Hypoxic sprint exercise as a complement to the “Live High‐Train Low” regimen

Despite decades of research and numerous studies, the evidence supporting altitude adaptation for lowlanders who intend to perform at or around sea level is still under debate. In a recent study, Girard and colleagues aimed to complement the general consensus that the “live high-train low” is the most advantageous regimen by adding either normoxic (LHTL) or hypoxic (LHTLH) repeated sprint sessions to improve team-athlete performance. The control group intervention consisted of 14 days “live low-train low” (LLTL) regimen, attending ordinary team training but without added sprint sessions. Both groups with the “live high” and added sprint sessions (LHTL and LHTLH) showed enhanced running performance 5 days and 3 weeks after the intervention. Sprint time was reduced at 5 days post-intervention in both groups, and this reduction was maintained at the 3 weeks post-intervention test in the LHTLH group only. Based on this 3-weeks post-intervention result, the authors suggest that LHTLH confers a sprint performance advantage. Unfortunately, the lack of a fourth intervention group (LLTL + sprint) makes the distinction between the effects of high-altitude residency and sprint exercises on performance difficult. With these performance data as a backdrop, the authors extended their study with descriptive analyses of skeletal muscle molecular adaptations. In summary, a set of gene transcripts associated with adaptations to exercise, including key angiogenic regulator Vegf, and regulators of mitochondrial biogenesis, Pgc-1a and Tfam, were significantly increased in the biopsy taken after the LHTLH intervention compared to the LHTL and LLTL interventions. These changes were suggested to reflect an enhanced skeletal muscle adaptation with the LHTLH regimen. The authors further speculate that these changes were dependent on differences in HIF activation as hif-1a mRNA also was higher in LHTLH group. It should, however, be noted that although the current literature proposes a primarily posttranslational regulation of HIF-1, HIF1a protein was not characterized in this study. Although Hif-1 is often introduced as a mediator of exercise adaptation, the story is likely more complex. Combining and/or comparing information from descriptive human intervention studies and experimental animal models can provide additional information on the role of hypoxia-induced mechanisms for performance and may aid in dissecting global (whole body) hypoxic response mechanisms involving peripheral muscle adaptation. For example, mice harbouring a skeletal muscle-specific deletion of Hif1a performed better in endurance trials and demonstrated several of the features associated with trained muscle, including mitochondrial adaptations. However, a recent study using an inducible global (whole body) deletion of PHD2 in mice (resulting in oxygen-independent Hif activation in multiple organs) exhibited elevated haematocrit, increased skeletal muscle capillarization and enhanced improvement in running time in response to training. These studies highlight the complexity of interpreting hypoxic regulating pathways in exercised and remodelling skeletal muscle. LHTLH and LLTL groups both showed increased protein levels and activity of citrate synthase, an indicator of muscle oxidative capacity, as compared to the LHTL + RSN group. Enhanced CS activity has been shown to be associated with improvements in aerobic performance, and sprint exercise can improve CS activity. Sustained environmental hypoxia as experienced in both LHTL and LHLTH conditions has been associated with an attenuation of oxidative processes. In line with this, a reduced CSA activity was observed in LHTL; however, notably, the repeated sprint intervention under hypoxia seems to have counteracted the detrimental effects of chronic hypoxia (LHTL) on oxidative capacity. This finding is supported by previous human studies showing an augmentation of peripheral adaptations during exercise with reduced oxygen delivery, which was associated with increases in Hif-1 and Pgc-1a activity. From a perspective of optimal performance, the use of hypoxic interventions is controversial and, as suggested in the current studies by Girard and Nunomiya, most likely expand beyond the effects of hypoxia on skeletal muscle tissue to comprise integration of multiple tissue adaptations, including buffering systems as well as ventilatory and cardiovascular responses. The current study utilizing DOI: 10.1111/apha.12989