Here an example, where we have with NIRS / MOXY a very different view and would have tested during this study very different.
Just because we have a normobaric hypoxic ( 12 % ) situation doe snot mean, that the muscle itself works hypoxic. It just means that the O2 situation during this workout is somewhat less "optimal".
The question during a workout is, whether we actually have a delivery limitation versus a utilization limitation.
So we have no real info on the muscle hypoxic reaction, when just looking at the O2 situation in % like in altitude or like in this study.
If we use hypoxic situation we as well do not benefit from a SpO2 sensor on the finger as we than only see the situation from lungs to blood but not in the active exchange area , where we use NIRS / MOXY.
In the above study we may simply had a situation, where the contraction forces was strong enough to create a delivery problem due to the muscle tension so the O2 utilization was depending on the local situation rather than the systemic O2 intake.
So when we like to use arguments like Hypoxia or ischemia as an important part of potential improvement in strength exercises we simply can't use 1 reps as 100 % nor can we use any outside information.
we now can use MOXY as a live feedback with instant information, whether we create a hypoxia and what causes the hypoxia. Now I do not argue, that the end result of this study is wrong, but I argue, that the end result may be as it is because they did not had a feedback, whether the muscel itself worked metabolically really different due to the O2 differing tested outside the muscle.
Effects of low-resistance/high-repetition strength training in hypoxia on muscle structure and gene expression.
Friedmann B1, Kinscherf R, Borisch S, Richter G, Bärtsch P, Billeter R.
To test the hypothesis that severe hypoxia during low-resistance/high-repetition strength training promotes muscle hypertrophy, 19 untrained males were assigned randomly to 4 weeks of low-resistance/high-repetition knee extension exercise in either normoxia or in normobaric hypoxia ( FiO(2) 0.12) with recovery in normoxia. Before and after the training period, isokinetic strength tests were performed, muscle cross-sectional area (MCSA) measured (magnetic resonance imaging) and muscle biopsies taken. The significant increase in strength endurance capacity observed in both training groups was not matched by changes in MCSA, fibre type distribution or fibre cross-sectional area. RT-PCR revealed considerable inter-individual variations with no significant differences in the mRNA levels of hypoxia markers, glycolytic enzymes and myosin heavy chain isoforms. We found significant correlations, in the hypoxia group only, for those hypoxia marker and glycolytic enzyme mRNAs that have previously been linked to hypoxia-specific muscle adaptations. This is interpreted as a small, otherwise undetectable adaptation to the hypoxia training condition. In terms of strength parameters, there were, however, no indications that low-resistance/high-repetition training in severe hypoxia is superior to equivalent normoxic training.