The high energy output seems to be the discriminating factor for top-class male marathon runners who trained at higher relative intensities.
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.
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 velocity at the VO2max is the main factor predicting the variance of the 10-km performance both in men and women, and high-intensity training contributes to this higher VO2max among men.
The purpose of this study was to implement a new method for assessing the ventilatory thresholds from heart rate variability (HRV) analysis. ECG, VO2, VCO2, and VE were collected from eleven well-trained subjects during an incremental exhaustive test performed on a cycle ergometer. The "Short-Term Fourier Transform" analysis was applied to RR time series to compute the high frequency HRV energy (HF, frequency range: 0.15 - 2 Hz) and HF frequency peak (fHF) vs. power stages. For all subjects, visual examination of ventilatory equivalents, fHF, and instantaneous HF energy multiplied by fHF (HF.fHF) showed two nonlinear increases. The first nonlinear increase corresponded to the first ventilatory threshold (VT1) and was associated with the first HF threshold (T(RSA1) from fHF and HFT1 from HF.fHF detection). The second nonlinear increase represented the second ventilatory threshold (VT2) and was associated with the second HF threshold (T(RSA2) from fHF and HFT2 from HF.fHF detection). HFT1 , T(RSA1), HFT2, and T(RSA2) were, respectively, not significantly different from VT1 (VT1 = 219 +/- 45 vs. HFT1 = 220 +/- 48 W, p = 0.975; VT1 vs. T(RSA1) = 213 +/- 56 W, p = 0.662) and VT2 (VT2 = 293 +/- 45 vs. HFT2 = 294 +/- - 48 W, p = 0.956; vs. T(RSA2) = 300 +/- 58 W, p = 0.445). In addition, when expressed as a function of power, HFT1, T(RSA1), HFT2, and T(RSA2) were respectively correlated with VT1 (with HFT1 r2 = 0.94, p < 0.001; with T(RSA1) r2 = 0.48, p < 0.05) and VT2 (with HFT2 r2 = 0.97, p < 0.001; with T(RSA2 )r2 = 0.79, p < 0.001). This study confirms that ventilatory thresholds can be determined from RR time series using HRV time-frequency analysis in healthy well-trained subjects. In addition it shows that HF.fHF provides a more reliable and accurate index than fHF alone for this assessment.
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.
This article traces the history of scientific and empirical interval training. Scientific research has shed some light on the choice of intensity, work duration and rest periods in so-called 'interval training'. Interval training involves repeated short to long bouts of rather high intensity exercise (equal or superior to maximal lactate steady-state velocity) interspersed with recovery periods (light exercise or rest). Interval training was first described by Reindell and Roskamm and was popularised in the 1950s by the Olympic champion, Emil Zatopek. Since then middle- and long- distance runners have used this technique to train at velocities close to their own specific competition velocity. In fact, trainers have used specific velocities from 800 to 5000m to calibrate interval training without taking into account physiological markers. However, outside of the competition season it seems better to refer to the velocities associated with particular physiological responses in the range from maximal lactate steady state to the absolute maximal velocity. The range of velocities used in a race must be taken into consideration, since even world records are not run at a constant pace.
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.
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