Females exposed to 24 h of sleep deprivation do not experience greater physiological strain, but do perceive heat illness symptoms more severely, during exercise-heat stress.

There is limited and inconclusive evidence surrounding the physiological and perceptual responses to heat stress while sleep deprived, especially for females. This study aimed to quantify the effect of 24 h sleep deprivation on physiological strain and perceptual markers of heat-related illness in females. Nine females completed two 30-min heat stress tests (HST) separated by 48 h in 39°C, 41% relative humidity at a metabolic heat production of 10 W · kg-1. The non-sleep deprived HST was followed by the sleep deprivation (SDHST) trial for all participants during the follicular phase of the menstrual cycle. Physiological and perceptual measures were recorded at 5 min intervals during the HSTs. On the cessation of the HSTs, heat illness symptom index (HISI) was completed. HISI scores increased after sleep deprivation by 28 ± 16 versus 20 ± 16 (P = 0.01). Peak (39.40 ± 0.35°C vs. 39.35 ± 0.33°C) and change in rectal temperature (1.91 ± 0.21 vs. 1.93 ± 0.34°C), and whole body sweat rate (1.08 ± 0.31 vs. 1.15 ± 0.36 L · h-1) did not differ (P > 0.05) between tests. No difference was observed in peak, nor rise in: heart rate, mean skin temperature, perceived exertion or thermal sensation during the HSTs. Twenty-four hours sleep deprivation increased perceptual symptoms associated with heat-related illness; however, no thermoregulatory alterations were observed.

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

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 FiO2: 0.21, n = 14), and normobaric hypoxic (HYP; SIT in FiO2: 0.15, n = 14). Participants completed a [Formula: see text] test, a time to exhaustion (TTE) trial (power = 80% [Formula: see text]) 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. [Formula: see text] (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 increased [Formula: see text], 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.