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Cerebrovascular and ventilatory responses to acute normobaric hypoxia in girls and women.

ABSTRACT: Physiological responses to hypoxia in children are incompletely understood. We aimed to characterize cerebrovascular and ventilatory responses to normobaric hypoxia in girls and women. Ten healthy girls (9.9 ± 1.7 years; mean ± SD; Tanner stage 1 and 2) and their mothers (43.9 ± 3.5 years) participated. Internal carotid (ICA) and vertebral artery (VA) velocity, diameter and flow (Duplex ultrasound) was recorded pre- and post-1 h of hypoxic exposure (FIO2 = 0.126;~4000 m) in a normobaric chamber. Ventilation (V˙E) and respiratory drive (VT/TI) expressed as delta change from baseline (∆%), and end-tidal carbon-dioxide (PETCO2) were collected at baseline (BL) and 5, 30 and 60 min of hypoxia (5/30/60 HYP). Heart rate (HR) and oxygen saturation (SpO2) were also collected at these time-points. SpO2 declined similarly in girls (BL-97%; 60HYP-80%, P < 0.05) and women (BL-97%; 60HYP-83%, P < 0.05). Global cerebral blood flow (gCBF) increased in both girls (BL-687; 60HYP-912 mL·min-1, P < 0.05) and women (BL-472; 60HYP-651 mL·min-1, P < 0.01), though the ratio of ICA:VA (%) contribution to gCBF differed significantly (girls, 75:25%; women, 61:39%). The relative increase in V˙E peaked at 30HYP in both girls (27%, P < 0.05) and women (19%, P < 0.05), as did ∆%VT/TI (girls, 41%; women, 27%, P's < 0.05). Tidal volume (VT) increased in both girls and women at 5HYP, remaining elevated above baseline in girls at 30 and 60 HYP, but declined back toward baseline in women. Girls elicit similar increases in gCBF and ventilatory parameters in response to acute hypoxia as women, though the pattern and contributions mediating these responses appear developmentally divergent.

SUBMITTER: Morris LE

PROVIDER: S-EPMC5555897 | biostudies-other | 2017 Aug

REPOSITORIES: biostudies-other

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Project description:The primary objective of the current study was to determine the effect of moderate normobaric hypoxia exposure during constant load cycling on post-exercise energy metabolism recorded in normoxia. Indirect calorimetry was used to examine whole body substrate oxidation before, during, 40-60 min post, and 22 h after performing 60 min of cycling exercise at two different fractions of inspired oxygen (FIO2): (i) FIO2 = 0.2091 (normoxia) and (ii) FIO2 = 0.15 (hypoxia). Seven active healthy male participants (26 ± 4 years of age) completed both experimental trials in randomized order with a 7-day washout period to avoid carryover effects between conditions. Resting energy expenditure was initially elevated following cycling exercise in normoxia and hypoxia (Δ 0.14 ± 0.05, kcal min-1, p = 0.037; Δ 0.19 ± 0.03 kcal min-1, p < 0.001, respectively), but returned to baseline levels the next morning in both conditions. Although, the same absolute workload was used in both environmental conditions (157 ± 10 W), a shift in resting substrate oxidation occurred after exercise performed in hypoxia while post-exercise measurements were similar to baseline after cycling exercise in normoxia. The additional metabolic stress of hypoxia exposure was sufficient to increase the rate of lipid oxidation (Δ 42 ± 11 mg min-1, p = 0.019) and tended to suppress carbohydrate oxidation (Δ -55 ± 26 mg min-1, p = 0.076) 40-60 min post-exercise. This shift in substrate oxidation persisted the next morning, where lipid oxidation remained elevated (Δ 9 ± 3 mg min-1, p = 0.0357) and carbohydrate oxidation was suppressed (Δ -22 ± 6 mg min-1, p = 0.019). In conclusion, prior exercise performed under moderate normobaric hypoxia alters post-exercise energy metabolism. This is an important consideration when evaluating the metabolic consequences of hypoxia exposure during prolonged exercise, and future studies should evaluate its role in the beneficial effects of intermittent hypoxia training observed in persons with obesity and insulin resistance.

Project description:BackgroundPhysical exercise is a source of stress to the human body, triggering different ventilatory responses through different regulatory mechanisms and the aquatic environment imposes several restrictions to the swimmer, particularly regarding the restricted ventilation. Thus, we aimed to assess the acute ventilatory responses and to characterize the adopted breathing patterns when swimming front crawl at increasing intensity domains.MethodsEighteen well-trained swimmers performed 7 × 200 m front crawl (0.05 m∙s-1 velocity increments) and a maximal 100 m (30 s rest intervals). Pulmonary gas exchange and ventilation were continuously measured (breath-by-breath) and capillary blood samples for lactate concentration ([La-]) analysis were collected at rest, during intervals and at the end of the protocol, allowing the identification of the low, moderate, heavy, severe and extreme intensity domains.ResultsWith the swimming velocity rise, respiratory frequency (f R), [La-] and stroke rate (SR) increased ([29.1-49.7] breaths∙min-1, [2.7-11.4] mmol∙L-1, [26.23-40.85] cycles; respectively) and stroke length (SL) decreased ([2.43-2.04] m∙min-1; respectively). Oxygen uptake (VO2), minute ventilation (VE), carbon dioxide production (VCO2) and heart rate (HR) increased until severe ([37.5-53.5] mL∙kg-1∙min-1, [55.8-96.3] L∙min-1, [32.2-51.5] mL∙kg-1∙min-1 and [152-182] bpm; respectively) and stabilized from severe to extreme (53.1 ± 8.4, mL∙kg-1∙min-1, 99.5 ± 19.1 L∙min-1, 49.7 ± 8.3 mL∙kg-1∙min-1 and 186 ± 11 bpm; respectively) while tidal volume (VT) was similar from low to severe ([2.02-2.18] L) and decreased at extreme intensities (2.08 ± 0.56 L). Lastly, the f R/SR ratio increased from low to heavy and decreased from severe to the extreme intensity domains (1.12 ± 0.24, 1.19 ± 0.25, 1.26 ± 0.26, 1.32 ± 0.26 and 1.23 ± 0.26).ConclusionsOur findings confirm a different ventilatory response pattern at extreme intensities when compared to the usually evaluated exertions. This novel insight helps to understand and characterize the maximal efforts in swimming and reinforces the importance to include extreme efforts in future swimming evaluations.

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Cerebrovascular and ventilatory responses to acute normobaric hypoxia in girls and women.

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