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Raffy Dotan

Exercise Science , the review misses out on the opportunity to provide a more complete and holistic explanation for the fundamental question on most readers’ minds: Why do children have faster VO 2 kinetics than adults? The child–adult differential muscle activation hypothesis, first proposed and reviewed

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Melitta A. McNarry

uptake and cardiac output at onset of arm exercise . Respir Physiol . 1996 ; 103 ( 2 ): 195 – 202 . PubMed ID: 8833551 doi:10.1016/0034-5687(95)00082-8 8833551 10.1016/0034-5687(95)00082-8 9. Koppo K , Bouckaert J. Prior arm exercise speeds the VO 2 kinetics during arm exercise above the

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Greg Doncaster, John Iga and Viswanath Unnithan

, when appropriately scaled. Similarly, it was hypothesized that less mature players would display superior VO 2 kinetics (faster taus ) than their more mature counterparts. Methods Participants and Anthropometry A total of 21 highly trained youth soccer players aged between 12 and 14 years volunteered

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Oliver Faude, Tim Meyer and Wilfried Kindermann

Purpose:

The work rate (WR) corresponding to ventilatory threshold (VT) is an appropriate intensity for regenerative and low-intensity training sessions. During incremental ramp exercise, VO2 increase lags behind WR increase. Traditionally, a VO2 time delay (t d) of 45 seconds is used to calculate the WR at VT from such tests. Considerable inaccuracies were observed when using this constant t d. Therefore, this study aimed at reinvestigating the temporal relationship between VO2 and WR at VT.

Methods:

20 subjects (VO2peak 49.9 to 72.6 mL · min–1 · kg–1) performed a ramp test in order to determine VT and a subsequent steady-state test during which WR was adjusted to elicit the VO2 corresponding to VT. The difference in WR and heart rate at VT was calculated between the ramp and the steady-state test (WRdiff, HRdiff) as well as the time delay corresponding to WRdiff during ramp exercise.

Results:

Mean values were t d = 85 ± 26 seconds (range 38 to 144), WRdiff = 45 ± 12 W (range 23 to 67), HRdiff = 1 ± 9 beats/min (range –21 to +15). The limits of agreement for the difference between WR at VT during ramp and steady-state exercise were ± 24 W. No signifi cant influence on t d, WRdiff, or HRdiff from differences in endurance capacity (VO2peak and VT; P > .10 for all correlations) or ramp increment (P = .26, .49, and .85, respectively) were observed.

Conclusion:

The wide ranges of t d, WRdiff, and HRdiff prevent the derivation of exact training guidelines from single-ramp tests. It is advisable to perform a steady-state test to exactly determine the WR corresponding to VT.

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Richard Latzel, Olaf Hoos, Sebastian Stier, Sebastian Kaufmann, Volker Fresz, Dominik Reim and Ralph Beneke

and P tot ), as well as energy share in terms of aerobic, anaerobic–lactic, and alactic energy, were calculated from VO 2 during exercise ( W aer ), net lactate production ( W blc ), and the fast component of postexercise VO 2 kinetics ( W PCr ). 14 Briefly, W aer was calculated from VO 2 above

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Stephen B. Draper, Dan M. Wood, Jo Corbett, David V.B. James and Christopher R. Potter

We tested the hypothesis that prior heavy-intensity exercise reduces the difference between asymptotic oxygen uptake (VO2) and maximum oxygen uptake (VO2max) during exhaustive severe-intensity running lasting ≍2 minutes. Ten trained runners each performed 2 ramp tests to determine peak VO2 (VO2peak) and speed at venti-latory threshold. They performed exhaustive square-wave runs lasting ≍2 minutes, preceded by either 6 minutes of moderate-intensity running and 6 minutes rest (SEVMOD) or 6 minutes of heavy-intensity running and 6 minutes rest (SEVHEAVY). Two transitions were completed in each condition. VO2 was determined breath by breath and averaged across the 2 repeats of each test; for the square-wave test, the averaged VO2 response was then modeled using a monoexponential function. The amplitude of the VO2 response to severe-intensity running was not different in the 2 conditions (SEVMOD vs SEVHEAVY; 3925 ± 442 vs 3997 ± 430 mL/min, P = .237), nor was the speed of the response (τ; 9.2 ± 2.1 vs 10.0 ± 2.1 seconds, P = .177). VO2peak from the square-wave tests was below that achieved in the ramp tests (91.0% ± 3.2% and 92.0% ± 3.9% VO2peak, P < .001). There was no difference in time to exhaustion between conditions (110.2 ± 9.7 vs 111.0 ± 15.2 seconds, P = .813). The results show that the primary VO2 response is unaffected by prior heavy exercise in running performed at intensities at which exhaustion will occur before a slow component emerges.

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Peter M. Christensen and Jens Bangsbo

Purpose:

To evaluate the influence of warm-up exercise intensity and subsequent recovery on intense endurance performance, selected blood variables, and the oxygen-uptake (VO2) response.

Methods:

Twelve highly trained male cyclists (VO2max 72.4 ± 8.0 mL · min−1 · kg−1, incremental-test peak power output (iPPO) 432 ± 31 W; mean ± SD) performed 3 warm-up strategies lasting 20 min before a 4-min maximal-performance test (PT). Strategies consisted of moderate-intensity exercise (50%iPPO) followed by 6 min of recovery (MOD6) or progressive high-intensity exercise (10–100%iPPO and 2 × 20-s sprints) followed by recovery for 6 min (HI6) or 20 min (HI20).

Results:

Before PT venous pH was lower (P < .001) in HI6 (7.27 ± 0.05) than in HI20 (7.34 ± 0.04) and MOD6 (7.35 ± 0.03). At the same time, differences (P < .001) existed for venous lactate in HI6 (8.2 ± 2.0 mmol/L), HI20 (5.1 ± 1.7 mmol/L), and MOD6 (1.4 ± 0.4 mmol/L), as well as for venous bicarbonate in HI6 (19.3 ± 2.6 mmol/L), HI20 (22.6 ± 2.3 mmol/L), and MOD6 (26.0 ± 1.4 mmol/L). Mean power in PT in HI6 (402 ± 38 W) tended to be lower (P = .11) than in HI20 (409 ± 34 W) and was lower (P = .007) than in MOD6 (416 ± 32 W). Total VO2 (15–120 s in PT) was higher in HI6 (8.18 ± 0.86 L) than in HI20 (7.85 ± 0.82 L, P = .008) and MOD6 (7.90 ± 0.74 L, P = .012).

Conclusions:

Warm-up exercise including race-pace and sprint intervals combined with short recovery can reduce subsequent performance in a 4-min maximal test in highly trained cyclists. Thus, a reduced time at high exercise intensity, a reduced intensity in the warm-up, or an extension of the recovery period after an intense warm-up is advocated.

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Joana F. Reis, Gregoire P. Millet, Davide Malatesta, Belle Roels, Fabio Borrani, Veronica E. Vleck and Francisco B. Alves

Purpose:

The aim of this study was to compare VO2 kinetics during constant power cycle exercise measured using a conventional facemask (CM) or a respiratory snorkel (RS) designed for breath-by-breath analysis in swimming.

Methods:

VO2 kinetics parameters—obtained using CM or RS, in randomized counterbalanced order—were compared in 10 trained triathletes performing two submaximal heavy-intensity cycling square-wave transitions. These VO2 kinetics parameters (ie, time delay: td1, td2; time constant: τ1, τ2; amplitude: A1, A2, for the primary phase and slow component, respectively) were modeled using a double exponential function. In the case of the RS data, this model incorporated an individually determined snorkel delay (ISD).

Results:

Only td1 (8.9 ± 3.0 vs 13.8 ± 1.8 s, P < .01) differed between CM and RS, whereas all other parameters were not different (τ1 = 24.7 ± 7.6 vs 21.1 ± 6.3 s; A1 = 39.4 ± 5.3 vs 36.8 ± 5.1 mL·min−1·kg−1; td = 107.5 ± 87.4 vs 183.5 ± 75.9 s; A2' (relevant slow component amplitude) = 2.6 ± 2.4 vs 3.1 ± 2.6 mL·min−1·kg−1 for CM and RS, respectively).

Conclusions:

Although there can be a small mixture of breaths allowed by the volume of the snorkel in the transition to exercise, this does not appear to significantly influence the results. Therefore, given the use of an ISD, the RS is a valid instrument for the determination of VO2 kinetics within submaximal exercise.

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Renato A.C. Caritá, Camila C. Greco and Benedito S. Denadai

Prior high-intensity exercise can improve exercise performance during severe-intensity exercise. These positive alterations have been attributed, at least in part, to enhancement of overall oxygen-uptake (VO2) kinetics.

Purpose:

To determine the effects of prior heavy-intensity exercise on VO2 kinetics and short-term high-intensity exercise performance in individuals with different aerobic-training statuses.

Methods:

Fifteen active subjects (UT; VO2max = 43.8 ± 6.3 mL · kg−1 · min−1) and 10 well-trained endurance cyclists (T; VO2max = 66.7 ± 6.7 mL · kg−1 · min−1) performed the following protocols: an incremental test to determine lactate threshold and VO2max, 4 maximal constant-load tests to estimate critical power, and two 3-min bouts of cycle exercise, involving 2 min of constant-work-rate exercise at severe intensity followed by a 1-min all-out sprint test. This trial was performed without prior intervention and 10 min after prior heavy-intensity exercise (ie, 6 min at 90% critical power).

Results:

The mean response time of VO2 was shortened after prior exercise for both UT (30.7 ± 9.2 vs 24.1 ± 7.2 s) and T (31.8 ± 5.2 vs 25.4 ± 4.3 s), but no group-by-condition interaction was detected. The end-sprint performance (ie, mean power output) was improved in both groups (UT ~4.7%, T ~2.0%; P < .05) by prior exercise.

Conclusion:

The effect of prior heavy-intensity exercise on overall VO2 kinetics and short-term high-intensity exercise performance is independent of aerobic-training status.

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Andrew M. Jones and Mark Burnley

The rate at which VO2 adjusts to the new energy demand following the onset of exercise strongly influences the magnitude of the “O2 defcit” incurred and thus the extent to which muscle and systemic homeostasis is perturbed. Moreover, during continuous high-intensity exercise, there is a progressive loss of muscle contractile efficiency, which is reflected in a “slow component” increase in VO2. The factors that dictate the characteristics of these fast and slow phases of the dynamic response of VO2 following a step change in energy turnover remain obscure. However, it is clear that these features of the VO2 kinetics have the potential to influence the rate of muscle fatigue development and, therefore, to affect sports performance. This commentary outlines the present state of knowledge on the characteristics of, and mechanistic bases to, the VO2 response to exercise of different intensities. Several interventions have been reported to speed the early VO2 kinetics and/or reduce the magnitude of the subsequent VO2 slow component, and the possibility that these might enhance exercise performance is discussed.