European Journal of Applied Physiology and Occupational Physiology最新文献

In this study, the influence of athletic training status and the contractile character of the active muscle on the magnitude of the pressor response (PR) to voluntary and electrically evoked isometric plantar flexion was investigated. Subjects were 10 sprint-trained athletes (sprint) (100-m, 200-m and 400-m) [mean (SD) age, 21 (2) years], 14 endurance trained athletes (distance) [22 (2) years] and 8 untrained men (control) [23 (3) years]. Twitch time to peak tension (TPT) in the sprint group [108 (7) ms] was significantly less (P<0.001) than that of the distance group [124 (10) ms]. During voluntary contraction, the mean change in systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (fc) was not significantly different between groups. During electrically evoked contractions, mean changes in SBP, DBP and fc were not significantly different between the sprint, distance and control groups. However, division of the sprint group into 400-m (sprint I) and 100/200-m athletes (sprint II) showed that an increase in DBP of 1.6 kPa (12 mm Hg) in sprint I was significantly less (P<0.05) than the 2.5 kPa (19 mm Hg) increase observed for both the distance and control groups. Prediction of the DBP response from our previously published relationship between TPT and DBP showed close agreement in all subject groups except sprint I; in these subjects the observed DBP response was only 55% of that predicted. Attenuation of the PR in the involuntary experiment suggests that some aspect of sprint training, but not endurance training, modifies the muscle afferent input to the PR in man.

It is commonly believed that during hyperbaric oxygen (HBO) treatment, in spite of the vasoconstriction induced by the increased O2 content in the breathing gas, the elevated carrying capacity of O2 in the arterial blood results in augmented O2 delivery to tissues. The experiments described here tested the hypothesis that HBO treatment would be more efficient in delivering O2 to poorly perfused tissues if the vasoconstriction induced by elevated O2 could be abolished or attenuated by adding CO2 to the breathing gas. Organ blood flow (QOBF), systemic hemodynamics, and arterial blood gases were measured before, during and after exposure to either 300 kPa O2 (group 1) or 300 kPa O2 with 2 kPa CO2 (group 2), in awake, instrumented rats. During the HBO exposure the respiratory frequency (fb) fell (4 breaths x min(-1) x 100 kPa O2(-1)), with no changes in arterial CO2 tension (PaCO2), but when CO2 was added, fb and PaCO2 increased. The left ventricular pressure (LVP) and the systolic arterial pressure (SBP) increased. The maximum velocity of LVP (+dP/dt) rose linearly with LVP whether CO2 was added or not (r2 = 0.72 and 0.75 respectively). Similarly, the cardiac output (Qc) and heart rate (fc) fell, while the stroke volume (SV) was unaltered, independent of PaCO2. There was a general vasoconstriction in most organs in both groups, with the exception of the central nervous system (CNS), eyes, and respiratory muscles. HBO reduced the blood flow to the CNS by 30%, but this vasoconstriction was diminished or eliminated when CO2 was added. In group 2, the blood flow to the CNS rose linearly with increased PaCO2 and decreased pH. After decompression fc and SBP stayed high, while Qc returned to control values by reducing the SV; CNS blood flow remained markedly elevated in group 2, while in group 1, it returned to control levels. We conclude that the changes in fc, Qc, LVP, dP/dt, SBP and most QOBF values induced by HBO were not changed by hypercapnia. Blood flow to the CNS decreased during HBO treatment at a constant PaCO2. Hypercapnia prevented this decline. Elevated PaCO2 augmented O2 delivery to the CNS and eyes, but increased the susceptibility to O2 poisoning. A prolonged suppression of O2 supply to the CNS occurred during the HBO exposure and in air following the decompression in the absence of CO2. This suppression was offset by the addition of CO2 to the breathing gas.

The effects of muscle fatigue on the temporal neuromuscular control of the vastus medialis (VM) muscle were investigated in 19 young male subjects. The electromyogram (EMG) activities of VM and the force generation capacities of the quadriceps muscle were monitored before and after a fatigue protocol. In response to light signals, which were triggered randomly, the subjects made three maximal isometric knee extensions. This was then followed by the fatigue protocol which consisted of 30 isometric maximal voluntary contractions at a sequence of 5-s on and 5-s off. Immediately after the exercise to fatigue, the subjects performed another three maximal isometric contractions in response to the light signals. The effects of fatigue on the temporal neuromuscular control were then investigated by dividing the total reaction time (TRT) into premotor time (PMT) and electromechanical delay (EMD). The TRT was defined as the time interval between the light signal and the onset of the knee extension force. The PMT was defined as the time from the light signal to the onset of EMG activities of VM, and EMD as the time interval between onset of EMG activities to that of force generation. Following the contractions to fatigue there was a significant decrease in peak force (Fpeak, P = 0.016), an increase in the root mean square (rms)-EMG: Fpeak quotient (P = 0.001) but an insignificant change in the median frequency (P = 0.062) and rms-EMG (P = 0.119). Significant lengthening of mean EMD was found after the fatigue protocol [0.0396 (SD 0.009) vs. 0.0518 (SD 0.016) s P<0.001]. The lengthening of EMD in VM would affect the stabilizing effect of the patella during knee extension. The faster mean PMT [0.2445 (SD 0.093) vs. 0.2075 (SD 0.074) s, P = 0.042] following the fatigue protocol might have compensated for the lengthened EMD and contributed to the insignificant change in the mean TRT [0.284 (SD 0.09) vs. 0.259 (SD 0.073) s, P = 0.164]. This was probably related to the low level of fatigue (15% decrease in force) and the stereotyped nature of the action such that the effects of the fatigue on neuromuscular control were likely to have been attributable to peripheral processes.

We have evaluated whether sodium bicarbonate, taken chronically (0.5 g x kg(-1) body mass) for a period of 5 days would improve the performance of eight subjects during 60 s of high-intensity exercise on an electrically braked cycle ergometer. The first test was performed prior to chronic supplementation (pre-ingestion) while the post-ingestion test took place 6 days later. A control test took place approximately 1 month after the cessation of all testing. Acid-base and metabolite data (n = 7) were measured from arterialised blood both pre- and post-exercise, as well as daily throughout the exercise period. The work completed by the subjects in the control and pre-ingestion test [21.1 (0.9) and 21.1 (0.9) MJ, respectively] was less than (P<0.05) that completed in the post-ingestion test [24.1 (0.9) MJ; F(2,21) = 3.4, P<0.05, power = 0.57]. Peak power was higher after the 5-day supplementation period (P<0.05). Ingestion of the sodium bicarbonate for a period of 5 days resulted in an increase in pH (F(5,36) = 12.5, P<0.0001, power = 1.0) over the 5-day period. The blood bicarbonate levels also rose during the trial (P<0.05) from a resting level of 22.8 (0.4) to 28.4 (1.1) mmol x l(-1) after 24 h of ingestion. In conclusion, the addition of sodium bicarbonate to a normal diet proved to be of ergogenic benefit in the performance of short-term, high-intensity work.

To test the hypothesis that a chronic expansion of extracellular water (ECW), usually observed during prolonged endurance exercise, is associated with an increase in intracellular water space (ICW), total body water (TBW) and ECW were estimated before (within a week, day C-7) and after (on the 1st day of recovery, R + 1) a competition lasting 7 consecutive days in nine healthy sportsmen. The competition involved running, cycling and cross-country skiing over 620 km. Between days C-7 and R + 1, the following increases occurred - mean TBW by 4.2 (SEM 1.1) l (i.e. +10%, P = 0.01, bioelectrical impedance analysis, BIA, at 100 kHz) and by 4.1 (SEM 0.7) l (P = 0.01, dilution of 18O); mean ECW by 2.2 (SEM 0.5) l (i.e. +14%, P = 0.01, BIA at 5 kHz), and mean plasma volume (PV) by 0.7 (SEM 0.1) l (i.e. +22%, Evans blue dye dilution, P = 0.008). Consequently, mean ICW had been expanded by 2.1 (SEM 0.6) l (i.e. +8%, P = 0.01). The intensity of daily exercise evaluated from recordings of heart rate varied between 49.0% to 57.8% of maximal oxygen consumption VO2max. Water retention was highly correlated with relative exercise intensity VO2max (ICW, r = 0.86; ECW, r = 0.93; TBW, r = 0.94). Total mean plasma content of sodium increased by 104 (SEM 17) mmol (P = 0.008) while albumin and total protein contents were unchanged. We concluded that prolonged and repeated exercise induced a chronic hyperhydration at both extracellular and intracellular levels, which was related to exercise intensity. Sodium retention was the major factor in the increase of PV.

This study tested that hypothesis that skeletal muscle within a year of spinal cord injury (SCI) would respond to intermittent high force loading by showing an increase in size. Three males about 46 weeks post clinically complete SCI underwent surface electrical stimulation of their left or right m. quadriceps femoris 2 days per week for 8 weeks to evoke 4 sets of ten isometric or dynamic actions each session. Conditioning increased average cross-sectional area of m. quadriceps femoris, assessed by magnetic resonance imaging, by 20+/-1% (p = 0.0103). This reversed 48 weeks of atrophy such that m. quadriceps femoris 54 weeks after SCI was the same size as when the patients were first studied 6 weeks after injury. The results suggest that skeletal muscle is remarkably responsive to intermittent, high force loading after almost one year of little if any contractile activity.

Cerebral blood flow increases on exposure to high altitude, and perhaps more so in subjects who develop acute mountain sickness. We determined cerebral blood flow by transcranial Doppler ultrasound of the middle cerebral artery at sea level, in normoxia (fraction of inspired O2, F(I)O2 0.21), and during 15-min periods of either hypoxic (F(I)O2 0.125) or hyperoxic (F(I)O2 1.0) breathing, in 7 subjects with previous high-altitude pulmonary oedema, 6 climbers who had previously tolerated altitudes between 6000 m and 8150 m, and in 20 unselected controls. Hypoxia increased mean middle cerebral artery flow velocity from 69 (3) to 83 (4) cm x s(-1) (P<0.001) in the controls, from 63 (3) to 75 (3) cm x s(-1) (P<0.001) in the high-altitude pulmonary-oedema-susceptible subjects, and from 58 (4) to 70 (4) cm x s(-1) (P<0.001) in the successful high-altitude climbers. Hyperoxia decreased mean middle cerebral flow velocity to 60 (3) cm x s(-1) (P<0.001), 53 (3) cm x s(-1) (P<0.01), and 49 (3) cm x s(-1) (P<0.01) in the controls, high-altitude pulmonary-oedema-susceptible, and high-altitude climbers, respectively. We conclude that a transcranial Doppler-based estimate of cerebral blood flow is affected by hypoxic and hyperoxic breathing, and that it is not predictive of tolerance to high altitude.

The contractile properties of muscle are usually investigated by analysing the force signal recorded during electrically elicited contractions. The electrically stimulated muscle shows surface oscillations that can be detected by an accelerometer; the acceleration signal is termed the surface mechanomyogram (MMG). In the study described here we compared, in the human tibialis anterior muscle, changes in the MMG and force signal characteristics before, and immediately after fatigue, as well as during 6 min of recovery, when changes in the contractile properties of muscle occur. Fatigue was induced by sustained electrical stimulation. The final aim was to evaluate the reliability of the MMG as a tool to follow the changes in the mechanical properties of muscle caused by fatigue. Because of fatigue, the parameters of the force peak, the peak rate of force production and the peak of the acceleration of force production (d2F/dt2) decreased, while the contraction time and the half-relaxation time (1/2-RT) increased. The MMG peak-to-peak (p-p) also decreased. The attenuation rate of the force oscillation amplitude and MMG p-p at increasing stimulation frequency was greater after fatigue. With the exception of 1/2-RT, all of the force and MMG parameters were restored within 2 min of recovery. A high correlation was found between MMG and d2F/dt2 in un-fatigued muscle and during recovery. In conclusion, the MMG reflects specific aspects of muscle mechanics and can be used to follow the changes in the contractile properties of muscle caused by localised muscle fatigue.

The purpose of this study was to show that velocity-specific training may be implicated in modifications in the level of coactivation of agonist and antagonist muscles. Healthy males (n = 20) were randomly placed in to two groups: one group trained using concentric contractions (n = 12), the other was an untrained control group (n = 8). The training group underwent unilateral resistance training at a level of 35 (5)% of a one-repetition maximal contraction of the elbow flexors, executed at maximal angular velocity. Training sessions consisted of six sets of eight consecutive elbow flexions, three times per weak for a total of seven weeks. The velocity of the ballistic movements executed during training were measured using an optoelectronic measuring device (Elite), both at the beginning and at the end of the training period. Subjects were tested pre- and post-training during isokinetic maximal elbow flexions with constant angular torque (CAT) at 90 degrees (0 degrees = full extension), and at different velocities (60, 120, 180, 240 and 300 degrees x s(-1)) for concentric actions, and -60 and -30 degrees x s(-1) for eccentric and isometric contractions at 90 degrees. In order to verify the levels of activation of the agonist biceps brachii (BB) muscles and antagonist triceps brachii (TB) muscles during maximal voluntary activation, their myoelectrical activities were recorded and quantified as root mean square (RMS) amplitudes, between angles of 75 and 105 degrees . The results show that mean angular velocities between elbow angles of 75 and 105 degrees were similar before [302 (32) degrees x s(-1)] and after [312 (27) degrees x s(-1)] the training period. CAT significantly increased measures at angular velocities of 240 and 300 degrees x s(-1) by 18.7% and 23.5%, respectively. The RMS activity of BB agonist muscles was not significantly modified by training. Post-training normalized RMS amplitudes of TB antagonist muscles were inferior to those observed at pre-training, but values were only significantly different at 300 x s(-1). In conclusion, in this study we attempted to show that an increase of CAT to 240 and 300 degrees x s(-1), though velocity-specific training, may be due, in part, to a lowering of the level of coactivation.

Resting energy expenditure, peak oxygen uptake (VO2peak) and the gas-exchange anaerobic threshold (Than) were measured during incremental arm cranking (15 W x min(-1)) in six able-bodied (AB) and six paraplegic (P) subjects. Only male subjects with traumatic spinal cord injuries in the area of the 10-12th thoracic segment were included in the P group. All AB and P subjects were physically active. Mean (SE) values for age and body mass were 28 (2) years and 78.9 (3.9) kg for the AB group and 32 (4) years and 70.8 (7.9) kg for the P group (P>0.05). Resting energy expenditure values were not found to be significantly different between AB [5.8 (0.2) kJ x min(-1)] and P [5.1 (0.3) kJ min(-1)] subjects. Mean VO2peak values were 29.3 (2.4) ml x kg(-1) min(-1) and 29.6 (2.2) ml x kg(-1) x min(-1) for the AB and P groups, respectively (P>0.05). Absolute oxygen uptake values measured at two gas-exchange anaerobic threshold (Than) were not significantly different between the two groups. However, the Than occurred at a significantly higher percentage of VO2peak in the P [58.9 (1.7)%] group than in the AB [50.0 (2.8)%] group (P<0.05). Moreover, respiratory exchange ratio (R) values obtained at the Than and at 15, 45, 60, 75 and 90 W of incremental exercise were significantly lower in the P group than in the AB group. Heart rates were significantly elevated at every submaximal work stage (15-120 W) in the P group compared to the AB group (P<0.05). These findings suggest that chronic daily wheelchair activity produces local adaptations in the functional upper-body musculature, which reduce glycogenolysis and increase the rate of lipid utilization (lower R) during arm exercise. These local adaptations may be in part responsible for the significantly higher Than observed for arm exercise in P subjects, even though VO2peak values were essentially the same for both groups.