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1.
The influence of artificially induced anaemia on thermal strain was evaluated in trained males. Heat stress trials (38.6°C, water vapour pressure 2.74 kPa) performed at the same absolute work rates [20 min of seated rest, 20 min of cycling at 30% peak aerobic power (O2peak), and 20 min cycling at 45% O2peak] were completed before (HST1) and 3–5 days after 3 units of whole blood were withdrawn (HST2). Mild anaemia did not elevate thermal strain between trials, with auditory canal temperatures terminating at 38.5°C [(0.16), HST1] and 38.6°C [(0.13), HST2; P > 0.05]. Given that blood withdrawal reduced aerobic power by 16%, this observation deviates from the close association often observed between core temperature and relative exercise intensity. During HST2, the absolute and integrated forearm sweat rate ( sw) exceeded control levels during exercise (P < 0.05), while a suppression of forehead sw occurred (P < 0.05). These observations are consistent with a possible peripheral redistribution of sweat secretion. It was concluded that this level of artificially induced anaemia did not impact upon heat strain during a 60-min heat stress test. Accepted: 17 April 1997  相似文献   

2.
A group of 12 healthy non-smoking men [mean age 22.3 (SD 1.1) years], performed an incremental exercise test. The test started at 30 W, followed by increases in power output (P) of 30 W every 3 min, until exhaustion. Blood samples were taken from an antecubital vein for determination of plasma concentration lactate [La]pl and acid-base balance variables. Below the lactate threshold (LT) defined in this study as the highest P above which a sustained increase in [La]pl was observed (at least 0.5 mmol · l−1 within 3 min), the pulmonary oxygen uptake (O2) measured breath-by-breath, showed a linear relationship with P. However, at P above LT [in this study 135 (SD 30) W] there was an additional accumulating increase in O2 above that expected from the increase in P alone. The magnitude of this effect was illustrated by the difference in the final P observed at maximal oxygen uptake (O2max) during the incremental exercise test (P max,obs at O2max) and the expected power output at O2max(P max,exp at O2max) predicted from the linear O2-P relationship derived from the data collected below LT. The P max,obs at O2max amounting to 270 (SD 19) W was 65.1 (SD 35) W (19%) lower (P<0.01) than the P max,exp at O2max . The mean value of O2max reached at P max,obs amounted to 3555 (SD 226) ml · min−1 which was 572 (SD 269) ml · min−1 higher (P<0.01) than the O2 expected at this P, calculated from the linear relationship between O2 and P derived from the data collected below LT. This fall in locomotory efficiency expressed by the additional increase in O2, amounting to 572 (SD 269) ml O2 · min−1, was accompanied by a significant increase in [La]pl amounting to 7.04 (SD 2.2) mmol · l−1, a significant increase in blood hydrogen ion concentration ([H+]b) to 7.4 (SD 3) nmol · l−1 and a significant fall in blood bicarbonate concentration to 5.78 (SD 1.7) mmol · l−1, in relation to the values measured at the P of the LT. We also correlated the individual values of the additional O2 with the increases (Δ) in variables [La]pl and Δ[H+]b. The Δ values for [La]pl and Δ[H+]b were expressed as the differences between values reached at the P max,obs at O2max and the values at LT. No significant correlations between the additional O2 and Δ[La]pl on [H+]b were found. In conclusion, when performing an incremental exercise test, exceeding P corresponding to LT was accompanied by a significant additional increase in O2 above that expected from the linear relationship between O2 and P occurring at lower P. However, the magnitude of the additional increase in O2 did not correlate with the magnitude of the increases in [La]pl and [H+]b reached in the final stages of the incremental test. Accepted: 30 October 1997  相似文献   

3.
The transient response of oxygen uptake (O2) to submaximal exercise, known to be abnormal in patients with cardiovascular disorders, can be useful in assessing the functional status of the cardiocirculatory system, however, a method for evaluating it accurately has not yet been established. As an alternative approach to the conventional test at constant exercise intensity, we applied a random stimulus technique that has been shown to provide relatively noise immune responses of system being investigated. In 27 patients with heart failure and 24 age-matched control subjects, we imposed cycle exercise at 50 W intermittently according to a pseudo-random binary (exercise-rest) sequence, while measuring breath-by-breath O2. After determining the transfer function relating exercise intensity () to O2 and attenuating the high frequency ranges (>6 exercise-rest cycles · min−1), we computed the high resolution band-limited (0–6 cycles · min−1) O2 response (0–120 s) to a hypothetical step exercise. The O2 response showed a longer time constant in the patients than in the control subjects [47 (SD 37) and 31 (SD 8) s, respectively, P < 0.05]. Furthermore, the amplitude of the O2 response after the initial response was shown to be significantly smaller in the patients than in the control subjects [176 (SD 50) and 267 (SD 54) ml · min−1 at 120 s]. The average amplitude over 120 s correlated well with peak O2 (r = 0.73) and ΔO2 (r = 0.70), both of which are well-established indexes of exercise tolerance. The data indicated that our band-limited V˙O2 step response using random exercise was more markedly attenuated and delayed in the patients with heart failure than in the normal controls and that it could be useful in quantifying the overall functional status of the cardiocirculatory system. Accepted: 6 January 1998  相似文献   

4.
This study compared the cardiorespiratory responses of eight healthy women (mean age 30.25 years) to submaximal exercise on land (LTm) and water treadmills (WTm) in chest-deep water (Aquaciser). In addition, the effects of two different water temperatures were examined (28 and 36°C). Each exercise test consisted of three consecutive 5-min bouts at 3.5, 4.5 and 5.5 km · h−1. Oxygen consumption (O2) and heart rate (HR), measured using open-circuit spirometry and telemetry, respectively, increased linearly with increasing speed both in water and on land. At 3.5 km · h−1 O2 was similar across procedures [χ = 0.6 (0.05) l · min−1]. At 4.5 and 5.5 km · h−1 O2 was significantly higher in water than on land, but there was no temperature effect (WTm: 0.9 and 1.4, respectively; LTm: 0.8 and 0.9 l · min−1, respectively). HR was significantly higher in WTm at 36°C compared to WTm at 28°C at all speeds, and compared to LTm at 4.5 and 5.5 km · h−1 (P ≤ 0.003). The HR-O2 relationship showed that at a O2 of 0.9 l · min−1, HR was higher in water at 36°C (115 beats · min−1) than either on land (100 beats · min−1) or in water at 28°C (99 beats · min−1). The Borg scale of perceived exertion showed that walking in water at 4.5 and 5.5 km · h−1 was significantly harder than on land (WTm: 11.4 and 14, respectively; LTm: 9.9 and 11, respectively; P ≤ 0.001). These cardiorespiratory changes occurred despite a slower cadence in water (the mean difference at all speeds was 27 steps/min). Thus, walking in chest-deep water yields higher energy costs than walking at similar speeds on land. This data has implications for therapists working in hydrotherapy pools. Accepted: 3 September 1997  相似文献   

5.
This study investigated the effects on running economy (RE) of ingesting either no fluid or an electrolyte solution with or without 6% carbohydrate (counterbalanced design) during 60-min running bouts at 80% maximal oxygen consumption (O2max). Tests were undertaken in either a thermoneutral (22–23°C; 56–62% relative humidity, RH) or a hot and humid natural environment (Singapore: 25–35°C; 66–77% RH). The subjects were 15 young adult male Singaporeans [O2max = 55.5 (4.4 SD) ml kg−1 min−1]. The RE was measured at 3 m s−1 [65 (6)% O2max] before (RE1) and after each prolonged run (RE2). Fluids were administered every 2 min, at an individual rate determined from prior tests, to maintain body mass (group mean = 17.4 ml min−1). The O2 during RE2 was higher (P < 0.05) than that during the RE1 test for all treatments, with no differences between treatments (ANOVA). The mean increase in O2 from RE1 to RE2 ranged from 3.4 to 4.7 ml kg−1 min−1 across treatments. In conclusion, the deterioration in RE at 3 m s−1 (65% O2max) after 60 min of running at 80% O2max appears to occur independently of whether fluid is ingested and regardless of whether the fluid contains carbohydrates or electrolytes, in both a thermoneutral and in a hot, humid environment. Accepted: 30 October 1997  相似文献   

6.
Oxygen toxicity of the central nervous system (CNS) can occur as convulsions and loss of consciousness, with no warning symptoms. A quantitative study of the effect of metabolic rate on sensitivity to oxygen toxicity was made in the rat. A group of 19 rats were exposed (126 exposures) to 12 combinations of four pressures (456, 507, 608 and 709 kPa) and three ambient temperatures (15, 23 and 29°C) until the appearance of the first electrical discharge (FED) preceding clinical convulsions. Carbon dioxide production (CO2) was also measured. A thermoneutral zone (mean CO2 0.87 ml · g−1 · h−1) existed between the temperatures of 24 and 29°C; at temperatures lower than this, the metabolic rate increased by 1.2 to 4 times the resting level. Latency of FED decreased linearly with the increase in CO2 at all four oxygen pressures. The slopes (absolute value) and intercepts decreased with the increase in oxygen pressure. This linear relationship made possible the derivation of an equation which described latency of the FED as a function of both oxygen pressure and metabolic rate. Various environmental and other physiological factors that have been said to influence sensitivity to CNS oxygen toxicity, enhancing the effect of the partial pressure of oxygen, can be explained by their effect on metabolic rate. It is suggested that in situations where there is a risk of oxygen toxicity of the CNS, that risk would be reduced by a lower metabolic rate. Accepted: 4 May 1998  相似文献   

7.
Specimens of Nautilus pompilius were trapped at depths of 225–300 m off the sunken barrier reef south-east of Port Moresby, Papua New Guinea. Animals transported to the Motupore Island laboratory were acclimated to normal habitat temperatures of 18 °C and then cannulated for arterial and venous blood sampling. When animals were forced to undergo a period of progressive hypoxia eventually to encounter ambient partial pressure of oxygen (PO2) levels of ∼10 mmHg (and corresponding arterial PO2's of ∼5 mmHg), they responded by lowering their aerobic metabolic rates to 5–10% of those seen in resting normoxic animals. Coincident with this profound metabolic suppression was an overall decrease in activity, with brief periods of jet propulsion punctuating long periods of rest. Below ambient PO2 levels of 30–40 mmHg, ventilatory movements became highly periodic and at the lowest PO2 levels encountered, ventilation occasionally ceased altogether. Cardiac output estimated by the Fick equation decreased during progressive hypoxia by as much as 75–80%, and in the deepest hypometabolic states heart rates slowed to one to two cycles of very low amplitude per minute. By the end of 500 min exposure to ambient PO2 levels of 10 mmHg or less, the anaerobic end products octopine and succinate had increased significantly in adductor muscle and heart, respectively. Increased concentrations of octopine in adductor muscle apparently contributed to a small intracellular acidosis and to the development of a combined respiratory and metabolic acidosis in the extracellular compartment. On the other hand, increases in succinate in heart muscle occurred in the absence of any change in cardiac pHi. Taken together, we estimate that these anaerobic end products would make up less than 2% of the energy deficit arising from the decrease in aerobic metabolism. Thus, metabolic suppression is combined with a massive downregulation of systemic O2 delivery to match metabolic supply to demand. Accepted: 26 January 2000  相似文献   

8.
The aims of the present study were: (1) to assess aerobic metabolism in paraplegic (P) athletes (spinal lesion level, T4–L3) by means of peak oxygen uptake (O2peak) and ventilatory threshold (VT), and (2) to determine the nature of exercise limitation in these athletes by means of cardioventilatory responses at peak exercise. Eight P athletes underwent conventional spirographic measurements and then performed an incremental wheelchair exercise on an adapted treadmill. Ventilatory data were collected every minute using an automated metabolic system: ventilation (l · min−1), oxygen uptake (O2, l · min−1, ml · min−1 · kg−1), carbon dioxide production (CO2, ml · min−1), respiratory exchange ratio, breathing frequency and tidal volume. Heart rate (HR, beats · min−1) was collected with the aid of a standard electrocardiogram. O2peak was determined using conventional criteria. VT was determined by the breakpoint in the CO2O2 relationship, and is expressed as the absolute VT (O2, ml · min−1 · kg−1) and relative VT (percentage of O2peak). Spirometric values and cardioventilatory responses at rest and at peak exercise allowed the measurement of ventilatory reserve (VR), heart rate reserve (HRr), heart rate response (HRR), and O2 pulse (O2 P). Results showed a O2peak value of 40.6 (2.5) ml · min−1 · kg−1, an absolute VT detected at 23.1 (1.5) ml · min−1 · kg−1 O2 and a relative VT at 56.4 (2.2)% O2peak. HRr [15.8 (3.2) beats · min−1], HRR [48.6 (4.3) beat · l−1], and O2 P [0.23 (0.02) ml · kg−1 · beat−1] were normal, whereas VR at peak exercise [42.7 (2.4)%] was increased. As wheelchair exercise excluded the use of an able-bodied (AB) control group, we compared our O2peak and VT results with those for other P subjects and AB controls reported in the literature, and we compared our cardioventilatory responses with those for respiratory and cardiac patients. The low O2peak values obtained compared with subject values obtained during an arm-crank exercise may be due to a reduced active muscle mass. Absolute VT was somewhat comparable to that of AB subjects, mainly due to the similar muscle mass involved in wheelchair and arm-crank exercise by P and AB subjects, respectively. The increased VR, as reported in patients with chronic heart failure, suggested that P athletes exhibited cardiac limitation at peak exercise, and this contributed to the lower O2peak measured in these subjects. Accepted: 22 April 1997  相似文献   

9.
The present experiment was designed to study the importance of strength and muscle mass as factors limiting maximal oxygen uptake (O2 max ) in wheelchair subjects. Thirteen paraplegic subjects [mean age 29.8 (8.7) years] were studied during continuous incremental exercises until exhaustion on an arm-cranking ergometer (AC), a wheelchair ergometer (WE) and motor-driven treadmill (TM). Lean arm volume (LAV) was estimated using an anthropometric method based upon the measurement of various circumferences of the arm and forearm. Maximal strength (MVF) was measured while pushing on the rim of the wheelchair for three positions of the hand on the rim (−30°, 0° and +30°). The results indicate that paraplegic subjects reached a similar O2 max [1.23 (0.34) l · min−1, 1.25 (0.38) l · min−1, 1.22 (0.18) l · min−1 for AC, TM and WE, respectively] and O2 max /body mass [19.7 (5.2) ml · min−1 · kg−1, 19.5 (6.14) ml · min−1 · kg−1, 19.18 (4.27) ml · min−1 · kg−1 for AC, TM and WE, respectively on the three ergometers. Maximal heart rate f c max during the last minute of AC (173 (17) beats · min−1], TM [168 (14) beats · min−1], and WE [165 (16) beats · min−1], were correlated, but f c max was significantly higher for AC than for TM (P<0.03). There were significant correlations between MVF and LAV (P<0.001) and between the MVF data obtained at different angles of the hand on the rim [311.9 (90.1) N, 313.2 (81.2) N, 257.1 (71) N, at −30°, 0° and +30°, respectively]. There was no correlation between O2 max and LAV or MVF. The relatively low values of f c max suggest that O2 max was, at least in part, limited by local aerobic factors instead of central cardiovascular factors. On the other hand, the lack of a significant correlation between O2 max and MVF or muscle mass was not in favour of muscle strength being the main factor limiting O2 max in our subjects. Accepted: 31 January 1997  相似文献   

10.
The ventilatory equivalent for CO2 defines ventilatory efficiency largely independent of metabolism. An impairment of ventilatory efficiency may be caused by an increase in either anatomical or physiological dead space, the latter being the most important mechanism in the hyperpnoea of heart failure, pulmonary embolism, pulmonary hypertension and the former in restrictive lung disease. However, normal values for ventilatory efficiency have not yet been established. We investigated 101 (56 men) healthy volunteers, aged 16–75 years, measuring ventilation and gas exchange at rest (n = 64) and on exercise (modified Naughton protocol, n = 101). Age and sex dependent normal values for ventilatory efficiency at rest defined as the ratio ventilation:carbon dioxide output ( E:CO2), exercise ventilatory efficiency during exercise, defined as the slope of the linear relationship between ventilation and carbon dioxide output ( E vs CO2 slope), oxygen uptake at the anaerobic threshold and at maximum (O2AT,O2max, respectively) and breathing reserve were established. Ventilatory efficiency at rest was largely independent of age, but was smaller in the men than in the women [ E:CO2 50.5 (SD 8.8) vs 57.6 (SD 12.6) P<0.05]. Ventilatory efficiency during exercise declined significantly with age and was smaller in the men than in the women (men: ( E vs CO2 slope = 0.13 × age + 19.9; women: E vs CO2 slope = 0.12 × age + 24.4). The O2AT and O2max were 23 (SD 5) and 39 (SD 7) ml O2 · kg · min−1 in the men and 18 (SD 4) and 32 (SD 7) in the women, respectively, and declined significantly with age. The O2AT was reached at 58 (SD 9)% O2max. Breathing reserve at the end of exercise was 41% and was independent of sex and age. It was concluded from this study that ventilatory efficiency as well as peak oxygen uptake are age and sex dependent in adults. Accepted: 11 June 1997  相似文献   

11.
The effects of whole-body exposure to ambient temperatures of −15°C and 23°C on selected performance-related physiological variables were investigated in elite nonasthmatic cross-country skiers. At an ambient temperature of −15°C we also studied the effects of the selective β2-adrenergic agonist Salbutamol (0.4 mg × 3) which was administered 10 min before the exercise test. Eight male cross-country skiers with known maximal oxygen uptakes (O2 max ) of more than 70 ml · kg−1 · min−1 participated in the study. Oxygen uptake (O2), heart rate (f c), blood lactate concentration ([La]b) and time to exhaustion were measured during controlled submaximal and maximal running on a treadmill in a climatic chamber. Lung function measured as forced expiratory volume in 1 s (FEV1) was recorded immediately before the warm-up period and at the conclusion of the exercise protocol. Submaximal O2 and [La]b at the two highest submaximal exercise intensities were significantly higher at −15°C than at 23°C. Time to exhaustion was significantly shorter in the cold environment. However, no differences in O2 max or f c were observed. Our results would suggest that exercise stress is higher at submaximal exercise intensities in a cold environment and support the contention that aerobic capacity is not altered by cold exposure. Furthermore, we found that after Salbutamol inhalation FEV1 was significantly higher than after placebo administration. However, the inhaled β2-agonist Salbutamol did not influence submaximal and maximal O2, f c, [La]b or time to exhaustion in the elite, nonasthmatic cross-country skiers we studied. Thus, these results did not demonstrate any ergogenic effect of the β2-agonist used. Accepted: 18 August 1997  相似文献   

12.
The purpose of this study was to develop a method to determine the power output at which oxygen uptake (O2) during an incremental exercise test begins to rise non-linearly. A group of 26 healthy non-smoking men [mean age 22.1 (SD 1.4) years, body mass 73.6 (SD 7.4) kg, height 179.4 (SD 7.5) cm, maximal oxygen uptake (O2max) 3.726 (SD 0.363) l · min−1], experienced in laboratory tests, were the subjects in this study. They performed an incremental exercise test on a cycle ergometer at a pedalling rate of 70 rev · min−1. The test started at a power output of 30 W, followed by increases amounting to 30 W every 3 min. At 5 min prior to the first exercise intensity, at the end of each stage of exercise protocol, blood samples (1 ml each) were taken from an antecubital vein. The samples were analysed for plasma lactate concentration [La]pl, partial pressure of O2 and CO2 and hydrogen ion concentration [H+]b. The lactate threshold (LT) in this study was defined as the highest power output above which [La]pl showed a sustained increase of more than 0.5 mmol · l−1 · step−1. The O2 was measured breath-by-breath. In the analysis of the change point (CP) of O2 during the incremental exercise test, a two-phase model was assumed for the 3rd-min-data of each step of the test: X i =at i +b i for i=1,2,…,T, and E(X i )>at i +b for i =T+1,…,n, where X 1, … , X n are independent and ɛ i ∼N(0,σ2). In the first phase, a linear relationship between O2 and power output was assumed, whereas in the second phase an additional increase in O2 above the values expected from the linear model was allowed. The power output at which the first phase ended was called the change point in oxygen uptake (CP-O2). The identification of the model consisted of two steps: testing for the existence of CP and estimating its location. Both procedures were based on suitably normalised recursive residuals. We showed that in 25 out of 26 subjects it was possible to determine the CP-O2 as described in our model. The power output at CP-O2 amounted to 136.8 (SD 31.3) W. It was only 11 W – non significantly – higher than the power output corresponding to LT. The O2 at CP-O2 amounted to 1.828 (SD 0.356) l · min−1 was [48.9 (SD 7.9)% O2 max ]. The [La]pl at CP-O2, amounting to 2.57 (SD 0.69) mmol · l−1 was significantly elevated (P<0.01) above the resting level [1.85 (SD 0.46) mmol · l−1], however the [H+]b at CP-O2 amounting to 45.1 (SD 3.0) nmol · l−1, was not significantly different from the values at rest which amounted to 44.14 (SD 2.79) nmol · l−1. An increase of power output of 30 W above CP-O2 was accompanied by a significant increase in [H+]b above the resting level (P=0.03). Accepted: 25 March 1998  相似文献   

13.
In a previous study, rectal temperature (T re) was found to be lower, and oxygen consumption (O2) and the respiratory exchange ratio (R) were higher in a cold (+5°C), wet and windy environment (COLD), compared with a thermoneutral environment during intermittent walking at ≈30% of peak O2 (Weller AS, Millard CE, Stroud MA et al. Am J Physiol 272:R226–R233, 1997). The aim of the present study was to establish whether these cold-induced responses are influenced by prior fasting, as impaired thermoregulation has been demonstrated in cold-exposed, resting men following a 48-h fast. To address this question, eight men attempted a 360-min intermittent (15 min rest, 45 min exercise) walking protocol under COLD conditions on two occasions. In one condition, the subjects started the exercise protocol ≈120 min after a standard meal (FED/COLD), whereas in the other the subjects had fasted for 36 h (FASTED/COLD). The first two exercise periods were conducted at a higher intensity (HIGHER, 6 km · h−1 and 10% incline), than the four subsequent exercise periods (LOW, 5 km · h−1 and 0% incline). There was no difference in the time endured in FED/COLD and FASTED/COLD. In FASTED/COLD com pared with FED/COLD, R was lower during HIGHER and LOW, and T re was lower during LOW, whereas there was no difference in O2, mean skin temperature and heart rate. Therefore, although the 36-h fast impaired temperature regulation during intermittent low-intensity exercise in the cold, wet and windy environment, it was unlikely to have been the principal factor limiting exercise performance under these experimental conditions. Accepted: 26 August 1997  相似文献   

14.
Heart rate (HR) monitoring is commonly used to assess 24-h energy expenditure (EE) in children but it has been found to overestimate the true values. One reason for this may be the effect of climatic heat stress on HR. An equation has been previously developed to adjust HR measured during continuous exercise for the influence of climate. Since play in children is rarely of a continuous pattern, one objective of this study was to compare the effects of climatic heat stress on the HR response to intermittent and to continuous exercise. A second objective was to determine whether the previously developed equation is suitable for intermittent exercise. A group of 12 boys and 8 girls (aged 8–11 years) cycled in a climatic chamber. The exercise consisted of continuous cycling for 5 min at 35%, 55%, and 75% of peak oxygen up take (random order) followed by alternating cycling at the same resistance and cadence (30 s) and rest (30 s) for 3 additional min. The oxygen uptake (O2) and HR were determined for 2 min at the end of continuous cycling and for 2 min during intermittent cycling. Climatic conditions (randomly assigned) were dry bulb temperature T db 22°C, 50% relative humidity (rh); T db 28°C, 55% rh; T db 32°C, 52% rh; or T db 35°C, 58% rh. The difference between HR measured at a given T db (HRmeas) and HR at 22°C and at the same O2 was then calculated (ΔHR). The ΔHR increased linearly with increasing temperature but was not related to O2 or to exercise type. However, a small but significant difference was found if the published equation was used with data from intermittent exercise. The accuracy of the existing equation adjusting HRmeas for the influence of T db (HRcorr) could be improved to HRcorr= HRmeas · (1.18308−(0.0083218 · T db)). In conclusion, the effects of climatic heat stress on HR were similar in continuous and intermittent exercise, and HR can be adjusted for the influence of climate in groups of pre- and early pubertal children during rest, intermittent and continuous exercise at ambient temperatures between 22°C and 35°C, thereby reducing the error in predicting EE from HR. Accepted: 13 January 1998  相似文献   

15.
Eight male endurance runners [mean ± (SD): age 25 (6) years; height 1.79 (0.06) m; body mass 70.5 (6.0) kg; % body fat 12.5 (3.2); maximal oxygen consumption (O2max 62.9 (1.7) ml · kg−1 · min−1] performed an interval training session, preceded immediately by test 1, followed after 1 h by test 2, and after 72 h by test 3. The training session was six 800-m intervals at 1 km · h−1 below the velocity achieved at O2max with 3 min of recovery between each interval. Tests 1, 2 and 3 were identical, and included collection of expired gas, measurement of ventilatory frequency (f v ), heart rate (f c), rate of perceived exertion (RPE), and blood lactate concentration ([La]B) during the final 5 min of 15 min of running at 50% of the velocity achieved at O2max (50% −O2max).␣Oxygen uptake (O2), ventilation ( E ), and respiratory exchange ratio (R) were subsequently determined from duplicate expired gas collections. Body mass and plasma volume changes were measured preceding and immediately following the training session, and before tests 1–3. Subjects ingested water immediately following the training session, the volume of which was determined from the loss of body mass during the session. Repeated measures analysis of variance with multiple comparison (Tukey) was used to test differences between results. No significant differences in body mass or plasma volume existed between the three test stages, indicating that the differences recorded for the measured parameters could not be attributed to changes in body mass or plasma volume between tests, and that rehydration after the interval training session was successful. A significant (P < 0.05) increase was found from test 1 to test 2 [mean (SD)] for O2 [2.128 (0.147) to 2.200 (0.140) 1 · min−1], f c [125 (17) to 132 (16) beats · min−1], and RPE [9 (2) to 11 (2)]. A significant (P < 0.05) decrease was found for submaximal R [0.89 (0.03) to 0.85 (0.04)]. These results suggest that alterations in O2 during moderate-intensity, constant-velocity running do occur following heavy-intensity endurance running training, and that this is due to factors in addition to changed substrate metabolism towards greater fat utilisation, which could explain only 31% of the increase in O2. Accepted: 8 December 1997  相似文献   

16.
Using 23 elite male athletes (8 cyclists, 7 kayakists, and 8 swimmers), the contribution of the anaerobic energy system to the time to exhaustion (t lim) at the minimal exercise intensity (speed or power) at which maximal oxygen uptake (O2 max) occurs (I V˙O2 max) was assessed by analysing the relationship between the t lim and the accumulated oxygen deficit (AOD). After 10-min warming up at 60% of O2 max, the exercise intensity was increased so that each subject reached his I V˙O2max in 30 s and then continued at that level until he was exhausted. Pre-tests included a continuous incremental test with 2 min steps for determining the I V˙O2max and a series of 5-min submaximal intensities to collect the data that would allow the estimation of the energy expenditure at I V˙O2max . The AOD for the t lim exercise was calculated as the difference between the above estimation and the accumulated oxygen uptake. The mean percentage value of energy expenditure covered by anaerobic metabolism was 15.2 [(SD 6)%, range 8.9–24.1] with significant differences between swimmers and kayakists (16.8% vs 11.5%, P≤0.05) and cyclists and kayakists (16.4% vs 11.5%, P≤0.05). Absolute AOD values ranged from 26.4 ml · kg−1 to 83.6 ml · kg−1 with a mean value of 45.9 (SD 18) ml · kg−1. Considering all the subjects, the t lim was found to have a positive and significant correlation with AOD (r = 0.62, P≤0.05), and a negative and significant correlation with O2 max (r = −0.46, P≤0.05). The data would suggest that the contribution of anaerobic processes during exercise performed at I V˙O2max should not be ignored when t lim is used as a supplementary parameter to evaluate specific adaptation of athletes. Accepted: 17 December 1996  相似文献   

17.
It has previously been demonstrated that metabolic heat production (M˙) during cold exposure at rest was related to maximal oxygen uptake (O2max). Consequently, an increase in O2max could allow an increase M˙ in the cold. The aim of the present study was therefore to test this hypothesis. Eight male volunteers undertook interval training (periods of 25% O2max of 30-s duration and 110% O2max of 60-s duration until exhaustion, five times a week over 8 weeks) to increase O2max. Both before and after this physical training, they were subjected to a 10, 5 and 1C 2-h cold air test in a climatic chamber. During the cold exposure, rectal temperature (T re), tympanic temperature (T ty), mean skin temperature () and M˙ were measured as well as the time to onset of shivering (t) and body temperatures () at t. The results showed that physical training involved an increase in O2max (14%–15%, P < 0.05). During the cold exposure, T re was higher after training both at 10,5 and 1C (P < 0.05) whereas were not significantly changed. However, an increase in the sensitivity of the thermoregulatory system was attested by a decreased t at higher These slight physiological changes found after training were not related to the increases in O2max. In conclusion, this study demonstrated that interval training induced slight thermoregulatory changes unrelated to changes in O2max and it suggested that M˙ during cold exposure could be related mainly to the level of O2max observed before training, since increases in O2max did not modify M˙. Accepted: 8 April 1998  相似文献   

18.
Fifteen young adult Singaporean male physical education students maximum oxygen consumption [(O2max) = 56 (4.7) ml · kg−1 · min−1] performed three prolonged runs in a counterbalanced design. The running bouts varied in time (40 vs 60 min) and intensity (70% vs 80% O2 max ). Each prolonged run was separated by 7 days. The running economy (RE) at 10.8 km · h−1 during 10-min running bouts was measured before (RE1) and after (RE2) each prolonged run. A control study involved monitoring RE at 10.8 km · h−1 before and after 60 min rest. There were no differences between RE1 and RE2 values during the control run. However, there were differences between RE1 and RE2 values when separated by a prolonged run. For example, the mean (SD) changes in oxygen consumption (ml · kg−1 · min−1) values were 38.2 (2.5) versus 40.1 (2.6) (40 min at 80% O2 max ), 38.9 (2.8) versus 41.5 (2.6) (60 min at 70% O2 max ), and 39.0 (3.1) versus 42.7 (2.9) (60 min at 80% O2 max ; P < 0.01). The results of this investigation support the hypothesis that RE deteriorates during prolonged running, and that the magnitude of the deterioration in RE increases with both increasing exercise intensity and duration. Accepted: 14 July 1997  相似文献   

19.
The purpose of this study was to compare the rates of muscle deoxygenation in the exercising muscles during incremental arm cranking and leg cycling exercise in healthy men and women. Fifteen men and 10 women completed arm cranking and leg cycling tests to exhaustion in separate sessions in a counterbalanced order. Cardiorespiratory measurements were monitored using an automated metabolic cart interfaced with an electrocardiogram. Tissue absorbency was recorded continuously at 760 nm and 850 nm during incremental exercise and 6 min of recovery, with a near infrared spectrometer interfaced with a computer. Muscle oxygenation was calculated from the tissue absorbency measurements at 30%, 45%, 60%, 75% and 90% of peak oxygen uptake (V˙O2) during each exercise mode and is expressed as a percentage of the maximal range observed during exercise and recovery (%Mox). Exponential regression analysis indicated significant inverse relationships (P < 0.01) between %Mox and absolute V˙O2 during arm cranking and leg cycling in men (multiple R = −0.96 and −0.99, respectively) and women (R =−0.94 and −0.99, respectively). No significant interaction was observed for the %Mox between the two exercise modes and between the two genders. The rate of muscle deoxygenation per litre of V˙O2 was 31.1% and 26.4% during arm cranking and leg cycling, respectively, in men, and 26.3% and 37.4% respectively, in women. It was concluded that the rate of decline in %Mox for a given increase in V˙O2 between 30% and 90% of the peak V˙O2 was independent of exercise mode and gender. Accepted: 31 March 1998  相似文献   

20.
This study investigated the question: is core temperature measurement influenced by whether exercise involves predominantly upper- or lower-body musculature? Healthy men were allocated to three groups: treadmill ergometry (T) n=4, cycle ergometry (C) n=6 and arm crank ergometry (AC) n=5. Subjects underwent an incremental exercise test to exhaustion on an exercise-specific ergometer to determine maximum/peak oxygen consumption (O2max). One week later subjects exercised for 36 min on the same ergometer at approximately 65% O2max while temperatures at the rectum (T re) and esophagus (T es) were simultaneously measured. The O2max (l · min−1) for groups T [4.76 (0.50)] and C [4.35 (0.30)] was significantly higher than that for the AC group [2.61 (0.24)]. At rest, T re was significantly higher than T es in all groups (P<0.05). At the end of submaximal exercise in the C group, T re [38.32 (0.11)°C] was significantly higher than T es [38.02 (0.12)°C, P<0.05]. No significant differences between T re and T es at the end of exercise were noted for AC and T groups. The temperature difference (T diff) between T re and T es was dissimilar at rest in the three groups; however, by the end of exercise T diff was approximately 0.2°C for each of the groups, suggesting that at the end of steady-state exercise T re can validly be used to estimate core temperature. Accepted: 3 November 1997  相似文献   

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