Analysis of epidermal oxygen supply by simulation of oxygen partial pressure fields under varying conditions

1981 ◽  
Vol 9 (10) ◽  
pp. 734-735 ◽  
Author(s):  
U. GROSSMANN ◽  
DIETRICH W. LÜBBERS
2021 ◽  
Vol 224 (8) ◽  
Author(s):  
Brad A. Seibel ◽  
Alyssa Andres ◽  
Matthew A. Birk ◽  
Alexandra L. Burns ◽  
C. Tracy Shaw ◽  
...  

ABSTRACT The critical oxygen partial pressure (Pcrit), typically defined as the PO2 below which an animal's metabolic rate (MR) is unsustainable, is widely interpreted as a measure of hypoxia tolerance. Here, Pcrit is defined as the PO2 at which physiological oxygen supply (α0) reaches its maximum capacity (α; µmol O2 g−1 h−1 kPa−1). α is a species- and temperature-specific constant describing the oxygen dependency of the maximum metabolic rate (MMR=PO2×α) or, equivalently, the MR dependence of Pcrit (Pcrit=MR/α). We describe the α-method, in which the MR is monitored as oxygen declines and, for each measurement period, is divided by the corresponding PO2 to provide the concurrent oxygen supply (α0=MR/PO2). The highest α0 value (or, more conservatively, the mean of the three highest values) is designated as α. The same value of α is reached at Pcrit for any MR regardless of previous or subsequent metabolic activity. The MR need not be constant (regulated), standardized or exhibit a clear breakpoint at Pcrit for accurate determination of α. The α-method has several advantages over Pcrit determination and non-linear analyses, including: (1) less ambiguity and greater accuracy, (2) fewer constraints in respirometry methodology and analysis, and (3) greater predictive power and ecological and physiological insight. Across the species evaluated here, α values are correlated with MR, but not Pcrit. Rather than an index of hypoxia tolerance, Pcrit is a reflection of α, which evolves to support maximum energy demands and aerobic scope at the prevailing temperature and oxygen level.


2019 ◽  
Author(s):  
Brad A. Seibel ◽  
Curtis Deutsch

AbstractPhysiological oxygen supply capacity is associated with athletic performance and cardiovascular health and is thought to cause hypometabolic scaling in diverse species. Environmental oxygen is widely believed to be limiting of metabolic rate and aerobic scope, setting thermal tolerance and body size limits with implications for species diversity and biogeography. Here we derive a quantifiable linkage between maximum and basal metabolic rate and their temperature, size and oxygen dependencies. We show that, regardless of size or temperature, the capacity for oxygen supply precisely matches the maximum evolved demand at the highest persistently available oxygen pressure which, for most species assessed, is the current atmospheric pressure. Any reduction in oxygen partial pressure from current values will result in a decrement in maximum metabolic performance. However, oxygen supply capacity does not constrain thermal tolerance and does not cause hypometabolic scaling. The critical oxygen pressure, typically viewed as an indicator of hypoxia tolerance, instead reflects adaptations for aerobic scope. This simple new relationship redefines many important physiological concepts and alters their ecological interpretation.One sentence summary: Metabolism is not oxygen limited


2020 ◽  
Author(s):  
B. A. Seibel ◽  
A. Andres ◽  
M. A. Birk ◽  
A. L. Burns ◽  
C. T. Shaw ◽  
...  

AbstractThe critical oxygen partial pressure (Pcrit) is most commonly defined as the oxygen partial pressure below which an animal’s standard metabolic rate can no longer be maintained. It is widely interpreted as measure of hypoxia tolerance, which influences a species’ aerobic scope and, thus, constrains biogeography. However, both the physiology underlying that interpretation and the methodology used to determine Pcrit remain topics of active debate. The debate remains unresolved in part because Pcrit, as defined above, is a purely descriptive metric that lacks a clear mechanistic basis. Here we redefine Pcrit as the PO2 at which physiological oxygen supply is maximized and refer to these values, thus determined, as Pcrit-α. The oxygen supply capacity (α) is a species- and temperature-specific coefficient that describes the slope of the relationship between the maximum achievable metabolic rate and PO2. This α is easily determined using respirometry and provides a precise and robust estimate of the minimum oxygen pressure required to sustain any metabolic rate. To determine α, it is not necessary for an individual animal to maintain a consistent metabolic rate throughout a trial (i.e. regulation) nor for the metabolic rate to show a clear break-point at low PO2. We show that Pcrit-α can be determined at any metabolic rate as long as the organisms’ oxygen supply machinery reaches its maximum capacity at some point during the trial. We reanalyze published representative Pcrit trials for 40 species across five phyla, as well as complete datasets from six additional species, five of which have not previously been published. Values determined using the Pcrit-α method are strongly correlated with Pcrit values reported in the literature. Advantages of Pcrit-α include: 1) Pcrit-α is directly measured without the need for complex statistics that hinder measurement and interpretation; 2) it makes clear that Pcrit is a measure of oxygen supply, which does not necessarily reflect hypoxia tolerance; 3) it alleviates many of the methodological constraints inherent in existing methods; 4) it provides a means of predicting the maximum metabolic rate achievable at any PO2, 5) Pcrit-α sheds light on the temperature- and size-dependence of oxygen supply and metabolic rate and 6) Pcrit-α can be determined with greater precision than traditional Pcrit.


2009 ◽  
Vol 87 (10) ◽  
pp. 835-851 ◽  
Author(s):  
A. P. Farrell ◽  
E. J. Eliason ◽  
E. Sandblom ◽  
T. D. Clark

This review examines selected areas of cardiovascular physiology where there have been impressive gains of knowledge and indicates fertile areas for future research. Because arterial blood is usually fully saturated with oxygen, increasing cardiac output is the only means for transferring substantially more oxygen to tissues. Consequently, any behavioural or environmental change that alters oxygen uptake typically involves a change in cardiac output, which in fishes can amount to a threefold change. During exercise, not all fishes necessarily have the same ability as salmonids to increase cardiac output by increasing stroke volume; they rely more on increases in heart rate instead. The benefits associated with increasing cardiac output via stroke volume or heart rate are unclear. Regardless, all fishes examined so far show an exquisite cardiac sensitivity to filling pressure and the cellular basis for this heightened cardiac stretch sensitivity in fish is being unraveled. Even so, a fully integrated picture of cardiovascular functioning in fishes is hampered by a dearth of studies on venous circulatory control. Potent positive cardiac inotropy involves stimulation of sarcolemmal β-adrenoceptors, which increases the peak trans-sarcolemmal current for calcium and the intracellular calcium transient available for binding to troponin C. However, adrenergic sensitivity is temperature-dependent in part through effects on membrane currents and receptor density. The membrane currents contributing to the pacemaker action potential are also being studied but remain a prime area for further study. Why maximum heart rate is limited to a low rate in most fishes compared with similar-sized mammals, even when Q10 effects are considered, remains a mystery. Fish hearts have up to three oxygen supply routes. The degree of coronary capillarization circulation is of primary importance to the compact myocardium, unlike the spongy myocardium, where venous oxygen partial pressure appears to be the critical factor in terms of oxygen delivery. Air-breathing fishes can boost the venous oxygen content and oxygen partial pressure by taking an air breath, thereby providing a third myocardial oxygen supply route that perhaps compensates for the potentially precarious supply to the spongy myocardium during hypoxia and exercise. In addition to venous hypoxemia, acidemia and hyperkalemia can accompany exhaustive exercise and acute warming, perhaps impairing the heart were it not for a cardiac protection mechanism afforded by β-adrenergic stimulation. With warming, however, a mismatch between an animal’s demand for oxygen (a Q10 effect) and the capacity of the circulatory and ventilatory systems to delivery this oxygen develops beyond an optimum temperature. At temperature extremes in salmon, it is proposed that detrimental changes in venous blood composition, coupled with a breakdown of the cardiac protective mechanism, is a potential mechanism to explain the decline in maximum and cardiac arrhythmias that are observed. Furthermore, the fall off in scope for heart rate and cardiac output is used to explain the decrease in aerobic scope above the optimum temperature, which may then explain the field observation that adult sockeye salmon ( Oncorhynchus nerka (Walbaum in Artedi, 1792)) have difficulty migrating to their spawning area at temperatures above their optimum. Such mechanistic linkages to lifetime fitness, whether they are cardiovascular or not, should assist with predictions in this era of global climate change.


1967 ◽  
Vol 45 (3) ◽  
pp. 543-549 ◽  
Author(s):  
Neri P. Segrem ◽  
J. S. Hart

Oxygen consumption, heart rate, and body temperature were measured at temperatures ranging from 27 °C to −28 °C and at oxygen partial pressure [Formula: see text] levels from 60 to 196 mm Hg. Temperature regulation and O2 uptake were progressively limited by reduction of [Formula: see text]. Limitation of O2 consumption by O2 supply was similar to that seen during exercise. The highest oxygen uptake during exposure to cold was greater than during exercise at the higher levels of [Formula: see text].


2008 ◽  
Vol 295 (5) ◽  
pp. R1631-R1639 ◽  
Author(s):  
Timothy D. Clark ◽  
Erik Sandblom ◽  
Georgina K. Cox ◽  
Scott G. Hinch ◽  
Anthony P. Farrell

This study was undertaken to provide a comprehensive set of data relevant to disclosing the physiological effects and possible oxygen transport limitations in the Chinook salmon (Oncorhynchus tshawytscha) during an acute temperature change. Fish were instrumented with a blood flow probe around the ventral aorta and catheters in the dorsal aorta and sinus venosus. Water temperature was progressively increased from 13°C in steps of 4°C up to 25°C. Cardiac output increased from 29 to 56 ml·min−1·kg−1 between 13 and 25°C through an increase in heart rate (58 to 105 beats/min). Systemic vascular resistance was reduced, causing a stable dorsal aortic blood pressure, yet central venous blood pressure increased significantly at 25°C. Oxygen consumption rate increased from 3.4 to 8.7 mg·min−1·kg−1 during the temperature increase, although there were signs of anaerobic respiration at 25°C in the form of increased blood lactate and decreased pH. Arterial oxygen partial pressure was maintained during the heat stress, although venous oxygen partial pressure (PvO2) and venous oxygen content were significantly reduced. Cardiac arrhythmias were prominent in three of the largest fish (>4 kg) at 25°C. Given the switch to anaerobic metabolism and the observation of cardiac arrhythmias at 25°C, we propose that the cascade of venous oxygen depletion results in a threshold value for PvO2 of around 1 kPa. At this point, the oxygen supply to systemic and cardiac tissues is compromised, such that the oxygen-deprived and acidotic myocardium becomes arrhythmic, and blood perfusion through the gills and to the tissues becomes compromised.


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