The vagal influence over large pulmonary arteries has been clearly demonstrated in Squamates. Additionally, diverse in situ experiments suggest that pulmonary circulation was either not responsive or much less responsive than the systemic circuit to known local, humoral, and nervous modulators. We suggest that the systemic alterations should be counterbalanced by pulmonary circuit modulation in awaken animals with a cardiac shunt, and the lack of pulmonary circuit responses is a collateral effect of the anesthesia used in in situ experiments. The use of a decerebrate experimental model allowed for diverse concomitant cardiovascular and respiratory measurements in two rattlesnake groups: left-vagotomized - LV (i.e. without vagal innervation of pulmonary arteries) and non-vagotomized (NV) at a range of body temperatures (Tb - 10, 20, and 30 °C). Aerobic metabolism increased proportionally to Tb. Unexpectedly, systemic conductance remained stable while the right-to-left shunt reduced. Therefore, inactive rattlesnakes change blood oxygenation rather than tissue perfusion to support alterations in aerobic demands. Peripheral pulmonary circulation was the main target of vascular modulatory adjustments following Tb change. Although LV snakes were unable to modulate pulmonary compliance, cardiac shunt was compensated as they reached the same O2 uptake, which was attained by the modulation of the pulmonary conductance. This was the first time such modulation was recorded. Our findings also suggest the presence of bilateral vagal innervation of the unique rattlesnake lung, in which the left vagus innervates the proximal arteries, while the right vagus modulates functioning of the distal vasculature.

Thirty-nine highly acknowledged experts in the areas of the physiology and the evolution of the vagus nerve and of vertebrate social behavior (many whose works have been cited in the polyvagal theory [PVT] literature as supporting the theory) were invited by the first author to participate as co-authors of this article. They were asked to evaluate the PVT and comment upon an overview of the theory written by its author (Porges, 2025a). All those invited, save one, accepted and co-authored the paper. The dissenting scholar was "unfamiliar with the PVT." This article specifically appraises--based upon the current state of knowledge of autonomic function and vertebrate evolution--several major elements of the PVT, as described in Porges (2025a) and elsewhere. These include: 1) the validity of PVT assumptions that respiratory sinus arrhythmia is a direct measure of the extent of central vagal drive to the heart; 2) PVT characterizations regarding the neuroanatomy and functions of two major brainstem vagal nuclei, the ventrally situated Nucleus Ambiguus and the Dorsal Motor Nucleus of the vagus nerve; 3) PVT assertions regarding the evolution of the vagus nerve; 4) PVT claims about the specificity of mammalian social behavior in relation to nonmammalian vertebrates, and 5) PVT interpretations of earlier seminal physiological literature. All co-authors agree that major tenets of the PVT are not supported by past or current knowledge and, in several instances, are inconsistent with the broader evidence base. Since the topics addressed constitute fundamental premises of the PVT, we conclude that the PVT is untenable, because it is not defensible based on existing neurophysiological and evolutionary evidence. The psychological elements composing the superstructure of the PVT are primarily derived from earlier psychological literature and are neither clarified nor strengthened by PVT constructs that lack evidence. This article does not intend to address alternative explanations about relations between vagal function and psychological processes, although such explanations do exist.

The variation of heart rate in phase with breathing, known as ‘respiratory sinus arrhythmia’ (RSA), is a physiological phenomenon present in all air-breathing vertebrates. RSA arises from the interaction of several physiological mechanisms but is primarily mediated by rhythmic changes in cardiac parasympathetic (vagal) activity, increasing heart rate during inspiration and decreasing heart rate during expiration. RSA amplitude is an indicator of autonomic and cardiac health; RSA is diminished or absent in common pathological conditions such as chronic heart failure and hypertension. In this Expert Recommendation, we argue that the term ‘RSA’, although historically important, is semantically inaccurate and carries misleading pathological connotations, contributing to misunderstanding and misinterpretation of the origin and the physiological importance of the phenomenon. We propose replacing ‘RSA’ with the term ‘respiratory heart rate variability’ (RespHRV), which avoids pathological connotations and emphasizes the specific respiratory contribution to heart rate variability. We clarify that RespHRV encompasses respiratory-related heart rate variations in both the low-frequency and high-frequency bands traditionally defined in heart rate variability analysis, and that its amplitude should not be misconstrued as a measure of vagal tone. Adopting the proposed term ‘RespHRV’ is expected to unify understanding and stimulate further experimental and clinical research into the physiological mechanisms and functional importance of this phenomenon. The physiological phenomenon whereby heart rate varies in phase with breathing in vertebrates has been known as ‘respiratory sinus arrhythmia’. In this Expert Recommendation, the authors argue that this terminology is potentially misleading and propose replacing it with the term ‘respiratory heart rate variability’, which avoids pathological connotations.

The metallurgy industry is a potent global source of particulate matter (PM) atmospheric emissions. A portion of this PM may settle in aquatic (SePM) carrying metal/metalloid particles and metallic nanoparticles. Surprisingly, this form of contamination has not received due attention from most environmental monitoring agencies. We analyzed the effect of exposure to SePM on shrimp post-larvae, a critical stage for the viability of shrimp populations and for the trophic chain. After acclimation, shrimp were exposed to contaminants using a randomized experimental design—a 4 × 4 factorial arrangement with 2 factors: exposure time (24, 48, 72, and 96 h) and SePM concentration (0.00, 0.01, 0.10, and 1.00 g L−1). The bioaccumulation of metals, contamination rates, mortality, and ROS-related biomarkers (lipid peroxidation – LPO; DNA strand breakage DNA SB and metallothionein content – MTs;) were evaluated. After contamination, the water contained 27 different metals/metalloids. Post-larvae accumulated metals, such as Cd, Pb, Al, As, Se, Sr, Zr, Ba, La, Ce, W, and Hg. However, the rise in SePM did not result in a proportional bioaccumulation rise, indicating that effective biological barriers may work for some metals. Although the different levels of SePM changed mortality dynamics, they resulted in a similar final lethality (60–80 %). SePM caused significant damage to lipids (increased LPO), genetic material (DNA SB), and increased Mts. Such effects may reflect a particularly deleterious ecological problem as it is present at such an early stage of life. These results identified a clear environmental risk since the lower level of exposure used was 102 times lower than that measured in the habitats affected by local industry. Consequently, our results emphasize the need for clear protocols for monitoring the effects of SePM in aquatic environments.

We evaluated interindividual variation in traits of warming and hypoxia tolerance in a cohort ( n = 24) of juvenile pacu Piaractus mesopotamicus , acclimated to 26°C, to investigate whether individuals tolerant to warming were also tolerant to hypoxia and whether individual tolerance depended on body mass or intrinsic traits of aerobic metabolism. Two traits of warming tolerance were measured, the critical thermal maximum (CT max ) in a static tank, with loss of equilibrium as the endpoint, and the critical thermal maximum for aerobic swimming (CTS max ) in a swim tunnel, with fatigue as the endpoint. Two traits of hypoxia tolerance were derived by static respirometry during progressive hypoxia, the critical saturation for regulation of standard metabolic rate (S crit ) and the regulation index (RI). At 39.7 ± 0.4°C (mean ± SD ), CT max was significantly higher than CTS max , at 38.0 ± 1.0°C. Both traits had very low coefficient of variation within the cohort (CV, 1.1 and 2.6%, respectively), and CT max was not correlated with any other trait. Individual S crit (18.5 ± 7.2% saturation, CV 38.9%) and RI (76.0 ± 16.1% regulation, CV 45.6%) were correlated ( R = 0.686), and both were significantly correlated with CTS max ( R = 0.472 and 0.475, respectively). This indicates that individuals tolerant to warming were also tolerant to hypoxia, although two individuals with low CTS max were drivers of the correlations against S crit and RI. The CT max , CTS max , and S crit showed no dependence on body mass, but RI increased with mass ( R 2 = 0.286), indicating that larger individuals were more tolerant to hypoxia. When corrected for body mass, RI was no longer correlated with CTS max , further revealing that the correlations were rather tenuous. Finally, we found no evidence that individual tolerance was dependent on intrinsic traits of aerobic metabolism. The results indicate that sublethal indicators, such as CTS max , S crit , and RI, can be useful in exploring correlations among traits of tolerance to warming and hypoxia in fishes, but more studies on more species with larger sample sizes are required to confirm these results and reveal if there are general patterns.

The steel industry is a significant worldwide source of atmospheric particulate matter (PM). Part of PM may settle (SePM) and deposit metal/metalloid and metallic nanoparticles in aquatic ecosystems. However, such an air -towater cross -contamination is not observed by most monitoring agencies. The region of Vitoria City is the main location of iron processing for exports in Brazil, and it has rivers, estuaries, and coastal areas affected by SePM. We have evaluated the effects of SePM on a local representative fish species, the fat snook, Centropomus parallelus . After acclimation, 48 fishes (61.67 +/- 27.83 g) were individually exposed for 96 h to diverse levels of SePM (0.0, 0.01, 0.1 and 1 g/L -1 ). The presence of metals in the blood and several blood biomarkers were analyzed to evaluate the impact of SePM on stress signaling, blood oxygen transport capacity, and innate immune activity. Metal bioaccumulation was measured from blood in two separately analyzed compartments: intracellular (erythrocytes plus white blood cells) and extracellular (plasma). The major metals present at all contamination levels in both compartments were Fe and Zn, followed by Al and Cu, plus traces of 'Emerging metals ': Ba, Ce, La, Rb, Se, Sr, and Ti. Emerging metals refer to those that have recently been identified in water as contaminants, encompassing rare earth elements and critical technology elements, as documented in previous studies (See REEs and TCEs in Cobelo-Garc & iacute;a et al., 2015; Batley et al., 2022). Multivariate analysis revealed that SePM had strong, dose -dependent correlations with all biomarker groups and indicated that blood oxygen -carrying capacity had the highest contamination responsiveness. Metal contamination also increased cortisol and blood glucose levels, attesting to increased stress signaling, and had a negative effect on innate immune activity. Knowledge of the risks related to SePM contamination remains rudimentary. However, the fact that there was metal bioaccumulation, causing impairment of fundamental physiological and cellular processes in this ecologically relevant fish species, consumed by the local human population, highlights the pressing need for further monitoring and eventual control of SePM contamination.

Studies on fish and mammals, and to a lesser extent on reptiles and amphibians, have shown that mean heart rate (HR) and heart rate variability (HRV) in vertebrates are determined predominantly by activity in the parasympathetic arm of the autonomic nervous system, originating in cardiac vagal preganglionic neurons (CVPN) located in the brainstem. A major feature of HRV in fish, as in all vertebrates, is beat-to-beat modulation of the heartbeat by the respiratory rhythm, termed cardiorespiratory interactions (CRI). This is generated by efferent activity in cardiac branches of the Xth cranial nerve, the vagus, which includes bursts of respiration-related activity delivered by fast-conducting, myelinated fibers. In elasmobranch fishes, this activity seems to originate primarily from central, stimulatory interactions between respiratory neurons and CVPN, and it is characterized by relatively low levels of vagal tone on the heart. In teleosts, there is evidence of a fundamental difference, with the bursts driven by feedback from peripheral chemoreceptors and mechanoreceptors located within the respiratory system responding to moderate hypoxia when respiratory drive and cardiac vagal tone are high. Ultimately, reflex control from peripheral receptors is important in determining heart rate in all fish. Evidence from current investigations suggests that there are elements of central feed-forward control of cardiorespiratory interactions in some teleosts. Consequently, it seems probable that a variable combination of feed-forward control via central interactions plus feedback from peripheral receptors determines activity in CVPN, and accordingly HRV, in all fishes. This includes CRI, which can recruit the heart to the respiratory rhythm, generating cardiorespiratory synchrony (CRS). However, this relationship may be differentially expressed in relation to conditions and possibly species differences. The release of an inhibitory parasympathetic, vagal supply to the heart determines the marked and instantaneous increase in HR at the onset of ram ventilation in swimming fish and at the point of surfacing in air-breathing teleost fishes. The changes in HR at the onset of each surface air breath in lungfish (an instantaneous increase in HR, accompanied by cardiac shunting, to increase blood flow to the lung) resemble the mechanisms generating CRI during discontinuous breathing in air-breathing vertebrates, such as reptiles. They may foreshadow the evolution of respiratory sinus arrhythmia (RSA) in mammals, which seems not to have a critical role in respiratory gas exchange, due to their completely divided circulation.

Cooperative ligand binding to linear polymers is fundamental in many scientific disciplines, particularly biological and chemical physics and engineering. Such ligand binding interactions have been widely modeled using infinite one-dimensional (1D) Ising models even in cases where the linear polymers are more complex (e.g. actin filaments and other double-stranded linear polymers). Here, we use sequence-generating and transfer matrix methods to obtain an analytical method for cooperative equilibrium ligand binding to double-stranded Ising lattices. We use this exact solution to evaluate binding properties and features and analyze experimental binding data of cooperative binding of the regulatory protein, cofilin, to actin filaments. This analysis, with additional experimental information about the observed bound cofilin cluster sizes and filament structure, reveals that a bound cofilin promotes cooperative binding to its longitudinal nearest-neighbors but has very modest effects on lateral nearest-neighbors. The bound cofilin cluster sizes calculated from the best fit parameters from the double-stranded model are considerably larger than when calculated with the 1D model, consistent with experimental observations made by electron microscopy and fluorescence imaging. The exact solution obtained and the method for using the solution developed here can be widely used for analysis of variety of multistranded lattice systems.

It is proposed that larger individuals within fish species may be more sensitive to global warming, due to limitations in their capacity to provide oxygen for aerobic metabolic activities. This could affect size distributions of populations in a warmer world but evidence is lacking. In Nile tilapia Oreochromis niloticus (n=18, mass range 21-313g), capacity to provide oxygen for aerobic activities (aerobic scope) was independent of mass at acclimation temperature (26°C). Tolerance of acute warming, however, declined significantly with mass when evaluated as critical temperature for fatigue from aerobic swimming (CT swim ). The CT swim protocol challenges a fish to meet the oxygen demands of constant intense aerobic exercise while their demands for basal metabolism are accelerated by incremental warming, culminating in fatigue. CT swim elicited pronounced increases in oxygen uptake but maximum rates achieved prior to fatigue declined very significantly with mass. Mass-related variation in CT swim and maximum oxygen uptake rates were positively correlated, which may indicate a causal relationship. When faced with acute thermal stress, larger fishes within populations may become constrained in their ability to swim at lower temperatures than smaller con-specifics. This could affect survival and fitness of larger fish in a world with more frequent and extreme heatwaves, with consequences for population productivity.

31 Atmospheric particulate matter (APM) emitted by iron ore processing industries has a 32 complex composition, including diverse metallic particles and nanoparticles. Such an 33 APM causes air to water cross-contamination and has recently been demonstrated to have 34 harmful sublethal impacts on fish, eliciting stress responses, affecting the immune system, 35 and reducing blood oxygen-carrying capacity. These findings imply potential 36 consequences for fish aerobic performance and energy allocation, particularly in their 37 ability to tolerate respiratory challenges such as aquatic hypoxia. To assess that potential 38 limitation, we analyzed metabolic, cardiorespiratory, and morphological responses to 39 progressive hypoxia in tilapia, Oreochromis niloticus , exposed for 96h to an 40 environmentally relevant concentration of settleable particulate matter (SePM) . This level 41 of SePM contamination initiate detectable gill damage, which reduced respiratory 42 efficiency, increased ventilatory effort and reduced fish capacity to deal with hypoxia. 43 The critical O 2 tension was increased (from 26 to 34% of O 2 / from 1.84 to 2.76 mg O 2 × 44 L -1 ). The resting normoxic respiratory frequency was elevated, limiting ventilatory 45 adjustments throughout hypoxia. Such ventilatory inefficacy is likely to increase 46 ventilatory cost and cause relevant alterations in energy allocation. We point up that a 47 potential progression in gill damage is potentially problematic in the long term as it could 48 result in infection, blood loss, ion imbalance, changes in the overall energy allocation and 49 hypoxia tolerance. Such an effect might not cause immediate lethality, but it might 50 threaten fish populations since the consequences limits physiological performance. This 51 was the first investigation to evaluate the physiological responses of fish to hypoxia after 52 SePM contamination. We suggest that the present level of environmental SePM deserves 53 attention. The present results base the need for extensive dedicated studies on SePM 54 effects in aquatic fauna.

Mammals show clear changes in heart rate linked to lung ventilation, characterized as respiratory sinus arrhythmia (RSA). These changes are controlled in part by variations in the level of inhibitory control exerted on the heart by the parasympathetic arm of the autonomic nervous system (PNS). This originates from preganglionic neurons in the nucleus ambiguous that supply phasic, respiration-related activity to the cardiac branch of the vagus nerve, via myelinated, efferent fibres with rapid conduction velocities. An elaboration of these central mechanisms, under the control of a ‘vagal system’ has been endowed by psychologists with multiple functions concerned with ‘social engagement’ in mammals and, in particular, humans. Long-term study of cardiorespiratory interactions (CRI) in other major groups of vertebrates has established that they all show both tonic and phasic control of heart rate, imposed by the PNS. This derives centrally from neurones located in variously distributed nuclei, supplying the heart via fast-conducting, myelinated, efferent fibres. Water-breathing vertebrates, which include fishes and larval amphibians, typically show direct, 1:1 CRI between heart beats and gill ventilation, controlled from the dorsal vagal motor nucleus. In air-breathing, ectothermic vertebrates, including reptiles, amphibians and lungfish, CRI mirroring RSA have been shown to improve oxygen uptake during phasic ventilation by changes in perfusion of their respiratory organs, due to shunting of blood over across their undivided hearts. This system may constitute the evolutionary basis of that generating RSA in mammals, which now lacks a major physiological role in respiratory gas exchange, due to their completely divided systemic and pulmonary circulations.

When snakes digest large meals, heart rate is accelerated by withdrawal of vagal tone and an increased non-adrenergic-non-cholinergic tone that seems to stem from circulating blood-borne factors exerting positive chronotropic effects. To investigate whether this tonic elevation of heart rate impairs the ability for autonomic regulation of heart during digestion, we characterised heart rate responses to pharmacological manipulation of blood pressure in the snake Boa constrictor through serial injections of sodium nitroprusside and phenylephrine. Both fasting and digesting snakes responded with a robust tachycardia to hypotension induced by sodium nitroprusside, with digesting snakes attaining higher maximal heart rates than fasting snakes. Both fasting and digesting snakes exhibited small reductions of the cardiac chronotropic response to hypertension, induced by injection of phenylephrine. All heart rate changes were abolished by autonomic blockade with the combination of atropine and propranolol. The digesting snakes retained the capacity for compensatory heart rate responses to hypotension, despite their higher resting values, and the upward shift of the barostatic response curve enables snakes to maintain the cardiac limb of barostatic regulation for blood pressure regulation.

Hypoxia and mercury contamination often co-occur in tropical freshwater ecosystems, but the interactive effects of these two stressors on fish populations are poorly known. The effects of mercury (Hg) on recorded changes in the detailed form of the electrocardiogram (ECG) during exposure to progressive hypoxia were investigated in two Neotropical freshwater fish species, matrinxã, Brycon amazonicus and traíra, Hoplias malabaricus . Matrinxã were exposed to a sublethal concentration of 0.1 mg L −1 of HgCl 2 in water for 96 h. Traíra were exposed to dietary doses of Hg by being fed over a period of 30 days with juvenile matrinxãs previously exposed to HgCl 2 , resulting in a dose of 0.45 mg of total Hg per fish, each 96 h. Both species showed a bradycardia in progressive hypoxia. Hg exposure impaired cardiac electrical excitability, leading to first-degree atrioventricular block, plus profound extension of the ventricular action potential (AP) plateau. Moreover, there was the development of cardiac arrhythmias and anomalies such as occasional absence of QRS complexes, extra systoles, negative Q-, R- and S-waves (QRS complex), and T wave inversion, especially in hypoxia below O 2 partial pressures (PO 2 ) of 5.3 kPa. Sub-chronic dietary Hg exposure induced intense bradycardia in normoxia in traira, plus lengthening of ventricular AP duration coupled with prolonged QRS intervals. This indicates slower ventricular AP conduction during ventricular depolarization. Overall, the data indicate that both acute waterborne and sub-chronic dietary exposure (trophic level transfer), at sublethal concentrations of mercury, cause damage in electrical stability and rhythm of the heartbeat, leading to myocardial dysfunction, which is further intensified during hypoxia. These changes could lead to impaired cardiac output, with consequences for swimming ability, foraging capacity, and hence growth and/or reproductive performance.

Vascular tone in the reptil-ian pulmonary vasculature is primarily under cholinergic, muscarinic control exerted via the vagus nerve. This control has been ascribed to a sphincter located at the arterial outflow, but we speculated whether the vascular control in the pulmonary artery is more widespread, such that responses to acetylcholine and electrical stimulation, as well as the expression of muscarinic receptors, are prevalent along its length. Working on the South American rattlesnake (Crotalus durissus), we studied four different portions of the pulmonary artery (truncus, proximal, distal, and branches). Acetylcholine elicited robust vaso-constriction in the proximal, distal, and branch portions, but the truncus vasodilated. Electrical field stimulation (EFS) caused contrac-tions in all segments, an effect partially blocked by atropine. We identified all five subtypes of muscarinic receptors (M1-M5). The expression of the M1 receptor was largest in the distal end and branches of the pulmonary artery, whereas expression of the musca-rinic M3 receptor was markedly larger in the truncus of the pulmonary artery. Application of the neural tracer 1,1'-dioctadecyl-3,3,3',3'- tetramethylindo-carbocyanine perchlorate (DiI) revealed widespread innervation along the whole pulmonary artery, and retrograde trans-port of the same tracer indicated two separate locations in the brainstem providing vagal innervation of the pulmonary artery, the medial dorsal motor nucleus of the vagus and a ventro-lateral location, possibly constituting a nucleus ambiguus. These results revealed parasympathetic innervation of a large portion of the pulmonary artery, which is responsible for regulation of vascular conductance in C. durissus, and implied its integration with cardiorespiratory control.

ABSTRACT We investigated whether fatigue from sustained aerobic swimming provides a sub-lethal endpoint to define tolerance of acute warming in fishes, as an alternative to loss of equilibrium (LOE) during a critical thermal maximum (CTmax) protocol. Two species were studied, Nile tilapia (Oreochromis niloticus) and pacu (Piaractus mesopotamicus). Each fish underwent an incremental swim test to determine gait transition speed (UGT), where it first engaged the unsteady anaerobic swimming mode that preceded fatigue. After suitable recovery, each fish was exercised at 85% of their own UGT and warmed 1°C every 30 min, to identify the temperature at which they fatigued, denoted as CTswim. Fish were also submitted to a standard CTmax, warming at the same rate as CTswim, under static conditions until LOE. All individuals fatigued in CTswim, at a mean temperature approximately 2°C lower than their CTmax. Therefore, if exposed to acute warming in the wild, the ability to perform aerobic metabolic work would be constrained at temperatures significantly below those that directly threatened survival. The collapse in performance at CTswim was preceded by a gait transition qualitatively indistinguishable from that during the incremental swim test. This suggests that fatigue in CTswim was linked to an inability to meet the tissue oxygen demands of exercise plus warming. This is consistent with the oxygen and capacity limited thermal tolerance (OCLTT) hypothesis, regarding the mechanism underlying tolerance of warming in fishes. Overall, fatigue at CTswim provides an ecologically relevant sub-lethal threshold that is more sensitive to extreme events than LOE at CTmax. Summary: Fatigue from sustained aerobic exercise can be used to measure sub-lethal tolerance of acute warming in fishes.

Significance Arp2/3 complex is an ATPase that binds to the side of a preexisting actin filament and nucleates an actin filament branch. Growing branched networks experience variable resistance and respond by adapting growth speed, power, and architecture. How force influences the dissociation of actin filament branches was not known. We used microfluidics to show that mechanical force promotes the dissociation of actin filament branches and that Arp2/3 complex adopts two distinct mechanical states with different responses to force. Phosphate release from Arp2/3 complex increases the sensitivity to both force and the debranching protein GMF. Thus, phosphate release from Arp2/3 complex may regulate debranching by force and debranching proteins.

ECG recordings were obtained using an implanted telemetry device from the South American rattlesnake, Crotalus durissus, held under stable conditions without restraining cables or interaction with researchers. Mean heart rate (f(H)) recovered rapidly (<24 h) from anaesthesia and operative procedures. This preceded a more gradual development of heart rate variability (HRV), with instantaneous f(H) increasing during each lung ventilation cycle. Atropine injection increased mean f(H) and abolished HRV. Complete autonomic blockade revealed a cholinergic tonus on the heart of 55% and an adrenergic tonus of 37%. Power spectral analysis of HRV identified a peak at the same frequency as ventilation. This correlation was sustained after temperature changes and it was more evident, marked by a more prominent power spectrum peak, when ventilation is less episodic. This HRV component is homologous to that observed in mammals, termed respiratory sinus arrhythmia (RSA). Evidence for instantaneous control of f(H) indicated rapid conduction of activity in the cardiac efferent nervous supply, as supported by the description of myelinated fibres in the cardiac vagus. Establishment of HRV 10 days after surgical intervention seems a reliable indicator of the re-establishment of control of integrative functions by the autonomic nervous system. We suggest that this criterion could be applied to other animals exposed to natural or imposed trauma, thus improving protocols involving animal handling, including veterinarian procedures.

Embryonic turtles have four distinct vascular beds that separately perfuse the developing embryo's body and the extra-embryonic yolk sac, amnion and chorioallantoic membrane (CAM). The mechanisms enabling differential regulation of blood flow through these separate beds, in order to meet the varying demands of the embryo during development, is of current interest. The present investigation followed the changes in blood flow distribution during an acute exposure to hypoxia and after α-adrenergic blockade. We monitored heart rate (fH), mean arterial pressure (Pm), and determined relative blood flow distribution (%Q̇sys) using colored microspheres. At 70% and 90% of the incubation period hypoxia elicited a bradycardia without changing Pm while %Q̇sys was altered only at 70%, increasing to the CAM and liver. Blockade of α-adrenergic responses with phentolamine did not change fH or Pm but increased %Q̇sys to the shell. These results show the capacity of embryos to redistribute cardiac output during acute hypoxia, however α-adrenergic receptors seemed to play a relatively small role in embryonic cardiovascular regulation.

Air-breathing and amphibious fishes are essential study organisms to shed insight into the required physiological shifts that supported the full transition from aquatic water-breathing fishes to terrestrial air-breathing tetrapods. While the origin of air-breathing in the evolutionary history of the tetrapods has received considerable focus, much less is known about the evolutionary physiology of air-breathing among fishes. This review summarizes recent advances within the field with specific emphasis on the cardiorespiratory regulation associated with air-breathing and terrestrial excursions, and how respiratory physiology of these living transitional forms are affected by development and personality. Finally, we provide a detailed and re-evaluated model of the evolution of air-breathing among fishes that serves as a framework for addressing new questions on the cardiorespiratory changes associated with it. This review highlights the importance of combining detailed studies on piscine air-breathing model species with comparative multi-species studies, to add an additional dimension to our understanding of the evolutionary physiology of air-breathing in vertebrates.