Middle distance (800–3000 m) running performance is dependent on the speed that an athlete can sustain for the duration of the event. This speed is dependent on the ability of the locomotor muscles to produce power and resist fatigue (di Prampero et al., 1986; Lacour et al., 1990). The relatively high speed sustained throughout middle distance running events results in an energy demand in excess of the maximal aerobic energy yield (~110–120%), as assessed via pulmonary oxygen uptake (V˙O2) and, thus necessitates the integrative contribution from both aerobic and anaerobic pathways (Lacour et al., 1990; Craig and Morgan, 1998; Spencer and Gastin, 2001; Duffield et al., 2005). The 800 m event, for example, requires an ~66 and 34% relative contribution from aerobic and anaerobic metabolism, respectively (Spencer and Gastin, 2001).

The overall energy demand of middle distance running events places these events within the severe, or possibly the extreme intensity domain (Jones and Burnley, 2009). It is assumed that during exercise within the severe or extreme intensity domain, V˙O2 will project exponentially toward the maximal rate of pulmonary oxygen uptake (V˙O2max) until V˙O2max is achieved, or exhaustion occurs (Whipp, 1994; Gaesser and Poole, 1996; Poole and Richardson, 1997; Hill and Ferguson, 1999; Jones and Burnley, 2009). However, research utilizing exhaustive constant work rate (CWR) treadmill running of ~2 min and highly aerobically trained middle distance runners (V˙O2max ≥ 60 ml.kg⁻¹.min⁻¹) has found that V˙O2 does not achieve V˙O2max despite sufficient time for the full response to develop (Draper and Wood, 2005a,b; Sandals et al., 2006; James et al., 2007a,b, 2008). Instead, a submaximal steady state V˙O2 is achieved following ~1 min of exercise with no evidence of a further increase in V˙O2 (Draper and Wood, 2005b).

Previous studies using cross-sectional designs have shown that individuals with a greater V˙O2max achieve a lower percentage of V˙O2max (V˙O2max) during exhaustive CWR treadmill running of ~2 min (Draper and Wood, 2005a; James et al., 2007a). However, it should be recognized that individuals with a larger V˙O2max typically have faster V˙O2 kinetics (Draper and Wood, 2005b; Kilding et al., 2006; Ingham et al., 2007; Marwood et al., 2010). It is therefore unclear why individuals whom possess a large V˙O2max and faster V˙O2 kinetics achieve a lower V˙O2max than lesser aerobically trained individuals during exercise of this type.

It is well-known that acute hypoxic exposure results in significant reductions in V˙O2max relative to values obtained in normoxic conditions (Dill et al., 1966; Dill and Adams, 1971; Engelen et al., 1996; Woorons et al., 2005; Calbet et al., 2015), and the decrement in V˙O2max is linearly associated to the fraction of inspired oxygen (FiO₂) (Lawler et al., 1988). Acute hypoxic exposure, therefore, allows the V˙O2max of highly aerobically trained individuals to be artificially and temporarily reduced. Whilst it is recognized that hypoxia may slow V˙O2 kinetics relative to normoxia (Engelen et al., 1996), the magnitude of slowing suggests that V˙O2 kinetics will remain sufficiently fast to permit the manifestation of its full response within <1 min, although evidence from exercise within the severe intensity domain is limited (Heubert et al., 2005). Therefore, hypoxia might provide the opportunity to explore whether highly aerobically trained individuals who are unable to achieve V˙O2max during an exhaustive (~2 min) CWR treadmill run in normoxia can achieve a hypoxia reduced V˙O2max during a time matched, thus relative intensity matched CWR treadmill run performed in hypoxia.

The purpose of this study, therefore, was to investigate the effect of artificially lowering V˙O2max in trained individuals on their ability to attain V˙O2max during an exhaustive treadmill run. We hypothesized that highly aerobically trained individuals would be unable to attain V˙O2max during a CWR run lasting ~2 min performed in normoxia, but would be able to achieve a hypoxic reduced V˙O2max.

The V˙O2max measured in the normoxic ramp incremental test was 4.40 ± 0.42 L.min⁻¹ (67.0 ± 5.2 ml.kg⁻¹.min⁻¹) and HR_max was 185 ± 7 bpm. Hypoxia reduced V˙O2max to 2.97 ± 0.27 L.min⁻¹ (45.1 ± 3.0 ml.kg⁻¹.min⁻¹; P < 0.001) and HR_max to 181 ± 6 bpm; P < 0.05).

The average speed utilized for the normoxic CWR trials was 22.0 ± 1.0 km.h⁻¹ which resulted in a trial duration of 114 ± 11 s (range: 100 s to 130 s). The speed of the hypoxic CWR trial was performed at a significantly slower speed (20.5 ± 1.0 km.h⁻¹; P < 0.001) to ensure a similar duration of trial between conditions. The duration of the hypoxic CWR trial (114 ± 11 s, range: 105 s to 135 s) was not significantly different to the duration of the normoxic CWR trial (114 ± 5 s, range: 105 s to 125 s) (P > 0.05). Normoxic V˙O2max was not achieved during the normoxic CWR trial (3.79 ± 0.47 L.min⁻¹; 86 ± 6% V˙O2max; P < 0.05; Figure 1).However, subjects attained hypoxic V˙O2max during the hypoxic CWR trial (3.02 ± 0.30 L.min⁻¹; 102 ± 8%; P > 0.05; Figure 1). V˙O2max was inversely associated with V˙O2max achieved during the normoxic (r = −0.64, P < 0.05) and hypoxic (r = −0.68, P < 0.01) CWR trials, and when the normoxic and hypoxic trials were combined (r = −0.85, P < 0.001; Figure 2). Condition-specific HR_max was attained during normoxic (189 ± 7 bpm) and hypoxic (181 ± 7 bpm) CWR trials (P > 0.05). The parameters of the modeled V˙O2 data are presented in Table 1. No relationships were observed between speed and % V˙O2 achieved during the CWR trials performed in normoxia (r = 0.34, P > 0.05), hypoxia (r = −0.16, P > 0.05), or the difference in speed and V˙O2 between the normoxic and hypoxic CWR trials (r = −0.05, P > 0.05).

No significant interaction effect was observed for V˙E (P > 0.05) with no significant main effect for condition (normoxia, 137.3 ± 17.5 L.min⁻¹; hypoxia 130 ± 16.2 L.min⁻¹; P > 0.05), but a significant main effect for test (ramp, 128.0 ± 16.6 L.min⁻¹; CWR, 139.2 ± 16.0 L.min⁻¹; P < 0.001). There was a significant interaction effect for V˙E/V˙O2 (P < 0.05) with significant main effects for condition (normoxia, 35.3 ± 6.7 L.min⁻¹; hypoxia 43.7 ± 4.7 L.min⁻¹; P < 0.001) and test (ramp, 128.0 ± 16.6 L.min⁻¹; CWR, 139.2 ± 16.0 L.min⁻¹; P < 0.001). There was a significant interaction effect for V˙E/V˙CO2 (P < 0.01) with significant main effects for condition (normoxia, 28.2 ± 3.7 L.min⁻¹; hypoxia 31.6 ± 6.0 L.min⁻¹; P < 0.05), but no significant difference for test (ramp, 29.8 ± 5.0 L.min⁻¹; CWR, 26.2 ± 3.4 L.min⁻¹; P > 0.05).

The principle novel finding of the current study was that despite being unable to attain V˙O2max during normoxic CWR running lasting ~2 min, highly aerobically trained individuals could achieve a hypoxia reduced V˙O2max during CWR running of a matched duration, thus of a similar relative intensity. This is the first study to demonstrate that subjects whose V˙O2 plateaued below V˙O2max during an exhaustive CWR run, were subsequently able to attain V˙O2max when the exercise bout was replicated in hypoxic conditions despite a slowed V˙O2 response.

Previous research has demonstrated that during normoxic CWR running lasting ~2 min, more highly aerobically trained individuals achieved a lower V˙O2max (Draper and Wood, 2005a; James et al., 2007a). In agreement with these findings, the current study reported an inverse association between V˙O2max and the V˙O2max achieved during the normoxic CWR trial (Figure 2). To gain further insight into the relationship between V˙O2max and V˙O2max achieved the present study investigated whether a hypoxia induced reduction in V˙O2max may permit highly aerobically trained individuals to attain V˙O2max during exhaustive CWR running at a matched relative intensity. The acute hypoxic exposure reduced V˙O2max by ~32%, consistent with previous reports (Engelen et al., 1996; Martin and O'Kroy, 1993; Woorons et al., 2005), and subject to this reduction V˙O2max was achieved (Figure 1B). No relationship was observed between % V˙O2max achieved and the running speed during the CWR tests in normoxia or hypoxia, nor the difference in speed between conditions (i.e., normoxia and hypoxia) and the difference in %VO_2max achieved (all P > 0.05), suggesting that V˙O2max may be an important parameter in determining whether an individual may be able to achieve their V˙O2max during this type of exercise. Furthermore, these findings highlight that further improvements in V˙O2max are of less benefit to high-intensity exercise performance compared to similar gains in anaerobic capability. These findings perhaps seem incongruous with the high V˙O2max values typically reported in elite 800 m runners (Svedenhag and Sjödin, 1984; Ingham et al., 2008) that they are apparently unable to fully utilize. However, such a high V˙O2max value may be due to the high volume of interval training performed by these athletes (Helgerud et al., 2007). There have certainly been instances where performance at altitude would indicate that the decrement in V˙O2max may not substantially impair performance. For example, Ralph Doubell equalled the World Record at the 1968 Mexico Olympics which was performed at an altitude of 2,240 m above sea level; a feat that would seem implausible if one's V˙O2max was a necessity for optimum performance.

The V˙O2 kinetics were similar to values previously reported during investigations utilizing similarly highly aerobically trained runners during CWR running lasting ~2 min (Draper and Wood, 2005a,b; Draper et al., 2008). The phase I time delays are also similar to those reported by Wilkerson et al. (2004). Consistent with Engelen et al. (1996), we found a slower phase II τ in the hypoxic condition (Table 1). However, it should be noted that despite a slower phase II τ, resulting in ~10 s difference in the attainment of the V˙O2 amplitude, hypoxic V˙O2max was achieved. Conversely, despite faster V˙O2 kinetics normoxic V˙O2max was not attained. Instead, there was an evident V˙O2 plateau in normoxia at ~86% normoxic V˙O2max. The occurrence of a V˙O2 plateau, rather than a continued trajectory toward V˙O2max and indeed the energy demands of the exercise, questions contemporary models of V˙O2 kinetics during CWR exercise lasting ~2 min in this highly aerobically trained group. Interestingly, this same response is not evident during exhaustive cycle ergometry of a similar duration whereby V˙O2 continues to increase throughout, although maximum values are not attained (Draper et al., 2003). At present the reasons for the differences between exercise modes in V˙O2 response to severe intensity exercise are unclear. Increasing oxygen uptake has been associated with reduced efficiency arising from factors, such as metabolite accumulation, limitations in substrate availability, pH disturbance, increased muscle temperature, and altered motor unit recruitment (Grassi et al., 2015). Indeed, it is well established that the patterns of muscle action, including the relative proportion of eccentric and concentric contraction and the contribution of the stretch-shortening cycle differ between running and cycling (van Ingen-Schenau et al., 1997; Bijker et al., 2002). These effects might, at least in part, contribute to the between mode differences in V˙O2 kinetics, particularly for higher work rates where the use of elastic energy is optimized (Dalleau et al., 1998); whether or not increased stored energy during the stretch shortening cycle can help maintain efficiency despite increased metabolic fatigue warrants further investigation.

Consistent with previous investigations, we found that HR_max was greater in normoxia than hypoxia (Benoit et al., 1995; Mollard et al., 2007). However, similar to our V˙O2 findings normoxic HR_max was not achieved during the normoxic CWR test (Draper and Wood, 2005a,b), but hypoxic HR_max could be achieved during the hypoxic CWR trial. Assuming HR_max is needed to achieve maximal cardiac output (Q_max), these findings suggest that Q_max was not achieved during the normoxic CWR test. Despite a lower HR_max in hypoxia relative to normoxia, previous findings have shown that hypoxia has no effect on Q_max (Mollard et al., 2007), implying a compensatory increase in maximal stroke volume in hypoxia. Therefore, the inability to achieve V˙O2max in the normoxic CWR trial may be associated with submaximal cardiac output. However, further investigation that assesses cardiac output and blood flow is necessary to gain insight into Q_max as a potential limiting factor in the attainment of V˙O2max during this type of exercise.

Although end exercise V˙E was greater during the CWR trials relative to the ramp incremental tests, this was not different between normoxia and hypoxia. Furthermore, we observed no differences in ventilatory equivalents between conditions (i.e., normoxia and hypoxia). These similar ventilatory responses might serve to attenuate or prevent the exercise induced arterial hypoxemia that has been described in highly aerobically trained individuals (Dempsey et al., 1984; Powers et al., 1988, 1992; Caillaud et al., 1993; review Prefaut et al., 2000). In normoxia, the increased V˙E during CWR exercise would likely increase the work of breathing thereby compromising limb muscle blood flow (Wetter et al., 1999). In hypoxia, the PO₂ is in the steep portion of the oxygen-hemoglobin dissociation curve and increased V˙E could have pronounced effects on arterial oxygen concentration and may help to preserve muscle V˙O2 despite reduced limb blood flow. However, in normoxia the PO₂ is in the flatter region of the oxygen-hemoglobin dissociation curve and the same increases in V˙E would be less effective in altering arterial oxygen concentration relative to hypoxia. As a consequence the increased work associated with breathing would result in little/small increases in arterial oxygen concentration and reduce muscle blood flow and thus muscle V˙O2. However, it should be noted that exercise induced arterial hypoxemia has also been reported during different exercise modalities, such as cycling (Powers et al., 1988), whereas the phenomenon whereby V˙O2 attains a plateau below V˙O2max has only been reported in highly aerobically trained individuals during CWR running exercise lasting ~2 min. The mechanistic origin(s) for this phenomenon is currently unknown and requires further research.

Despite only one transition to the CWR trial in each condition, due to the large amplitude of the V˙O2 response during this intensity of exercise there is a much greater signal/noise ratio when compared to exercise of a lower intensity (Lamarra et al., 1987). In lesser trained individuals with smaller V˙O2 amplitude, thus smaller signal to noise ratio, Draper et al. (2008) demonstrated that two transitions would at worst (i.e., smallest signal to noise ratio) provide 95% confidence intervals of 1 s. Given that the current study recruited more highly aerobically trained individuals than Draper et al. (2008), thus a greater signal to noise ratio, it would be reasonable to expect 95% confidence intervals of better than 2 s for τ. Furthermore, the current study design was sufficiently sensitive and had adequate power to detect differences in τ between conditions.

In conclusion, the results of the present study demonstrate that highly aerobically trained individuals whom are unable to achieve V˙O2max during an exhaustive CWR run lasting ~2 min, are able to achieve a hypoxia reduced V˙O2max despite exhibiting slower V˙O2 kinetics. These data further support the notion that V˙O2max is an important determinant of the V˙O2max that can be achieved during a short duration exhaustive CWR run. The present data demonstrate that ventilatory differences are unable to explain the inability to attain V˙O2max during normoxic CWR trials. Future research should explore the possibility of an O₂ delivery or blood perfusion limitation during this type of exercise in highly aerobically trained runners. Future research should also consider utilizing an experimental condition in normoxia which uses gradient on the treadmill (or weighted vest) instead of hypoxia to slow the running speed down and induce task failure in ~2 min. This would aid in deciphering the novel finding of this study.

The study was approved by University of Gloucestershire Ethics Committee. All participants were provided with verbal and written information that detailed the rationale of the study, the test procedures, and any risks and benefits of participation. Participants were informed of their right to withdraw from the study at any time without penalty. All participants provided written informed consent detailing that they were willing to take part.

MB, CP, SD, JC, and CC were involved in conceptual design, data collection, interpretation, and manuscript preparation. All authors approve the submission of this work and agree to be accountable for all aspects of the work.