Academic literature on the topic 'Device-guided slow breathing'

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Journal articles on the topic "Device-guided slow breathing"

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Oneda, Bruna, Kátia C. Ortega, Josiane L. Gusmão, Tatiana G. Araújo, and Décio Mion. "Sympathetic nerve activity is decreased during device-guided slow breathing." Hypertension Research 33, no. 7 (June 3, 2010): 708–12. http://dx.doi.org/10.1038/hr.2010.74.

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Viskoper, R. "Nonpharmacologic treatment of resistant hypertensives by Device-Guided slow breathing exercises." American Journal of Hypertension 16, no. 6 (June 2003): 484–87. http://dx.doi.org/10.1016/s0895-7061(03)00571-5.

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Adler, Tessa E., Yasmine Coovadia, Domenica Cirone, Maha L. Khemakhem, and Charlotte W. Usselman. "Device-guided slow breathing reduces blood pressure and sympathetic activity in young normotensive individuals of both sexes." Journal of Applied Physiology 127, no. 4 (October 1, 2019): 1042–49. http://dx.doi.org/10.1152/japplphysiol.00442.2019.

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Slow breathing (SLOWB) is recommended for use as an adjuvant treatment for hypertension. However, the extent to which blood pressure (BP) responses to SLOWB differ between men and women are not well-established. Therefore, we tested the hypothesis that an acute bout of SLOWB would induce larger decreases in BP in males than in females, given that males typically have higher resting BP. We also examined autonomic contributors to reduced BP during SLOWB; that is, muscle sympathetic nerve activity and spontaneous cardiovagal (sequence method) and vascular sympathetic baroreflex sensitivity. We tested normotensive females ( n = 10, age: 22 ± 2 y, body mass index: 22 ± 2 kg/m2) and males ( n = 12, age: 23 ± 3 y, body mass index: 26 ± 4 kg/m2). Subjects were tested at baseline and during the last 5 min of a 15-min RESPeRATE-guided SLOWB session. Overall, SLOWB reduced systolic BP by 3.2 ± 0.8 mmHg (main effect, P < 0.01). Females had lower systolic BP (main effect, P = 0.02); we observed no interaction between sex and SLOWB. SLOWB also reduced muscle sympathetic nerve activity burst incidence by −5.0 ± 1.4 bursts/100 heartbeats (main effect, P < 0.01). Although females tended to have lower burst incidence (main effect, P = 0.1), there was no interaction between sex and SLOWB. Cardiovagal baroreflex sensitivity improved during SLOWB (21.0 vs. 36.0 ms/mmHg, P = 0.03) with no effect of sex. Despite lower overall BP in females, our data support a lack of basement effect on SLOWB-induced reductions in BP, as SLOWB was equally effective in reducing BP in males and females. Our findings support the efficacy of the RESPeRATE device for reducing BP in both sexes, even in young, normotensive individuals. NEW & NOTEWORTHY We provide support for the effectiveness of device-guided slow breathing for blood pressure reduction in young normotensive women and men. Despite having lower baseline blood pressure and sympathetic nerve activity, women experienced equivalent reductions in both measures in response to RESPeRATE-guided slow breathing as men. Thus, slow breathing appears to be effective in young healthy normotensive individuals of both sexes and may be an ideal preventative therapy against future hypertension.
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de Jong, Maartje Cathelijne, and Cornelis Hendrikus Boersma. "Device-guided breathing as a possible tool to improve the outcome of exposure therapy." Mental Illness 2, no. 1 (January 25, 2010): 25–27. http://dx.doi.org/10.4081/mi.2010.e6.

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Exposure therapy is a widely used treatment for patients with post-traumatic stress dis -order. It involves reduction of fear through progressive exposure to frightening stimuli in a therapeutic environment. Here we propose a new method designed to improve the effectiveness of exposure therapy. We hypothesized that device-guided breathing during exposure therapy can increase the capability of the patient to undergo effective exposure. The successful application of the method is described for a single patient. Using a device to slow and regularize breathing, the patient was calmed and experienced a greater sense of control and a profound effect of the exposure. The use of the breathing-guiding device is believed to reduce arousal level and excitability of sympathetic “fight-flight” behaviors. The present study suggests that device-guided breathing integrated with exposure therapy may provide a practically feasible and potentially promising non-pharmacological treatment after trauma.
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Anderson, D. E., J. D. McNeely, and B. G. Windham. "Device-guided slow-breathing effects on end-tidal CO2and heart-rate variability." Psychology, Health & Medicine 14, no. 6 (December 2009): 667–79. http://dx.doi.org/10.1080/13548500903322791.

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van Dijk, Peter R., Kornelis J. J. van Hateren, Nanne Kleefstra, and Gijs W. D. Landman. "It is time to close the book on device-guided slow breathing." Blood Pressure 27, no. 3 (February 6, 2018): 181–82. http://dx.doi.org/10.1080/08037051.2018.1435260.

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Chaddha, Ashish, Daniel Modaff, Christopher Hooper-Lane, and David A. Feldstein. "Device and non-device-guided slow breathing to reduce blood pressure: A systematic review and meta-analysis." Complementary Therapies in Medicine 45 (August 2019): 179–84. http://dx.doi.org/10.1016/j.ctim.2019.03.005.

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Kim, Jang-Young, Byung-Su Yoo, Seung-Hwan Lee, Junghan Yoon, and Kyung-Hoon Choe. "The Changes of Noninvasive Hemodynamic Parameters after Device-Guided Slow Breathing Exercise in Hypertensive Patients." Journal of the Korean Society of Hypertension 19, no. 2 (2013): 55. http://dx.doi.org/10.5646/jksh.2013.19.2.55.

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Gavish, Benjamin. "Device-guided slow breathing as a nonpharmacological approach to antihypertensive treatment in type 2 diabetics." Journal of Hypertension 25, no. 8 (August 2007): 1742. http://dx.doi.org/10.1097/hjh.0b013e3282094181.

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Logtenberg, Susan JJ, Nanne Kleefstra, Sebastiaan T. Houweling, Klaas H. Groenier, and Henk JG Bilo. "Device-guided slow breathing as a nonpharmacological approach to antihypertensive treatment in type 2 diabetics." Journal of Hypertension 25, no. 8 (August 2007): 1742–43. http://dx.doi.org/10.1097/hjh.0b013e32820941a1.

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Dissertations / Theses on the topic "Device-guided slow breathing"

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Barros, Silvana de. "Efeito da respiração lenta na pressão arterial e na função autonômica em hipertensos." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-22092017-134829/.

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INTRODUÇÃO: A respiração lenta é indicada como tratamento não medicamentoso da hipertensão arterial. Porém, os mecanismos fisiológicos envolvidos na redução da pressão arterial (PA) ainda são desconhecidos. A redução na atividade nervosa simpática (ANS) pode ser um dos mecanismos envolvidos na redução da PA. OBJETIVOS: Avaliar o efeito crônico da respiração lenta na PA e na ANS em hipertensos. MÉTODOS: Foram randomizados hipertensos, com e sem uso de anti-hipertensivos, em grupo controle (GC), orientados a ouvir músicas serenas com uso de aparelho de MP3, ou grupo respiração lenta (GRL), treinados a reduzir a frequência respiratória com auxílio de um dispositivo eletrônico, tendo como alvo terapêutico uma frequência respiratória menor que 10 respirações por minuto, por um período de 15 minutos diários, durante 8 semanas. Antes e após o período de intervenção, foi realizada monitorização ambulatorial da pressão arterial (MAPA), dosagem de catecolaminas plasmáticas e medida da atividade nervosa simpática periférica (ANSP) pela técnica da microneurografia. RESULTADOS: Completaram o estudo 17 voluntários no GRL e 15 no GC. Não houve mudança na PA de consultório antes e após a intervenção nos dois grupos. Observou-se redução na pressão arterial sistólica (PAS) e diastólica (PAD) na vigília entre os períodos pré e pós-intervenção apenas no GC (131±10 / 92±9 vs 128±10 / 88±8 mmHg, p < 0,05). Não foi observada diferença na concentração de catecolaminas plasmáticas (pg/ml) em ambos os grupos entre os períodos pré e pós-intervenção: GRL 302 (220-256) vs 234 (156-318), p=0,35; e GC 201 (144-230) vs 221 (179-274), p=0,97. Nos voluntários que realizaram microneurografia, GRL (n=10) e GC (n=10), observou-se redução significativa da PAD de sono entre os períodos pré e pós- intervenção apenas no GC (83±6 vs 79±4 mmHg, p < 0,05) A ANSP (impulsos/minuto) medida pela microneurografia apresentou elevação no período pós-intervenção em comparação ao período pré-intervenção nos dois grupos: GRL (16±6 vs 22±8, p < 0,05) e GC (20±5 vs 23±5, p < 0,05). CONCLUSÕES: A respiração lenta, realizada por 15 minutos diários durante 8 semanas, não reduziu a pressão arterial, os níveis de catecolaminas plasmáticas e a atividade nervosa simpática periférica de hipertensos
INTRODUCTION: Slow breathing is indicated as nonpharmacological treatment of hypertension. However, the physiological mechanisms involved in blood pressure (BP) reduction are still unknown. The decrease in sympathetic nerve activity (SNA) may be one of the mechanisms involved in BP reduction. OBJECTIVES: To evaluate the chronic effect of slow breathing on BP and SNS in hypertensive patients. METHODS: Hypertensive patients, with or without use of antihypertensive drugs, were randomized to listen serene songs using an MP3 player (Control Group - CG) or device-guided slow breathing group (DGB), who were trained to reduce respiratory rate with assistance of an electronic device, targeting a respiratory rate of less than 10 breaths per minute, for a period of 15 minutes per day for 8 weeks. Before and after the intervention period, ambulatory blood pressure monitoring (ABPM), plasma catecholamines concentration and muscle sympathetic nerve activity (MSNA) using the microneurography technique were performed. RESULTS: 17 volunteers in the DGB and 15 in the CG completed the study. There was no change in office BP before and after intervention in both groups. There was a reduction in daytime systolic (SBP) and diastolic (DBP) before and after intervention only in the CG (131±10 / 92±9 vs 128±10 / 88±8 mmHg, p < 0,05). No difference in plasma catecholamines concentration (pg/ml) was observed in both groups before and after intervention: DGB 302 (220-256) vs 234 (156-318), p = 0.35; CG 201 (144-230) vs 221 (179-274), p=0.97. In the volunteers who underwent microneurography, DGB (n=10) and CG (n=10), there was a significant reduction in sleep DBP only in the CG: 83±6 vs 79±4 mmHg, p < 0,05. The MSNA (bursts/minute) measured by the microneurography showed a rise after the intervention in both groups: DGB (16±6 vs 22±8, p < 0.05) and CG (20±5 vs 23±5, p < 0.05). CONCLUSIONS: Slow breathing, performed for 15 minutes daily for 8 weeks, did not reduce blood pressure, plasma catecholamine concentration and muscle sympathetic nerve activity in hypertensive patients
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