As the submaximal workload was controlled using HR, the uniformity of the submaximal exercise heart rate between baseline and post-intervention measurements in all three groups indicates good consistency in the exercise test between baseline and post-intervention trials. The within group differences between baseline and post-intervention oxygen efficiency, as assessed by V˙O2submax,
suggested that the IHE3 remained largely unchanged following the 5-week intervention, and the IHE5 group improved efficiency (see Table 23 in Appendix C). As the decrease in V˙O2submax in IHE5 (-1.2
mlmin-1kg-1) was similar to the change in the control group (-0.8 mlmin-1kg-1), it is unlikely that the improved oxygen efficiency could be attributable to the intermittent hypoxic exposure. Despite
113 improved familiarity with the researchers and exercise testing protocols. Thus, neither group (IHE3 nor IHE5) demonstrated any advantage attributable to the IHE treatment over the control group during submaximal exercise.
During the maximal assessment, the results were somewhat conflicting. The IHE3 group likely improved V˙O2peak but did not demonstrate any other improvement to support an improvement in
exercise tolerance (such as improved timeex, or resmax). Conversely, the IHE5 group did demonstrate
increased timeex and resmax but did not demonstrate any improvement in V˙O2peak, despite an increase
in Hb. The findings from the IHE5 group are similar to those of Burtscher et al. (2009) who reported improved exercise time, time to anaerobic threshold, and increased total haemoglobin mass, but no clear improvement in V˙O2peak in his population of patients at risk for coronary pulmonary obstructive
disease. Burtscher et al. (2009) suggests, that the exercise time reflects greater sensitivity to training effects than V˙O2peak. So, while participants in the IHE5 group did not improve exercise tolerance to the
point of improving V˙O2peak, exercise capacity was improved sufficiently to alter more sensitive
markers of exercise tolerance. Contrary to the findings of other researchers (Calbet et al., 2006), the 1.75% increase (within group) in Hb in the IHE5 group following the 5 weeks of IHE treatment was not sufficient to alter the V˙O2peak of our participants in a meaningful way. Similarly, Clark et al. (2009)
reported no change in V˙O2peak in their cohort of well-trained male cyclists following an increase of
3.3% Hbmass, and only a trivial correlation (r = 0.09) between the change in Hbmass and V˙O2peak. Our
research supports the idea of a minimum dose required in a hypoxic environment for an increase in haemoglobin (the Control and IHE3 groups exhibited no change, but there was a clear, possible increase in Hbmass in IHE5). However, it does not support an automatic improvement in V˙O2peak with
an increase in Hbmass. The question arises of whether in addition to recommendations for a minimum
time spent in hypoxic exposure for an increase in Hbmass (Rusko et al., 2004), there is also a minimum
worthwhile increase in Hbmass required before a practical increase in V˙O2peak is achieved.
Alternatively, the increased workload and higher time to exhaustion in the IHE5 group may indicate a greater anaerobic tolerance. Findings such as these have also been observed by other researchers (Hamlin et al., 2010) who posit that mechanisms such a shift to glycolytic energy pathways (Hamlin et al., 2010), and improved skeletal muscle buffer capacity (Mizuno et al., 1990) are responsible for the improvements in anaerobic performance.
The improvement of V˙O2peak in the IHE3 group without any other supporting evidence of improved
exercise tolerance is confusing. It is possible that ‘upstream changes’ in response to hypoxic exposure (Garvican et al., 2011) may be responsible for the increase in V˙O2peak in the IHE3 group in
114 adaptations associated with an up regulation of HIF-1α and an adaptation of the hypoxic sensing system (Vogt et al., 2001, Hoppeler et al., 2003). However, if this were the case, it is unlikely that these adaptations would occur in the group receiving 2 – 3 IHE sessions per week, and not in the group receiving 5 IHE sessions per week.
Blood pressure
Resting systolic blood pressure decreased in both the IHE3 (9.6 mmHg) and IHE5 (5.2 mmHg) groups compared to negligible change in the control group (0.2 mmHg). However, when the baseline was added as a covariate the changes between groups were unclear. The improved HRV as indicated by increased parasympathetic activity (rMSSD) in IHE3 (small) and IHE5 (moderate – large) following the 5 weeks of IHE may be linked to the improved resting SBP in the IHE3 and IHE5 groups. However, as the SBP at baseline in the IHE3 and IHE5 groups was substantially higher than the C group, it is possible that the improvements reflect a regression to the mean, as opposed to a true change (Hopkins, 2006). Therefore, the ‘unclear’ outcome is appropriate in this regard, and more
information is needed before a confident statement can be made regarding the effect of IHE on SBP.
Muscle mass and fat mass
There were no meaningful differences between groups in either the fat mass or muscle mass measurements following the intervention when compared to the control group. The absence in any notable changes between groups pre- and post-intervention supports both the study by Balykin et al. (2004) and our earlier study (see Chapter 3) and suggests that an IHE protocol in this format, without an additional exercise component, is insufficient to induce any beneficial alteration in muscle mass or fat mass.