Degree of arterial desaturation in normoxia influences VO2max decline in mild hypoxia.

PURPOSE: Elite endurance athletes display varying degrees of pulmonary gas exchange limitations during maximal normoxic exercise and many demonstrate reduced arterial O2 saturations (SaO2) at VO2max--a condition referred to as exercise induced arterial hypoxemia (EIH). We asked whether mild hypoxia would cause significant declines in SaO2 and VO2max in EIH athletes while non-EIH athletes would be unaffected. METHODS: Nineteen highly trained males were divided into EIH (N = 8) or Non-EIH (N = 6) groups based on SaO2 at VO2max (EIH <90%, Non-EIH >92%). Athletes with intermediate SaO2 values (N = 5) were only included in correlational analyses. Two randomized incremental treadmill tests to exhaustion were completed--one in normoxia, one in mild hypoxia (FIO2 = 0.187; approximately 1,000 m). RESULTS: EIH subjects demonstrated a significant decline in VO2max from normoxia to mild hypoxia (71.1+/-5.3 vs. 68.1+/-5.0 mL x kg(-1) min(-1), P<0.01), whereas the non-EIH group did not show a significant deltaVO2max (67.2+/-7.6 vs. 66.2+/-8.4 mL x kg(-1) x min(-1)). For all 19 athletes, SaO2 during maximal exercise in normoxia correlated with the change in VO2max from normoxia to mild hypoxia (r = -0.54, P<0.05). However, the change in SaO2 and arterial O2 content from normoxia to mild hypoxia was equal for both EIH and Non-EIH (deltaSaO2 = 5.2% for both groups), bringing into question the mechanism by which changes in SaO2 affect VO2max in mild hypoxia. CONCLUSIONS: We conclude that athletes who display reduced measures of SaO2 during maximal exercise in normoxia are more susceptible to declines in VO2max in mild hypoxia compared with normoxemic athletes.     

Evidence of exercise-induced O2 arterial desaturation in non-elite sportsmen and sportswomen following high-intensity interval-training

The aim of this study was to investigate the development of exercise-induced hypoxemia (EIH defined as an exercise decrease > 4 % in oxygen arterial saturation, i. e. SaO (2) measured with a portable pulse oximeter) in twelve sportsmen and ten sportswomen (18.5 +/- 0.5 years) who were non-elite and not initially engaged in endurance sport or training. They followed a high-intensity interval-training program to improve V.O (2)max for eight weeks. The training running speeds were set at approximately 140 % V.O (2)max running speed up to 100 % 20-m maximal running speed. Pre- and post-training pulmonary gas exchanges and SaO (2) were measured during an incremental running field-test. After the training period, men and women increased their V.O (2)max (p < 0.001) by 10.0 % and 7.8 %, respectively. Nine subjects (seven men and two women) developed EIH. This phenomenon appeared even in sportsmen with low V.O (2)max from 45 ml x min (-1) x kg (-1) and seemed to be associated with inadequate hyperventilation induced by training: because only this hypoxemic group showed 1) a decrease in maximal ventilatory equivalent in O (2) (V.E/V.O (2), p < 0.01) although maximal ventilation increased (p < 0.01) with training, i. e. in EIH-subjects the ventilatory response increased less than the metabolic demand after the training program; 2) a significant relationship between SaO (2) at maximal workload and the matched V.E/V.O (2) (p < 0.05, r = 0.67) which strengthened a relative hypoventilation implication in EIH. In conclusion, in this field investigation the significant decrease in the minimum SaO (2) inducing the development of EIH after high-intensity interval-training indicates that changes in training conditions could be accompanied in approximately 40 % non-endurance sportive subjects by alterations in the degree of arterial oxyhemoglobin desaturation developing during exercise.     

Effect of intensity of aerobic training on VO2max

PURPOSE: To determine whether various intensities of aerobic training differentially affect aerobic capacity as well as resting HR and resting blood pressure (BP). METHODS: Sixty-one health young adult subjects were matched for sex and VO2max and were randomly assigned to a moderate- (50% VO2 reserve (VO2R), vigorous (75% VO2R), near-maximal-intensity (95% VO2R), or a nonexercising control group. Intensity during exercise was controlled by having the subjects maintain target HR based on HR reserve. Exercise volume (and thus energy expenditure) was controlled across the three training groups by varying duration and frequency. Fifty-five subjects completed a 6-wk training protocol on a stationary bicycle ergometer and pre- and posttesting. During the final 4 wk, the moderate-intensity group exercised for 60 min, 4 d.wk the vigorous-intensity group exercised for 40 min, 4 d.wk and the near-maximal-intensity group exercised 3 d.wk performing 5 min at 75% VO2R followed by five intervals of 5 min at 95% VO2R and 5 min at 50% VO2R. RESULTS: VO2max significantly increased in all exercising groups by 7.2, 4.8, and 3.4 mL.min.kg in the near-maximal-, the vigorous-, and the moderate-intensity groups, respectively. Percent increases in the near-maximal- (20.6%), the vigorous- (14.3%), and the moderate-intensity (10.0%) groups were all significantly different from each other (P < 0.05). There were no significant changes in resting HR and BP in any group. CONCLUSION: When volume of exercise is controlled, higher intensities of exercise are more effective for improving VO2max than lower intensities of exercise in healthy, young adults.     

Effect of training on VO2max, thigh strength, and muscle morphology in septuagenarian women

The purpose of this study was to determine the effects of a long-term (50 wk) combined aerobic-resistance training program on maximal oxygen consumption (VO2max, thigh strength, and vastus lateralis fiber morphology in healthy septuagenarian women (mean age = 72 +/- 6 yr). Subjects volunteered to be in either an exercise (Ex; N = 17) or control (Con; N = 10) group. Con subjects were 34% less active in winter than in summer, Ex subjects maintained their summer activity level on exercise days in winter. Initial, intermediate (20 wk), and final (50 wk) measurements were made for isokinetic knee extension/flexion strength; VO2max and morphological measurements from a muscle biopsy were made at the initial and final times only. Both groups gained in leg strength (Ex = +6.5%; Con = +7.8%; P less than or equal to 0.05) during the summer; in the winter the Ex group maintained leg strength and the Con group declined 12.2% (P less than or equal to 0.05). The fast-twitch muscle fiber area (Type IIb) increased 29% (P less than or equal to 0.001) in the Ex group and declined 26% (P = 0.014) in the Con group. VO2max increased only in the Ex group (16%; P less than 0.001). We conclude that healthy septuagenarian women can increase aerobic capacity, leg strength, and Type IIb muscle fiber area with a long-duration, combined aerobic-resistance exercise program.     

O2 arterial desaturation in endurance athletes increases muscle deoxygenation

PURPOSE: The aim of this study was to compare the muscle deoxygenation measured by near infrared spectroscopy in endurance athletes who presented or not with exercise-induced hypoxemia (EIH) during a maximal incremental test in normoxic conditions. METHODS: Nineteen male endurance sportsmen performed an incremental test on a cycle ergometer to determine maximal oxygen consumption (VO2max) and the corresponding power output (P(max)). Arterial O2 saturation (SaO2) was measured noninvasively with a pulse oxymeter at the earlobe to detect EIH, which was defined as a drop in SaO2 > 4% between rest and the end of the exercise. Muscle deoxygenation of the right vastus lateralis was monitored by near infrared spectroscopy and was expressed in percentage according to the ischemia-hyperemia scale. RESULTS: Ten athletes exhibited arterial hypoxemia (EIH group) and the nine others were nonhypoxemic (NEIH group). Training volume, competition level, VO2max, Pmax, and lactate concentration were similar in the two groups. Nevertheless, muscle deoxygenation at the end of the exercise was significantly greater in the EIH group (P < 0.05). CONCLUSION: Greater muscle deoxygenation at maximal exercise in hypoxemic athletes seems to be due, at least in part, to reduced oxygen delivery--that is, exercise-induced hypoxemia--to working muscle added to the metabolic demand. In addition, our finding is also consistent with the hypothesis of greater muscle oxygen extraction in order to counteract reduced O2 availability.     

VO2 responses to running speeds above VO2max

This study compared VO2, heart rate (HR) and electromyographic (iEMG) responses to speeds above the velocity associated with VO2max (v-VO2max). Eight male, middle-distance runners performed a graded exercise test to determine VO2max and v-VO2max and runs to fatigue at 100 % and 110 % v-VO2max. Breath-by-breath VO2 and HR were continuously recorded; lactate [La (-)] measured pre- and post-run and iEMG measures of rectus femoris (RF) and vastus lateralis were recorded during the first and last 20 s of each run. Analysis indicated longer time to fatigue in the 100 % v-VO2max run with no differences between conditions for VO2 or HR amplitudes or post-run [La (-)] (p > 0.05). There were significantly faster tau values (p < 0.05) in the 110 % condition in VO2 and HR. No significant correlations were observed between VO2 or HR tau values and time to fatigue. RF iEMG was significantly larger in 110 % compared to 100 % run in the first 20 s (p < 0.05). While no association between treadmill performance and VO2 response was evident, faster running speeds resulted in faster VO2 and HR responses, with no difference in amplitude or % VO2max attained. This may potentially be as a result of an increased muscle fibre recruitment stimulus during the faster running velocity resulting in faster cardiodynamic responses.     

Long-term intermittent hypoxia increases O2-transport capacity but not VO2max

Long-term intermittent hypoxia, characterized by several days or weeks at altitude with periodic stays at sea level, is a frequently occurring pattern of life in mountainous countries demanding a good state of physical performance. The aim of the study was to determine the effects of a typical South American type of long-term intermittent hypoxia on VO2max at altitude and at sea level. We therefore compared an intermittently exposed group of soldiers (IH) who regularly (6 months) performed hypoxic-normoxic cycles of 11 days at 3550 m and 3 days at sea level with a group of soldiers from sea level (SL, control group) at 0 m and in acute hypoxia at 3550 m. VO2max was determined in both groups 1 day after arrival at altitude and at sea level. At altitude, the decrease in VO2max was less pronounced in IH (10.6 +/- 4.2%) than in SL (14.1 +/- 4.7%). However, no significant differences in VO2max were found between the groups either at sea level or at altitude, although arterial oxygen content (Ca(O(2) )) at maximum exercise was elevated (p < 0.001) in IH compared to SL by 11.7% at sea level and by 8.9% at altitude. This higher Ca(O(2) ) mainly resulted from augmented hemoglobin mass (IH: 836 +/- 103 g, SL: 751 +/- 72 g, p < 0.05) and at altitude also from increased arterial O(2)-saturation. In conclusion, acclimatization to long-term intermittent hypoxia substantially increases Ca(O(2) ), but has no beneficial effects on physical performance either at altitude or at sea level.     

New ideas on limitations to VO2max

VO2max indicates maximal oxidative metabolic capacity (unfit subjects) or maximal O2 supply (athletes). The latter reflects integration of all transport steps from air to cytochromes. Every step contributes something; the importance of each contribution varies with conditions. Cardiac output seems most important at sea level; at higher altitudes, lung/muscle diffusion are more critical.     

Effect of aerobic training quantity on the VO2 max of circumpubertal swimmers

Maximal oxygen uptake (VO2 max) was measured in 38 swimmers aged 10-14 years. Thirty of 38 boys participated in this study for at least 2 consecutive years. Group 1 consisted of 23 subjects (48 measures) who trained for 7 h/week while group 2 consisted of 15 subjects (27 measures) who trained for 14 h/week. In group 2, VO2 max normalized to body weight was significantly higher at 14 years of age than at 10, whereas the increase was nonsignificant during this period in group 1. The subjects of group 2 showed a large increase of VO2 max/kg body weight from the age of 13, which corresponded in this study to the age of peak height growth velocity. The differences between the two groups were statistically significant at both 13 (P less than 0.02) and 14 years of age (P less than 0.05). At 13 and 14, the most trained subjects also showed significantly higher (P less than 0.05) values of maximal oxygen pulse/kg body weight (VO2 max/kg/HR max). Maximal heart rate (HR max) was similar in the two groups between 10 and 14 years of age. Therefore, we conclude that an increase in a training program of the aerobic type induces a large increase in VO2 max from the age of peak height growth velocity. This is likely due to an increase in the stroke volume.     

Role of maximal heart rate and arterial O2 saturation on the decrement of VO2max in moderate acute hypoxia in trained and untrained men

We aimed to evaluate 1) the altitude where maximal heart rate (HR (max)) decreases significantly in both trained and untrained subjects in moderate acute hypoxia, and 2) if the HR (max) decrease could partly explain the drop of V.O (2max). Seventeen healthy males, nine trained endurance athletes (TS) and eight untrained individuals (US) were studied. Subjects performed incremental exercise tests at sea level and at 5 simulated altitudes (1000, 1500, 2500, 3500, 4500 meters). Power output (PO), heart rate (HR), arterial oxygen saturation (SaO (2)), oxygen uptake (V.O (2)), arterialized blood pH and lactate were measured. Both groups showed a progressive reduction in V.O (2max). The decrement in HR (max) (DeltaHR (max)) was significant from 1000 m for TS and 2500 m for US and more important in TS than US (at 1500 m and 3500 m). At maximal exercise, TS had a greater reduction in SaO (2) (DeltaSaO (2)) at each altitude. DeltaHR (max) observed in TS was correlated with DeltaSaO (2). When the two groups were pooled, simple regressions showed that DeltaV.O (2max) was correlated with both DeltaSaO (2) and DeltaHR (max). However, a multiple regression analysis demonstrated that DeltaSaO (2) alone may account for DeltaV.O (2max). Furthermore, in spite of a greater reduction in SaO (2) and HR (max) in TS, no difference was evidenced in relative DeltaV.O (2max) between groups. Thus, in moderate acute hypoxia, the reduction in SaO (2) is the primary factor to explain the drop of V.O (2max) in trained and untrained subjects.     

Effect of exercise intensity on relationship between VO2max and cardiac output

PURPOSE: The purpose of this study was to determine whether the maximal oxygen uptake (VO2max) is attained with the same central and peripheral factors according to the exercise intensity. METHODS: Nine well-trained males performed an incremental exercise test on a cycle ergometer to determine the maximal power associated with VO2max (pVO2max) and maximal cardiac output (Qmax). Two days later, they performed two continuous cycling exercises at 100% (tlim100 = 5 min 12 s +/- 2 min 25 s) and at an intermediate work rate between the lactate threshold and pVO2max (tlimDelta50 +/- 12 min 6 s +/- 3 min 5 s). Heart rate and stroke volume (SV) were measured (by impedance) continuously during all tests. Cardiac output (Q) and arterial-venous O2 difference (a-vO2 diff) were calculated using standard equations. RESULTS: Repeated measures ANOVA indicated that: 1) maximal heart rate, VE, blood lactate, and VO2 (VO2max) were not different between the three exercises but Q was lower in tlimDelta50 than in the incremental test (24.4 +/- 3.6 L x min(-1) vs 28.4 +/- 4.1 L x min(-1); P < 0.05) due to a lower SV (143 +/- 27 mL x beat(-1) vs 179 +/- 34 mL x beat(-1); P < 0.05), and 2) maximal values of a-vO2 diff were not significantly different between all the exercise protocols but reduced later in tlimDelta50 compared with tlim100 (6 min 58 s +/- 4 min 29 s vs 3 min 6 s +/- 1 min 3 s, P = 0.05). This reduction in a-vO2 diff was correlated with the arterial oxygen desaturation (SaO2 = -15.3 +/- 3.9%) in tlimDelta50 (r = -0.74, P = 0.05). CONCLUSION: VO2max was not attained with the same central and peripheral factors in exhaustive exercises, and tlimDelta50 did not elicit the maximal Q. This might be taken into account if the training aim is to enhance the central factors of VO2max using exercise intensities eliciting VO2max but not necessarily Qmax.     

VO2max, protocol duration, and the VO2 plateau

PURPOSE: The purpose of this study was to compare VO2max, VO2-time slopes at the end of the protocol (last 30 s), and the presence of a VO2 plateau (VO2-time slope < 0.05 L.min(-1) during the last 30 s) across four protocol durations (5, 8, 12, and 16 min) during incremental cycling exercise to VO2max. METHODS: Eight male (23.8 +/- 3.2 yr) and eight female (26.0 +/- 8.9 yr) subjects of moderate to high fitness levels participated in the study. RESULTS: VO2max was significantly higher in men than in women for each protocol duration, with main effect means of 4.23 versus 2.84 L.min(-1), respectively. For women, VO2max did not differ between any protocol duration. For men, VO2max for the 8-min protocol (4.44 +/- 0.39 L.min(-1)) was significantly higher than for all other protocol durations. Analysis of covariance, using the highest VO2max as the covariate, removed all protocol-duration significance for men. The VO2 slope for the final 30 s of each test was significantly lower for the 16-min protocol compared with the 5-min protocol, for both men and women. The ventilation threshold across four protocols was similar, at approximately 76% of VO2max for both men and women. CONCLUSIONS: The protocol duration of tests to VO2max should be between 8 and 10 min for healthy, moderately to highly trained subjects.     

Prevalence of exercise-induced arterial hypoxemia in healthy women

PURPOSE: Exercise-induced arterial hypoxemia (EIAH) is reported to occur in approximately 50% of highly trained male endurance athletes. Few studies have examined EIAH in women and the prevalence remains unclear. It has been reported that some female subjects who develop EIAH possess maximal oxygen consumption (VO2max) values that are within 15% of their predicted value. This is unique to women, where EIAH has generally been reported in men who have a high VO2max. The primary objective of this investigation was to determine the prevalence of EIAH in a large female population with a wide range of VO2max values. It was hypothesized that EIAH would occur with a greater prevalence and at relatively lower predicted VO2max than that previously reported in males. METHODS: Young women (N = 52; 26.5 +/- 4.9 yr) performed a cycle test to exhaustion to determine VO2max, and oxyhemoglobin saturation (SaO2) was monitored via pulse oximetry. All subjects were tested during the early follicular phase of their menstrual cycle. A >/= 4% drop in SaO2 represented EIAH. RESULTS: Values for VO2max were variable (VO2max range: 28.0-61.3 mL x kg(-1) x min(-1)). EIAH was present in 67% of the women with N = 19 displaying mild EIAH (92-94%SaO2) and N = 16 displaying moderate EIAH (87-91%SaO2). CONCLUSION: It appears that the prevalence of EIAH in women is slightly greater than the 50% prevalence value that is typically reported for highly fit men.     

Validation of a new method for estimating VO2max based on VO2 reserve

PURPOSE: The American College of Sports Medicine's (ACSM) preferred method for estimating maximal oxygen consumption (VO2max) has been shown to overestimate VO2max, possibly due to the short length of the cycle ergometry stages. This study validates a new method that uses a final 6-min stage and that estimates VO2max from the relationship between heart rate reserve (HRR) and VO2 reserve. METHODS: A cycle ergometry protocol was designed to elicit 65-75% HRR in the fifth and sixth minutes of the final stage. Maximal workload was estimated by dividing the workload of the final stage by %HRR. VO2max was then estimated using the ACSM metabolic equation for cycling. After the 6-min stage was completed, an incremental test to maximal effort was used to measure actual VO2max. Forty-nine subjects completed a pilot study using one protocol to reach the 6-min stage, and 50 additional subjects completed a modified protocol. RESULTS: The pilot study obtained a valid estimate of VO2max (r = 0.91, SEE = 3.4 mL x min(-1) x kg-1) with no over- or underestimation (mean estimated VO2max = 35.3 mL x min(-1) x kg(-1), mean measured VO2max = 36.1 mL x min(-1) x kg(-1)), but the average %HRR achieved in the 6-min stage was 78%, with several subjects attaining heart rates considered too high for submaximal fitness testing. The second study also obtained a valid estimate of VO2max (r = 0.89, SEE = 4.0 mL x min(-1) x kg(-1)) with no over- or underestimation (mean estimated VO2max = 36.7 mL x min(-1) x kg(-1), mean measured VO2max = 36.9 mL x min(-1) x kg(-1), and the average %HRR achieved in the 6-min stage was 64%. CONCLUSIONS: A new method for estimating VO2max from submaximal cycling based on VO2 reserve has been found to be valid and more accurate than previous methods.     

Maximal endurance time at VO2max

INTRODUCTION: There has been significant recent interest in the minimal running velocity which elicits VO2max. There also exists a maximal velocity, beyond which the subject becomes exhausted before VO2max is reached. Between these limits, there must be some velocity that permits maximum endurance at VO2max, and this parameter has also been of recent interest. This study was undertaken to model the system and investigate these parameters. METHODS: We model the bioenergetic process based on a two-component (aerobic and anaerobic) energy system, a two-component (fast and slow) oxygen uptake system, and a linear control system for maximal attainable velocity resulting from declining anaerobic reserves as exercise proceeds. Ten male subjects each undertook four trials in random order, running until exhaustion at velocities corresponding to 90, 100, 120, and 140% of the minimum velocity estimated as being required to elicit their individual VO2max. RESULTS: The model development produces a skewed curve for endurance time at VO2max, with a single maximum. This curve has been successfully fitted to endurance data collected from all 10 subjects (R2 = 0.821, P < 0.001). For this group of subjects, the maximal endurance time at VO2max can be achieved running at a pace corresponding to 88% of the minimal velocity, which elicits VO2max as measured in an incremental running test. Average maximal endurance at VO2max is predicted to be 603 s in a total endurance time of 1024 s at this velocity. CONCLUSION: Endurance time at VO2max can be realistically modeled by a curve, which permits estimation of several parameters of interest; such as the minimal running velocity sufficient to elicit VO2max, and that velocity for which endurance at VO2max is the longest.     

Hemoglobin, muscle oxidative capacity, and VO2max in African-American and Caucasian women

PURPOSE: The purpose of this paper was to determine whether differences in hemoglobin (Hb) and muscle aerobic capacity exist between African-American (AA) and Caucasian (CA) premenopausal women and to determine whether Hb and aerobic capacity of the muscle are associated with the racial differences in maximum oxygen uptake (VO2max). METHODS: 43 AA and 46 CA sedentary premenopausal women were subjects. Percent body fat was determined by four-compartment model, leg lean tissue by dual energy x-ray absorptiometry, VO2max during a graded exercise test, aerobic capacity of the calf muscle by 31P magnetic resonance spectroscopy, and serum Hb by the cyanide method. RESULTS: AA women had reduced VO2max (AA 29.3 +/- 3.0 vs CA 33.6 +/- 5.6 mL.kg(-1) bdw(-1).min, P < 0.01), reduced muscle aerobic capacity (AA 24.3 +/- 5.8 vs CA 21.3 +/- 4.8 s, P = 0.01, where lower values indicate higher aerobic capacity), and reduced Hb (AA 11.8 +/- 1.3 vs CA 12.9 +/- 0.8 g.dL(-1), P < 0.01). The racial difference in VO2max persisted whether the values were unadjusted or adjusted for fat-free mass or leg lean tissue. Multiple regression analysis revealed that both Hb and muscle aerobic capacity were related to VO2max after adjusting for each other, race, and either fat-free mass or leg lean tissue. Being AA was associated with reduced VO2max in mL O2.kg leg lean tissue(-1).min(-1) (zero-order simple Pearson-product correlation -0.60, P < 0.01). When multiple regression was used, the correlation between race and VO2max decreased but persisted (-0.40, <0.01) after adjusting for Hb and muscle aerobic capacity. CONCLUSIONS: These data suggest that differences in Hb and aerobic capacity of muscle are related to reduced VO2max in AA women. However, Hb and aerobic capacity of the muscle can only partially explain the racial differences in VO2max.     

Accurate prediction of VO2max in cycle ergometry

Numerous equations exist for predicting VO2max from the duration (an analog of maximal work rate, Wmax) of a treadmill graded exercise test (GXT). Since a similar equation for cycle ergometry (CE) was not available, we saw the need to develop such an equation, hypothesizing that CE VO2max could be accurately predicted due to its more direct relationship with W. Thus, healthy, sedentary males (N = 115) and females (N = 116), aged 20-70 yr, were given a 15 W.min-1 CE GXT. The following multiple linear regression equations which predict VO2max (ml.min-1) from the independent variables of Wmax (W), body weight (kg), and age (yr) were derived from our subjects: Males: Y = 10.51 (W) + 6.35 (kg) - 10.49 (yr) + 519.3 ml.min-1; R = 0.939, SEE = 212 ml.min-1. Females: Y = 9.39 (W) + 7.7 (kg) - 5.88 (yr) + 136.7 ml.min-1; R = 0.932, SEE = 147 ml.min-1 Using the 95% confidence limits as examples of worst case errors, our equations predict VO2max to within 10% of its true value. Internal (double cross-validation) and external cross-validation analyses yielded r values ranging between 0.920 and 0.950 for the male and female regression equations. These results indicate that use of the equations generated in this study for a 15 W.min-1 CE GXT provides accurate estimates of VO2max.     

Time limit and VO2 slow component at intensities corresponding to VO2max in swimmers

The purpose of this study was to measure, in swimming pool conditions and with high level swimmers, the time to exhaustion at the minimum velocity that elicits maximal oxygen consumption (TLim at vVO(2)max), and the corresponding VO(2) slow component (O(2)SC). The vVO(2)max was determined through an intermittent incremental test (n = 15). Forty-eight hours later, TLim was assessed using an all-out swim at vVO(2)max until exhaustion. VO(2) was measured through direct oximetry and the swimming velocity was controlled using a visual light-pacer. Blood lactate concentrations and heart rate values were also measured. Mean VO(2)max for the incremental test was 5.09 +/- 0.53 l/min and the corresponding vVO(2)max was 1.46 +/- 0.06 m/s. Mean TLim value was 260.20 +/- 60.73 s and it was inversely correlated with the velocity of anaerobic threshold (r = -0.54, p < 0.05). This fact, associated with the inverse relationship between TLim and vVO(2)max (r = -0.47, but only for p < 0.10), suggested that swimmers' lower level aerobic metabolic rate might be associated with a larger capacity to sustain that exercise intensity. O(2)SC reached 274.11 +/- 152.83 l/min and was correlated with TLim (r = 0.54), increased ventilation in TLim test (r = 0.52) and energy cost of the respiratory muscles (r = 0.51), for p < 0.05. These data suggest that O(2)SC was also observed in the swimming pool, in high level swimmers performing at vVO(2)max, and that higher TLim seems to correspond to higher expected O(2)SC amplitude. These findings seem to bring new data with application in middle distance swimming.