min) in exercise. Peak PSD in the early phase was significantly higher than that at rest. There were at least three peaks of PSD in exercise. The highest peak was a band around 0.01 Hz, the next peak was a band around 0.04 Hz, and the lowest peak was a band around 0.06 Hz. PSD in the early phase was not significantly different from that in the late phase in exercise. Heart rate (HR) showed a continuous significant increase from 3 min in exercise until the end of exercise. Skin blood flow (SBF) around the early phase was significantly lower than that around the late phase. It was concluded that oscillation of oxygenation in the muscle oxygen system in the early phase is not different from that in the late phase in prolonged exercise despite cardiovascular drift.

Oscillation of oxygenation in skeletal muscle at rest and in light exercise.

The aim of the present study was to compare the frequency of oxygenation determined in the vastus lateralis by near-infrared spectroscopy (NIRS) in light exercise with that at rest. A subject rested in a recumbent position for 5 min and changed body position to a sitting position on a cycle ergometer for 9 min. Then exercise with low intensity (work rate of 60% of maximal oxygen uptake) was carried out for 30 min. Total hemoglobin and myoglobin (THb/Mb) suddenly decreased after the start of exercise and gradually increased for 6 min. Oxygenated hemoglobin and myoglobin (Hb/MbO2) suddenly decreased and returned to a steady-state after the start of exercise. The difference between Hb/MbO2 and THb/Mb showed a sudden decrease and then a steady-state. This difference was analyzed by fast Fourier transform. The peak frequencies of the power spectrum density (PSD) were 0.0169 ± 0.0076 Hz at rest and 0.0117 ± 0.0042 Hz in exercise. The peak frequency of PSD was significantly decreased in exercise. In exercise, the range of frequencies was expanded. It is concluded that there are oscillations at rest as well as in exercise and that the frequency of peak PSD becomes lower in exercise than at rest.