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Aim: Sympathoexcitation and sleep‐disordered breathing are common contributors for disease progression. Catecholaminergic neurons from the rostral ventrolateral medulla (RVLM‐C1) modulate sympathetic outflow and have anatomical projections to respiratory neurons; however, the contribution of highly selective activation of RVLM‐C1 neurons on long‐term autonomic and breathing (dys)regulation remains to be understood. Methods: To explore this relationship, a lentiviral vector carrying the light‐sensitive cation channel channelrhodopsin‐2 (LVV‐PRSX8‐ChR2‐YFP) was unilaterally injected into the RVLM of healthy rats. On the contralateral side, LVV‐PRSX8‐ChR2‐YFP was co‐injected with a specific immunotoxin (DβH‐SAP) targeted to eliminate C1 neurons. Results: Intermittent photostimulation of RVLM‐C1 in vivo, in unrestrained freely moving rats, elicited long‐term facilitation of the sympathetic drive, a rise in blood pressure and sympatho‐respiratory coupling. In addition, photoactivation of RVLM‐C1 induced long‐lasting ventilatory instability, characterized by oscillations in tidal volume and increased breathing variability, but only during non‐rapid eye movement sleep. These effects were not observed when photostimulation of the RVLM was performed in the presence of DβH‐SAP toxin. Conclusions: The finding that intermittent activation of RVLM‐C1 neurons induces autonomic and breathing dysfunction suggest that episodic stimulation of RVLM‐C1 may serve as a pathological substrate for the long‐term development of cardiorespiratory disorders. [ABSTRACT FROM AUTHOR]

We investigated the extent to which the facultative air‐breathing fish, the striped catfish (Pangasianodon hypophthalmus), uses air‐breathing to cope with aquatic hypercarbia, and how air‐breathing is influenced by the experimental exposure protocol and level of hypercarbia. We exposed individuals to severe aquatic hypercarbia (up to PwCO2 = 81 mmHg) using step‐wise and progressive exposure protocols while measuring gill ventilation rate, heart rate, mean arterial blood pressure, and air‐breathing frequency, as well as arterial blood pH and PCO2. We confirm that P. hypophthalmus is tolerant of hypercarbia. Under both protocols gill ventilation rate, heart rate, and mean arterial blood pressure were maintained near control levels even at very high CO2 levels. We observed a marked amount of individual variation in the PwCO2 at which air‐breathing was elicited, with some individuals not responding at all. The experimental protocol also influenced the onset of air‐breathing. Air‐breathing began at lower PwCO2 in the step‐wise protocol (23 ± 4.1 mmHg) compared with the progressive protocol (46 ± 7.8 mmHg). Air‐breathing was often followed by aquatic surface respiration, at higher PCO2 (71 ± 5.2 mmHg) levels. On average, the blood PCO2 was approximately 43% lower (46 ± 2.5 mmHg) than water PwCO2 (~81 mmHg) at our highest tested CO2 level. While this suggests that aerial CO2 elimination is an effective, and perhaps critical, respiratory strategy used by P. hypophthalmus to cope with severe hypercarbia, this observation may also be explained by a long lag time required for equilibration. Research Highlights: Pangasianodon hypophthalmus are tolerant of high aquatic CO2 (hypercarbia) but use air‐breathing and aquatic surface respiration to cope with severe levels.The onset of hypercarbia induced air‐breathing depends on the level and, importantly, the rate of PCO2 increase. [ABSTRACT FROM AUTHOR]

The aim of the present study was to determine the roles that externally versus internally oriented CO2/H+-sensitive chemoreceptors might play in promoting cardiorespiratory responses to environmental hypercarbia in the air-breathing fish, Hoplerythrinus unitaeniatus (jeju). Fish were exposed to graded hypercarbia (1, 2.5, 5, 10 and 20% CO2) and also to graded levels of environmental acidosis (pH -7.0, 6.0, 5.8, 5.6, 5.3 and 4.7) equal to the pH levels of the hypercarbic water to distinguish the relative roles of CO2 versus H+. We also injected boluses of CO2-equilibrated solutions (5, 10 and 20% CO2) and acid solutions equilibrated to the same pH as the CO2 boluses into the caudal vein (internal) and buccal cavity (external) to distinguish between internal and external stimuli. The putative location of the chemoreceptors was determined by bilateral denervation of branches of cranial nerves IX (glossopharyngeal) and X (vagus) to the gills. The data indicate that the chemoreceptors eliciting bradycardia, hypertension and gill ventilatory responses (increased frequency and amplitude) to hypercarbia are exclusively branchial, externally oriented and respond specifically to changes in CO2 and not H+. Those involved in producing the cardiovascular responses appeared to be distributed across all gill arches while those involved in the gill ventilatory responses were located primarily on the first gill arch. Higher levels of aquatic CO2 depressed gill ventilation and stimulated air breathing. The chemoreceptors involved in producing air breathing in response to hypercarbia also appeared to be branchial, distributed across all gill arches and responded specifically to changes in aquatic CO2. This would suggest that chemoreceptor groups with different orientations (blood versus water) are involved in eliciting air-breathing responses to hypercarbia in jeju. [ABSTRACT FROM AUTHOR]

Heart rate variability (HRV) at rest and heart rate recovery after exercise reflect cardiac vagal activity. The aim of this study was to determine whether increasing HRV during involuntary respiratory training induced by rebreathing air using a Hepburn heart and lung exerciser (HHALE) could, like exercise, improve vagal tone. Eighteen subjects (36–88 years) underwent a 6-week control period, then a 6-week training period with the HHALE following which half continued training for 6 weeks and half ceased training. Measurements were made of HRV, work at 60% predicted heart rate max for 15 min, heart rate recovery after exercise, resting blood pressure, heart rate, vital capacity and forced expiratory volume. After the first 6-week HHALE training, there was a significant increase of 13.2±5.7 ν in the high frequency peak of the power spectrum of HRV at rest, whereas, the low frequency peak decreased. Similarly, exercise performance showed a significant improvement of 0.031±0.012 J per heartbeat from a pre-training 0.128±0.022. Also, heart rate recovery after exercise significantly faster (drop in the first 20 s improving by 3.3±1.5 beats from a pre-training 12.9±1.6). The subgroup that continued training maintained or slightly improved these values. In those that ceased training the speed of heart rate recovery at the end of the exercise test returned to pre-trained levels, whereas, other responses were either maintained or decreased slightly. We conclude that training with the HHALE can, without additional exercise, increase cardiac vagal tone and exercise performance. [ABSTRACT FROM AUTHOR]

Despite being obligate air breathers, many species of marine mammal are capable of spending most of their lives submerged in water. How they do this has been a subject of intense interest to physiologists for over a century, yet we still do not have a detailed understanding of the physiological mechanisms underlying this behaviour. What are the proximate mechanisms that trigger the ‘decisions’ to submerge and return to the surface? The present study proposes a model intended to address this question, based on fundamental concepts of cardiorespiratory control. Two basic hypotheses are examined by computer simulation, using a mathematical model of the mammalian cardiorespiratory control system with parameter values for an adult Weddell seal: (1) that the control of diving can be considered to be a respiratory control problem, and (2) that dives are initiated and maintained by disfacilitation of respiratory drive, not inhibition. Computer simulations confirmed the plausibility of these hypotheses. Simulated diving behaviour and physiological responses (ventilation, cardiac output, blood and tissue gas tensions) were consistent with published data from freely diving Weddell seals. Dives up to the estimated aerobic dive limit (ADL, 18–25 min) could be simulated without the need for active inhibition of breathing in this model. This theoretical analysis suggests that the most important physiological adjustments occur during the surface interval phase of the dive cycle and include hyperventilation accompanied by high cardiac output, appropriate regulation of cerebral blood flow and central chemoreceptor threshold shifts. During dives, cardiac output, distribution of peripheral blood flow, splenic contraction and peripheral chemoreflex drives were found to modulate physiological and behavioural responses, but were not essential for simulated dives to occur. The main conclusion from this study is that the central chemoreceptor may be an important mechanism involved in the regulation of diving behaviour, implying that CO2, not O2, is the key regulatory variable in this model. This model includes and extends the ADL concept and suggests an explicit mechanism by which the respiratory control system may play a central role in the regulation of diving behaviour. It is likely that respiratory mechanisms are an important component of a hierarchical behavioural control system and further studies are required to test the qualitative and quantitative validity of the model. [ABSTRACT FROM AUTHOR]

During the nursing period seals undergo several physiological and behavioural changes. A key component of development is increased cardiorespiratory control, fundamental for breath-holding and thus diving. This study focused on the ontogenetic changes in cardiac responses to respiration in quietly resting, pre-weaned harbour seal pups (Phoca vitulina). During periods of quiet rest, breathing became episodic, eupnoea interspersed with periods of apnoea. Little change was observed in respiration (∼35 breaths min-1) and eupnoeic heart rate (∼160 beats min-1) throughout the nursing period. However, apnoea duration increased (from ∼20 to 40 s), while apnoeic heart rate decreased with age (from ∼150 to 90 beats min-1). The observed decline in apnoeic heart rate resulted from an increase in cardiorespiratory control as pups approached weaning, evident by the ability to maintain a lower heart rate more consistently. Similar changes in cardiorespiratory patterns have been reported for elephant and Weddell seals. Due to the early onset of independent foraging, however, the rate of cardiorespiratory control development was more rapid in harbour seals. Our findings suggest that by 1 month of age, harbour seal pups possess the cardiorespiratory control necessary to sustain long-duration apnoeas, fundamental for proficient diving and successful foraging upon weaning. [ABSTRACT FROM AUTHOR]