Effect of Heat Acclimatization, Heat Acclimation, and Intermittent Heat Training on Maximal Oxygen Uptake.

BACKGROUND: Maximal oxygen uptake (VO2max) is an important determinant of endurance performance. Heat acclimation/acclimatization (HA/HAz) elicits improvements in endurance performance. Upon heat exposure reduction, intermittent heat training (IHT) may alleviate HA/HAz adaptation decay; however, corresponding VO2max responses are unknown. HYPOTHESIS: VO2max is maintained after HAz/HA; IHT mitigates decrements in aerobic power after HAz/HA. STUDY DESIGN: Interventional study. LEVEL OF EVIDENCE: Level 3. METHODS: A total of 27 male endurance runners (mean ± SD; age, 36 ± 12 years; body mass, 73.03 ± 8.97 kg; height, 178.81 ± 6.39 cm) completed VO2max testing at 5 timepoints; baseline, post-HAz, post-HA, and weeks 4 and 8 of IHT (IHT4, IHT8). After baseline testing, participants completed HAz, preceded by 5 days of HA involving exercise to induce hyperthermia for 60 minutes in the heat (ambient temperature, 39.13 ± 1.37°C; relative humidity, 51.08 ± 8.42%). Participants were assigned randomly to 1 of 3 IHT groups: once-weekly, twice-weekly, or no IHT. Differences in VO2max, velocity at VO2max (vVO2), and maximal heart rate (HRmax) at all 5 timepoints were analyzed using repeated-measure analyses of variance with Bonferroni corrections post hoc. RESULTS: No significant VO2max or vVO2 differences were observed between baseline, post-HAz, or post-HA (P = 0.36 and P = 0.09, respectively). No significant group or time effects were identified for VO2max or vVO2 at post-HA, IHT4, and IHT8 (P = 0.67 and P = 0.21, respectively). Significant HRmax differences were observed between baseline and post-HA tests (P < 0.01). No significant group or time HRmax differences shown for post-HA, IHT4, and IHT8 (P = 0.59). CONCLUSION: VO2max was not reduced among endurance runners after HA/HAz and IHT potentially due to participants' similar aerobic training status and high aerobic fitness levels. CLINICAL RELEVANCE: HAz/HA and IHT maintain aerobic power in endurance runners, with HAz/HA procuring reductions in HRmax.

Eccentric muscle-damaging exercise in the heat lowers cellular stress prior to and immediately following future exertional heat exposure.

Muscle-damaging exercise (e.g., downhill running [DHR]) or heat exposure bouts potentially reduce physiological and/or cellular stress during future exertional heat exposure; however, the true extent of their combined preconditioning effects is unknown. Therefore, this study investigated the effect of muscle-damaging exercise in the heat on reducing physiological and cellular stress during future exertional heat exposure. Ten healthy males (mean ± Standard Definition; age, 23 ± 3 years; body mass, 78.7 ± 11.5 kg; height, 176.9 ± 4.7 cm) completed this study. Participants were randomly assigned into two preconditioning groups: (a) DHR in the heat (ambient temperature [Tamb], 35 °C; relative humidity [RH], 40%) and (b) DHR in thermoneutral (Tamb, 20 °C; RH, 20%). Seven days following DHR, participants performed a 45-min flat run in the heat (FlatHEAT [Tamb, 35 °C; RH, 40%]). During exercise, heart rate and rectal temperature (Trec) were recorded at baseline and every 5-min. Peripheral blood mononuclear cells were isolated to assess heat shock protein 72 (Hsp72) concentration between conditions at baseline, immediately post-DHR, and immediately pre-FlatHEAT and post-FlatHEAT. Mean Trec during FlatHEAT between hot (38.23 ± 0.38 °C) and thermoneutral DHR (38.26 ± 0.38 °C) was not significantly different (P = 0.68), with no mean heart rate differences during FlatHEAT between hot (172 ± 15 beats min-1) and thermoneutral conditions (174 ± 8 beats min-1; P = 0.58). Hsp72 concentration change from baseline to immediately pre-FlatHEAT was significantly lower in hot (-51.4%) compared to thermoneutral (+24.2%; P = 0.025) DHR, with Hsp72 change from baseline to immediately post-FlatHEAT also lower in hot (-52.6%) compared to thermoneutral conditions (+26.3%; P = 0.047). A bout of muscle-damaging exercise in the heat reduces cellular stress levels prior to and immediately following future exertional heat exposure.

Storing urine samples with moisture preserves urine hydration marker stability up to 21 days.

INTRODUCTION: To assess hydration status, hydration markers [urine color, osmolality, and urine-specific gravity (USG)] are used. Urine color, osmolality, and USG have shown to be stable for 7, 7, and 3 days, respectively, at 4 °C. However, refrigeration could produce a dry environment which enhances evaporation and potentially affects urine hydration markers. PURPOSE: To examine the effect of duration and moisture on urine markers with refrigeration. METHODS: 24 participants provided urine samples between 9 and 10 AM. Urine color, osmolality, and USG were analyzed within 2 h (baseline). Then, each urine sample was divided into two urine cups and placed in a storage container with (moisture condition) and without (no moisture condition) water bath at 3 °C. Hydration markers were analyzed at day 1(D1), D2, D7, D10, D14, and D21. A two-way ANOVA (time x condition) and repeated-measures ANOVA on time were performed to examine differences. RESULTS: No significant (p > 0.05) condition x time effect was observed for urine color (p = 0.363), urine osmolality (p = 0.358), and USG (p = 0.248). When urine samples were stored in moisture condition, urine color (p = 0.126) and osmolality (p = 0.053) were stable until D21, while USG was stable until D2 (p = 0.394). CONCLUSION: When assessing hydration status, it appears that the urine color and osmolality were stable for 21 days, while USG was stable for 2 days when stored with moisture at 3 °C. Our results provide guidelines for practitioners regarding urine storage duration and conditions when urine cannot be analyzed immediately.

Supplemental CO2 improves oxygen saturation, oxygen tension, and cerebral oxygenation in acutely hypoxic healthy subjects.

Oxygen is viewed in medicine as the sole determinant of tissue oxygenation, though carbon dioxide homeostasis is equally important and clinically often ignored. The aims of this study were as follows: (a) to examine the effects of different acute hypoxic conditions on partial pressure of arterial oxygen ( PaO2 ), arterial oxygen saturation of hemoglobin ( SaO2 ), and regional cerebral saturation of hemoglobin (rSO2 ); and (b) to evaluate supplemental CO2 as a tool to improve oxygenation in acutely hypoxic individuals. We hypothesized that exposure to gas mixtures with added CO2 would improve oxygenation in hypoxic human subjects. Twenty healthy subjects were exposed to 5-min intervals of two gas mixtures: hypoxic gas mixture containing 8% oxygen, and a CO2 -enriched mixture containing 8% oxygen plus either 3% or 5% CO2 . Ten subjects received the 3% CO2 -enriched mixture, and the remaining 10 subjects received the 5% CO2 -enriched mixture. The order of exposure was randomized. Blood gases, pulse oximetry, end-tidal CO2 , and cerebral oximetry were measured. Compared to the purely hypoxic gas group, PaO2 was increased in the 3% and 5% CO2 -enriched groups by 14.9 and 9.5 mmHg, respectively. Compared to pure hypoxia, SaO2 was increased in the 3% and 5% CO2 -enriched groups by 16.8% and 12.9%, respectively. Both CO2 -enriched gas groups had significantly higher end-exposure rSO2 and recovered to baseline rSO2 within 1 min, compared to the pure hypoxic gas group, which returned to baseline in 5 min. These results suggest that in acutely hypoxic subjects, CO2 supplementation improves blood oxygen saturation and oxygen tension as well as cerebral oxygenation measures.