Journal articles: 'Respiration physiology'

1

Ward, Susan A. "Physiology of Respiration." Medicine &amp Science in Sports &amp Exercise 29, no. 6 (June 1997): 844. http://dx.doi.org/10.1097/00005768-199706000-00017.

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Harris, Dnf. "The physiology of respiration." Perfusion 9, no. 3 (May 1994): 159–62. http://dx.doi.org/10.1177/026765919400900302.

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Orlikoff, Robert F. "Anatomy and physiology of respiration." Current Opinion in Otolaryngology & Head and Neck Surgery 2 (June 1994): 220–25. http://dx.doi.org/10.1097/00020840-199406000-00002.

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Hoover, Jan Jeffrey, Kenneth L. Gage, and Mark S. Paulissen. "Hellgrammite Respiration: Temperature's Role in Ectotherm Physiology." American Biology Teacher 50, no. 1 (January 1, 1988): 39–42. http://dx.doi.org/10.2307/4448631.

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Remmers, J. E., F. G. Issa, and P. M. Suratt. "Sleep and respiration." Journal of Applied Physiology 68, no. 3 (March 1, 1990): 1286–89. http://dx.doi.org/10.1152/jappl.1990.68.3.1286.

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6

Safonov, V. A., and N. N. Tarasova. "Nervous control of respiration." Human Physiology 32, no. 4 (July 2006): 429–39. http://dx.doi.org/10.1134/s0362119706040086.

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Daimon, Shigeru, and Kazunori Yamaguchi. "Changes in respiratory activity induced by mastication during oral breathing in humans." Journal of Applied Physiology 116, no. 11 (June 1, 2014): 1365–70. http://dx.doi.org/10.1152/japplphysiol.01236.2013.

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We examined the effect of oral breathing on respiratory movements, including the number of respirations and the movement of the thoracic wall at rest and while chewing gum. Forty normal nose breathers were selected by detecting expiratory airflow from the mouth using a CO2 sensor. Chest measurements were recorded using a Piezo respiratory belt transducer, and electromyographic (EMG) activity of the masseter and trapezius muscles were recorded at rest and while chewing gum during nasal or oral breathing. Oral breathing was introduced by completely occluding the nostrils with a nose clip. During oral breathing, the respiration rate was significantly lower while chewing gum than while at rest ( P < 0.05). While chewing gum, the respiration rate was significantly lower during oral breathing than during nasal breathing ( P < 0.05). During oral breathing, thoracic movement was significantly higher while chewing gum than while at rest ( P < 0.05). Thoracic movement was significantly greater during oral breathing than during nasal breathing ( P < 0.05). The trapezius muscle exhibited significant EMG activity when chewing gum during oral breathing. The activity of the trapezius muscle coincided with increased movement of the thoracic wall. Chewing food while breathing through the mouth interferes with and decreases the respiratory cycle and promotes unusual respiratory movement of the thoracic wall, which is directed by the activity of accessory muscles of respiration.

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Pelavski, Andrés. "PHYSIOLOGY IN PLATO'S TIMAEUS: IRRIGATION, DIGESTION AND RESPIRATION." Cambridge Classical Journal 60 (September 15, 2014): 61–74. http://dx.doi.org/10.1017/s1750270514000086.

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The third part of the Timaeus, where the account is focused on the cooperation of reason and necessity, has received far less attention than the opening two sections. Particularly, the description of irrigation, digestion and respiration constitutes a challenging passage that has been conspicuously overlooked by scholarly research. Virtually the only modern explanation for the passage was devised by Cornford, and despite several inaccuracies it has been unanimously accepted by all commentators. This paper will challenge Cornford's interpretation, and use some modern biological concepts to provide an alternative approach to the passage more compatible with an actual human body.

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Subotyalov, M. A. "DEVELOPMENT OF IDEAS ABOUT THE PHYSIOLOGY OF RESPIRATION." Vestnik of the Kyrgyz-Russian Slavic University 22, no. 10 (2022): 32–40. http://dx.doi.org/10.36979/1694-500x-2022-22-10-32-40.

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10

Shaik, Zabeena P., E. Kim Fifer, and Grażyna Nowak. "Akt activation improves oxidative phosphorylation in renal proximal tubular cells following nephrotoxicant injury." American Journal of Physiology-Renal Physiology 294, no. 2 (February 2008): F423—F432. http://dx.doi.org/10.1152/ajprenal.00463.2007.

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Previously, we showed that protein kinase B (Akt) activation increases intracellular ATP levels and decreases necrosis in renal proximal tubular cells (RPTC) injured by the nephrotoxicant S-(1, 2-dichlorovinyl)-l-cysteine (DCVC) (Shaik ZP, Fifer EK, Nowak G. Am J Physiol Renal Physiol 292: F292–F303, 2007). This study examined the role of Akt in improving mitochondrial function in DCVC-injured RPTC. Our data show a novel observation that phosphorylated (active) Akt is localized in mitochondria of noninjured RPTC, both in mitoplasts and the mitochondrial outer membrane. Mitochondrial levels of active Akt decreased in nephrotoxicant-injured RPTC, and this decrease was associated with mitochondrial dysfunction. DCVC decreased basal, uncoupled, and state 3 respirations; ATP production; activities of complexes I, II, and III; the mitochondrial membrane potential (ΔΨm); and F0F1-ATPase activity. Expressing constitutively active Akt in DCVC-injured RPTC increased the levels of phosphorylated Akt in mitochondria, reduced the decreases in basal and uncoupled respirations, increased complex I-coupled state 3 respiration and ATP production, enhanced activities of complex I, complex III, and F0F1-ATPase, and improved ΔΨm. In contrast, inhibiting Akt activation by expressing dominant negative (inactive) Akt or using 20 μM LY294002 exacerbated decreases in electron transport rate, state 3 respiration, ATP production, ΔΨm, and activities of complex I, complex III, and F0F1-ATPase. In conclusion, our data show that Akt activation promotes mitochondrial respiration and ATP production in toxicant-injured RPTC by 1) improving integrity of the respiratory chain and maintaining activities of complex I and complex III, 2) reducing decreases in ΔΨm, and 3) restoring F0F1-ATPase activity.

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Harrison, Jon F., and Stephen P. Roberts. "Flight Respiration and Energetics." Annual Review of Physiology 62, no. 1 (March 2000): 179–205. http://dx.doi.org/10.1146/annurev.physiol.62.1.179.

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12

Hedges, C. P., J. S. T. Woodhead, H. W. Wang, C. J. Mitchell, D. Cameron-Smith, A. J. R. Hickey, and T. L. Merry. "Peripheral blood mononuclear cells do not reflect skeletal muscle mitochondrial function or adaptation to high-intensity interval training in healthy young men." Journal of Applied Physiology 126, no. 2 (February 1, 2019): 454–61. http://dx.doi.org/10.1152/japplphysiol.00777.2018.

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Measurement of skeletal muscle mitochondrial respiration requires invasive biopsy to obtain a muscle sample. Peripheral blood mononuclear cell (PBMC) mitochondrial protein content appears to reflect training status in young men; however, no studies have investigated whether there are training-induced changes in PBMC mitochondrial respiration. Therefore, we determined whether PBMC mitochondrial respiration could be used as a marker of skeletal muscle mitochondrial respiration in young healthy men and whether PBMC mitochondrial respiration responds to short-term training. Skeletal muscle and PBMC samples from 10 healthy young (18–35 yr) male participants were taken before and after a 2-wk high-intensity interval training protocol. High-resolution respirometry was used to determine mitochondrial respiration from muscle and PBMCs, and Western blotting and quantitative PCR were used to assess mitochondrial biogenesis in PBMCs. PBMC mitochondrial respiration was not correlated with muscle mitochondrial respiration at baseline ( R2 = 0.012–0.364, P > 0.05). While muscle mitochondrial respiration increased in response to training (32.1–61.5%, P < 0.05), PBMC respiration was not affected by training. Consequently, PBMCs did not predict training effect on muscle mitochondrial respiration ( R2 = 0.024–0.283, P > 0.05). Similarly, gene and protein markers of mitochondrial biogenesis did not increase in PBMCs following training. This suggests PBMC mitochondrial function does not reflect that of skeletal muscle and does not increase following short-term high-intensity training. PBMCs are therefore not a suitable biomarker for muscle mitochondrial function in young healthy men. It may be useful to study PBMC mitochondrial function as a biomarker of muscle mitochondrial function in pathological populations with different respiration capacities. NEW & NOTEWORTHY Research in primates has suggested that peripheral blood mononuclear cells (PBMCs) may provide a less-invasive alternative to a muscle biopsy for measuring muscle mitochondrial function. Furthermore, trained individuals appear to have greater mitochondrial content in PBMCs. Here we show that in healthy young men, PBMCs do not reflect skeletal muscle mitochondrial function and do not adapt in response to a training intervention that increases muscle mitochondrial function, suggesting PBMCs are a poor marker of muscle mitochondrial function in humans.

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13

Gurner, Ryan. "Physiology of Woody Plants." Pacific Conservation Biology 4, no. 3 (1998): 272. http://dx.doi.org/10.1071/pc980272.

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Plant physiology is the scientific study of how plants grow and respond to environmental factors and cultural treatments in terms of their physiological processes and conditions. This book aims to explain how physiological processes (such as photosynthesis, respiration, transpiration, carbohydrate, nitrogen and mineral relations) are involved in the growth of woody plants and how they are affected by the environment, in addition to explaining the mechanisms of the processes themselves.

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14

Kanters, J. K., M. V. Hojgaard, E. Agner, and N. H. Holstein-Rathlou. "Influence of forced respiration on nonlinear dynamics in heart rate variability." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 4 (April 1, 1997): R1149—R1154. http://dx.doi.org/10.1152/ajpregu.1997.272.4.r1149.

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Although it is doubtful whether the normal sinus rhythm can be described as low-dimensional chaos, there is evidence for inherent nonlinear dynamics and determinism in time series of consecutive R-R intervals. However, the physiological origin for these nonlinearities is unknown. The aim of this study was to test whether the known nonlinear input from spontaneous respiration is a source for the nonlinearities in heart rate variability. Twelve healthy subjects were examined in supine position with 3-h electrocardiogram recordings during both spontaneous and forced respiration in accordance with a metronome set to 12 min(-1). Nonlinear dynamics were measured as the correlation dimension and the nonlinear prediction error. Complexity expressed as correlation dimension was unchanged from normal respiration, 9.1 +/- 0.5, compared with forced respiration, 9.3 +/- 0.6. Also, nonlinear determinism expressed as the nonlinear prediction error did not differ between spontaneous respiration, 32.3 +/- 3.4 ms, and forced respiration, 31.9 +/- 5.7. It is concluded that the origin of the nonlinear dynamics in heart rate variability is not a nonlinear input from the respiration into the cardiovascular oscillator. Additional studies are needed to elucidate the mechanisms behind the nonlinear dynamics in heart rate variability.

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15

MacDonald, J. R., M. Oellermann, S. Rynbeck, G. Chang, K. Ruggiero, G. J. S. Cooper, and A. J. R. Hickey. "Transmural differences in respiratory capacity across the rat left ventricle in health, aging, and streptozotocin-induced diabetes mellitus: evidence that mitochondrial dysfunction begins in the subepicardium." American Journal of Physiology-Cell Physiology 300, no. 2 (February 2011): C246—C255. http://dx.doi.org/10.1152/ajpcell.00294.2010.

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In diabetic cardiomyopathy, ventricular dysfunction occurs in the absence of hypertension or atherosclerosis and is accompanied by altered myocardial substrate utilization and depressed mitochondrial respiration. It is not known if mitochondrial function differs across the left ventricular (LV) wall in diabetes. In the healthy heart, the inner subendocardial region demonstrates higher rates of blood flow, oxygen consumption, and ATP turnover compared with the outer subepicardial region, but published transmural respirometric measurements have not demonstrated differences. We aim to measure mitochondrial function in Wistar rat LV to determine the effects of age, streptozotocin-diabetes, and LV layer. High-resolution respirometry measured indexes of respiration in saponin-skinned fibers dissected from the LV subendocardium and subepicardium of 3-mo-old rats after 1 mo of streptozotocin-induced diabetes and 4-mo-old rats following 2 mo of diabetes. Heart rate and heartbeat duration were measured under isoflurane-anesthesia using a fetal-Doppler, and transmission electron microscopy was employed to observe ultrastructural differences. Heart rate decreased with age and diabetes, whereas heartbeat duration increased with diabetes. While there were no transmural respirational differences in young healthy rat hearts, both myocardial layers showed a respiratory depression with age (30–40%). In 1-mo diabetic rat hearts only subepicardial respiration was depressed, whereas after 2 mo diabetes, respiration in subendocardial and subepicardial layers was depressed and showed elevated leak (state 2) respiration. These data provide evidence that mitochondrial dysfunction is first detectable in the subepicardium of diabetic rat LV, whereas there are measureable changes in LV mitochondria after only 4 mo of aging.

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16

Franklin, Karl A., Erik Sandström, Göran Johansson, and Eva M. Bålfors. "Hemodynamics, cerebral circulation, and oxygen saturation in Cheyne-Stokes respiration." Journal of Applied Physiology 83, no. 4 (October 1, 1997): 1184–91. http://dx.doi.org/10.1152/jappl.1997.83.4.1184.

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Franklin, Karl A., Erik Sandström, Göran Johansson, and Eva M. Bålfors. Hemodynamics, cerebral circulation, and oxygen saturation in Cheyne-Stokes respiration. J. Appl. Physiol. 83(4): 1184–1191, 1997.—Because cardiovascular disorders and stroke may induce Cheyne-Stokes respiration, our purpose was to study the interaction among cerebral activity, cerebral circulation, blood pressure, and blood gases during Cheyne-Stokes respiration. Ten patients with heart failure or a previous stroke were investigated during Cheyne-Stokes respiration with recordings of daytime polysomnography, cerebral blood flow velocity, intra-arterial blood pressure, and intra-arterial oxygen saturation with and without oxygen administration. There were simultaneous changes in wakefulness, cerebral blood flow velocity, and respiration with accompanying changes in blood pressure and heart rate ∼10 s later. Cerebral blood flow velocity, blood pressure, and heart rate had a minimum occurrence in apnea and a maximum occurrence during hyperpnea. The apnea-induced oxygen desaturations were diminished during oxygen administration, but the hemodynamic alterations persisted. Oxygen desaturations were more severe and occurred earlier according to intra-arterial measurements than with finger oximetry. It is not possible to explain Cheyne-Stokes respiration by alterations in blood gases and circulatory time alone. Cheyne-Stokes respiration may be characterized as a state of phase-linked cyclic changes in cerebral, respiratory, and cardiovascular functions probably generated by variations in central nervous activity.

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17

Fritzen, Björn. "Vocal fold physiology: laryngeal function in phonation and respiration." Journal of Phonetics 16, no. 4 (October 1988): 463–65. http://dx.doi.org/10.1016/s0095-4470(19)30523-6.

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18

Webster, Lynn R., and Suzanne Karan. "The Physiology and Maintenance of Respiration: A Narrative Review." Pain and Therapy 9, no. 2 (October 6, 2020): 467–86. http://dx.doi.org/10.1007/s40122-020-00203-2.

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Eldridge, F. L., D. E. Millhorn, and J. P. Kiley. "Antagonism by theophylline of respiratory inhibition induced by adenosine." Journal of Applied Physiology 59, no. 5 (November 1, 1985): 1428–33. http://dx.doi.org/10.1152/jappl.1985.59.5.1428.

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The effects on respiration of an analogue of adenosine, L-2-N6-(phenylisopropyl)adenosine (PIA), and of the methylxanthine, theophylline, were determined in 19 vagotomized glomectomized cats whose end-tidal PCO2 was kept constant by means of a servo-controlled ventilator. Integrated phrenic nerve activity was used to represent respiratory output. Our results show that PIA, whether given systemically or into the third cerebral ventricle, depressed respiration. Systemically administered theophylline stimulated respiration. Theophylline given intravenously, or into the third ventricle not only reversed the depressive effects of previously administered PIA but caused further increases of respiration above the control level. Prior systemic administration of theophylline blocked both respiratory and hypotensive effects of subsequently administered PIA. Effects of either agent on medullary extracellular fluid pH did not explain the results. We conclude that the adenosine analogue PIA, acts to inhibit neurons in the brain that are involved in the control of respiration and that its effects are blocked by theophylline. We suggest that adenosine acts as a tonic modulator of respiration and that theophylline stimulates breathing by competitive antagonism of adenosine at neuronal receptor sites.

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Ljubicic, Vladimir, Peter J. Adhihetty, and David A. Hood. "Role of UCP3 in state 4 respiration during contractile activity-induced mitochondrial biogenesis." Journal of Applied Physiology 97, no. 3 (September 2004): 976–83. http://dx.doi.org/10.1152/japplphysiol.00336.2004.

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In an effort to better characterize uncoupling protein-3 (UCP3) function in skeletal muscle, we assessed basal UCP3 protein content in rat intermyofibrillar (IMF) and subsarcolemmal (SS) mitochondrial subfractions in conjunction with measurements of state 4 respiration. UCP3 content was 1.3-fold ( P < 0.05) greater in IMF compared with SS mitochondria. State 4 respiration was 2.6-fold greater ( P < 0.05) in the IMF subfraction than in SS mitochondria. GDP attenuated state 4 respiration by ∼40% ( P < 0.05) in both subfractions. The UCP3 activator oleic acid (OA) significantly increased state 4 respiration in IMF mitochondria only. We used chronic electrical stimulation (3 h/day for 7 days) to investigate the relationship between changes in UCP3 protein expression and alterations in state 4 respiration during contractile activity-induced mitochondrial biogenesis. UCP3 content was increased by 1.9- and 2.3-fold in IMF and SS mitochondria, respectively, which exceeded the concurrent 40% ( P < 0.05) increase in cytochrome- c oxidase activity. Chronic contractile activity increased state 4 respiration by 1.4-fold ( P < 0.05) in IMF mitochondria, but no effect was observed in the SS subfraction. The uncoupling function of UCP3 accounted for 50–57% of the OA-induced increase in state 4 respiration in IMF mitochondria, which was independent of the induced twofold difference in UCP3 content due to chronic contractile activity. Thus modifications in UCP3 function are more important than changes in UCP3 expression in modifying state 4 respiration. This effect is evident in IMF but not SS mitochondria. We conclude that UCP3 at physiological concentrations accounts for a significant portion of state 4 respiration in both IMF and SS mitochondria, with the contribution being greater in the IMF subfraction. In addition, the contradiction between human and rat training studies with respect to UCP3 protein expression may partly be explained by the greater than twofold difference in mitochondrial UCP3 content between rat and human skeletal muscle.

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Bigatello, Luca, and Antonio Pesenti. "Respiratory Physiology for the Anesthesiologist." Anesthesiology 130, no. 6 (June 1, 2019): 1064–77. http://dx.doi.org/10.1097/aln.0000000000002666.

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Abstract Respiratory function is fundamental in the practice of anesthesia. Knowledge of basic physiologic principles of respiration assists in the proper implementation of daily actions of induction and maintenance of general anesthesia, delivery of mechanical ventilation, discontinuation of mechanical and pharmacologic support, and return to the preoperative state. The current work provides a review of classic physiology and emphasizes features important to the anesthesiologist. The material is divided in two main sections, gas exchange and respiratory mechanics; each section presents the physiology as the basis of abnormal states. We review the path of oxygen from air to the artery and of carbon dioxide the opposite way, and we have the causes of hypoxemia and of hypercarbia based on these very footpaths. We present the actions of pressure, flow, and volume as the normal determinants of ventilation, and we review the resulting abnormalities in terms of changes of resistance and compliance.

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Chamberlin, M. E. "Top-down control analysis of the effect of temperature on ectotherm oxidative phosphorylation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 4 (October 2004): R794—R800. http://dx.doi.org/10.1152/ajpregu.00240.2004.

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Top-down control and elasticity analysis was conducted on mitochondria isolated from the midgut of the tobacco hornworm ( Manduca sexta) to assess how temperature affects oxidative phosphorylation in a eurythermic ectotherm. Oxygen consumption and protonmotive force (measured as membrane potential in the presence of nigericin) were monitored at 15, 25, and 35°C. State 4 respiration displayed a Q10 of 2.4–2.7 when measured over two temperature ranges (15–25°C and 25–35°C). In state 3, the Q10s for respiration were 2.0 and 1.7 for the lower and higher temperature ranges, respectively. The kinetic responses (oxygen consumption) of the substrate oxidation system, proton leak, and phosphorylation system increased as temperature rose, although the proton leak and substrate oxidation system showed the greatest thermal sensitivity. Whereas there were temperature-induced changes in the activities of the oxidative phosphorylation subsystems, there was no change in the state 4 membrane potential and little change in the state 3 membrane potential. Top-down control analysis revealed that control over respiration did not change with temperature. In state 4, control of respiration was shared nearly equally by the proton leak and the substrate oxidation system, whereas in state 3 the substrate oxidation system exerted over 90% of the control over respiration. The proton leak and phosphorylation system account for <10% of the temperature-induced change in the state 3 respiration rate. Therefore, when the temperature is changed, the state 3 respiration rate is altered primarily because of temperature's effect on the substrate oxidation system.

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Brown, Jason C. L., Alexander R. Gerson, and James F. Staples. "Mitochondrial metabolism during daily torpor in the dwarf Siberian hamster: role of active regulated changes and passive thermal effects." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 5 (November 2007): R1833—R1845. http://dx.doi.org/10.1152/ajpregu.00310.2007.

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During daily torpor in the dwarf Siberian hamster, Phodopus sungorus, metabolic rate is reduced by 65% compared with the basal rate, but the mechanisms involved are contentious. We examined liver mitochondrial respiration to determine the possible role of active regulated changes and passive thermal effects in the reduction of metabolic rate. When assayed at 37°C, state 3 (phosphorylating) respiration, but not state 4 (nonphosphorylating) respiration, was significantly lower during torpor compared with normothermia, suggesting that active regulated changes occur during daily torpor. Using top-down elasticity analysis, we determined that these active changes in torpor included a reduced substrate oxidation capacity and an increased proton conductance of the inner mitochondrial membrane. At 15°C, mitochondrial respiration was at least 75% lower than at 37°C, but there was no difference between normothermia and torpor. This implies that the active regulated changes are likely more important for reducing respiration at high temperatures (i.e., during entrance) and/or have effects other than reducing respiration at low temperatures. The decrease in respiration from 37°C to 15°C resulted predominantly from a considerable reduction of substrate oxidation capacity in both torpid and normothermic animals. Temperature-dependent changes in proton leak and phosphorylation kinetics depended on metabolic state; proton leakiness increased in torpid animals but decreased in normothermic animals, whereas phosphorylation activity decreased in torpid animals but increased in normothermic animals. Overall, we have shown that both active and passive changes to oxidative phosphorylation occur during daily torpor in this species, contributing to reduced metabolic rate.

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Liu, Binbin, Saisai Yan, Xiaoni Wang, Lin Xie, Jie Tong, Fadong Zhao, Xiaohui Di, Xiangguo Yan, and Jianbao Zhang. "An improved method to evaluate heart rate variability based on time-variant cardiorespiratory relation." Journal of Applied Physiology 127, no. 2 (August 1, 2019): 320–27. http://dx.doi.org/10.1152/japplphysiol.00125.2019.

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Frequency domain analysis of heart rate variability (HRV) is a noninvasive method to evaluate the autonomic nervous system (ANS), but the traditional parameters of HRV, i.e., the power spectra of the high-frequency (HF) and low-frequency bands (LF), cannot estimate the activity of the parasympathetic (PNS) and sympathetic nervous systems (SNS) well. The aim of our study was to provide a corrected method to better distinguish the contributions of the PNS and SNS in the HRV spectrum. Respiration has a gating effect on cardiac vagal efferent activity, which induces respiration-locked heart rate (HR) changes because of the fast effect of the PNS. So the respiration-related heart rate (HRr) is closely related to PNS activity. In this study, HR was decomposed into HRr and the respiration-unrelated component (HRru) based on empirical mode decomposition (EMD) and the relationship between HR and respiration. Time-frequency analysis of HRr and HRru was defined as HFr and LFru, respectively, with specific adaptive bands for every signal. Two experimental data sets, representing SNS and PNS activation, respectively, were used for efficiency analysis of our method. Our results show that the corrected HRV predicted ANS activity well. HFr could be an index of PNS activity, LFru mainly reflected SNS activity, and LFru/HFr could be more accurate in representing the sympathovagal balance. NEW & NOTEWORTHY This study includes the time-varying relationship between respiration and heart rate in the analysis of heart rate variability. Correction for low-frequency and high-frequency components based on respiration significantly improved evaluation of the sympathetic and parasympathetic nervous systems.

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Nowak, Grażyna, Diana Bakajsova, and Ginger L. Clifton. "Protein kinase C-ϵ modulates mitochondrial function and active Na+ transport after oxidant injury in renal cells." American Journal of Physiology-Renal Physiology 286, no. 2 (February 2004): F307—F316. http://dx.doi.org/10.1152/ajprenal.00275.2003.

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The aim of this study was to determine whether protein kinase C-ϵ (PKC-ϵ) is involved in the repair of mitochondrial function and/or active Na+ transport after oxidant injury in renal proximal tubular cells (RPTC). Sublethal injury was produced in primary cultures of RPTC using tert-butylhydroperoxide (TBHP), and the recovery of functions was examined. PKC-ϵ was activated three- to fivefold after injury. Active PKC-ϵ translocated to the mitochondria. Basal oxygen consumption (Qo2), uncoupled Qo2, and ATP production decreased 58, 60, and 41%, respectively, at 4 h and recovered by day 4 after injury. At 4 h, complex I-coupled respiration decreased 50% but complex II- and IV-coupled respirations were unchanged. Inhibition of PKC-ϵ translocation using a peptide selective inhibitor, PKC-ϵV1-2, reduced decreases in basal and uncoupled Qo2 values and increased complex I-linked respiration in TBHP-injured RPTC at 4 h of recovery. Furthermore, PKC-ϵV1-2 prevented decreases in ATP production in injured RPTC. Na+-K+-ATPase activity and ouabain-sensitive 86Rb+ uptake were decreased by 60 and 53%, respectively, at 4 h of recovery. Inhibition of PKC-ϵ activation prevented a decline in Na+-K+-ATPase activity and reduced decreases in ouabain-sensitive 86Rb+ uptake. We conclude that during early repair after oxidant injury in RPTC 1) PKC-ϵ is activated and translocated to mitochondria; 2) PKC-ϵ activation decreases mitochondrial respiration, electron transport rate, and ATP production by reducing complex I-linked respiration; and 3) PKC-ϵ mediates decreases in active Na+ transport and Na+-K+-ATPase activity. These data show that PKC-ϵ activation after oxidant injury in RPTC is involved in the decreases in mitochondrial function and active Na+ transport and that inhibition of PKC-ϵ activation promotes the repair of these functions.

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XYLOURI-FRAGIADAKI (Ε. ΞΥΛΟΥΡΗ-ΦΡΑΓΚΙΑΔΑΚΗ), E., E. GOLIDI (Ε. ΓΟΛΙΔΗ), I. MENEGATOS (Ι. ΜΕΝΕΓΑΤΟΣ), and F. LUZI. "Influence of high ambient temperature on reproductive performance and physiology of rabbit does in a commercial rabbitry in Greece." Journal of the Hellenic Veterinary Medical Society 54, no. 2 (January 25, 2018): 119. http://dx.doi.org/10.12681/jhvms.15247.

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The reproductive performance and physiological traits of intensively raised does were evaluated under farm conditions in Greece, during the hot (average farm temperature 19.5°C) and cold period (average farm temperature 12.4°C). The size of litter at birth (6.94 vs. 7.84 alive pups, P<0.001), the size of litter at weaning (5.95 vs. 7.06, P<0.001), the pre-weaning mortality rate (16.94% vs. 9.60%, P<0.001, the number of born dead (0.39 vs. 0.19, P<0.001) and the number of stillborn (0,05 vs 0,02 P<0.01) were significantly affected during the hot period, while litter weight and individual weight at birth did not seem to differ between hot and cold period (461 g vs. 466 g (P<0.05) and 68 vs. 65 g (P<0.05), respectively). Rectal temperature of does and respiration rate were higher in the hot period (39.09°C vs. 38.93°C (NS) and 128.08 respirations/min vs. 115.37 respirations/min; P<0.001). The effects of parity order and animals were also studied revealing that parity order influenced significantly total born, born alive, stillborn and weaned rabbits, litter weight and individual weight at birth, as well as the does' respiration rate. The interaction between parity and period was not significant for any of the recorded parameters. In conclusion, high ambient temperature impaired does' reproductive and physiological traits under those conditions, similar to most natural environmental conditions in Greece.

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Darszon, A., A. Guerrero, A. Lievano, M. Gonzalez-Martinez, and E. Morales. "Ionic Channels in Sea Urchin Sperm Physiology." Physiology 3, no. 5 (October 1, 1988): 181–85. http://dx.doi.org/10.1152/physiologyonline.1988.3.5.181.

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In sea urchin sperm, ionic fluxes modulate the activation of respiration and motility and the acrosome reaction, a prerequisite for egg fertilization. Ionic channels are present in the plasma membrane of these cells, and there is good evidence indicating that they are deeply involved in these processes.

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Neubauer, J. A., J. E. Melton, and N. H. Edelman. "Modulation of respiration during brain hypoxia." Journal of Applied Physiology 68, no. 2 (February 1, 1990): 441–51. http://dx.doi.org/10.1152/jappl.1990.68.2.441.

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This review is a summary of the effects of brain hypoxia on respiration with a particular emphasis on those studies relevant to understanding the cellular basis of these effects. Special attention is given to mechanisms that may be responsible for the respiratory depression that appears to be the primary sequela of brain hypoxia in animal models. Although a variety of potential mechanisms for hypoxic respiratory depression are considered, emphasis is placed on changes in the neuromodulator constituency of the respiratory neuron microenvironment during hypoxia as the primary cause of this phenomenon. Hypoxia is accompanied by a net increase in neuronal inhibition due to both decreased excitatory and increased inhibitory neuromodulator levels. A survey of hypoxia-tolerant cellular systems and organisms suggests that hypoxic respiratory depression may be a manifestation of the depression of cellular metabolism, which appears to be a major adaptation to limited oxygen availability in these systems.

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Shishkin, G. S., N. V. Ustyuzhaninova, and N. D. Umantseva. "Standardized estimation of external respiration function." Human Physiology 33, no. 1 (February 2007): 125–28. http://dx.doi.org/10.1134/s0362119707010215.

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Li, Lai-tien. "Comparative Physiology on "The Lung Controls the Skin and Hair"." American Journal of Chinese Medicine 15, no. 01n02 (January 1987): 13–18. http://dx.doi.org/10.1142/s0192415x87000035.

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"The lung is connected with skin and hair" is a theory of traditional Chinese medicine. From the view of comparative physiology we researched the inter-relation of lung and skin and hair and found it in water. From living protein to fish respiration is by the structure corresponding to the skin and the organ which originated skin. Though amphibia have lung respiratory effect of skin still locate 2/3. Aves. Mammals and human beings use lungs to respire. In fact air exchanges from nature through the thin water molecular layer of the surface of the pulmonary alveoli. So the lung is derived from "skin and hair" to adapt to inter-respiration.

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Israel, D. J., and R. S. Pozos. "Synchronized slow-amplitude modulations in the electromyograms of shivering muscles." Journal of Applied Physiology 66, no. 5 (May 1, 1989): 2358–63. http://dx.doi.org/10.1152/jappl.1989.66.5.2358.

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The electromyograms (EMG) of shivering human subjects exposed to 0 degrees C air in an environmental chamber were analyzed to detect slow-amplitude modulations (SAMs, less than 1 Hz) in the EMGs of widely separated muscles and to study the relationship of these SAMs to respiration rate and skin temperature. Distinct amplitude modulations were observed in the raw EMGs during shivering. The peaks in EMG activity occurred simultaneously in the majority of the monitored muscles in all subjects. Pearson correlations between the average rectified EMGs of 93% of the muscles were significant (P less than 0.05). Visual analysis of the EMG and respiration signals indicated that the peaks in muscular activity occurred 6–12 times/min, whereas respiration ranged from 10 to 23 cycles/min. For all subjects respiration was at a higher frequency than amplitude modulation in the EMG. Comparison of EMG records with expiratory flow rate traces in shivering subjects indicated no one-to-one correlation between the occurrence of respiration and EMG amplitude modulations. Respiratory flow rate and average rectified EMG showed significant correlation in only 33% of the cases. In addition, skin temperature changes could not be correlated with the SAMS.

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Cohen, Gerald, and Natasa Kesler. "MAO inhibits mitochondrial respiration." Free Radical Biology and Medicine 25 (January 1998): S110. http://dx.doi.org/10.1016/s0891-5849(98)90337-9.

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Kovac, Helmut, Anton Stabentheiner, Stefan K. Hetz, Markus Petz, and Karl Crailsheim. "Respiration of resting honeybees." Journal of Insect Physiology 53, no. 12 (December 2007): 1250–61. http://dx.doi.org/10.1016/j.jinsphys.2007.06.019.

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Leung, Richard S. T., Michael E. Bowman, Tung M. Diep, Geraldo Lorenzi-Filho, John S. Floras, and T. Douglas Bradley. "Influence of Cheyne-Stokes respiration on ventricular response to atrial fibrillation in heart failure." Journal of Applied Physiology 99, no. 5 (November 2005): 1689–96. http://dx.doi.org/10.1152/japplphysiol.00027.2005.

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In subjects with sinus rhythm, respiration has a profound effect on heart rate variability (HRV) at high frequencies (HF). Because this HF respiratory arrhythmia is lost in atrial fibrillation (AF), it has been assumed that respiration does not influence the ventricular response. However, previous investigations have not considered the possibility that respiration might influence HRV at lower frequencies. We hypothesized that Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) would entrain HRV at very low frequency (VLF) in AF by modulating atrioventricular (AV) nodal refractory period and concealed conduction. Power spectral analysis of R-wave-to-R-wave (R-R) intervals and respiration during sleep were performed in 13 subjects with AF and CSR-CSA. As anticipated, no modulation of HRV was detected at HF during regular breathing. In contrast, VLF HRV was entrained by CSR-CSA [coherence between respiration and HRV of 0.69 (SD 0.22) at VLF during CSR-CSA vs. 0.20 (SD 0.19) at HF during regular breathing, P < 0.001]. Comparison of R-R intervals during CSR-CSA demonstrated a shorter AV node refractory period during hyperpnea than apnea [minimum R-R of 684 (SD 126) vs. 735 ms (SD 147), P < 0.001] and a lesser degree of concealed conduction [scatter of 178 (SD 56) vs. 246 ms (SD 72), P = 0.001]. We conclude that CSR-CSA entrains the ventricular response to AF, even in the absence of HF respiratory arrhythmia, by inducing rhythmic oscillations in AV node refractoriness and the degree of concealed conduction that may be a function of autonomic modulation of the AV node.

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35

Weaver, Ryan J., Gina Carrion, Rachel Nix, Gerald P. Maeda, Samantha Rabinowitz, Erik N. K. Iverson, Kiley Thueson, and Justin C. Havird. "High mitochondrial mutation rates in Silene are associated with nuclear-mediated changes in mitochondrial physiology." Biology Letters 16, no. 9 (September 2020): 20200450. http://dx.doi.org/10.1098/rsbl.2020.0450.

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Mitochondrial (mt) respiration depends on proteins encoded both by the mitochondrial and nuclear genomes. Variation in mt-DNA mutation rates exists across eukaryotes, although the functional consequences of elevated mt mutation rates in some lineages remain underexplored. In the angiosperm genus Silene , closely related, ecologically similar species have either ‘fast' or ‘slow' mt-DNA mutation rates. Here, we investigated the functional consequences of elevated mt-DNA mutation rates on mt respiration profiles of Silene mitochondria. Overall levels of respiration were similar among Species. Fast species had lower respiration efficiency than slow species and relied up to 48% more on nuclear-encoded respiratory enzymes alternative oxidase (AOX) and accessory dehydrogenases (DHex), which participate in stress responses in plants. However, not all fast species showed these trends. Respiratory profiles of some enzymes were correlated, most notably AOX and DHex. We conclude that subtle differences in mt physiology among Silene lineages with dramatically different mt mutation rates may underly similar phenotypes at higher levels of biological organization, betraying the consequences of mt mutations.

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Martin, B. J., J. A. Logemann, R. Shaker, and W. J. Dodds. "Coordination between respiration and swallowing: respiratory phase relationships and temporal integration." Journal of Applied Physiology 76, no. 2 (February 1, 1994): 714–23. http://dx.doi.org/10.1152/jappl.1994.76.2.714.

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The coordination of breathing and swallowing was studied in 13 young healthy adult subjects during the administration of graduated volumes of water (3, 10, and 20 ml). Simultaneous submental electromyography, respiratory plethysmography, and fiber-optic endoscopy revealed a well-timed pattern between physiological respiratory events and related swallowing events. Expiration was the phase of respiration that was most closely associated with deglutition. Respiration was usually maintained at the onset of deglutition and halted before the onset of laryngeal elevation. The apneic interval was approximately 1 s for the 3-, 10-, and 20-ml boluses. A large-volume (100-ml) straw swallow resulted in variable respiration-swallowing patterns and in statistically significant differences (P < 0.01) in the duration of apneic pause and laryngeal excursion. The expiratory phase of respiration resumed nearly 0.50 s before the completion of swallowing. Clinical implications of the findings are addressed and related to aspiration and pulmonary complications in dysphagic patients.

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YAMAMOTO, Y., M. RUNOLD, N. PRABHAKAR, T. PANTALEO, and H. LAGERCRANTZ. "Somatostatin in the control of respiration." Acta Physiologica Scandinavica 134, no. 4 (December 1988): 529–33. http://dx.doi.org/10.1111/j.1365-201x.1988.tb10631.x.

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YAMAMOTO, Y., M. RUNOLD, N. PRABHAKAR, T. PANTALEO, and H. LAGERCRANTZ. "Somatostatin in the control of respiration." Acta Physiologica Scandinavica 134, no. 4 (December 1998): 529–33. http://dx.doi.org/10.1111/j.1748-1716.1998.tb08527.x.

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Wibking, Katie. "Gas Exchange Gamified: Teaching Respiration Physiology with a Novel Board Game." American Biology Teacher 82, no. 3 (March 1, 2020): 175–77. http://dx.doi.org/10.1525/abt.2020.82.3.175.

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Pulmonary gas exchange is a complex component of respiratory physiology. For many students, the movement of unseen gases can seem abstract and confusing. The “Gas Exchange Game” is a novel board game designed for use in a second-semester anatomy and physiology course. Students apply textbook knowledge of the laws of gas exchange and use the game board and pieces to see concrete examples of how gases move in the human body.

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Chen, Pei-Chung. "Physiology of Nitrogen Fixation in Two New Strains of Anabaena." Zeitschrift für Naturforschung C 40, no. 5-6 (June 1, 1985): 406–8. http://dx.doi.org/10.1515/znc-1985-5-620.

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Abstract Two different cyanobacteria, Anabaena CH 1 and CH2, were isolated from Taiwan paddy soils. Both strains can grow well with daily dilution method. Anabaena CH1 shows a blue-green color and Anabaena CH2 a green brownish one. Nitrogenase activity decreased as cultures were transferred from light to dark. When a darkened culture was placed again into the light, nitrogenase activity recovered within two hours, but not in the presence of chloramphenicol. Energy supply for nitrogenase within both strains was different. Nitrogenase activity of Anabaena CH1 was light-dependent and oxygen in heterocyst was exhausted through oxyhydrogen reaction. Except photosynthesis, respiration may be used as energy source for nitrogenase in Anabaena CH2. Respiration was the major one to protect nitrogenase against oxygen.

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Laaß, Michael, Oliver Hampe, Michael Schudack, Corinna Hoff, Nikolay Kardjilov, and André Hilger. "New insights into the respiration and metabolic physiology of Lystrosaurus." Acta Zoologica 92, no. 4 (October 1, 2010): 363–71. http://dx.doi.org/10.1111/j.1463-6395.2010.00467.x.

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42

Novak, V., P. Novak, J. de Champlain, A. R. Le Blanc, R. Martin, and R. Nadeau. "Influence of respiration on heart rate and blood pressure fluctuations." Journal of Applied Physiology 74, no. 2 (February 1, 1993): 617–26. http://dx.doi.org/10.1152/jappl.1993.74.2.617.

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The dynamics of the respiratory and cardiovascular systems were studied by continuously slowing respiration from 0.46 to 0.05 Hz. The time-frequency distribution and global spectral analysis were used to assess the R-R interval (R-R) and the systolic and diastolic blood pressure fluctuations in 16 healthy subjects. During rest, the nonrespiratory-to-respiratory frequency ratios were not affected by occasional slow breathing, whereas the low- (0.01–0.15 Hz) to high- (0.15–0.3 Hz) frequency indexes for blood pressure were increased (P < 0.05). The respiratory fluctuations in R-R and the systolic and diastolic pressures were paced over the 0.46- to 0.05-Hz range. As respiration slowed to 0.07–0.09 Hz, the frequency content of the respiration and cardiovascular variables increased sharply and nonlinearly to a maximum that exceeded values at higher frequencies (P < 0.001). The nonrespiratory frequency content remained stable in the 0.01- to 0.05-Hz range and did not significantly differ from that at rest. In contrast, the nonstable 0.05- to 0.1-Hz component was suppressed. A slow 0.012- to 0.017-Hz rhythm modulated respiration and hemodynamic fluctuations at both respiratory and nonrespiratory frequencies. The study indicated that respiration input should be considered in the interpretation of global spectra. Furthermore the time-frequency distributions demonstrated that a close nonlinear coupling exists between the respiratory and cardiovascular systems.

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Nowak, Grażyna, Ginger L. Clifton, Malinda L. Godwin, and Diana Bakajsova. "Activation of ERK1/2 pathway mediates oxidant-induced decreases in mitochondrial function in renal cells." American Journal of Physiology-Renal Physiology 291, no. 4 (October 2006): F840—F855. http://dx.doi.org/10.1152/ajprenal.00219.2005.

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Previously, we showed that oxidant exposure in renal proximal tubular cells (RPTC) induces mitochondrial dysfunction mediated by PKC-ε. This study examined the role of ERK1/2 in mitochondrial dysfunction induced by oxidant injury and whether PKC-ε mediates its effects on mitochondrial function through the Raf-MEK1/2-ERK1/2 pathway. Sublethal injury produced by tert-butylhydroperoxide (TBHP) resulted in three- to fivefold increase in phosphorylation of ERK1/2 and p38 but not JNK. This was followed by decreases in basal and uncoupled respirations (41%), state 3 respiration and ATP production coupled to complex I (46%), and complex I activity (42%). Oxidant exposure decreased aconitase activity 30% but not pyruvate, α-ketoglutarate, and malate dehydrogenase activities. Inhibition of ERK1/2 restored basal and state 3 respirations, ΔΨm, ATP production, and complex I activity but not aconitase activity. In contrast, activation of ERK1/2 by expression of constitutively active MEK1 suppressed basal, uncoupled, and state 3 respirations in noninjured RPTC to the levels observed in TBHP-injured RPTC. MEK1/2 inhibition did not change Akt or p38 phosphorylation, demonstrating that the protective effect of MEK1/2 inhibitor was not due to activation of Akt or inhibition of p38 pathway. Inhibition of PKC-ε did not block TBHP-induced ERK1/2 phosphorylation in whole RPTC or in mitochondria. We conclude that 1) oxidant-induced activation of ERK1/2 but not p38 or JNK reduces mitochondrial respiration and ATP production by decreasing complex I activity and substrate oxidation through complex I, 2) citric acid cycle dehydrogenases are not under control of the ERK1/2 pathway in oxidant-injured RPTC, 3) the protective effects of ERK1/2 inhibition are not due to activation of Akt, and 4) ERK1/2 and PKC-ε mediate oxidant-induced mitochondrial dysfunction through independent pathways.

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Rannels, D. Eugene. "Cellular neurobiology of respiration." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 1 (July 1, 1995): L1. http://dx.doi.org/10.1152/ajplung.1995.269.1.l1.

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45

Holmqvist, Fredrik, Martin Stridh, Johan E. P. Waktare, Johan Brandt, Leif Sörnmo, Anders Roijer, and Carl J. Meurling. "Rapid fluctuations in atrial fibrillatory electrophysiology detected during controlled respiration." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 2 (August 2005): H754—H760. http://dx.doi.org/10.1152/ajpheart.00075.2005.

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Heart rate during sinus rhythm is modulated through the autonomic nervous system, which generates short-term oscillations. The high-frequency components in these oscillations are associated with respiration, causing sinus arrhythmia, mediated by the parasympathetic nervous system. In this study, we evaluated whether slow, controlled respiration causes cyclic fluctuations in the frequency of the fibrillating atria. Eight patients (four women; median age 63 yr, range 53–68 yr) with chronic atrial fibrillation (AF) and third-degree atrioventricular block treated by permanent pacemaker were studied. ECG was recorded during baseline rest, during 0.125-Hz frequency controlled respiration, and finally during controlled respiration after full vagal blockade. We calculated fibrillatory frequency using frequency analysis of the fibrillatory ECG for overlapping 2.5-s segments; spectral analysis of the resulting frequency trend was performed to determine the spectrum of variations of fibrillatory frequency. Normalized spectral power at respiration frequency increased significantly during controlled respiration from 1.4 (0.76–2.0) (median and range) at baseline to 2.7 (1.2–5.8) ( P = 0.01). After vagal blockade, the power at respiration frequency decreased to 1.2 (0.23–2.8) ( P = 0.01). Controlled respiration causes cyclic fluctuations in the AF frequency in patients with long-duration AF. This phenomenon seems to be related to parasympathetic modulations of the AF refractory period.

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Liang, Li Ya, Zhao Jin, Li Ping Hao, and Shi Jie Yan. "Effects of Different Cooling Methods on Postharvest Physiology of Yali Pears during Ice Temperature Storage." Advanced Materials Research 554-556 (July 2012): 1072–75. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1072.

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The effects of slow and rapid cooling methods on the postharvest physiology of Yali pears during ice temperature (-0.5°C) storage were investigated. Respiration rate, ethylene production, browning index and polyphenol oxidase(PPO) activity were used to evaluate the quality of Yali pears. The results showed that the slow cooling treatment decreased the levels of respiration rate，ethylene production，and PPO activity of Yali pears, and delayed the occurrence of the respiration, ethylene, and PPO activity peak compared to the rapid cooling treatment. The browning indexes of Yali pears with slow cooling treatment were lower than that of rapid cooling treatment. The results indicate that the cooling method may be an important factor affecting the storage quality of Yali pears. The slow cooling can delay the occurrence of physiological disorder during ice temperature storage.

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Donina, Zh A. "Intersystem relationship between respiration and blood circulation." Human Physiology 37, no. 2 (March 2011): 229–39. http://dx.doi.org/10.1134/s0362119711020034.

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48

Decker, M. J., J. Haaga, J. L. Arnold, D. Atzberger, and K. P. Strohl. "Functional electrical stimulation and respiration during sleep." Journal of Applied Physiology 75, no. 3 (September 1, 1993): 1053–61. http://dx.doi.org/10.1152/jappl.1993.75.3.1053.

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During obstructive sleep apnea (OSA), respiratory activation of upper airway muscles, particularly genioglossus, is ineffective during sleep. Functional electrical stimulation (FES) of muscles reportedly reduces the number and length of OSAs. Our goals were to examine the effect of FES on sensation during wakefulness and on OSA events. Studies were performed in 11 subjects: 4 healthy asymptomatic subjects and 7 patients with OSA. Surface electrodes placed on the submental region produced discomfort; however, during sleep, the stimulus intensity producing arousal was significantly greater than that producing barely tolerable discomfort during wakefulness. Additionally, we developed a protocol for placement of fine-wire electrodes into the neurovascular bundle of the hypoglossal nerve, using recognizable radiographic features and computerized axial tomography as guides. In these patients, while awake, optimal wire placement was associated with visible tongue protrusion without discomfort. With both surface stimulation and fine-wire FES, during sleep the stimulus intensity required to produce obvious electroencephalographic arousal was significantly greater than that producing a barely tolerable sensation while awake. During apneic events, the application of surface stimulation had an inconsistent effect, terminating 22% of the apneas, and fine-wire FES also had a limited impact, terminating 23% of the apneic events. We conclude from our studies that subjects tolerate surface and fine-wire FES to higher stimulus parameters during sleep than during wakefulness but that both approaches have an inconsistent effect on apneas during sleep.

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Jennings, Donald B., and Heather J. Lockett. "Angiotensin stimulates respiration in spontaneously hypertensive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 5 (May 1, 2000): R1125—R1133. http://dx.doi.org/10.1152/ajpregu.2000.278.5.r1125.

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Spontaneously hypertensive rats (SHR) have an activated brain angiotensin system. We hypothesized 1) that ventilation (V˙) would be greater in conscious SHR than in control Wistar-Kyoto (WKY) rats and 2) that intravenous infusion of the ANG II-receptor blocker saralasin would depress respiration in SHR, but not in WKY. Respiration and oxygen consumption (V˙o 2) were measured in conscious aged-matched groups ( n = 16) of adult female SHR and WKY. For protocol 1, rats were habituated to a plethysmograph and measurements obtained over 60–75 min. After installation of chronic intravenous catheters, protocol 2consisted of 30 min of saline infusion (∼14 μl ⋅ kg− 1 ⋅ min− 1) followed by 40 min of saralasin (1.3 μg ⋅ kg− 1 ⋅ min− 1).V˙, tidal volume (VT), inspiratory flow [VT/inspiratory time (Ti)], breath expiratory time, and V˙o 2 were higher, and breath Ti was lower in “continuously quiet” SHR. In SHR, but not in WKY rats, ANG II-receptor block decreasedV˙, VT, and VT/Ti and increased breath Ti. During ANG II-receptor block, an average decrease in V˙o 2 in SHR was not significant. About one-half of the higherV˙ in SHR appears to be accounted for by an ANG II mechanism acting either via peripheral arterial receptors or circumventricular organs.

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Kutsch, Werner L., Arne Staack, Jörg Wötzel, Ulrike Middelhoff, and Ludger Kappen. "Field measurements of root respiration and total soil respiration in an alder forest." New Phytologist 150, no. 1 (April 2001): 157–68. http://dx.doi.org/10.1046/j.1469-8137.2001.00071.x.

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Journal articles on the topic 'Respiration physiology'

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