Abstract
While intermittent hypoxic training (IHT) has been reported to evoke cellular responses via hypoxia inducible factors (HIFs) but without substantial performance benefits in endurance athletes, we hypothesized that repeated sprint training in hypoxia could enhance repeated sprint ability (RSA) performed in normoxia via improved glycolysis and O2 utilization. 40 trained subjects completed 8 cycling repeated sprint sessions in hypoxia (RSH, 3000 m) or normoxia (RSN, 485 m). Before (Pre-) and after (Post-) training, muscular levels of selected mRNAs were analyzed from resting muscle biopsies and RSA tested until exhaustion (10-s sprint, work-to-rest ratio 1∶2) with muscle perfusion assessed by near-infrared spectroscopy. From Pre- to Post-, the average power output of all sprints in RSA was increased (p<0.01) to the same extent (6% vs 7%, NS) in RSH and in RSN but the number of sprints to exhaustion was increased in RSH (9.4±4.8 vs. 13.0±6.2 sprints, p<0.01) but not in RSN (9.3±4.2 vs. 8.9±3.5). mRNA concentrations of HIF-1α (+55%), carbonic anhydrase III (+35%) and monocarboxylate transporter-4 (+20%) were augmented (p<0.05) whereas mitochondrial transcription factor A (−40%), peroxisome proliferator-activated receptor gamma coactivator 1α (−23%) and monocarboxylate transporter-1 (−36%) were decreased (p<0.01) in RSH only. Besides, the changes in total hemoglobin variations (Δ[tHb]) during sprints throughout RSA test increased to a greater extent (p<0.01) in RSH. Our findings show larger improvement in repeated sprint performance in RSH than in RSN with significant molecular adaptations and larger blood perfusion variations in active muscles.
Highlights
Hypoxic conditions can be characterized in working muscle by a decreased oxygen tension [1]
There are some evidences that exercising in hypoxia affects muscular functions [2] and a large number of genes mediated by hypoxia-inducible factors (HIFs) [3]
Total work and training intensity during supervised repeated sprints (RS) training were similar during RSN and RS training in hypoxia (RSH), with only the mean heart rate being higher in RSH (Table 2)
Summary
Hypoxic conditions can be characterized in working muscle by a decreased oxygen tension (e.g. lower myoglobin oxygen saturation and intramyocellular oxygen partial pressure) [1]. There are some evidences that exercising in hypoxia affects muscular functions [2] and a large number of genes mediated by hypoxia-inducible factors (HIFs) [3] These transcription factors have been demonstrated to control the expression of over 70 targets in response to a reduction in oxygen concentration. Any limitation in O2 availability (e.g. exercising in hypoxia) induces a compensatory vasodilation shifting blood flow upward to keep constant O2 delivery to the muscle. This later mechanism is influenced by the exercise intensity [10]. During supramaximal efforts, an increase in skeletal muscle blood flow allows matching the augmented O2 demand tightly [11]
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