European Journal of Applied Physiology and Occupational Physiology最新文献

In this study we investigated the effects of underwater exercise in warm water (34 degrees C) on physiological and psychological relaxation. Eight healthy young men (aged 20-26 years) volunteered for the experiment. The experiment consisted of the following three successive segments: a pre-exercise period of 20 min, during which the subjects rested in a semi-supine posture with their eyes closed for the final 10 min; an underwater exercise period of approximately 60 min, during which the subjects performed gymnastic exercises or aerobic dancing with occasional movements or jumping; a post-exercise recovery of 20 min, which was similar to the pre-exercise rest period. We compared the relative power values (power %) of the electroencephalogram alpha bands (8-13 Hz) and profile of moods states (POMS) before and after the underwater exercise. We also estimated the percentage of maximal heart rate (%HRmax) throughout the experiment to ascertain the intensity of the underwater exercise. The results of %HRmax indicated that the intensity of underwater exercises practised in the experiments ranged from low to moderate. The power % of EEG alpha bands had increased significantly after the underwater exercise compared with the pre-exercise rest (P<0.05). From the POMS results, we observed that positive mood (vigour) increased and negative mood (tension and anxiety, depression and dejection) decreased significantly after the underwater exercise (P<0.05). This study found that the subjects showed increased physiological and psychological indices of relaxation after underwater exercise.

In this study we examined the influence of complete spinal cord injury (SCI) on affected skeletal muscle morphology within 6 months of SCI. Magnetic resonance (MR) images of the leg and thigh were taken as soon as patients were clinically stable, on average 6 weeks post injury, and 11 and 24 weeks after SCI to assess average muscle cross-sectional area (CSA). MR images were also taken from nine able-bodied controls at two time points separated from one another by 18 weeks. The controls showed no change in any variable over time. The patients showed differential atrophy (P = 0.0001) of the ankle plantar or dorsi flexor muscles. The average CSA of m. gastrocnemius and m. soleus decreased by 24% and 12%, respectively (P = 0.0001). The m. tibialis anterior CSA showed no change (P = 0.3644). As a result of this muscle-specific atrophy, the ratio of average CSA of m. gastrocnemius to m. soleus, m. gastrocnemius to m. tibialis anterior and m. soleus to m. tibialis anterior declined (P = 0.0001). The average CSA of m, quadriceps femoris, the hamstring muscle group and the adductor muscle group decreased by 16%, 14% and 16%, respectively (P< or =0.0045). No differential atrophy was observed among these thigh muscle groups, thus the ratio of their CSAs did not change (P = 0.6210). The average CSA of atrophied skeletal muscle in the patients was 45-80% of that of age- and weight-matched able-bodied controls 24 weeks after injury. In conclusion, the results of this study suggest that there is marked loss of contractile protein early after SCI which differs among affected skeletal muscles. While the mechanism(s) responsible for loss of muscle size are not clear, it is suggested that the development of muscular imbalance as well as diminution of muscle mass would compromise force potential early after SCI.

In human locomotion, the metabolic power required (E) to cover a given distance d, in the time t is set by the product of the energy cost of the locomotion (C), i.e. the amount of metabolic energy spent to move over one unit of distance, and the speed (v = d t(-1)): E = Cv = Cdt(-1). Since, for any given d, v is a decreasing function of t and C is either constant or increases with v, it necessarily follows that E is larger the smaller the value of t. Thus, for any given distance and subject, the shortest time will be achieved when E is equal to the individual maximal metabolic power (Emax). In turn, Emax is a decreasing function of t: it depends upon the subject's maximal aerobic power (MAP) and on the maximal amount of energy derived from the full utilisation of anaerobic energy stores (AnS). So, if the relationship between C and (v) in the locomotion at stake and the subject's MAP and AnS are known, his best performance time (BPT) over any given distance can be obtained by solving the equality Emax(t) = E(t). This approach has been applied to estimate individual BPTs in running and cycling. In this paper, the above approach will be used to quantify the role of C, MAP, and AnS in determining BPTs for running, track cycling and swimming. This has been achieved by calculating the changes in BPT obtained when each variable, or a combination thereof, is changed by a given percentage. The results show that in all the three types of locomotion, regardless of the speed, the changes in BPT brought about by changes of C alone account for 45-55% of the changes obtained when all three variables (C, MAP and AnS) are changed by the same amount.

In this study, we examined whether athletes, who typically replace only approximately 50% of their fluid losses during moderate-duration endurance exercise, should attempt to replace their Na+ losses to maintain extracellular fluid volume. Six male cyclists performed three 90-min rides at 65% of peak O2 uptake in a 32 degrees C environment and ingested either no fluid (NF), 1.21 of water (W), or saline (S) containing 100 mmol of NaCl x l(-1) to replace their electrolyte losses. Both W and S conditions decreased final heart rates by approximately 10 betas min(-1) (P<0.005) and reduced falls in plasma volume (PV) by approximately 4% (P<0.05). Maintenance of PV after 10 min in the W trial prevented further rises in plasma concentrations of Na+ [Na+], Cl- and protein but in the S and NF trials, plasma [Na+] continued to increase by approximately 4 mEq x l(-1). Differences in plasma [Na+] had little effect on the approximately 2.4 l fluid, approximately 120 mEq Na+ and approximately 50 mEq K+ losses in sweat and urine in the three trials. The main effects of W and S were on body fluid shifts. During the NF trial, PV and interstitial fluid (ISF) and intracellular fluid (ICF) volumes decreased by approximately 0.1, 1.2 and 1.0 l, respectively. In the W trial, the approximately 1.2 l fluid and approximately 120 mEq Na+ losses contracted the ISF volume, and in the S trial, ISF volume was maintained by the movement of water from the ICF. Since the W and S trials were equally effective in maintaining PV, Na+ ingestion may not be of much advantage to athletes who typically replace only approximately 50% of their fluid losses during competitive endurance exercise.

This experiment was performed to study the effects on femoral bone of endurance training performed during the 3 months before orchidectomy in rats which were then killed 90 days later. A total of 70 male Wistar rats were used at 8 weeks old. One day 0 of the experiment, 10 rats were killed by cervical dislocation and used as first controls. Among the 60 others, 30 were selected for treadmill running (60% maximal oxygen uptake, 1 h x day(-1), 6 days x week(-1) for 90 days). The 30 other rats remained at rest. On day 90, 10 exercised (IE) and resting (IR) rats were killed and used as intermediary controls. Among the 20 other animals of each group, 10 were surgically castrated (CXE, CXR) or 10 sham-operated (SHE, SHR) and killed on day 180. On day 90 femoral failure load (three-point bending test) was greater in IE than in IR. Simultaneously, the deoxypyridinolinuria was lower in IE than in IR. On day 180, femoral bones were thinner in CXR than in CXE. The lowest values for trabecular bone are in the distal femoral metaphysis were measured in CXE and CXR rats, but the value measured in CXE was no different from that measured in SHR. Simultaneously total femoral bone density was lower in CXR than in SHE, while no difference concerning femoral metaphyseal density was observed between CXE and SHR. These results confirmed that endurance running increased femoral bone growth and modelling and femoral trabecular area, and thereby peak bone mass, in 8-month-old male rats. In resting animals, castrated after the training period, androgen deficiency decreased femoral density, mineral content and trabecular area. This decrease was not observed in castrated but previously exercised rats. Thus, by increasing peak bone mass, it was considered that endurance training may have a preventive effect against orchidectomy-induced bone loss.

The coordination between breathing and other motor activities usually implies that the respiratory rhythm has become entrained by the rhythm of the simultaneous movement. Our hypothesis was that by increasing the respiratory drive, e.g. by hypercapnia, we would be able to reduce the subordination of breathing to other movements and, on the other hand, enhance effects of breathing on those movements. We investigated interactions between breathing and finger flexion movements in a visually controlled step-tracking procedure which allowed us to distinguish the mutual effects and to detect the dependence of these effects on the phase-relationship between breathing and movement. In contrast to our hypothesis, we found no large increase of the respiratory influences on finger movements during hypercapnia. A noteworthy difference to normocapnia was a shortening of the finger flexion time during the final stage of expiration which was associated with an increased frequency of coincidence between the end of flexion time and the transition from expiration to inspiration. On the other hand, the response of breathing to the finger movement increased when the tracking signal was presented at the beginning of inspiration. The results of the study disproved our hypothesis and demonstrated that, during hypercapnia, breathing can be even more susceptible to influences originating from motor control. Thus, they are in agreement with the findings of a previous study that the coordination between breathing and rhythmic limb movements becomes closer during hypercapnia.

The purpose of the study was to obtain force/velocity relationships for electrically stimulated (80 Hz) human adductor pollicis muscle (n = 6) and to quantify the effects of fatigue. There are two major problems of studying human muscle in situ; the first is the contribution of the series elastic component, and the second is a loss of force consequent upon the extent of loaded shortening. These problems were tackled in two ways. Records obtained from isokinetic releases from maximal isometric tetani showed a late linear phase of force decline, and this was extrapolated back to the time of release to obtain measures of instantaneous force. This method gave usable data up to velocities of shortening equivalent to approximately one-third of maximal velocity. An alternative procedure (short activation, SA) allowed the muscle to begin shortening when isometric force reached a value that could be sustained during shortening (essentially an isotonic protocol). At low velocities both protocols gave very similar data (r2 = 0.96), but for high velocities only the SA procedure could be used. Results obtained using the SA protocol in fresh muscle were compared to those for muscle that had been fatigued by 25 s of ischaemic isometric contractions, induced by electrical stimulation at the ulnar nerve. Fatigue resulted in a decrease of isometric force [to 69 (3)%], an increase in half-relaxation time [to 431 (10)%], and decreases in maximal shortening velocity [to 77 (8)%] and power [to 42 (5)%]. These are the first data for human skeletal muscle to show convincingly that during acute fatigue, power is reduced as a consequence of both the loss of force and slowing of the contractile speed.

In this study we compared substrate use at submaximal intensities of a maximal graded exercise test (GXT) with that derived from equivalent intensities during continuous submaximal steady-state exercise in obese and normal-weight women. Sedentary obese (n = 20, body fat > 30%) and normal-weight (n = 15, body fat < or =30%) women performed three treadmill tests with concurrent metabolic measurements. Maximal oxygen consumption (VO2max) was determined using the Bruce protocol, followed by two, randomly assigned, continuous 15-min, steady-state exercise bouts, on different days; one bout at 50% and one bout at 75% VO2max. Analysis of variance revealed no significant differences between groups for blood lactate or respiratory exchange ratio (R) values at any point during exercise. Therefore, obese and normal-weight group data were combined for subsequent analyses. The R at 50% VO2max from the GXT [0.83 (0.01)] was significantly (P < 0.05) lower than at 8 min [0.90 (0.01)] and 15 min [0.89 (0.01)] of steady-state exercise, whereas at 75% VO2max, the GXT R [0.96 (0.01)] was similar to that seen at 8 min [0.96 (0.01)] and at 15 min of steady-state exercise [0.93 (0.01)]. Blood lactate values at 50% VO2max were similar between the GXT [1.66 (0.10) mM] and steady-state exercise [1.65 (0.09) mM], but at 75% VO2max the GXT blood lactate values [2.58 (0.21) mM] were lower than after 15 min of steady-state exercise [4.65 (0.46) mM]. Total exercise fat oxidation was greater at 50% compared to 75% VO2max. There was no difference in substrate use between sedentary obese and normal-weight women either at rest or during steady-state exercise at the same relative intensity. Total fat oxidation was greater during low- (50% VO2max) compared to high-intensity (75% VO2max) exercise. Data from a GXT cannot be used to predict R or substrate utilization values for the purpose of exercise prescription.

The purpose of this study was to investigate the cardiovascular and haemodynamic responses that occur during moderate orthostatic challenge in people with paraplegia, and the effect of electrical stimulation (ES)-induced leg muscle contractions on their responses to orthostatic challenge. Eight males with complete spinal lesions between the 5th and 12th thoracic vertebrae (PARA) and eight able-bodied individuals (AB) volunteered for this study. Changes in heart rate (fc), stroke volume (SV), cardiac output (Qc), mean arterial pressure (MAP), total peripheral resistance (TPR), limb volumes and indices of neural modulation of fc, [parasympathetic (PNS) and sympathetic (SNS) nervous system indicators] were assessed during: (1) supine rest (REST), (2) REST with lower-body negative pressure at -30 torr (LBNP -30, where 1 torr = 133.32 N/m2), and (3) for PARA only, LBNP -30 with ES-induced leg muscle contractions (LBNP + ES). LBNP -30 elicited a decrease in SV (by 23% and 22%), Qc (by 15% and 18%) and the PNS indicator, but an increase in fc (by 10% and 9%), TPR (by 23% and 17%) and calf volume (by 1.51% and 4.04%) in both PARA and AB subjects, respectively. The SNS indicator was increased in the AB group only. Compared to LBNP -30, LBNP + ES increased SV (by 20%) and Qc (by 16%), and decreased TPR (by 12%) in the PARA group. MAP was unchanged from REST during all trials, for both groups. The orthostatic challenge induced by LBNP -30 elicited similar cardiovascular adaptations in PARA and AB subjects. ES-induced muscle contractions during LBNP -30 augmented the cardiovascular responses exhibited by the PARA group, probably via reactivation of the skeletal muscle pump and improved venous return.

The mechanisms responsible for the oxygen uptake (VO2) slow component during high-intensity exercise have yet to be established. In order to explore the possibility that the VO2 slow component is related to the muscle contraction regimen used, we examined the pulmonary VO2 kinetics during constant-load treadmill and cycle exercise at an exercise intensity that produced the same level of lactacidaemia for both exercise modes. Eight healthy subjects, aged 22-37 years, completed incremental exercise tests to exhaustion on both a cycle ergometer and a treadmill for the determination of the ventilatory threshold (defined as the lactate threshold, Th1a) and maximum VO2 (VO2max). Subsequently, the subjects completed two "square-wave" transitions from rest to a running speed or power output that required a VO2 that was halfway between the mode-specific Th1a and VO2max. Arterialised blood lactate concentration was determined immediately before and after each transition. The VO2 responses to the two transitions for each exercise mode were time-aligned and averaged. The increase in blood lactate concentration produced by the transitions was not significantly different between cycling [mean (SD) 5.9 (1.5) mM] and running [5.5 (1.6) mM]. The increase in VO2 between 3 and 6 min of exercise; (i.e. the slow component) was significantly greater in cycling than in running, both in absolute terms [290 (102) vs 200 (45) ml x min(-1); P<0.05] and as a proportion of the total VO2 response above baseline [10 (3)% vs 6 (1)%; P < 0.05]. These data indicate that: (a) a VO2 slow component does exist for high-intensity treadmill running, and (b) the magnitude of the slow component is less for running than for cycling at equivalent levels of lactacidaemia. The greater slow component observed in cycling compared to running may be related to differences in the muscle contraction regimen that is required for the two exercise modes.