A modified 2-min CO-rebreathing procedure using capillary or venous blood sampled 8 and 10 min after starting CO-rebreathing allows complete circulatory mixing and provides an accurate and reliable estimate of Hbmass.

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.

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.

There is evidence to suggest athletes have adopted recombinant human erythropoietin (rHuEPO) dosing regimens that diminish the likelihood of being caught by direct detection techniques. However, the temporal response in physiology, performance, and Athlete Biological Passport (ABP) parameters to such regimens is not clearly understood. Participants were assigned to a high-dose only group (HIGH, n = 8, six rHuEPO doses of 250 IU/kg over two weeks), a combined high micro-dose group (COMB, n = 8, high-dose plus nine rHuEPO micro-doses over a further three weeks), or one of two placebo control groups who received saline in the same pattern as the HIGH (HIGH-PLACEBO, n = 4) or COMB (COMB-PLACEBO, n = 4) groups. Temporal changes in physiology and performance were tracked by graded exercise test (GXT) and haemoglobin mass assessment at baseline, after high dose, after micro-dose (COMB and COMB-PLACEBO only) and after a four-week washout. Venous blood samples were collected throughout the baseline, rHuEPO administration, and washout periods to determine the haematological and ABP response to each dosing regimen. Physiological adaptations induced by a two-week rHuEPO high-dose were maintained by rHuEPO micro-dosing for at least three weeks. However, all participants administered rHuEPO registered at least one suspicious ABP value during the administration or washout periods. These results indicate there is sufficient sensitivity in the ABP to detect use of high rHuEPO doping regimens in athletic populations and they provide important empirical examples for use by anti-doping experts. Copyright © 2017 John Wiley & Sons, Ltd.

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)