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Sprint interval training (SIT) is an efficient intervention capable of improving aerobic capacity and exercise performance. This experiment aimed to determine differences in training adaptations and the inflammatory responses following 2 weeks of SIT (30 s maximal work, 4 min recovery; 4–7 repetitions) performed in normoxia or hypoxia. Forty-two untrained participants [(mean ±  SD ), age 21 ±1 years, body mass 72.1 ±11.4 kg, and height 173 ±10 cm] were equally and randomly assigned to one of three groups; control (CONT; no training,  n  = 14), normoxic (NORM; SIT in FiO 2 : 0.21,  n  = 14), and normobaric hypoxic (HYP; SIT in FiO 2 : 0.15,  n  = 14). Participants completed aV  ˙    O   2  peaktest, a time to exhaustion (TTE) trial (power = 80%V  ˙    O   2  peak) and had hematological [hemoglobin (Hb), haematocrit (Hct)] and inflammatory markers [interleukin-6 (IL-6), tumor necrosis factor-α (TNFα)] measured in a resting state, pre and post SIT.V  ˙    O   2  peak(mL.kg −1 .min −1 ) improved in HYP (+11.9%) and NORM (+9.8%), but not CON (+0.9%). Similarly TTE improved in HYP (+32.2%) and NORM (+33.0%), but not CON (+3.4%) whilst the power at the anaerobic threshold (AT; W.kg −1 ) also improved in HYP (+13.3%) and NORM (+8.0%), but not CON (–0.3%). AT (mL.kg −1 .min −1 ) improved in HYP (+9.5%), but not NORM (+5%) or CON (–0.3%). No between group change occurred in 30 s sprint performance or Hb and Hct. IL-6 increased in HYP (+17.4%) and NORM (+20.1%), but not CON (+1.2%), respectively. TNF-α increased in HYP (+10.8%) NORM (+12.9%) and CON (+3.4%). SIT in HYP and NORM increasedV  ˙    O   2  peak, power at AT and TTE performance in untrained individuals, improvements in AT occurred only when SIT was performed in HYP. Increases in IL-6 and TNFα reflect a training induced inflammatory response to SIT; hypoxic conditions do not exacerbate this.

Similar Inflammatory Responses following Sprint Interval Training Performed in Hypoxia and Normoxia