The effect of acute simulated moderate altitude on power, performance and pacing strategies in well-trained cyclists.

Athletes regularly compete at 2,000-3,000 m altitude where peak oxygen consumption (VO2peak) declines approximately 10-20%. Factors other than VO2peak including gross efficiency (GE), power output, and pacing are all important for cycling performance. It is therefore imperative to understand how all these factors and not just VO2peak are affected by acute hypobaric hypoxia to select athletes who can compete successfully at these altitudes. Ten well-trained, non-altitude-acclimatised male cyclists and triathletes completed cycling tests at four simulated altitudes (200, 1,200, 2,200, 3,200 m) in a randomised, counter-balanced order. The exercise protocol comprised 5 x 5-min submaximal efforts (50, 100, 150, 200 and 250 W) to determine submaximal VO2 and GE and, after 10-min rest, a 5-min maximal time-trial (5-minTT) to determine VO2peak and mean power output (5-minTT(power)). VO2peak declined 8.2 +/- 2.0, 13.9 +/- 2.9 and 22.5 +/- 3.8% at 1,200, 2,200 and 3,200 m compared with 200 m, respectively, P < 0.05. The corresponding decreases in 5-minTT(power) were 5.8 +/- 2.9, 10.3 +/- 4.3 and 19.8 +/- 3.5% (P < 0.05). GE during the 5-minTT was not different across the four altitudes. There was no change in submaximal VO2 at any of the simulated altitudes, however, submaximal efficiency decreased at 3,200 m compared with both 200 and 1,200 m. Despite substantially reduced power at simulated altitude, there was no difference in pacing at the four altitudes for athletes whose first trial was at 200 or 1,200 m; whereas athletes whose first trial was at 2,200 or 3,200 m tended to mis-pace that effort. In conclusion, during the 5-minTT there was a dose-response effect of hypoxia on both VO2peak and 5-minTT(power) but no effect on GE.

Effect of pedal cadence on the accumulated oxygen deficit, maximal aerobic power and blood lactate transition thresholds of high-performance junior endurance cyclists.

In this study we investigated the effect of pedal cadence on the cycling economy, accumulated oxygen deficit (AOD), maximal oxygen consumption (VO2max) and blood lactate transition thresholds of ten high-performance junior endurance cyclists [mean (SD): 17.4 (0.4) years; 183.8 (3.5) cm, 71.56 (3.75) kg]. Cycling economy was measured on three ergometers with the specific cadence requirements of: 90-100 rpm for the road dual chain ring (RDCR90-100 rpm) ergometer, 120-130 rpm for the track dual chain ring (TDCR120-130 rpm) ergometer, and 90-130 rpm for the track single chain ring (TSCR90-130 rpm) ergometer. AODs were then estimated using the regression of oxygen consumption (VO2) on power output for each of these ergometers, in conjunction with the data from a 2-min supramaximal paced effort on the TSCR90-130 rpm ergometer. A regression of VO2 on power output for each ergometer resulted in significant differences (P<0.001) between the slopes and intercepts that produced a lower AOD for the RDCR90-100 rpm [2.79 (0.43) l] compared with those for the TDCR120-130 rpm [4.11 (0.78) l] and TSCR90-130 rpm [4.06 (0.84) l]. While there were no statistically significant VO2max differences (P = 0.153) between the three treatments [RDCR90-100 rpm: 5.31 (0.24) l x min(-1); TDCR120-130 rpm; 5.33 (0.25) 1 x min(-1); TSCR90-130 rpm: 5.44 (0.27) l x min(-1)], all pairwise comparisons of the power output at which VO2max occurred were significantly different (P<0.001). Statistically significant differences were identified between the RDCR90-100 rpm and TDCR120-130 rpm tests for power output (P = 0.003) and blood lactate (P = 0.003) at the lactate threshold (Thla-), and for power output (P = 0.005) at the individual anaerobic threshold (Thiat). Our findings emphasise that pedal cadence specificity is essential when assessing the cycling economy, AOD and blood lactate transition thresholds of high-performance junior endurance cyclists.

Altitude training at 2690m does not increase total haemoglobin mass or sea level VO2max in world champion track cyclists.

Haemoglobin mass (Hb mass), maximum oxygen consumption (VO2max), simulated 4000 m individual pursuit cycling performance (IP4000), and haematological markers of red blood cell (RBC) turnover were measured in 8 male cyclists before and after (A) 31 d of altitude training at 2690 m. The dependent variables were measured serially after altitude on d A3-4, A8-9 and A20-21. There was no significant change in Hb mass over the course of the study and VO2max at d A9 was significantly lower than the baseline value (79.3 +/- 0.7 versus 81.4 +/- 0.6 ml x kg(-1) x min(-1), respectively). No increase in Hb mass or VO2max was probably due to initial values being close to the natural physiological limit with little scope for further change. When the IP4000 was analysed as a function of the best score on any of the three test days after altitude training there was a 4% improvement that was not reflected in a corresponding change in VO2max or Hb mass. RBC creatine concentration was significantly reduced after altitude training, suggesting a decrease in the average age of the RBC population. However, measurement of reticulocyte number and serum concentrations of erythropoietin, haptoglobin and bilirubin before and after altitude provided no evidence of increased RBC turnover. The data suggest that for these elite cyclists any benefit of altitude training was not from changes in VO2max or Hb mass, although this does not exclude the possibility of improved anaerobic capacity.

Reduced performance of male and female athletes at 580 m altitude.

This study examined the effect of mild hypobaria (MH) on the peak oxygen consumption (VO2peak) and performance of ten trained male athletes [x (SEM); VO2peak = 72.4 (2.2) ml x kg(-1) x min(-1)] and ten trained female athletes [VO2peak = 60.8 (2.1) ml x kg(-1) x min(-1)]. Subjects performed 5-min maximal work tests on a cycle ergometer within a hypobaric chamber at both normobaria (N, 99.33 kPa) and at MH (92.66 kPa), using a counter-balanced design. MH was equivalent to 580 m altitude. VO2peak at MH decreased significantly compared with N in both men [-5.9 (0.9)%] and women [-3.7 (1.0)%]. Performance (total kJ) at MH was also reduced significantly in men [-3.6 (0.8)%] and women [-3.8 (1.2)%]. Arterial oxyhaemoglobin saturation (SaO2) at VO2peak was significantly lower at MH compared with N in both men [90.1 (0.6)% versus 92.0 (0.6)%] and women [89.7 (3.1)% versus 92.1 (3.0)%]. While SaO2 at VO2peak was not different between men and women, it was concluded that relative, rather than absolute. VO2peak may be a more appropriate predictor of exercise-induced hypoxaemia. For men and women, it was calculated that 67-76% of the decrease in VO2peak could be accounted for by a decrease in O2 delivery, which indicates that reduced O2 tension at mild altitude (580 m) leads to impairment of exercise performance in a maximal work bout lasting approximately 5 min.

Influence of test duration and event specificity on maximal accumulated oxygen deficit of high performance track cyclists.

This study examined the relationship between the time required to fully utilise the maximal accumulated oxygen deficit (MAOD) and event specificity of track cyclists. Twelve track endurance and 6 sprint high performance track cyclists performed four treatments of 70 s, 120 s, 300 s and 115% VO2max of maximal cycling on an air-braked ergometer. Peak blood lactate was measured immediately after each test with VO2 kinetics being assessed during the 115% VO2max time to exhaustion test. When the two cycling groups were combined there was no significant difference in the MAOD when assessed under the four different exercise durations. However, when the groups were analysed separately the following results were apparent: (1) the sprint cyclists achieved a significantly greater MAOD (66.9 +/- 2.2 ml.kg-1) compared to the track endurance cyclists (57.6 +/- 6.7 ml.kg-1) when a 70 s test duration was employed (2) even though the track endurance cyclists achieved their greatest MAOD during the 300 s test protocol (62.1 +/- 11.0 ml.kg-1), it was not significantly different to the MAOD's measured during the three other test durations and (3) the sprint cyclists recorded their greatest MAOD during the 70 s supramaximal test protocol (66.9 +/- 2.2 ml.kg-1). This was not significantly different to the 120 s test MAOD, but it was significantly higher than the MAOD values recorded during the 115% VO2max and 300 s test durations. There was no significant difference between the two groups in the peak post-exercise blood lactate concentrations for any of the tests and only the 70 s test produced a significant correlation between peak blood lactate and the MAOD. The VO2 kinetics (VO2 t1/2) of the sprinters was significantly slower than that of the track endurance cyclists (26.3 +/- 2.3 vs 23.9 +/- 2.8 s.). The findings of this study demonstrate that sprint cyclists can fully express their anaerobic capacity within an event specific 70 s all-out test and that these cyclists progressively decrease their anaerobic capacity during a 120 s, 115% VO2max (mean time = 210 s) or 300 s test, despite giving all-out efforts. Conversely, track endurance cyclists achieve their highest mean score during an event specific 300 s test and their lowest during a 70 s test. These findings have important implications when testing high performance cyclists for determination of MAOD, with the implication that it is necessary to assess MAOD under exercise conditions (i.e., duration, pacing) specific to the cyclist's chosen event.

Aerobic and anaerobic indices contributing to track endurance cycling performance.

A group of 18 male high performance track endurance and sprint cyclists were assessed to provide a descriptive training season specific physiological profile, to examine the relationship between selected physiological and anthropometric variables and cycling performance in a 4000-m individual pursuit (IP4000) and to propose a functional model for predicting success in the IP4000. Anthropometric characteristics, absolute and relative measurements of maximal oxygen uptake (VO2max), blood lactate transition thresholds (Thla- and Th(an),i), VO2 kinetics, cycling economy and maximal accumulated oxygen deficit (MAOD) were assessed, with cyclists also performing a IP4000 under competition conditions. Peak post-competition blood lactate concentrations and acid-base values were measured. Although all corresponding indices of Thla- and Th(an),i occurred at significantly different intensities there were high intercorrelations between them (0.51-0.85). There was no significant difference in MAOD when assessed using a 2 or 5 min protocol (61.4 vs 60.2 ml.kg-1, respectively). The highest significant correlations were found among IP4000 and the following: VO2max (ml.kg-2/3.min-1; r = -0.79), power output at lactate threshold (Wthla) (W; r = -0.86), half time of VO2 response whilst cycling at 115% VO2max (s; r = 0.48) and MAOD when assessed using the 5 min protocol (ml.kg-1; r = -0.50). A stepwise multiple regression yielded the following equation, which had an r of 0.86 and a standard error of estimate of 5.7 s: IP4000 (s) = 462.9 - 0.366 x (Wthla) - 0.306 x (MAOD) - 0.438 x (VO2max) where Wthla is in W, MAOD is in ml.kg-1 and VO2max is in ml.kg-1 x min-1.(ABSTRACT TRUNCATED AT 250 WORDS)