European Journal of Applied Physiology and Occupational Physiology最新文献

The responses of serum myocellular proteins and hormones to exercise were studied in ten well-trained middle-distance runners [maximal oxygen consumption (VO(2max)) = 69.4 (5.1) ml x kg(-1) x min(-1)] during 3 recovery days and compared to various measures of physical performance. The purpose was to establish the duration of recovery from typical intermittent middle-distance running exercises. The subjects performed, in random, order two 28-min treadmill running exercises at a velocity associated with VO(2max): 14 bouts of 60-s runs with 60 s of rest between each run (IR(60)) and 7 bouts of 120-s runs with 120 s of rest between each run (IR(120)). Before the exercises (pre- exercise), 2 h after, and 1, 2 and 3 days after the exercises, the same series of measurements were performed, including those for serum levels of the myocellular proteins creatine kinase, myoglobin and carbonic anhydrase III (S-CK, S-Mb and S-CA III, respectively), serum hormones testosterone, Luteinizing hormone, follicle-stimulating hormone and cortisol (S-testosterone, S-LH, S-FSH and S-cortisol, respectively) and various performance parameters: maximal vertical jump height (CMJ) and stride length, heart rate and ratings of perceived exertion during an 8-min run at 15 km x h(-1) (SL(15 km x h(-1)), HR(15 km x h(-1)) and RPE(15 km x h(-1)), respectively). Two hours after the end of both exercise bouts the concentration of each measured serum protein had increased significantly (P < 0.001) compared to the pre-exercise level, but there were no changes in SL(15 km x h(-1)) or CMJ. During the recovery days only S-CK was significantly raised (P < 0.01), concomitant with a decrease in CMJ (P < 0.01) and an increase in RPE(15 km x h(-1)) (P < 0.01). Hormone levels remained unchanged compared to the pre-exercise levels during the recovery days and there were no significant differences between the two exercise bouts in any of the observed post-exercise day-to-day responses. With the exception of S-CK, after IR(120) the post-exercise responses returned to their pre-exercise levels within the 3 days of recovery. The present findings suggest that a single 28-min intermittent middle-distance running exercise does not induce changes in serum hormones of well-trained runners during recovery over 3 days, while changes in S-CK, CMJ and RPE(15 km x h(-1)) indicate that 2-3 days of light training may be needed before the recovery at muscle level is complete.

Diurnal variations in ventilatory and cardiorespiratory responses to submaximal treadmill exercise were analysed in 11 eumenorrhoeic women and in 10 women using monophasic oral contraceptives. Subjects performed submaximal treadmill exercise at three intensities averaging 7, 8, and 9 km x h(-1), each for 4 min at 0800, 1300 and 1700 hours, assigned randomly on 3 separate days. Rectal temperature was measured before (T(rec(b))) and after (T(rec(a))) exercise. Cardiac frequency (f(c)), ventilation (V(E)), oxygen uptake (VO(2)), carbon dioxide output (VCO(2)), and respiratory exchange ratio (R) were assessed in the last minute of each stage of the exercise. Both T(rec(b)) and T(rec(a)) increased from 0800 to 1700 hours (P < 0.001). For a given submaximal work rate, VO(2) and VCO(2) were higher in the afternoon compared to the morning. Similarly, R was increased at 1700 hours compared to 0800 hours during the recovery period following exercise (P < 0.05). However, V(E) did not vary significantly during the day at any of the running intensities. No significant interactions (group x time of day) were observed in any of the studied parameters. In contrast to ventilation, the VO(2) and VCO(2) of the females during submaximal exercise were both affected by the time of day, without any differences between eumenorrhoeic women and users of oral contraceptives.

The distribution of oxygen tension (PO(2)) in microvessels and in the tissues of the rat brain cortex on inhaling air (normoxia) and pure oxygen at atmospheric pressure (normobaric hyperoxia) was studied with the aid of oxygen microelectrodes (diameter = 3-6 microm), under visual control using a contact optic system. At normoxia, the PO(2) of arterial blood was shown to decrease from [mean (SE)] 84.1 (1.3) mmHg in the aorta to about 60.9 (3.3) mmHg in the smallest arterioles, due to the permeability of the arteriole walls to oxygen. At normobaric hyperoxia, the PO(2) of the arterial blood decreased from 345 (6) mmHg in the aorta to 154 (11) mmHg in the smallest arterioles. In the blood of the smallest venules at normoxia and at normobaric hyperoxia, the differences between PO(2) values were smoothed out. Considerable differences between PO(2) values at normoxia and at normobaric hyperoxia were found in tissues at a distance of 10-50 microm from the arteriole walls (diameter = 10-30 microm). At hyperbaric hyperoxia these values were greater than at normoxia, by 100-150 mmHg. In the long-run, thorough measurements of PO(2) in the blood of the brain microvessels and in the tissues near to the microvessels allowed the elucidation of quantitative changes in the process of oxygen transport from the blood to the tissues after changing over from the inhalation of air to inhaling oxygen. The physiological, and possibly pathological significance of these changes requires further analysis.

The bilateral patterns of physiological tremor in the upper limb of adults were examined under conditions where eight combinations of the elbow, wrist and index-finger joints of the right arm were braced using individually molded splints. The hypotheses tested were that: (a) coordination of upper-limb tremor involves (compensatory) coupling of intra- but not inter-limb segments, (b) splinting the respective joints of the right arm changes the organization of this synergy in both limbs, and (c) reducing the involvement of joint-space degrees of freedom through restricting their motion (by splinting) results in increased tremor in the distal segments. Under no-splinting conditions, significant relationships were only observed between adjacent (intra-limb) effector units, with the strength of the correlation increasing from proximal to distal. Splinting the right limb resulted in an increase in the strength and number of significant intra-limb relationships in both limbs. No inter-limb tremor relationships were found between any segment during this task, irrespective of the splinting condition. The frequency profile for the tremor in each limb segment showed two prominent frequency peaks (at 2-4 Hz and 8-12 Hz). A third, higher frequency peak (18-22 Hz) was observed in the index fingers only. Splinting the right limb produced a general increase in the amplitude and variability of tremor in the fingertip of both arms. This effect was particularly strong under conditions where the more proximal joints were splinted. The lack of any between-limb relationships, coupled with the fact that splinting one limb influenced both limbs, suggests that some form of linkage does exist between the limbs. It is unlikely that mechanical linkages can explain fully these relationships. It is proposed that the tremor observed in either limb represents the output of a central oscillatory mechanism(s), but that this output is subsequently independently filtered in a parallel fashion on its way to each respective limb. A common bilateral (compensatory) strategy is employed to minimize the tremor in either limb during this multiple-degrees-of-freedom task.

The purpose of this study was to investigate the effect of strength training (12 weeks, 3 days/week, four lower-body exercises) of young individuals (mean age 23.6 years) on estimates of mitochondrial distribution throughout muscle fibres. A control group (mean age 21. 7 years) was followed simultaneously. Skeletal muscle biopsy samples were obtained from the vastus lateralis, pre- and post-training. The regional distribution of subsarcolemmal and intermyofibrillar mitochondrial populations was determined using quantitative histochemical staining of succinate dehydrogenase (SDH) in type I and II muscle fibres. Strength training resulted in significant increases of 26% and 28% in the cross-sectional area of type I and II fibres, respectively (P < 0.05). Overall SDH activity decreased by 13% with strength training (P < 0.05). The decrease in SDH activity with strength training between fibre types and between subsarcolemmal and intermyofibrillar regions of muscle fibres was not different. Fibre area and SDH activity was unchanged in the control group. We conclude that the muscle hypertrophy associated with strength training results in reduced density of regionally distributed mitochondria, as indicated by the reduction in the activity of SDH.

We have used a new approach to study the effects of overload on skeletal muscle phenotype in mice. The method used avoids any traumatising contact with muscles and the inflammatory reaction that this may provoke. Blocks of lead embedded in silicone were inserted under the skin of the lower part of the back. After 1 month, a 17% hypertrophy was found to have occurred in the tonic soleus muscle, but no change was observed in the fast-twitch extensor digitorum longus (EDL) muscle. The main effects on the contractile properties of the soleus muscle were a decrease in the tetanic relaxation rate and a reduction in the maximal velocity of shortening. Immunohistological analysis of the soleus muscles revealed an increase in the proportion of fibres that express myosin heavy chain (MHC) 1, from 54.2% to 73.9%, with a reduction in the proportion of MHC2a-positive fibres, from 45.8% to 30.2%. These changes were accompanied by an increase in the proportion of fibres that express the slow type of sarcoplasmic reticulum calcium pump (SERCA2a), from 61.8% to 84.7%. In EDL muscles, overload induced only minor changes. Thus, this method of overload affected the soleus muscle in particular. The observed changes in the control of muscle contraction were significantly larger than the changes in typical myofibrillar properties that were observed. These results indicate that there is a temporal dissociation between the relative expression of MHCs and SERCAs.

We have investigated the effects of quasi-total-body exposure of healthy volunteers to either an oxygen-ozone mixture (O(2)-O(3)) or to oxygen (O(2)) alone during a short period in a sauna cabin. The subjects underwent both an experimental and a control examination, separated by a 3.5-month interval. Body mass, blood pressure, body temperature changes, electrocardiograms, venous blood gas and haemocytometric analyses, total antioxidant status and plasma levels of protein thiol groups, thiobarbituric acid reactive substances (TBARS), plasma cytokine, hepatic enzymes and creatine were determined before, immediately after the 20-min period in the cabin and then 0.5, 1.0 and 24 h afterwards. We observed statistically significant variations of body temperature, venous partial pressure of O(2) values, TBARS and plasma levels of interleukin 8, particularly after O(2)-O(3) exposure. The increase in TBARS plasma levels concomitant with protein oxidation has been tentatively interpreted as being attributable to the transcutaneous passage of some reactive O(2) species, which should be considered if this approach is to be used as a biological response modifier. However, in the present study no adverse effects were noted after one session.

Fatigue Profile, a new numerical method for characterising fatigue in isokinetic cycle ergometry is presented and compared with the conventional fatigue index (FI). The new method describes the temporal development of muscle fatigue based on the decline of peak power output throughout a whole trial. The advantage of this method is demonstrated by the analysis of two 25 s maximum trials, separated by 90 s recovery, performed by a well-trained athlete at a pedal frequency of 120 revolutions per minute. A fourth degree polynomial was fitted to model the peak power data. Using the polynomial model coefficients the first derivative represented the rate of changing peak power which represented the Fatigue Profile. The conventional FI was calculated as -35 Ws(-1) and -32 Ws(-1) for trials 1 and 2 respectively, indicating minor differences in fatigue between trials. In contrast the Fatigue Profile revealed important numeric and temporal differences between the trials. For trial 1 a maximum rate of peak power decline of -65 Ws(-1) was reached at approximately 6 s into the trial. In marked contrast, in trial 2, maximum rate of peak power decline (-146 Ws(-1)) occurred immediately. The Fatigue Profile approach allows the characterisation of the temporal development of fatigue under different experimental conditions and in combination with other techniques may yield further insight into the underlying mechanisms of fatigue.

We have tested the hypothesis that agonist and antagonist muscle fatigue could affect the final position of rapid, discrete movements. Six subjects performed consecutive elbow flexion and extension movements between two targets, with their eyes closed prior to, and after fatiguing the elbow extensor muscles. The results demonstrate that elbow extension movements performed in the post-test period systematically undershot the final position as compared to pre-test movements. However, attainment of the aimed final position in elbow flexion movements was unaffected by fatiguing of the extensor muscles. Undershoot of the final position obtained in extension movements was associated with agonist muscle fatigue, a result that was expected from the point of view of current motor control theories, and that could be explained by a reduced ability of the shortening muscle to exert force. On the other hand, the absence of the expected overshoot of the final position when the antagonist is fatigued, indicates the involvement of various reflex and/or central mechanisms operating around the stretched muscle that could contribute to returning the limb to the standard final position after a brief prominent overshoot.

Eight competitive cyclists [mean peak oxygen consumption, (VO2(peak)) = 65 ml x min(-1) x kg(-1)] undertook two 60-min cycle ergometer time trials at 32 degrees C and 60% relative humidity. The time trials were split into two 30-min phases: a fixed-workload phase and a variable-workload phase. Each trial was preceded by ingestion of either a glycerol solution [1 g x kg(-1) body mass (BM) in a diluted carbohydrate (CHO)-electrolyte drink] or a placebo of equal volume (the diluted CHO-electrolyte drink). The total fluid intake in each trial was 22 ml x kg(-1) BM. A repeated-measures, double blind, cross over design with respect to glycerol was employed. Glycerol ingestion expanded body water by approximately 600 ml over the placebo treatment. Glycerol treatment significantly increased performance by 5% compared with the placebo group, as assessed by total work in the variable-workload phase (P < 0.04). There were no significant differences in rectal temperature, sweat rate or cardiac frequency between trials. Data indicate that the glycerol-induced performance increase did not result from plasma volume expansion and subsequently lower core temperature or lower cardiac frequencies at a given power output as previously proposed. However, during the glycerol trial, subjects maintained a higher power output without increased perception of effort or thermal strain.