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The purpose of this study was to examine the physiological characteristics of an elite centenarian cyclist who, at 101 yr old, established the 1-h cycling record for individuals ≥100 yr old (24.25 km) and to determine the physiological factors associated with his performance improvement 2 yr later at 103 yr old (26.92 km; +11%). Before each record, he performed an incremental test on a cycling ergometer. For 2 yr, he trained 5,000 km/yr with a polarized training that involved cycling 80% of mileage at "light" rate of perceived exertion (RPE) ≤12 and 20% at "hard" RPE ≥15 at a cadence between 50 and 70 rpm. His body weight and lean body mass did not change, while his maximal oxygen consumption (V̇o 2max ) increased (31-35 ml·kg -1 ·min -1 ; +13%). Peak power output increased from 90 to 125 W (+39%), mainly because of increasing the maximal pedaling frequency (69-90 rpm; +30%). Maximal heart rate did not change (134-137 beats/min) in contrast to the maximal ventilation (57-70 l/min, +23%), increasing with both the respiratory frequency (38-41 cycles/min; +8%) and the tidal volume (1.5-1.7 liters; +13%). Respiratory exchange ratio increased (1.03-1.14) to the same extent as tolerance to V̇co 2 In conclusion, it is possible to increase performance and V̇o 2max with polarized training focusing on a high pedaling cadence even after turning 100 yr old. NEW & NOTEWORTHY This study shows, for the first time, that maximal oxygen consumption (+13%) and performance (+11%) can still be increased between 101 and 103 yr old with 2 yr of training and that a centenarian is able, at 103 yr old, to cover 26.9 km/h in 1 h., (Copyright © 2017 the American Physiological Society.)

Purpose: Despite the increasing popularity of marathon running, there are no data on the responses of stroke volume (SV) and cardiac output (CO) to exercise in this context. We sought to establish whether marathon performance is associated with the ability to sustain high fractional use of maximal SV and CO (i.e, cardiac endurance) and/or CO, per meter (i.e., cardiac cost)., Methods: We measured the SV, heart rate (HR), CO, and running speed of 14 recreational runners in an incremental, maximal laboratory test and then during a real marathon race (mean performance: 3 hr 30 min ± 45 min)., Results: Our data revealed that HR, SV and CO were all in a high but submaximal steady state during the marathon (87.0 ± 1.6%, 77.2 ± 2.6%, and 68.7 ± 2.8% of maximal values, respectively). Marathon performance was inversely correlated with an upward drift in the CO/speed ratio (mL of CO × m(-1)) (r = -0.65, P < 0.01) and positively correlated with the runner's ability to complete the race at a high percentage of the speed at maximal SV (r = 0.83, P < 0.0002)., Conclusion: Our results showed that marathon performance is inversely correlated with cardiac cost and positively correlated with cardiac endurance. The CO response could be a benchmark for race performance in recreational marathon runners.

The purpose of this study was to test the hypothesis that mountaineering experience decreases the net oxygen cost of uphill walking (OCw) on steep mountain trails and in ice and snow conditions. OCw was measured during an ascent of Mont Blanc in eight experienced alpinists and eight non-alpinists who were matched for sex (4 + 4) and low-altitude aerobic power (V(O)(2)(max) 50-55 ml kg(-1) min(-1)). Subjects carried a breath-by-breath gas exchange analyzer and a GPS. V(O)(2)(max) at altitude was estimated from measured low-altitude V(O)(2)(max) using Bassett's equation to calculate fractional use of V(O)(2)(max) during the ascent (FV(O)(2)(max)). OCw was calculated as the difference between V(O)(2) while climbing minus resting V(O)(2). At all elevations, Alpinists exhibited a lower OCw (P < 0.01). In all subjects, OCw increased when encountering ice and snow conditions. FV(O)(2)(max) remained stable around 75% at all elevations independent of experience or sex. In conclusion, the OCw is lower in experienced mountaineers compared to non-experienced subjects, and increases when going from steep rocky mountain terrain to ice and snow conditions, independent of mountaineering experience or sex.

This study examined the hypothesis that running speed over 800- and 1,500-m races is regulated by the prevailing anaerobic (oxygen independent) store (ANS) at each instant of the race up until the all-out phase of the race over the last several meters. Therefore, we hypothesized that the anaerobic power that allows running above the speed at maximal oxygen uptake (VO2max) is regulated by ANS, and as a consequence the time limit at the anaerobic power (tlim PAN=ANS/PAN) is constant until the final sprint. Eight 800-m and seven 1,500-m male runners performed an incremental test to measure VO2max and the minimal velocity associated with the attainment of VO2max (vVO2max), referred to as maximal aerobic power, and ran the 800-m or 1,500-m race with the intent of achieving the lowest time possible. Anaerobic power (PAN) was measured as the difference between total power and aerobic power, and instantaneous ANS as the difference between end-race and instantaneous accumulated oxygen deficits. In 800 m and 1,500 m, tlim PAN was constant during the first 70% of race time in both races. Furthermore, the 1,500-m performance was significantly correlated with tlim PAN during this period (r=-0.92, P<0.01), but the 800-m performance was not (r=-0.05, P=0.89), although it was correlated with the end-race oxygen deficit (r=-0.70, P=0.05). In conclusion, this study shows that in middle-distance races over both 800 m and 1,500 m, the speed variations during the first 70% of the race time serve to maintain constant the time to exhaustion at the instantaneous anaerobic power. This observation is consistent with the hypothesis that at any instant running speed is controlled by the ANS remaining.

To examine the fatigue response during an exhaustive heavy exercise performed under control of oxygen uptake (SS@V.O (2)Delta50) or power output (SS@pDelta50), eleven trained male subjects performed an incremental test to determine the peak of the oxygen uptake value (V.O (2peak)) and lactate threshold and two exhaustive steady-state cycling exercises at the intermediate value between the lactate threshold and V.O (2peak) (SS@V.O (2)Delta50 and SS@pDelta50). The control of V.O (2) induced an oscillation of the power output, which lowered the average power output (276 +/- 47 vs. 315 +/- 40 W, p = 0.004) and cancelled the slow component of oxygen kinetics. However, all subjects reached maximal cardiac output (CO) and heart rate (HR) values which were sustained almost two times longer in SS@V.O (2)Delta50 compared to SS@pDelta50 (979 +/- 854 vs. 475 +/- 236 s, p = 0.046 for CO and 1050 +/- 890 vs. 513 +/- 288 s, p = 0.037 for HR). Furthermore, SS@pDelta50 elicited V.O (2peak) but not SS@V.O (2)Delta50 (4963 +/- 434 vs. 4723 +/- 460 mL . min (-1), p = 0.026). Finally, the time spent at the maximal CO and HR values is correlated with time to exhaustion at V.O (2)Delta50. In conclusion, the cause of fatigue does not seem to have the same origin during exhaustive supra-lactate threshold exercise under control of V.O (2) (V.O (2)Delta50) compared to constant power output (pDelta50), while both elicit the maximal HR and CO values.

We hypothesized that a freely paced 10,000 m running race would induce a smaller physiological strain (heart rate and oxygen uptake) compared with one performed at the same average speed but with an imposed constant pace. Furthermore, we analyzed the scaling properties with a wavelet transform algorithm computed log2 (wavelet transform energy) vs. log2 (scale) to get slope alpha, which is the scaling exponent, a measure of the irregularity of a time series. HR was sampled beat by beat and V2O, breath by breath. The enforced constant pace run elicited a significantly higher mean VO2 value (53 +/- 4 vs. 48 +/- 5 ml kg(-1) min(-1), P < 0.001), HR (169 +/- 13 vs. 165 +/- 14 bpm, P < 0.01), and blood lactate concentration (6.6 +/- 0.9 vs. 7.5 +/- 1 mM, P < 0.001) than the freely paced run. HR and VO2 signals showed a scaling behavior, which means that the signals have a similar irregularity (a self-similarity) whatever the scale of analysis may be, in both constant and free-paced 10,000 m runs. The scaling exponent was not significantly different according to the type of run (free vs. constant, P > 0.05) and the signal (HR vs. VO2, P > 0.05). The higher metabolic cost of constant vs. free paced run did not affect the self-similarity of HR and VO2, in either run. The HR signal only kept its scaling behavior only with a distance run, no matter the type of run (free or constant). The results suggest that the larger degree of pace variation in freely paced races may be an intentionally chosen strategy designed to minimize the physiological strain during severe exercise and to prevent a premature termination of effort, even if the variability of the heart rate and VO2, are comparable in an enforced constant vs. a freely paced run and if HR keeps the same variability until the arrival.

The purpose of this study was to examine the influence of hypoxia on the O2 uptake response, on the arterial and muscular desaturation and on the test duration and test duration at VO2max during exhaustive exercise performed in normoxia and hypoxia at the same relative workload. Nine well-trained males cyclists performed an incremental test and an exhaustive constant power test at 90 % of maximal aerobic power on a cycling ergometer, both in normoxia and hypoxia (inspired O2 fraction = 16 %). Hypoxic normobar conditions were obtained using an Alti Trainer200 and muscular desaturation was monitored by near-infrared spectroscopy instrument (Niro-300). The mean response time (66 +/- 4 s vs. 44 +/- 7 s) was significantly lower in hypoxia caused by the shorter time constant of the VO2 slow component. This result was due to the lower absolute work rate in hypoxia which decreased the amplitude of the VO2 slow component. The arterial (94.6 +/- 0.3 % vs. 84.2 +/- 0.7 %) and muscular desaturation (in the vastus lateralis and the lateral gastrocnemius) were reduced by hypoxia. The test duration (440 +/- 31 s vs. 362 +/- 36 s) and the test duration at VO2max (286 +/- 53 s vs. 89 +/- 33 s) were significantly shorter in hypoxia. Only in normoxia, the test duration was correlated with arterial and muscular saturation (r = 0.823 and r = 0.828; p < 0.05). At the same relative workload, hypoxia modified performance, arterial and muscular oxygen desaturation but not the oxygen uptake response. In normoxia, correlation showed that desaturation seems to be a limiting factor of performance.

The relationships between both metabolic (E) and mechanical (W) energy expended and exhaustion time (t(e)), was determined for 11 well-trained subjects during constant load cycloergometric exercises at 95, 100, 110, 115 % maximal aerobic power performed both from rest and, without interruption, after an all-out sprint of 7 s. These relationships were well described by straight lines: y = a + bt(e), where b was taken as the critical power (metabolic and mechanical) that can be sustained for long periods of time. b was unaffected by the exercise conditions and amounted to 82 - 94 % of maximal aerobic metabolic and mechanical power. The constant a was taken as the anaerobic stores capacity in excess of the O2 deficit. When the test was preceded by the sprint, a (metabolic and mechanical) was reduced to about 60 - 70 % of control values. This reduction was essentially equal to the corresponding E and W output during the sprint. These data support the view that the slope of linear regressions of E and W on t(e) is indeed a measure of the critical power, whereas the y intercept of these same regressions is a measure of the anaerobic capacity.

The purpose of this study was to examine whether the heart rate (HR) deflection point (HRDP) in the HR-power relationship is concomitant with the maximal stroke volume (SV(max)) value achievement in endurance-trained subjects. Twenty-two international male cyclists (30.3 +/- 7.3 yr, 179.7 +/- 7.2 cm, 71.3 +/- 5.5 kg) undertook a graded cycling exercise (50 W every 3 min) in the upright position. Thoracic impedance was used to measure continuously the HR and stroke volume (SV) values. The HRDP was estimated by the third-order curvilinear regression method. As a result, 72.7% of the subjects (HRDP group, n = 16) presented a break point in their HR-work rate curve at 89.9 +/- 2.8% of their maximal HR value. The SV value increased until 78.0 +/- 9.3% of the power associated with maximal O(2) uptake (Vo(2 max)) in the HRDP group, whereas it increased until 94.4 +/- 8.6% of the power associated with Vo(2 max) in six other subjects (no-HRDP group, P = 0.004). Neither SV(max) (ml/beat or ml.beat(-1).m(-2)) nor Vo(2 max) (ml/min or ml.kg(-1).min(-1)) were different between both groups. However, SV significantly decreased before exhaustion in the HRDP group (153 +/- 44 vs. 144 +/- 40 ml/beat, P = 0.005). In the HRDP group, 62% of the variance in the power associated with the SV(max) could also be predicted by the power output at which HRDP appeared. In conclusion, in well-trained subjects, the power associated with the SV(max)-HRDP relationship supposed that the HR deflection coincided with the optimal cardiac work for which SV(max) was attained.

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.

The aim of this study was to determine the energetic factors of middle-distance running performance in junior elite runners according to gender and by using measurements from on-track performances. Fifteen elite runners (8 males and 7 females) were investigated by means of an incremental test and an all-out run over 600 m performed with a 2-d interval. We calculated (1) the aerobic maximal power (E(r max aero), in W kg(-1)), including VO(2 max) and the delay of attainment of VO(2 max) in the 600 m run; (2) the anaerobic power (E(r max anaero)), i.e., the oxygen deficit (J kg(-1)) divided by the duration of the 600 m run. Despite the difference in race duration (87 +/- 3 vs. 102 +/- 2 s), the 600 m run was made at the same relative value of the velocity associated with VO(2 max) (VVO(2 )max) in males and females (121.6 +/- 7 vs. 120 +/- 8% VO(2 max), p = 0.7). E(r max aero) explained most of the variance in the performance (the personal best performed 8 weeks later) between genders: 65 and 79% over 800 m (T(800)) and 1,500 m (T(1,500)). For females, E(r max aero) explained most of the variance of T(1,500) (r(2) = 0.66), and E(r max anaero) improved this prediction (r(2) = 0.84). No energetic factor predicted the performance on 800 m run in males. In elite junior athletes, the energetic model with individual data measured over an all-out 600 m performed on a track, provides an explanation for most of the variance in middle-distance running performances between genders. The distinction between aerobic power and anaerobic power allowed an improvement in the prediction of middle-distance running performances.

Purpose: To examine whether differences in heart rate variability (HRV) can distinguish sub- from supra-ventilatory-threshold exercise and whether the exercise duration at supra-threshold intensity alters cardiorespiratory synchronization., Methods: Beat-to-beat RR interval, VO2, VCO2, VE, and blood lactate concentration of 11 healthy well-trained young subjects were collected during two exercise tests: 1) a moderate-intensity test: 15 min performed below the power at ventilatory threshold (pVT); and 2) a heavy-intensity test: above pVT until exhaustion. Fast Fourier transform, smoothed pseudo Wigner-Ville distribution, and complex demodulation were applied to RR time series., Results: 1) Moderate exercise shows a prevalence of low-frequency (LF) spectral energy compared with the high-frequency (HF) one (LF = 80 +/- 10% vs HF = 20 +/- 10%, P < 0.001), whereas the reverse is observed during heavy exercise (LF = 11 +/- 8% vs HF = 89 +/- 8%, P < 0.001). 2) During heavy exercise, the HF amplitude and the tidal volume (Vt) remained constant, whereas the breathing frequency (BF) increased (BF: 0.70 +/- 0.18 vs 0.93 +/- 0.31, P < 0.01) and mean RR decreased (342 +/- 15 vs 317 +/- 16, P < 0.01). Despite the RR series and the breathing signal remaining synchronized, HR/BF ratio decreased and stabilized at 3 RR for one breathing cycle, whatever the initial ratio., Conclusion: 1) HRV allows us to differentiate sub- from supra-ventilatory-threshold exercise and 2) exercise duration at supra-threshold intensity does not alter the cardiorespiratory synchronization.

Training effects on time-to-exhaustion, substrate and blood lactate balances at the maximal lactate steady state velocity (MLSSv) were examined. Eleven male, veteran, long-distance runners performed three tests before and after 6 weeks of training at MLSSv: an incremental test to determine maximum O2 uptake (VO(2,max)) and the velocity at the lactate threshold (vLT), a sub-maximal test of two stages of 20 min at 95 and 105% of vLT separated by 40 min rest to determine the MLSSv and the corresponding lactate concentration (MLSSc) and a time-to-exhaustion run at MLSSv for which the substrate balance was calculated. Duration and distance run at MLSSv increased dramatically respectively from 44+/-10 to 63+/-12 min and from 10.4 to 15.7 km respectively (P<0.01). MLSSv increased significantly with training but the relative fraction of VO(2,max) remained the same (85.2+/-4.5 vs. 85.3+/-5.2%, P=0.93). MLSSc was unaffected by training as determined from the percentage of energy yielded by carbohydrates (80%) during the exhaustive run at MLSSv. These findings show that training at MLSS elicits small increases in MLSSv and VO(2,max), but enhances time-to-exhaustion (endurance) at MLSSv substantially (+50%). Training does not change the proportion of carbohydrate oxidized, which is the major substrate used during an exhaustive run at MLSS lasting 1 h.

The purpose of this study was to examine the effect of 4 weeks training in running on the time spent at VO2max (tlim VO2max). Eight athletes carried out, before and after an aerobic training, an incremental and five exhaustive tests at 90, 95, 100, 115% vVO2max and at the critical power at VO2max (CV'; slope of the linear relation between the tlim VO2max and the distance limit at VO2max). This training did not significantly improve VO2max (p = 0.17) or tlim VO2max (p = 0.72). However, the "tlim VO2max-intensity" curve was shifted toward the right, meaning that the athlete had to run at a higher intensity after training to obtain the same tlim VO2max. Tlim VO2max at CV' before training was significantly higher than tlim VO2max at 90, 95, 100, and 115% vVO2max (p < 0.05). This training increased CV' in absolute value (13.9 +/- 1.3 vs. 14.9 +/- 1.2 km.h-1, p < 0.05; n = 6) but not in relative value (86 +/- 4 vs. 86 +/- 5% vVO2max; p = 0.9). In conclusion, in spite of the shift of the "tlim VO2max-intensity" curve, tlim VO2max was not significantly increased by this training. Furthermore, CV' allowed subjects to spend the longest time of exercise at VO2max during a continuous exercise with constant speed, but CV', expressed in % vVO2max, did not improve with this training.

The aim of this study was to examine (i) the effects of a severe interval training period on oxygen pulse kinetics (O2-p, the ratio between VO2 and heart rate), and (ii) to study the consequences of these effects on the variation of performance (time to exhaustion) during severe runs. Seven athletes were tested before and after an eight-weeks period of a specific intermittent training at v Delta 50, i.e., the intermediate velocity between the lactate threshold (vLT) and the velocity associated with VO2max (vVO2max ). During the test sessions, athletes performed an incremental test and an all-out test at the pretraining v Delta 50. After the training period they also completed an additional all-out test at the posttraining v Delta 50 (v Delta 50bis). Results showed that after training there was i) an increase in the O2-p maximal value during the incremental test (22.7 +/- 1.5 mlO2.b-1 vs. 20.6 +/- 1.5 mlO2.b-1; p < 0.04), ii) a decrease in the time to reach the O2-p steady state (TRO2-p ) at the same absolute v Delta 50 (33 +/- 7 s vs. 60 +/- 27 s; p < 0.04) and iii) an increase in the O2-p steady state duration (TSSO2-p) at the same absolute v Delta 50 (552 +/- 201 s vs. 407 +/- 106 s; p < 0.04). However, there was no relationship between the improvement of these two O 2 -p kinetics parameters (TRO2-p and TSS O2-p) and those of the performance. This study found that after an individualised interval-training program conducted at the same absolute velocity, the O2-p kinetics reached a steady state quicker and for a longer duration than before training. This is however not related with the improvement of performance.

The first purpose of this study was to assess the eventual training adaptations in the time to exhaustion at the same severe velocity occurring after severe interval-training programs in few- and well-trained subjects. In the event of such training adaptations, the second purpose was to identify the discriminant factors of performance improvement according to the initial training status. Seven few- and six well-trained subjects performed: firstly, an incremental test to determine the maximal oxygen consumption (VO2max), the energy cost of running (ECR), the velocity associated with the achievement of VO2max (vVO2max) and the lactate threshold (LT expressed in VO2, km x h(-1), % vVO2max); secondly, an all-out test at the velocity corresponding to the midway between vLT and vVO2max (vdelta50) to determine the time to exhaustion (tmax); such tests were carried out before and after 4- and 8-week severe interval-training programs. In the few-trained subjects, all factors of performance (i.e., VO2max, ECR, vVO2max, LT expressed in VO2, km x h(-1), % vVO2max) and tmax at the pre-training vdelta50 were improved after training (+8, -8, +7, +9, +14, +6% and +79%, respectively); only the increase in vLT was related to the one in tmax (r = 0.714, p < or = 0.05, n = 7). In the well-trained subjects, only vVO2max was improved (+3%) due to the decrease in ECR (-3%), tmax at the pre-training vdelta50 did not vary after training; only the three subjects (over six) who improved their vLT (+0.5, +0.5, +0.8 km x h(-1), respectively) improved their tmax (+10, +24, +101%, respectively) (r = 0.895, p < or = 0.01, n = 6). So, whichever the initial training status, any training-induced adaptation in vLT appeared as a major factor of performance improvement especially at supra-LT velocities.

Eight unacclimatized long-distance runners performed, on a level treadmill, an incremental test to determine the maximal oxygen uptake (VO2max) and the minimal velocity eliciting VO2max (vVO2max) in normoxia (N) and acute moderate hypoxia (H) corresponding to an altitude of 2,400 m (PIO 2 of 109 mmHg). Afterwards, on separate days, they performed two all-out constant velocity runs at vO2 max in a random order (one in N and the other in H). The decrease in VO2max between N and H showed a great degree of variability amongst subjects as VO2max decreased by 8.9 +/- 4 ml x min(-1) x kg)(-1) in H vs. N conditions (-15.3 +/- 6.3 % with a range from -7.9 % to -23.8 %). This decrease in VO2max was proportional to the value of VO2max (VO2max vs. delta VO2max N-H, r = 0.75, p = 0.03). The time run at vVO2max was not affected by hypoxia (483 +/- 122 vs. 506 +/- 148 s, in N and H, respectively, p = 0.37). However, the greater the decrease in vVO2max during hypoxia, the greater the runners increased their time to exhaustion at vVO2max (vVO2max N-H vs. tlim @vVO2max N-H, r = -0.75, p = 0.03). In conclusion, this study showed that there was a positive association between the extent of decrease in vVO2max, and the increase in run time at vVO2max in hypoxia.

The maximal lactate steady state (MLSS) is defined as the highest blood lactate concentration (MLSSc) and work load (MLSSw) that can be maintained over time without a continual blood lactate accumulation. A close relationship between endurance sport performance and MLSSw has been reported and the average velocity over a marathon is just below MLSSw. This work rate delineates the low- to high-intensity exercises at which carbohydrates contribute more than 50% of the total energy need and at which the fuel mix switches (crosses over) from predominantly fat to predominantly carbohydrate. The rate of metabolic adenosine triphosphate (ATP) turnover increases as a direct function of metabolic power output and the blood lactate at MLSS represents the highest point in the equilibrium between lactate appearance and disappearance both being equal to the lactate turnover. However, MLSSc has been reported to demonstrate a great variability between individuals (from 2-8 mmol/L) in capillary blood and not to be related to MLSSw. The fate of enhanced lactate clearance in trained individuals has been attributed primarily to oxidation in active muscle and gluconeogenesis in liver. The transport of lactate into and out of the cells is facilitated by monocarboxylate transporters (MCTs) which are transmembrane proteins and which are significantly improved by training. Endurance training increases the expression of MCT1 with intervariable effects on MCT4. The relationship between the concentration of the two MCTs and the performance parameters (i.e. the maximal distance run in 20 minutes) in elite athletes has not yet been reported. However, lactate exchange and removal indirectly estimated with velocity constants of the individual blood lactate recovery has been reported to be related to time to exhaustion at maximal oxygen uptake.

The purpose of this study was to examine the influence of time run at maximal oxygen uptake (VO2 max) on the off-transient pulmonary oxygen uptake phase after supra-lactate threshold runs. We hypothesised: 1) that among the velocities eliciting VO2 max there is a velocity threshold from which there is a slow component in the VO2-off transient, and 2) that at this velocity the longer the duration of this time at VO2 max (associated with an accumulated oxygen kinetics since VO2 can not overlap VO2 max), the longer is the off-transient phase of oxygen uptake kinetics. Nine long-distance runners performed five maximal tests on a synthetic track (400 m) while breathing through the COSMED K4b2 portable, telemetric metabolic analyser: i) an incremental test which determined VO2 max, the minimal velocity associated with VO2 max (vVO2 max) and the velocity at the lactate threshold (vLT), ii) and in a random order, four supra-lactate threshold runs performed until exhaustion at vLT + 25, 50, 75 and 100% of the difference between vLT and vVO2 max (vdelta25, vdelta50, vdelta75, vdelta100). At vdelta25, vdelta50 (= 91.0 +/- 0.9% vVO2 max) and vdelta75, an asymmetry was found between the VO2 on (double exponential) and off-transient (mono exponential) phases. Only at vdelta75 there was at positive relationship between the time run at VO2 max (%tlimtot) and the VO2 recovery time constant (Z = 1.8, P = 0.05). In conclusion, this study showed that among the velocities eliciting VO2 max, vdelta75 is the velocity at which the longer the duration of the time at VO2 max, the longer is the off-transient phase of oxygen uptake kinetics. It may be possible that at vdelta50 there is not an accumulated oxygen deficit during the plateau of VO2 at VO2 max and that the duration of the time at VO2 max during the exhaustive runs at vdelta100, could be too short to induce an accumulating oxygen deficit affecting the oxygen recovery.

The purpose of this study was to examine the effect of 4 weeks of intense interval-training on the pulmonary off-transient oxygen uptake (V*O2) after running until exhaustion at the same absolute speed. Seven physical education students ran as follows in three maximal tests on a synthetic track (400 m) whilst breathing through a portable, telemetric metabolic analyser: firstly, in an incremental test which determined maximal oxygen uptake (V*O2max), the minimal speed associated with V*O2max (vV*O2max) and the speed at the lactate threshold ( v(LT)). Secondly, in two continuous severe intensity runs at 90% (R90) and 95% (R95) of vV*O2max. After training, the times to exhaustion ( t(lim)) at these two speeds (i.e. the time limits t(lim90) and t(lim95), respectively), were significantly increased at both speeds (+37% and +66% for t(lim90) and t(lim95), P=0.04 and 0.01, respectively) and v(LT) and vV*O2max were increased by 8% and 5%, respectively ( P<0.02). The time constants of the cardio-dynamic added to the metabolic phase (phases I+II) and of the slow phase (phase III) of oxygen kinetics in the on-transient phase decreased significantly after training ( P=0.05). However, the decrease in the time constants of oxygen kinetics in the on-transient phases II and III were not correlated with the improvement in performance (i.e. increase in t(lim)). After training the V*O2 off-transient phase was significantly faster [off-time constant (tau(off)) decreased significantly both after R90 and R95, P=0.03]. This decrease in tau(off) was correlated with the increase in t(lim90) ( r=0.795, P=0.03). The physiological factors best correlated with the increased performance after training were v(LT) for t(lim90) and vV*O2max for t(lim95).

This study examined the effect of 8 weeks of specific marathon training before the Olympic trials on the physiological factors of the marathon performance in top-class marathon runners. Five males and four females, age 34 +/- 6 yr (+/- SD) with a marathon performance time of 2 h 11 min 40 s +/- 2 min 27 s for males and 2 h 35 min 34 s +/- 2 min 54 s for females, performed one test ten and two weeks before the trials. Between this period they trained weekly 180 +/- 27 km and 155 +/- 19 km with 11 +/- 7 and 7 +/- 0% of this distance at velocity over 10000 m for males and females, respectively. The purpose of this test was to determine in real conditions i. e. on level road: VO2 peak, the energy cost of running and the fractional utilisation of VO2 peak at the marathon velocity (vMarathon). They ran 10 km at the speed of their personal best marathon performance on a level road and after a rest of 6 min they ran an all-out 1000 m run. VO2 peak increased after the 8 weeks of pre-competitive training (66.3 +/- 9.2 vs 69.9 +/- 9.4 ml x min(-1) x kg(-1), p = 0.01). Moreover, since the oxygen cost of running at vMarathon did not change after this training, the fractional utilization (F) of VO2 peak during the 10 km run at vMarathon decreased significantly after training (94.6 +/- 6.2% VO2 peak vs 90.3 +/- 9.5% VO2 peak, p = 0.04). The high intensity of pre-competitive training increased VO2 peak and did not change the running economy at vMarathon and decreased the fractional utilization of VO2 peak at vMarathon.

Best performances in middle-distance running are characterized by coefficients of variation of the velocity ranging from 1% to 5%. This seems to suggest that running at constant velocity is a strain inducing an increase in physiological variables such as oxygen uptake. This study tested three questions. (l) Does velocity variability during a middle-distance all-out run increase with fatigue? (2) Does velocity variability alter the slow phase of the oxygen kinetic because of small spontaneous recoveries, compared with the same distance run at constant velocity? (3) Is a maintained average velocity over a given distance enhanced by a variable-pace rather than by a constant-pace? Ten long-distance runners performed two series of all-out runs over the distance (previously determined) which they could cover maintaining a velocity equal to 90% of that eliciting maximal oxygen consumption. In the first series ( free-pace) the subjects were asked to run as fast as possible, without any predetermined velocity profile. In the second series, the same distance was covered at a constant velocity (equal to the average in the previous free-pace run), set by a cyclist preceding the runner. Short-term Fourier transform was used to analyse velocity oscillations. Our results show that: (1) for all subjects, the mean energy spectrum did not change throughout the free-pace runs, suggesting that velocity variability did not increase with fatigue (2-way ANOVA, P=0.557); (2) the kinetic of oxygen uptake and its asymptote were not changed during the free-pace runs compared to the constant-velocity run; (3) performance was not significantly improved by free-pace average velocity [mean (SD) 4.22 (0.47) compared to 4.25 (0.52) m x s(-1) for constant and free-pace respectively, t=-0.58, P=0.57]. These results indicate that during middle-distance running, fatigue does not increase variations in velocity, and free-pace changes neither performance nor the oxygen kinetic.

Purpose: This study compares the physical and training characteristics of top-class marathon runners (TC), i.e., runners having a personal best of less than 2 h 11 min for males and 2 h 32 min for females, respectively, versus high-level (HL) (< 2 h 16 min and < 2 h 38 min)., Methods: Twenty marathon runners (five TC and HL in each gender) ran 10 km at their best marathon performance velocity (vMarathon) on a level road. This velocity was the target velocity for the Olympic trials they performed 8 wk later. After a rest of 6 min, they ran an all-out 1000-m run to determine the peak oxygen consumption on flat road (.VO(2peak))., Results: Marathon performance time (MPT) was inversely correlated with .VO(2peak). (r = -0.73, P < 0.01) and predicted 59% of the variance of MPT. Moreover, TC male marathon runners were less economical because their energy cost of running (Cr) at marathon velocity was significantly higher than that of their counterparts (212 +/- 17 vs 195 +/- 14 mL.km(-1).kg(-1), P = 0.03). For females, no difference was observed for the energetic characteristics between TC and HL marathon runners. However, the velocity reached during the 1000-m run performed after the 10-km run at vMarathon was highly correlated with MPT (r = -0.85, P < 0.001). Concerning training differences, independent of the gender, TC marathon runners trained for more total kilometers per week and at a higher velocity (velocity over 3000 m and 10,000 m)., Conclusion: The high energy output seems to be the discriminating factor for top-class male marathon runners who trained at higher relative intensities.

The aim of this study was to determine the effect of endurance training on the relationship between mechanical stride descriptors (stride rate and stride rate variability) and the aerobic energy cost that would be decreased by training in an all-out supra-lactate threshold run. Six long distance runners (175 +/- 6 cm; 72 +/- 9 kg; 27 +/- 4 years) performed two identical track tests before and after 8 weeks of supra-lactate threshold training: an incremental test and a constant load test at 50% of the velocity difference between the lactate threshold and *VO2max (vdelta50). During the constant load test, aerobic energy cost (EC), stride rate (SR) and stride rate variability (SRV) were measured. The constant load tests were carried out before and after training at the same absolute intensity, in order to compare stride mechanical descriptors. Our results show that after eight weeks of intermittent running at vdelta50, the velocity associated with *VO2max (v *V02max) increases (p = 0.03) due to the decrease of running economy (RE, p = 0.02), and not due to an increase in *VO2max (p = 0.5). EC remained unchanged with training (p > 0.1), but SRV was significantly reduced (p < 0.03). No relationship was observed before and after training between the stride rate variability and the aerobic energetic cost (rs < 0.5; p > 0.05). This study indicates that because of the initial level of the runners, endurance training has not induced an increased *VO2max but a decrease of the SRV. Further studies have to be conducted with more subjects in order to elucidate the mechanisms underlying this decrease in SRV which is observed with training.

The purpose of this study was to compare the effectiveness of three very short interval training sessions (15-15 s of hard and easier runs) run at an average velocity equal to the critical velocity to elicit VO2 max for more than 10 minutes. We hypothesized that the interval with the smallest amplitude (defined as the ratio between the difference in velocity between the hard and the easy run divided by the average velocity and multiplied by 100) would be the most efficient to elicit VO2 max for the longer time. The subjects were middle-aged runners (52 +/- 5 yr, VO2 max of 52.1 +/- 6 mL x min(-1) x kg(-1), vVO2 max of 15.9 +/- 1.8 km x h(-1), critical velocity of 85.6 +/- 1.2% vVO2 max) who were used to long slow distance-training rather than interval training. They performed three interval-training (IT) sessions on a synthetic track (400 m) whilst breathing through the COSMED K4b2 portable metabolic analyser. These three IT sessions were: A) 90-80% vVO2 max (for hard bouts and active recovery periods, respectively), the amplitude= (90-80/85) 100=11%, B) 100-70% vVO2 max amplitude=35%, and C) 60 x 110% vVO2 max amplitude = 59%. Interval training A and B allowed the athlete to spend twice the time at VO2 max (14 min vs. 7 min) compared to interval training C. Moreover, at the end of interval training A and B the runners had a lower blood lactate than after the procedure C (9 vs. 11 mmol x l(-1)). In conclusion, short interval-training of 15s-15s at 90-80 and 100-70% of vVO2 max proved to be the most efficient in stimulating the oxygen consumption to its highest level in healthy middle-aged long-distance runners used to doing only long slow distance-training.

The main purpose of this study was to investigate the effects of an 8-wk severe interval training program on the parameters of oxygen uptake kinetics, such as the oxygen deficit and the slow component, and their potential consequences on the time until exhaustion in a severe run performed at the same absolute velocity before and after training. Six endurance-trained runners performed, on a 400-m synthetic track, an incremental test and an all-out test, at 93% of the velocity at maximal oxygen consumption, to assess the time until exhaustion. These tests were carried out before and after 8 wk of a severe interval training program, which was composed of two sessions of interval training at 93% of the velocity at maximal oxygen consumption and three recovery sessions of continuous training at 60--70% of the velocity at maximal oxygen consumption per week. Neither the oxygen deficit nor the slow component were correlated with the time until exhaustion (r = -0.300, P = 0.24, n = 18 vs. r = -0.420, P = 0.09, n = 18, respectively). After training, the oxygen deficit significantly decreased (P = 0.02), and the slow component did not change (P = 0.44). Only three subjects greatly improved their time until exhaustion (by 10, 24, and 101%). The changes of oxygen deficit were significantly correlated with the changes of time until exhaustion (r = -0.911, P = 0.01, n = 6). It was concluded that the decrease of oxygen deficit was a potential factor for the increase of time until exhaustion in a severe run performed after a specific endurance-training program.

Background: The purpose of this study was to examine the influence of prior intermittent running at VO2max on oxygen kinetics during a continuous severe intensity run and the time spent at VO2max., Methods: Eight long-distance runners performed three maximal tests on a synthetic track (400 m) whilst breathing through the COSMED K4 portable telemetric metabolic analyser: i) an incremental test which determined velocity at the lactate threshold (vLT), VO2max and velocity associated with VO2max (vVO2max), ii) a continuous severe intensity run at vLT+50% (vdelta50) of the difference between vLT and vVO2max (91.3+/-1.6% VO2max)preceded by a light continuous 20 minute run at 50% of vVO2max (light warm-up), iii) the same continuous severe intensity run at vdelta50 with a prior interval training exercise (hard warm-up) of repeated hard running bouts performed at 100% of vVO2max and light running at 50% of vVO2max (of 30 seconds each) performed until exhaustion (on average 19+/-5 min with 19+/-5 interval repetitions). This hard warm-up speeded the VO2 kinetics: the time constant was reduced by 45% (28+/-7 sec vs 51+/-37 sec) and the slow component of VO2 (deltaVO2 6-3 min) was deleted (-143+/-271 ml x min(-1) vs 291+/-153 ml x min(-1)). In conclusion, despite a significantly lower total run time at vdelta50 (6 min 19+/-0) min 17 vs 8 min 20+/-1 min 45, p=0.02) after the intermittent warm-up at VO2max, the time spent specifically at VO2max in the severe continuous run at vdelta50 was not significantly different.

This study examined the influence of light additional arm cranking exercise on the VO2 slow component observed during severe cycling exercise. During incremental tests, eleven triathletes exercised to exhaustion cycling with leg, cranking with arm and combined arm and leg cranking and cycling (arm work-rates being set at the third of leg work rates) to determine arm, leg and combined arm and leg lactate threshold and VO2max. After these incremental tests subjects performed in random order severe exercises until exhaustion at work-rates corresponding to the lactate threshold + 50% of the difference to the work rate associated with VO2max and the lactate threshold, i.e., delta50: 1) with legs only (leg delta50) 2) leg delta50 plus a very light arm cranking exercise at 25 % of the arm lactate threshold (Ldelta50 + A25). VO2 slow component was the increase of VO2 (in ml x min(-1)) between the third and the sixth minute of exercise (deltaVO2 63 min). Results showed 1) Nine of the eleven triathletes had a VO2 slow component in arm delta50; 2) a light cycle arm exercise (25% of lactate threshold) added to a severe leg cycle exercise did not decrease time to exhaustion in severe exercise (493 +/- 154s vs 418 +/- 84, P=0.4); 3) For the five subjects who had a VO2 slow component in leg cycling, the addition of a light arm exercise (25% of arm LT) decreased the VO2 slow component significantly (from 457 +/- 173 ml x min(-1) for leg delta50 to 111 +/- 150 ml x min(-1) for Ldelta50 + A25, Z = -2.0, P = 0.04). In conclusion, light additional arm cranking decreases the VO2 slow component in severe cycling. Further studies are needed to confirm the hypothesis that extra work due to an increasing handgrip on the handlebars may contribute to the VO2 slow component in cycling.

Background: The purpose of this study was to verify, by track field tests, whether sub-elite runners (n=15) could (i) reach their VO2max while running at v50%delta, i.e. midway between the speed associated with lactate threshold (vLAT) and that associated with maximal aerobic power (vVO2max), and (ii) if an intermittent exercise provokes a maximal and/or supra maximal oxygen consumption longer than a continuous one., Methods: Within three days, subjects underwent a multistage incremental test during which their vVO2max and vLAT were determined; they then performed two additional testing sessions, where continuous and intermittent running exercises at v50%delta were performed up to exhaustion. Subject's gas exchange and heart rate were continuously recorded by means of a telemetric apparatus. Blood samples were taken from fingertip and analysed for blood lactate concentration., Results: In the continuous and the intermittent tests peak VO2 exceeded VO2max values, as determined during the incremental test. However in the intermittent exercise, peak VO2, time to exhaustion and time at VO2max reached significantly higher values, while blood lactate accumulation showed significantly lower values than in the continuous one., Conclusions: The v50%delta is sufficient to stimulate VO2max in both intermittent and continuous running. The intermittent exercise results better than the continuous one in increasing maximal aerobic power, allowing longer time at VO2max and obtaining higher peak VO2 with lower lactate accumulation.

The purpose of this study was to characterise the relationship between running velocity and the time for which a subject can run at maximal oxygen uptake (VO2max), (tlimVO2max). Seven physical education students ran in an incremental test (3-min stages) to determine VO2max and the minimal velocity at which it was elicited (vVO2max). They then performed four all-out running tests on a 200-m indoor track every 2 days in random order. The mean times to exhaustion tlim at 90%, 100%, 120% and 140% vVO2max were 13 min 22 s (SD 4 min 30 s), 5 min 47 s (SD 1 min 50 s), 2 min 11 s (SD 38 s) and 1 min 12 s (SD 18 s), respectively. Five subjects did not reach VO2max in the 90% vVO2max test. All the subjects reached VO2max in the runs at 100% vVO2max. All the subjects, except one, reached VO2max in the runs at 120% vVO2max. Four subjects did not reach VO2max in the 140% vVO2max test. Time to achieve VO2max was always about 50% of the time to exhaustion irrespective of the intensity. The time to exhaustion-velocity relationship was better fitted by a 3- than by a 2-parameter critical power model for running at 90%, 100%, 120%, 140% vVO2max as determined in the previous incremental test. In conclusion, tlimVO2max depended on a balance between the time to attain VO2max and the time to exhaustion tlim. The time to reach VO2max decreased as velocity increased. The tlimVO2max was a bi-phasic function of velocity, with a peak at 100% vVO2max.

The aim was to compare physiologic responses during exhaustive runs performed on a treadmill at 100 and 120% maximal aerobic speed (MAS: the minimum speed that elicits VO2max). Fourteen subelite male runners (mean +/- SD; age = 27+/-5 years; VO2max = 68.9+/-4.6 ml/kg(-1)/min(-1); MAS = 21.5+/-1 km/h(-1)) participated. Mean time to exhaustion tlim100% at 100% MAS (269+/- 77s) was similar to those reported in other studies. However, there was large variability in individual tlim100% MAS (CV = 29%). MAS was positively correlated with VO2max (r = 0.66, p<0.05) but not with tlim100%) MAS (r = -0.50, p<0.05). tlim100% MAS was correlated with t(lim) at 120% MAS (r = 0.52, p < 0.05) and to blood pH following the rest at 120% MAS (r = -0.68, p<0.05). The data suggest that running time to exhaustion at MAS in subelite male runners is related to time limit at 120% (tlim120%) MAS. Moreover, anaerobic capacity determined by the exercise to exhaustion at 120% MAS can be defined as the variable 'a' in the model of Monod and Scherrer (1954).

Interval training consisting of brief high intensity repetitive runs (30 s) alternating with periods of complete rest (30 s) has been reported to be efficient in improving maximal oxygen uptake (VO2max) and to be tolerated well even by untrained persons. However, these studies have not investigated the effects of the time spent at VO2max which could be an indicator of the benefit of training. It has been reported that periods of continuous running at a velocity intermediate between that of the lactate threshold (vLT) and that associated with VO2max (vVO2max) can allow subjects to reach VO2max due to an additional slow component of oxygen uptake. Therefore, the purpose of this study was to compare the times spent at VO2max during an interval training programme and during continuous strenuous runs. Eight long-distance runners took part in three maximal tests on a synthetic track (400 m) whilst breathing through a portable, telemetric metabolic analyser: they comprised firstly, an incremental test which determined vLT, VO2max [59.8 (SD 5.4) ml.min-1; kg-1], vVO2max [18.5 (SD 1.2) km.h-1], secondly, an interval training protocol consisting of alternately running at 100% and at 50% of vVO2max (30 s each); and thirdly, a continuous high intensity run at vLT + 50% of the difference between vLT and vVO2max [i.e. v delta 50: 16.9 (SD 1.00) km.h-1 and 91.3 (SD 1.6)% vVO2max]. The first and third tests were performed in random order and at 2-day intervals. In each case the subjects warmed-up for 15 min at 50% of vVO2max. The results showed that in more than half of the cases the v delta 50 run allowed the subjects to reach VO2max, but the time spent specifically at VO2max was much less than that during the alternating low/high intensity exercise protocol [2 min 42 s (SD 3 min 09 s) for v delta 50 run vs 7 min 51 s (SD 6 min 38 s) in 19 (SD 5) interval runs]. The blood lactate responses were less pronounced in the interval runs than for the v delta 50 runs, but not significantly so [6.8 (SD 2.2) mmol.l-1 vs 7.5 (SD 2.1) mmol.l-1]. These results do not allow us to speculate as to the chronic effects of these two types of training at VO2max.

The purpose of this study was to compare the effect of two different types of cyclic severe exercise (running and cycling) on the VO2 slow component. Moreover we examined the influence of cadence of exercise (freely chosen [FF] vs. low frequency [LF]) on the hypothesis that: 1) a stride frequency lower than optimal and 2) a pedalling frequency lower than FF one could induce a larger and/or lower VO2 slow component. Eight triathletes ran and cycled to exhaustion at a work-rate corresponding to the lactate threshold + 50% of the difference between the work-rate associated with VO2max and the lactate threshold (delta 50) at a freely chosen (FF) and low frequency (LF: - 10 % of FF). The time to exhaustion was not significantly different for both types of exercises and both cadences (13 min 39 s, 15 min 43 s, 13 min 32 s, 15 min 05 s for running at FF and LF and cycling at FF and LF, respectively). The amplitude of the VO2 slow component (i.e. difference between VO2 at the last and the 3rd min of the exercise) was significantly smaller during running compared with cycling, but there was no effect of cadence. Consequently, there was no relationship between the magnitude of the VO2 slow component and the time to fatigue for a severe exercise (r = 0.20, p = 0.27). However, time to fatigue was inversely correlated with the blood lactate concentration for both modes of exercise and both cadences (r = - 0.42, p = 0.01). In summary, these data demonstrate that: 1) in subjects well trained for both cycling and running, the amplitude of the VO2 slow component at fatigue was larger in cycling and that it was not significantly influenced by cadence; 2) the VO2 slow component was not correlated with the time to fatigue. If the nature of the linkage between the VO2 slow component and the fatigue process remains unclear, the type of contraction regimen depending on exercise biomechanic characteristics seems to be determinant in the VO2 slow component phenomenon for a same level of training.

The purpose of this study was to show the relationship between oxygen deficit and the time to exhaustion (tlim) at maximal aerobic speed (MAS). The minimum speed that elicits VO(2max) was assumed to be the maximal aerobic speed (MAS). Fourteen subelite male runners (mean (SD: age = 27 +/- 5 yrs: VO(2max) = 68.9 +/- 4.6 ml kg (-1). min ( -1); MAS = 21.5 +/- 1 km h (-1) ) participated in the study. Each subject performed an incremental test to determine and MAS. The subjects ran to exhaustion at velocities corresponding to 100 and 120 % MAS. Oxygen deficit was measured during the period exercise to exhaustion at 120% of MAS and was calculated from the difference between O(2) demand and the accumulated O 2 uptake. The tlim values at 100% MAS were correlated with the values of tlim at 120% MAS (r = 0.52). The results reveal that the oxygen deficit was related to the time to exhaustion at MAS and indicate that the greater the oxygen deficit, the greater the time to exhaustion at MAS. It was also noted that the adjustment of oxygen consumption is related to the oxygen deficit. In other words, the subjects who have an important anaerobic capacity are the most efficient during an exercise time to exhaustion at MAS. The time limit values can be expressed by a linear regression making intervene MAS and anaerobic capacity. This conclusion could be of great interest in the training of middle distance runners.

This article traces the study of interrelationships between power output, work done, velocity maintained or distance covered and the endurance time taken to achieve that objective. During the first half of the twentieth century, scientists examined world running records for distances from < 100 m to > 1000 km. Such examinations were empirical in nature, involving mainly graphical and crude curve-fitting techniques. These and later studies developed the use of distance/time or power/time models and attempted to use the parameters of these models to characterise the endurance capabilities of athletes. More recently, physiologists have proposed theoretical models based on the bioenergetic characteristics of humans (i.e. maximal power, maximal aerobic and anaerobic capacity and the control dynamics of the system). These models have become increasingly complex but they do not provide sound physiological and mathematical descriptions of the human bioenergetic system and its observed performance ability. Finally, we are able to propose new parameters that can be integrated into the modelling of the power/time relationship to explain the variability in endurance time limit at the same relative exercise power (e.g. 100% maximal oxygen uptake).

Purpose: Between inefficient training and overtraining, an appropriate training stimulus (in terms of intensity and duration) has to be determined in accordance with individual capacities. Interval training at the minimal velocity associated with VO2max (vVO2max) allows an athlete to run for as long as possible at VO2max. Nevertheless, we don't know the influence of a defined increase in training volume at vVO2max on aerobic performance, noradrenaline, and heart rate., Methods: Eight subjects performed 4 wk of normal training (NT) with one session per week at vVO2max, i.e., five repetitions run at 50% of the time limit at vVO2max, with recovery of the same duration at 60% vVO2max. They then performed 4 wk of overload training (OT) with three interval training sessions at vVO2max., Results: Normal training significantly improved their velocity associated with VO2max (20.5+/-0.7 vs 21.1+/-0.8 km x h(-1), P = 0.02). As a result of improved running economy (50.6+/-3.5 vs 47.5+/-2.4 mL x min(-1) x kg(-1), P = 0.02), VO2max was not significantly different (71.6+/-4.8 vs 72.7+/-4.8 mL x min(-1) x kg(-1)). Time to exhaustion at vVO2max was not significantly different (301+/-56 vs 283+/-41 s) as was performance (i.e., distance limit run at vVO2max: 2052.2+/-331 vs 1986.2+/-252.9 m). Heart rate at 14 km x h(-1) decreased significantly after NT (162+/-16 vs 155+/-18 bpm, P < 0.01). Lactate threshold remained the same after normal training (84.1+/-4.8% vVO2max). Overload training changed neither the performance nor the factors concerning performance. However, the submaximal heart rate measured at 14 km x h(-1) decreased after overload training (155+/-18 vs 150+/-15 bpm). The maximal heart rate was not significantly different after NT and OT (199+/-9.5, 198+/-11, 194+/-10.4, P = 0.1). Resting plasma norepinephrine (veinous blood sample measured by high pressure liquid chromatography), was unchanged (2.6 vs 2.4 nm x L(-1), P = 0.8). However, plasma norepinephrine measured at the end of the vVO2max test increased significantly (11.1 vs 26.0 nm x L(-1), P = 0.002)., Conclusion: Performance and aerobic factors associated with the performance were not altered by the 4 wk of intensive training at vVO2max despite the increase of plasma noradrenaline.

The purpose of this study was to examine the influence of the type of exercise (running vs. cycling) on the O2 uptake V(O2) slow component. Ten triathletes performed exhaustive exercise on a treadmill and on a cycloergometer at a work rate corresponding to 90% of maximal VO2 (90% work rate maximal V(O2)). The duration of the tests before exhaustion was superimposable for both type of exercises (10 min 37 s +/- 4 min 11 s vs. 10 min 54 s +/- 4 min 47 s for running and cycling, respectively). The V(O2) slow component (difference between V(O2) at the last minute and minute 3 of exercise) was significantly lower during running compared with cycling (20.9 +/- 2 vs. 268.8 +/- 24 ml/min). Consequently, there was no relationship between the magnitude of the V(O2) slow component and the time to fatigue. Finally, because blood lactate levels at the end of the tests were similar for both running (7.2 +/- 1.9 mmol/l) and cycling (7.3 +/- 2.4 mmol/l), there was a clear dissociation between blood lactate and the V(O2) slow component during running. These data demonstrate that 1) the V(O2) slow component depends on the type of exercise in a group of triathletes and 2) the time to fatigue is independent of the magnitude of the V(O2) slow component and blood lactate concentration. It is speculated that the difference in muscular contraction regimen between running and cycling could account for the difference in the V(O2) slow component.

During prolonged and intense running exercises beyond the critical power level, a VO2 slow component elevates VO2 above predicted VO2-work rates calculated from exercise performed at intensities below the lactate threshold. In such cases, the actual VO2 value will increase over time until it reaches VO2max. The aims of the present study were to examine whether the VO2 slow component is a major determinant of VO2 over time when running at a speed beyond critical velocity, and whether the exhaustion latency period at such intensity correlates with the magnitude of the VO2 slow component. Fourteen highly trained long-distance runners performed four exhaustive runs, each separated by one week of light training. VO2 and the velocity at VO2max (vVO2max) were determined for each by a graded treadmill exercise. The critical velocity (86.1 +/- 1.5% vVO2max) of each runner was calculated from exhaustive treadmill runs at 90, 100 and 105% of vVO2max. During supra-critical velocity runs at 90% of vVO2max, there was no significant rise in VO2max (20.9 +/- 2.1 ml min-1 kg-1 between the third and last min of tlim 90), such that the runners reached a VO2 steady-state, but did not reach their vVO2max level over time (69.5 +/- 5.0 vs 74.9 +/- 3.0 ml min-1 kg-1). Thus, subjects' time to exhaustion at 90% of vVO2max was not correlated with the VO2max slow component (r = 0.11, P = 0.69), but significantly correlated with the lactate threshold (r = 0.54, P = 0.04) and the critical velocity (% vVO2max; r = 0.65, P = 0.01). In conclusion, the present study demonstrates that for highly trained long-distance runners performing exhaustive, supra-critical velocity runs at 90% of vVO2max, there was not a VO2 slow component tardily completing the rise of VO2. Instead, runners will maintain a VO2 steady-state below VO2max, such that the time to exhaustion at 90% of vVO2max for these runners is positively correlated with the critical velocity expressed as % of vVO2max.

Recent studies reported good intra-individual reproducibility, but great inter-individual variation in a sample of elite athletes, in time to exhaustion (tlim) at the maximal aerobic speed (MAS: the lowest speed that elicits VO2max in an incremental treadmill test). The purpose of the present study was, on the one hand, to detect modifications of kinematic variables at the end of the tlim of the VO2max test and, on the other hand, to evaluate the possibility that such modifications were factors responsible for the inter-individual variability in tlim. Eleven sub-elite male runners (Age = 24 +/- 6 years; VO2max = 69.2 +/- 6.8 ml kg-1 min-1; MAS = 19.2 +/- 1.45 km h-1; tlim = 301.9 +/- 82.7 s) performed two exercise tests on a treadmill (0% slope): an incremental test to determine VO2max and MAS, and an exhaustive constant velocity test to determine tlim at MAS. Statistically significant modifications were noted in several kinematic variables. The maximal angular velocity of knee during flexion was the only variable that was both modified through the tlim test and influenced the exercise duration. A multiple correlation analysis showed that tlim was predicted by the modifications of four variables (R = 0.995, P < 0.01). These variables are directly or indirectly in relation with the energic cost of running. It was concluded that runners who demonstrated stable running styles were able to run longer during MAS test because of optimal motor efficiency.

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 (VO2max) occurs (IVO2max) was assessed by analysing the relationship between the t(lim) and the accumulated oxygen deficit (AOD). After 10-min warming up at 60% of VO2max, the exercise intensity was increased so that each subject reached his IVO2max 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 IVO2max and a series of 5-min submaximal intensities to collect the data that would allow the estimation of the energy expenditure at IVO2max. 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 < or = 0.05) and cyclists and kayakists (16.4% vs 11.5%, P < or = 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 < or = 0.05), and a negative and significant correlation with VO2max (r = -0.46, P < or = 0.05). The data would suggest that the contribution of anaerobic processes during exercise performed at IVO2max should not be ignored when t(lim) is used as a supplementary parameter to evaluate specific adaptation of athletes.

In 1923, Hill and Lupton pointed out that for Hill himself, 'the rate of oxygen intake due to exercise increases as speed increases, reaching a maximum for the speeds beyond about 256 m/min. At this particular speed, for which no further increases in O2 intake can occur, the heart, lungs, circulation, and the diffusion of oxygen to the active muscle-fibres have attained their maximum activity. At higher speeds the requirement of the body for oxygen is far higher but cannot be satisfied, and the oxygen debt continuously increases'. In 1975, this minimal velocity which elicits maximal oxygen uptake (VO2max) was called 'critical speed' and was used to measure the maximal aerobic capacity (max Eox), i.e. the total oxygen consumed at VO2max. This should not be confused with the term 'critical power' which is closes to the power output at the 'lactate threshold'. In 1984, the term 'velocity at VO2max' and the abbreviation 'vVO2max' was introduced. It was reported that vVO2max is a useful variable that combines VO2max and economy into a single factor which can identify aerobic differences between various runners or categories of runners. vVO2max explained individual differences in performance that VO2max or running economy alone did not. Following that, the concept of a maximal aerobic running velocity (Vamax in m/sec) was formulated. This was a running velocity at which VO2max occurred and was calculated as the ratio between VO2max (ml/kg/min) minus oxygen consumption at rest, and the energy cost of running (ml/kg/sec). There are many ways to determine the velocity associated with VO2max making it difficult to compare maintenance times. In fact, the time to exhaustion (tlim) at vVO2max is reproducible in an individual, however, there is a great variability among individuals with a low coefficient of variation for vVO2max. For an average value of about 6 minutes, the coefficient of variation is about 25%. It seems that the lactate threshold which is correlated with the tlim at vVO2max can explain this difference among individuals, the role of the anaerobic contribution being significant. An inverse relationship has been found between tlim at vVO2max and VO2max, and a positive one between vVO2max and the velocity at the lactate threshold expressed as a fraction of vVO2max. These results are similar for different sports (e.g. running, cycling, kayaking, swimming). It seems that the real time spent at VO2max is significantly different from an exhaustive run at a velocity close to vVO2max (105% vVO2max). However, the minimal velocity which elicits VO2max, and the tlim at this velocity appear to convey valuable information when analysing a runner's performance over 1500m to a marathon.

A recent study has shown the reproducibility of time to exhaustion (time limit: tlim) at the lowest velocity that elicits the maximal oxygen consumption (vVO2 max). The same study found an inverse relationship between this time to exhaustion at vVO2 max and vVO2 max among 38 élite long-distance runners (Billat et al. 1994b). The purpose of the present study was to compare the time to exhaustion at the power output (or velocity) at VO2 max for different values of VO2 max, depending on the type of exercise and not only on the aerobic capacity. The time of exhaustion at vVO2 max (tlim) has been measured among 41 élite (national level) sportsmen: 9 cyclists, 9 kayak paddlers, 9 swimmers and 14 runners using specific ergometers. Velocity or power at VO2 max (vVO2 max) was determined by continuous incremental testing. This protocol had steps of 2 min and increments of 50 W, 30 W, 0.05 m s-1 and 2 km-1 for cyclists, kayak paddlers, swimmers and runners, respectively. One week later, tlim was determined under the same conditions. After a warm-up of 10 min at 60% of their vVO2 max, subjects were concluded (in less than 45 s) to their vVO2 max and then had to sustain it as long as possible until exhaustion. Mean values of vVO2 max and tlim were respectively equal to 419 +/- 49 W (tlim = 222 +/- 91 s), 239 +/- 56 W (tlim = 376 +/- 134 s), 1.46 +/- 0.09 m s-1 (tlim = 287 +/- 160 s) and 22.4 +/- 0.8 km h-1 (tlim = 321 +/- 84 s), for cyclists, kayak paddlers, swimmers and runners. Time to exhaustion at vVO2 max was only significantly different between cycling and kayaking (ANOVA test, p < 0.05). Otherwise, VO2 max (expressed in ml min-1 kg-1) was significantly different between all sports except between cycling and running (p < 0.05). In this study, time to exhaustion at vVO2 max was also inversely related to VO2 max for the entire group of élite sportsmen (r = -0.320, p < 0.05, n = 41). The inverse relationship between VO2 max and tlim at vVO2 max has to be explained, it seems that tlim depends on VO2 max regardless of the type of exercise undertaken.

The velocity associated with the achievement of VO2 max during an incremental treadmill test (v VO2 max) has been reported to be an indicator of performance in middle distance running events. Previous study has shown the reproducibility of the time to exhaustion (time limit: tlim) at v VO2 max performed by well-trained males in the same condition at one week of interval (Billat et al., 1994b). It is essential in studies involving tlim at v VO2 max that the v VO2 max be precisely determined, or else the measured tlim will be meaningless. The purpose of this study was to examine the influence of the stage duration and velocity incrementation on the velocity at VO2 max and, consequently, on the two times to exhaustion (tlim) associated with the two v VO2 max generated by the two protocols. v VO2 max was determined in 15 trained male endurance athletes as the lowest speed at which VO2 max was attained in speed-incremented 0%-slope treadmill tests. For one test, increments were 1.0 km.h-1 and stages were 2 min in duration; for the other test, increments were 0.5 km.h-1 and stages were 1 min in duration. Results of paired means t-tests revealed no difference in v VO2 max obtained using the two protocols. v VO2 max was 20.7 +/- 1.0 km.h-1 with the 1.0 km.h-1 x 2 min protocol and 20.8 +/- 0.9 km.h-1 with the 0.5 km.h-1 x 1 min protocol. In addition, VO2, VCO2, VE, VE/VO2 and respiratory exchange ratio at the submaximal intensities that were common to both protocols (e.g., 17.0 km.h-1, 18.0 km.h-1, 19.0 km.h-1, 20.0 km.h-1) did not differ. Times to exhaustion at the two v VO2 max demonstrated a high degree of inter-individual variability (coefficients of variation were 35% and 45%) but did not differ (345 +/- 120 s versus 373 +/- 169 s). These results demonstrated that small changes in protocol have no significant impact on the value of v VO2 max and in consequence on tlim v VO2 max.