It has been established that Wingate-based high-intensity training (HIT) consisting of 4 to 6 x 30-s all-out sprints interspersed with 4-min recovery is an effective training paradigm. Despite the increased utilisation of Wingate-based HIT to bring about training adaptations, the majority of previous studies have been conducted over a relatively short timeframe (2 to 6 weeks). However, activity during recovery period, intervention duration or sprint length have been overlooked. In study 1, the dose response of recovery intensity on performance during typical Wingate-based HIT (4 x 30-s cycle all-out sprints separated by 4-min recovery) was examined and active recovery (cycling at 20 to 40% of V̇O2peak) has been shown to improve sprint performance with successive sprints by 6 to 12% compared to passive recovery (remained still), while increasing aerobic contribution to sprint performance by ~15%. In the following study, 5 to 7% greater endurance performance adaptations were achieved with active recovery (40%V̇O2peak) following 2 weeks of Wingate-based HIT. In the final study, shorter sprint protocol (4 to 6 x 15-s sprints interspersed with 2 min of recovery) has been shown to be as effective as typical 30-s Wingate-based HIT in improving cardiorespiratory function and endurance performance over 9 weeks with the improvements in V̇O2peak being completed within 3 weeks, whereas exercise capacity (time to exhaustion) being increased throughout 9 weeks. In conclusion, the studies demonstrate that active recovery at 40% V̇O2peak significantly enhances endurance adaptations to HIT. Further, the duration of the sprint does not seem to be a driving factor in the magnitude of change with 15 sec sprints providing similar adaptations to 30 sec sprints. Taken together, this suggests that the arrangement of recovery mode should be considered to ensure maximal adaptation to HIT, and the practicality of the training would be enhanced via the reduction in sprint duration without diminishing overall training adaptations.

京都大学 / 0048 / 新制・課程博士 / 博士(農学) / 甲第20429号 / 農博第2214号 / 新制||農||1048(附属図書館) / 学位論文||H29||N5050(農学部図書室) / 京都大学大学院農学研究科森林科学専攻 / (主査)教授 吉村 剛, 教授 藤井 義久, 教授 矢野 浩之 / 学位規則第4条第1項該当 / Doctor of Agricultural Science / Kyoto University / DFAM

Introduction: There have been few well controlled altitude and hypoxic training studies to date. This thesis investigated the effects of altitude and (sham controlled) intermittent hypoxic training (IHT) on exercise capacity, and the associated physiological adaptations. Methods: Chapter 3 investigated how living and training at 2320 m or at sea level affected total haemoglobin mass (tHb) and race performance in highly trained swimmers. Chapter 4 investigated how IHT or normoxic training affected cardiopulmonary variables and the incremental exercise limit of tolerance (T-Lim), in highly trained runners. Chapter 5 investigated how single-legged IHT or normoxic training affected phosphorus-31 nuclear magnetic resonance spectroscopy assessed muscle energetics. Results: In Chapter 3, tHb increased significantly more after altitude (+0.6 ± 0.4 g•kg-1, or +4.4 ± 3.2%) than after sea level (+0.03 ± 0.1 g•kg-1, or +0.3 ± 1.0%), but the changes in swimming performances were not different between groups, and there were no correlations between tHb and performance changes. In Chapter 4, submaximal heart rate in normoxia decreased significantly more after IHT than after normoxic training (-5 ± 5 vs. -1 ± 5 b∙min-1), and submaximal "V" ̇O2 in hypoxia significantly decreased, only after IHT. T-Lim in hypoxia significantly increased post-IHT, but there were no between group differences. In Chapter 5, the phosphocreatine recovery time constant was speeded significantly more in the IHT compared to the normoxic trained leg, when tested in hypoxia (-25 ± 8% vs. -13 ± 6%), but not in normoxia (-16 ± 15% vs. -9 ± 10%). Conclusions: Altitude training likely increases tHb, but this is not necessarily associated with improved athletic performance. IHT may induce other non-haematological adaptations; potentially an enhanced skeletal muscle oxidative capacity, but evidence for exercise capacity gains is lacking. The precise underlying causes for these adaptations require further investigation, as does any translation to athletic performance.