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Hypoxia is common in aquatic environments and has substantial effects on development, metabolism and survival of aquatic organisms. To understand the physiological effects of hypoxia and its dependence on temperature, metabolic rate ( [Formula: see text] ) and cardiorespiratory function were studied in response to acute hypoxia (21→5kPa) at different measurement temperatures (T a ; 4, 8 and 12°C) in Salmo salar alevins that were incubated under normoxic conditions (P O 2 =21kPa) or following hypoxic acclimation (P O 2 =10kPa) as well as two different temperatures (4°C or 8°C). Hypoxic acclimation lead to a developmental delay manifested through slower yolk absorption. The general response to acute hypoxia was metabolic depression (~60%). Hypoxia acclimated alevins had higher [Formula: see text] s when measured in normoxia than alevins acclimated to normoxia. [Formula: see text] s were elevated to the same degree (~30% per 4°C change) irrespective of T a . Under severe, acute hypoxia (~5kPa) and irrespective of T a or acclimation, [Formula: see text] s were similar between most groups. This suggests that despite different acclimation regimes, O 2 transport was limited to the same degree. While cardiorespiratory function (heart-, ventilation rate) was unchanged in response to acute hypoxia after normoxic acclimation, hypoxic acclimation led to cardiorespiratory changes predominantly in severe hypoxia, indicating earlier onset and plasticity of cardiorespiratory control mechanisms. Although [Formula: see text] in normoxia was higher after hypoxic acclimation, at the respective acclimation P O 2 , [Formula: see text] was similar in normoxia and hypoxia acclimated alevins. This is indicative of metabolic compensation to an intrinsic [Formula: see text] at the acclimation condition in hypoxia-acclimated alevins after re-exposure to normoxia., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Most experiments examining acid-base regulation of chicken embryos have employed static, single time point measurements rather than dynamic, multiple time point measurements that might reveal additional components of developing acid-base regulation. Thus, we studied blood acid-base balance and hematology of day 15 chicken embryos under 24h exposure to graded hypercapnia (1%-7% CO 2 ) accompanied by graded hypoxia (20% O 2 down to 13% O 2 ). Across all hypercapnic/hypoxic environments, respiratory acidosis occurred 2h after exposure in proportion to the magnitude of hypercapnia. An additional metabolic alkalosis occurred in ≥16% O 2 , and metabolic acidosis in ≤14% O 2 . As exposure progressed, compensatory metabolic alkalosis occurred in all groups at 6h, but partial metabolic compensation could not be preserved as hypoxia increased (≤18% O 2 ). Across all hypercapnic/hypoxic groups, hematocrit, mean corpuscular volume and red blood cell concentration significantly increased by 24h, most likely due to hypoxia rather than hypercapnia. Overall, day 15 chicken embryos cannot maintain even partial compensation in their acid-base physiology after 24h exposure to hypercapnic/hypoxic environments of ≥5% CO 2 +≤15% O 2 ., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Steele, Andrew R., Philip N. Ainslie, Rachel Stone, Kaitlyn Tymko, Courtney Tymko, Connor A. Howe, David MacLeod, James D. Anholm, Christopher Gasho, and Michael M. Tymko. Global REACH 2018: characterizing acid–base balance over 21 days at 4,300 m in lowlanders. High Alt Med Biol. 23:185–191, 2022. Introduction: High altitude exposure results in hyperventilatory-induced respiratory alkalosis, followed by metabolic compensation to return arterial blood pH (pHa) toward sea level values. However, previous work has limited sample sizes, short-term exposure, and pharmacological confounders (e.g., acetazolamide). The purpose of this investigation was to characterize acid–base balance after rapid ascent to high altitude (i.e., 4,300 m) in lowlanders. We hypothesized that despite rapid bicarbonate ([HCO3−]) excretion during early acclimatization, partial respiratory alkalosis would still be apparent as reflected in elevations in pHa compared with sea level after 21 days of acclimatization to 4,300 m. Methods: In 16 (3 female) healthy volunteers not taking any medications, radial artery blood samples were collected and analyzed at sea level (150 m; Lima, Peru), and on days 1, 3, 7, 14, and 21 after rapid automobile (∼8 hours) ascent to high altitude (4,300 m; Cerro de Pasco, Peru). Results and Discussion: Although reductions in [HCO3−] occurred by day 3 (p < 0.01), they remained stable thereafter and were insufficient to fully normalize pHa back to sea level values over the subsequent 21 days (p < 0.01). These data indicate that only partial compensation for respiratory alkalosis persists throughout 21 days at 4,300 m. [ABSTRACT FROM AUTHOR]

Embryos of Austrofundulus limnaeus are exceptional in their ability to tolerate prolonged bouts of complete anoxia. Hypoxia and anoxia are a normal part of their developmental environment. Here, we exposed embryos to a range of PO levels at two different temperatures (25 and 30 °C) to study the combined effects of reduced oxygen and increased temperature on developmental rate, heart rate, and metabolic enzyme capacity. Hypoxia decreased overall developmental rate and caused a stage-specific decline in heart rate. However, the rate of early development prior to the onset of organogenesis is insensitive to PO. Increased incubation temperature caused an increase in the developmental rate at high POs, but hindered developmental progression under severe hypoxia. Embryonic DNA content in pre-hatching embryos was positively correlated with PO. Citrate synthase, lactate dehydrogenase, and phosphoenolpyruvate carboxykinase capacity were all reduced in embryos developing under hypoxic conditions. Embryos of A. limnaeus are able to develop normally across a wide range of POs and contrary to most other vertebrates severe hypoxia is not a teratogen. Embryos of A. limnaeus do not respond to hypoxia through an increase in the capacity for enzymatic activity of the metabolic enzymes lactate dehydrogenase, citrate synthase, or phosphoenolpyruvate carboxykinase. Instead they appear to adjust whole-embryo metabolic capacity to match oxygen availability. However, decreased DNA content in hypoxia-reared embryos suggests that cellular enzymatic capacity may remain unchanged in response to hypoxia, and the reduced capacity may rather indicate reduced cell number in hypoxic embryos. [ABSTRACT FROM AUTHOR]

Abstract: In day 15 chicken embryos, we determined the time course responses of acid–base balance and hematological respiratory variables during 24h exposure to 15, 20, 40 or 90% O2, in the presence of 5% CO2. Hypercapnic respiratory acidosis was initially (2h) only slightly (∼20%) compensated by metabolic alkalosis in normoxic/hyperoxic embryos. After 6h, respiratory acidosis was partially (∼40–50%) compensated not only in normoxic/hyperoxic embryos, but also in hypoxic embryos. However, partial metabolic compensation in 15% O2 could not be preserved after 24h. Preservation of metabolic compensation required oxygen concentration ([O2]) above 20%, but the magnitude of partial metabolic compensation was unrelated to [O2]. Hematocrit (Hct), together with mean corpuscular volume (MCV), markedly increased in hypercapnic hypoxia, and was maintained at 24h due to a subsequent increase in red blood cell concentration ([RBC]). In contrast, Hct, together with MCV, decreased in hypercapnic normoxia/hyperoxia accompanied by a subsequent decrease in [RBC] at 24h. Regulation of variables takes place similarly irrespective of environmental [O2] above 20%, matching acid–base regulation. [Copyright &y& Elsevier]