scholarly journals Evolved changes in breathing and CO2 sensitivity in deer mice native to high altitudes

2018 ◽  
Vol 315 (5) ◽  
pp. R1027-R1037 ◽  
Author(s):  
Catherine M. Ivy ◽  
Graham R. Scott
Keyword(s):  
High Altitude ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Deer Mice ◽  
Hypoxic Ventilatory Response ◽  
Ventilatory Responses ◽  
In Captivity ◽  
Generation Progeny ◽  
First And Second Generation ◽  
Hypoxia Acclimation

We examined the control of breathing by O2 and CO2 in deer mice native to high altitude to help uncover the physiological specializations used to cope with hypoxia in high-altitude environments. Highland deer mice ( Peromyscus maniculatus) and lowland white-footed mice ( P. leucopus) were bred in captivity at sea level. The first and second generation progeny of each population was raised to adulthood and then acclimated to normoxia or hypobaric hypoxia (12 kPa O2, simulating hypoxia at ~4,300 m) for 6–8 wk. Ventilatory responses to poikilocapnic hypoxia (stepwise reductions in inspired O2) and hypercapnia (stepwise increases in inspired CO2) were then compared between groups. Both generations of lowlanders appeared to exhibit ventilatory acclimatization to hypoxia (VAH), in which hypoxia acclimation enhanced the hypoxic ventilatory response and/or made the breathing pattern more effective (higher tidal volumes and lower breathing frequencies at a given total ventilation). In contrast, hypoxia acclimation had no effect on breathing in either generation of highlanders, and breathing was generally similar to hypoxia-acclimated lowlanders. Therefore, attenuation of VAH may be an evolved feature of highlanders that persists for multiple generations in captivity. Hypoxia acclimation increased CO2 sensitivity of breathing, but in this case, the effect of hypoxia acclimation was similar in highlanders and lowlanders. Our results suggest that highland deer mice have evolved high rates of alveolar ventilation that are unaltered by exposure to chronic hypoxia, but they have preserved ventilatory sensitivity to CO2.

scholarly journals Coordinated changes across the O 2 transport pathway underlie adaptive increases in thermogenic capacity in high-altitude deer mice

2020 ◽  
Vol 287 (1927) ◽  
pp. 20192750 ◽  
Author(s):  
Kevin B. Tate ◽  
Oliver H. Wearing ◽  
Catherine M. Ivy ◽  
Zachary A. Cheviron ◽  
Jay F. Storz ◽  
...  
Keyword(s):  
High Altitude ◽  
Complex Traits ◽  
Deer Mice ◽  
Transport Pathway ◽  
Physiological Mechanisms ◽  
Critical Determinant ◽  
In Captivity ◽  
Low Altitude ◽  
Hypoxia Acclimation ◽  
Thermogenic Capacity

Animals native to the hypoxic and cold environment at high altitude provide an excellent opportunity to elucidate the integrative mechanisms underlying the adaptive evolution and plasticity of complex traits. The capacity for aerobic thermogenesis can be a critical determinant of survival for small mammals at high altitude, but the physiological mechanisms underlying the evolution of this performance trait remain unresolved. We examined this issue by comparing high-altitude deer mice ( Peromyscus maniculatus ) with low-altitude deer mice and white-footed mice ( P. leucopus ). Mice were bred in captivity and adults were acclimated to each of four treatments: warm (25°C) normoxia, warm hypoxia (12 kPa O 2 ), cold (5°C) normoxia or cold hypoxia. Acclimation to hypoxia and/or cold increased thermogenic capacity in deer mice, but hypoxia acclimation led to much greater increases in thermogenic capacity in highlanders than in lowlanders. The high thermogenic capacity of highlanders was associated with increases in pulmonary O 2 extraction, arterial O 2 saturation, cardiac output and arterial–venous O 2 difference. Mechanisms underlying the evolution of enhanced thermogenic capacity in highlanders were partially distinct from those underlying the ancestral acclimation responses of lowlanders. Environmental adaptation has thus enhanced phenotypic plasticity and expanded the physiological toolkit for coping with the challenges at high altitude.

scholarly journals Ventilatory responses to acute hypoxia and hypercapnia in humans with a patent foramen ovale

2019 ◽  
Vol 126 (3) ◽  
pp. 730-738 ◽  
Author(s):  
James T. Davis ◽  
Lindsey M. Boulet ◽  
Alyssa M. Hardin ◽  
Alex J. Chang ◽  
Andrew T. Lovering ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
High Altitude ◽  
Patent Foramen Ovale ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Acute Exposure ◽  
Foramen Ovale ◽  
Hypoxic Ventilatory Response ◽  
Ventilatory Responses ◽  
Peripheral Chemoreflex

Subjects with a patent foramen ovale (PFO) have blunted ventilatory acclimatization to high altitude compared with subjects without PFO. The blunted response observed could be because of differences in central and/or peripheral respiratory chemoreflexes. We hypothesized that compared with subjects without a PFO (PFO−), subjects with a PFO (PFO+) would have blunted ventilatory responses to acute hypoxia and hypercapnia. Sixteen PFO+ subjects (9 female) and 15 PFO− subjects (8 female) completed four 20-min trials on the same day: 1) normoxic hypercapnia (NH), 2) hyperoxic hypercapnia (HH), 3) isocapnic hypoxia (IH), and 4) poikilocapnic hypoxia (PH). Hypercapnic trials were completed before the hypoxic trials, the order of the hypercapnic (NH & HH) and hypoxic (IH & PH) trials were randomized, and trials were separated by ≥40 min. During the NH trials but not the HH trials subjects who were PFO+ had a blunted hypercapnic ventilatory response compared with subjects who were PFO− (1.41 ± 0.46 l·min−1·mmHg−1 vs. 1.98 ± 0.71 l·min−1·mmHg−1, P = 0.02). There were no differences between the PFO+ and PFO− subjects with respect to the acute hypoxic ventilatory response during IH and PH trials. Hypoxic ventilatory depression was similar between subjects who were PFO+ and PFO− during IH. These data suggest that compared with subjects who were PFO−, subjects who were PFO+ have normal ventilatory chemosensitivity to acute hypoxia but blunted ventilatory chemosensitivity to carbon dioxide, possibly because of reduced carbon dioxide sensitivity of either the central and/or the peripheral chemoreceptors. NEW & NOTEWORTHY Patent foramen ovale (PFO) is found in ~25%–40% of the population. The presence of a PFO appears to be associated with blunted ventilatory responses during acute exposure to normoxic hypercapnia. The reason for this blunted ventilatory response during acute exposure to normoxic hypercapnia is unknown but may suggest differences in either central and/or peripheral chemoreflex contribution to hypercapnia.

Blunted hypoxic ventilatory drive in subjects susceptible to high-altitude pulmonary edema

1989 ◽  
Vol 66 (3) ◽  
pp. 1152-1157 ◽  
Author(s):  
Y. Matsuzawa ◽  
K. Fujimoto ◽  
T. Kobayashi ◽  
N. R. Namushi ◽  
K. Harada ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Pulmonary Function Test ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
High Altitude Pulmonary Edema ◽  
Function Test ◽  
History Of ◽  
Low Altitude

It has been proposed that subjects susceptible to high-altitude pulmonary edema (HAPE) show exaggerated hypoxemia with relative hypoventilation during the early period of high-altitude exposure. Some previous studies suggest the relationship between the blunted hypoxic ventilatory response (HVR) and HAPE. To examine whether all the HAPE-susceptible subjects consistently show blunted HVR at low altitude, we evaluated the conventional pulmonary function test, hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) in ten lowlanders who had a previous history of HAPE and compared these results with those of eight control lowlanders who had no history of HAPE. HVR was measured by the progressive isocapnic hypoxic method and was evaluated by the slope relating minute ventilation to arterial O2 saturation (delta VE/delta SaO2). HCVR was measured by the rebreathing method of Read. All measurements were done at Matsumoto, Japan (610 m). All the HAPE-susceptible subjects showed normal values in the pulmonary function test. In HCVR, HAPE-susceptible subjects showed relatively lower S value, but there was no significant difference between the two groups (1.74 +/- 1.16 vs. 2.19 +/- 0.4, P = NS). On the other hand, HAPE-susceptible subjects showed significantly lower HVR than control subjects (-0.42 +/- 0.23 vs. -0.87 +/- 0.29, P less than 0.01). These results suggest that HAPE-susceptible subjects more frequently show low HVR at low altitude. However, values for HVR were within the normal range in 2 of 10 HAPE-susceptible subjects. It would seem therefore that low HVR alone need not be a critical factor for HAPE. This could be one of several contributing factors.

scholarly journals Plasticity of non-shivering thermogenesis and brown adipose tissue in high-altitude deer mice

2021 ◽  
Author(s):  
Soren Z. Coulson ◽  
Cayleih E. Robertson ◽  
Sajeni Mahalingam ◽  
Grant B. McClelland
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Altitude ◽  
Heat Production ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Deer Mice ◽  
Brown Adipose ◽  
Hypoxia Acclimation ◽  
Shivering Thermogenesis

High altitude environments challenge small mammals with persistent low ambient temperatures that require high rates of aerobic heat production in face of low O2 availability. An important component of thermogenic capacity in rodents is non-shivering thermogenesis (NST) mediated by uncoupled mitochondrial respiration in brown adipose tissue (BAT). NST is plastic, and capacity for heat production increases with cold acclimation. However, in lowland native rodents, hypoxia inhibits NST in BAT. We hypothesize that highland deer mice (Peromyscus maniculatus) overcome the hypoxic inhibition of NST through changes in BAT mitochondrial function. We tested this hypothesis using lab born and raised highland and lowland deer mice, and a lowland congeneric (P. leucopus), acclimated to either warm normoxia (25°C, 760 mmHg) or cold hypoxia (5°C, 430 mmHg). We determined the effects of acclimation and ancestry on whole-animal rates of NST, the mass of interscapular BAT (iBAT), and uncoupling protein (UCP)-1 protein expression. To identify changes in mitochondrial function, we conducted high-resolution respirometry on isolated iBAT mitochondria using substrates and inhibitors targeted to UCP-1. We found that rates of NST increased with cold hypoxia acclimation but only in highland deer mice. There was no effect of cold hypoxia acclimation on iBAT mass in any group, but highland deer mice showed increases in UCP-1 expression and UCP-1 stimulated mitochondrial respiration in response to these stressors. Our results suggest that highland deer mice have evolved to increase the capacity for NST in response to chronic cold hypoxia, driven in part by changes in iBAT mitochondrial function.

Time course of augmentation and depression of hypoxic ventilatory responses at altitude

1994 ◽  
Vol 77 (1) ◽  
pp. 313-316 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
P. Bickler
Keyword(s):  
Pulse Oximetry ◽  
Sea Level ◽  
Time Course ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Ventilatory Response ◽  
Set Point ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

Hypoxic ventilatory response (HVR) and hypoxic ventilatory depression (HVD) were measured in six subjects before, during, and after 12 days at 3,810-m altitude (barometric pressure approximately 488 Torr) with and without 15 min of preoxygenation. HVR was tested by 5-min isocapnic steps to 75% arterial O2 saturation measured by pulse oximetry (Spo2) at an isocapnic PCO2 (P*CO2) chosen to set hyperoxic resting ventilation to 140 ml.kg-1.min-1. Hypercapnic ventilatory response (HCVR, 1.min-1.Torr-1) was tested at ambient and high SPO2 6–8 min after a 6- to 10-Torr step increase of end-tidal PCO2 (PETCO2) above P*CO2. HCVR was independent of preoxygenation and was not significantly increased at altitude (when corrected to delta logPCO2). Preoxygenated HVR rose from -1.13 +/- 0.23 (SE) l.min-1.%SPO2(-1) at sea level to -2.17 +/- 0.13 by altitude day 12, without reaching a plateau, and returned to control after return to sea level for 4 days. Ambient HVR was measured at P*CO2 by step reduction of SPO2 from its ambient value (86–91%) to approximately 75%. Ambient HVR slope was not significantly less, but ventilation at equal levels of SPO2 and PCO2 was lower by 13.3 +/- 2.4 l/min on day 2 (SPO2 = 86.2 +/- 2.3) and by 5.9 +/- 3.5 l/min on day 12 (SPO2 = 91.0 +/- 1.5; P < 0.05). This lower ventilation was estimated (from HCVR) to be equivalent to an elevation of the central chemoreceptor PCO2 set point of 9.2 +/- 2.1 Torr on day 2 and 4.5 +/- 1.3 on day 12.(ABSTRACT TRUNCATED AT 250 WORDS)

An assessment of nasal functions in control of breathing

1988 ◽  
Vol 65 (4) ◽  
pp. 1520-1524 ◽  
Author(s):  
Y. Tanaka ◽  
T. Morikawa ◽  
Y. Honda
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Airway Resistance ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Control Of Breathing ◽  
Mouth Breathing ◽  
Occlusion Pressure ◽  
Ventilatory Responses ◽  
End Tidal

Breathing pattern and steady-state CO2 ventilatory response during mouth breathing were compared with those during nose breathing in nine healthy adults. In addition, the effect of warming and humidification of the inspired air on the ventilatory response was observed during breathing through a mouthpiece. We found the following. 1) Dead space and airway resistance were significantly greater during nose than during mouth breathing. 2) The slope of CO2 ventilatory responses did not differ appreciably during the two types of breathing, but CO2 occlusion pressure response was significantly enhanced during nose breathing. 3) Inhalation of warm and humid air through a mouthpiece significantly depressed CO2 ventilation and occlusion pressure responses. These results fit our observation that end-tidal PCO2 was significantly higher during nose than during mouth breathing. It is suggested that a loss of nasal functions, such as during nasal obstruction, may result in lowering of CO2, fostering apneic spells during sleep.

Hypocapnia and sustained hypoxia blunt ventilation on arrival at high altitude

1984 ◽  
Vol 56 (3) ◽  
pp. 602-606 ◽  
Author(s):  
S. Y. Huang ◽  
J. K. Alexander ◽  
R. F. Grover ◽  
J. T. Maher ◽  
R. E. McCullough ◽  
...  
Keyword(s):  
High Altitude ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Ventilatory Responses ◽  
Low Altitude ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

Hypoxia at high altitude stimulates ventilation, but inhibitory influences in the first days after arrival limit the ventilatory response. Possible inhibitory influences include hypocapnia and depression of ventilation during sustained hypoxia. Our approach was to compare hypoxic ventilatory responses at low altitude with ventilation at high altitude. In 12 subjects we compared responses both to isocapnic hypoxia and poikilocapnic (no CO2 added) hypoxia during acute (less than 10 min) and sustained (30 min) hypoxia in Denver (1,600 m) with ventilations measured on each of 5 days on Pikes Peak (4,300 m). On Pikes Peak, day 1 ventilation [minute ventilation = 10.0 1/min, BTPS; arterial O2 saturation (Sao2) = 82%] was less than predicted by either acute isocapnic or poikilocapnic tests. However, sustained poikilocapnic hypoxia (Sao2 approximately = 82%) in Denver yielded ventilation similar to that on Pikes Peak on day 1. By Pikes Peak days 4 and 5, endtidal PCO2, pHa, and Sao2 approached plateaus, and ventilation (12.4 1/min, BTPS) on these days was as predicted by the acute isocapnic test. Thus the combination of hypocapnia and sustained hypoxia may have blunted the ventilatory increase on Pikes Peak day 1 but apparently not after 4 or 5 days of acclimatization.

Role of glutamate and serotonin on the hypoxic ventilatory response in high-altitude-adapted plateau Pika

2015 ◽  
Vol 212-214 ◽  
pp. 39-45 ◽  
Author(s):  
Zhenzhong Bai ◽  
Nicolas Voituron ◽  
Tana Wuren ◽  
Florine Jeton ◽  
Guoen Jin ◽  
...  
Keyword(s):  
High Altitude ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Plateau Pika

Effect of prior O2 breathing on ventilatory response to sustained isocapnic hypoxia in adult humans

1996 ◽  
Vol 81 (4) ◽  
pp. 1627-1632 ◽  
Author(s):  
Y. Honda ◽  
H. Tani ◽  
A. Masuda ◽  
T. Kobayashi ◽  
T. Nishino ◽  
...  
Keyword(s):  
Response Pattern ◽  
Excitatory Amino Acid ◽  
Ventilatory Response ◽  
Random Order ◽  
Relative Magnitude ◽  
Hypoxic Ventilatory Response ◽  
Biphasic Response ◽  
Ventilatory Responses ◽  
Adult Humans ◽  
Neurotransmitter Glutamate

Honda, Y., H. Tani, A. Masuda, T. Kobayashi, T. Nishino, H. Kimura, S. Masuyama, and T. Kuriyama. Effect of prior O2 breathing on ventilatory response to sustained isocapnic hypoxia in adult humans. J. Appl. Physiol. 81(4): 1627–1632, 1996.—Sixteen healthy volunteers breathed 100% O2 or room air for 10 min in random order, then their ventilatory response to sustained normocapnic hypoxia (80% arterial O2saturation, as measured with a pulse oximeter) was studied for 20 min. In addition, to detect agents possibly responsible for the respiratory changes, blood plasma of 10 of the 16 subjects was chemically analyzed. 1) Preliminary O2 breathing uniformly and substantially augmented hypoxic ventilatory responses. 2) However, the profile of ventilatory response in terms of relative magnitude, i.e., biphasic hypoxic ventilatory depression, remained nearly unchanged. 3) Augmented ventilatory increment by prior O2 breathing was significantly correlated with increment in the plasma glutamine level. We conclude that preliminary O2administration enhances hypoxic ventilatory response without affecting the biphasic response pattern and speculate that the excitatory amino acid neurotransmitter glutamate, possibly derived from augmented glutamine, may, at least in part, play a role in this ventilatory enhancement.

Sign in / Sign up

Export Citation Format

Share Document