本研究嘗試檢視原發性失眠 (Primary insomnia) 患者在接受完認知行為治療後，其生理激發系統與恆定系統相關生理指標的改變，並探討其主、客觀睡眠改善與生理指標變化之間的關聯，藉以瞭解不同的生理系統在影響原發性失眠患者其主、客觀睡眠改善程度上可能的重要性。本研究透過醫師轉介，共18名原發性失眠患者 (男5人，女13人，平均年齡37.4歲) 接受7週6次的失眠認知行為治療，在接受治療的前後，分別進行一個晚上的多頻道睡眠記錄檢查與主、客觀睡眠評估。再進一步分析高頻率腦波Beta波 (14~35Hz) ，用來反應其中樞神經系統的激發，低頻率腦波Delta波 (0.5~2.5Hz) 則用來反應個案的恆定系統；另外，透過心跳變異率分析得出的參數，包括低頻率 (Low frequency，簡稱LF) 功率與高頻率 (High frequency，簡稱HF) 功率，以LF/HF的比率值測量其交感神經系統的活動，而HF/ (LF+HF) 則是測量副交感神經系統的活動。研究結果顯示個案的失眠問題在主觀睡眠評估指標上有顯著改善，而客觀睡眠評估指標與睡眠結構於入睡時間與入睡後清醒時間有顯著降低，其餘則無顯著改善。而各項生理系統指標，僅後半夜階段二的腦波的Delta波有顯著上升，其餘均無顯著地改善，而LF/HF的下降與失眠嚴重度的下降有顯著地關聯。因此，本研究顯示原發性失眠患者接受認知行為治療前後，其交感神經系統的下降與失眠嚴重度之改善有明顯關聯，推論失眠認知行為治療對於原發性失眠患者的交感神經活動的改善，可能是使其失眠嚴重度改善的關鍵。 / The present study evaluated the changes in beta and delta ranges of electroencephalogram (EEG) power and heart rate variability (HRV) after cognitive behavioural therapy for insomnia (CBT-I) to understand the effect of CBT-I on arousal system and homeostatic system. The study also examined the correlations between change of sleep measurement and the physiological index to clarify underlying mechanisms of sleep improved by CBT-I. Eighteen primary insomnia patients (5 males, 13 female, mean age = 37.4) participated in this study. The participants were scheduled to come to the sleep laboratory for polysomnographic (PSG) recording twice, one prior to CBT-I and one following CBT-I. A course of 6-session CBT-I was conducted during a period of seven weeks. Subjects’ changes in subjective ratings of sleep quality and quantity and sleep parameters in PSG were calculated. Spectrum analyses were conducted for their EEG and electrocardiogram (EKG). Beta EEG activity (14~35 Hz) was used to indicate the central nervos system (CNS) arousal level and Delta EEG activity (0.5~2.5 Hz) for the intensity of homeostatic system. Low frequency power (LF) and high frequency power (HF) of the R-R interval were calculated for heart rate variability (HRV). LF/HF ratio was used as a index of sympathetic nervous system activity and the HF/ (LF+HF) ratio as a index of parasympathetic nervous system activity. The results show subjective sleep quality of subjects were significantly improved after CBT-I. PSG shows shortened sleep onset latency and decreased wake time after sleep onset, but not in the other measures. For EEG spectrum and HRV parameters, only Delta EEG activity in stage2 of the second half of the night was significantly improved. In addition, the decrease of LF/HF significantly correlated with the improvement of the insomnia severity index. Thus, the results suggests that sleep improvements by CBT-I may be associated with the reduction of sympathetic arousal.

Estudou-se o efeito do treinamento físico sobre a freqüência cardíaca (FC), a freqüência cardíaca intrínseca (FCI), o efeito vagal (EV), o tônus vagal (TV), o efeito simpático (ES) e o tônus simpático (TS), de ratos idosos em repouso volitivo, na esteira, e durante o exercício de intensidade progressiva (4 estágios de 5 min à 5; 7,5; 10 e 15 m.min-1). Verificaram-se, também, as respostas da FC à doses crescentes de agonistas ?-adrenérgico (isoproterenol) e muscarínico (metacolina). Utilizaram-se 20 ratos Wistar machos, aleatoriamente divididos em dois grupos: Treinado (T, 28+2 meses, 460+36 g), submetido a 10 semanas de treinamento físico de moderada intensidade; e Sedentário-controle (S, 28+2 meses, 461+43 g), apenas manipulado, três a cinco vezes por semana, durante nove semanas, e submetido a cinco minutos de exercício diário, na décima semana, para habituação ao pesquisador e ao ambiente experimental. Utilizaram-se duplos bloqueios farmacológicos (propranolol/atropina e atropina/propranolol) para determinação da FCI, bem como bloqueios farmacológicos autonômicos unilaterais que permitiram a medida do EV, do TV, do ES e do TS. Definições: EV = FC após atropina - FC controle, ES = FC controle - FC após propranolol, TV = FCI - FC após propranolol, TS = FC após atropina - FCI. Registros: batimento-a-batimento, 500Hz (AT/CODAS). Para comparação realizou-se análise de variância de dois caminhos para medidas repetidas, com contraste. Significância estatística, P<0,05. FC e FCI foram menores em T que S, em repouso e nos quatro estágios estudados: FC = 296+6, T vs. 325+16, S; 374+33, T vs. 420+29, S; 380+ 39, T vs. 423+29, S; 407+46, T vs. 434+25, S; 441+48, T vs. 455+30, S; e FCI = 288+28, T vs. 312+18, S; 302+27, T vs. 332+24, S; 301+30, T vs. 339+26, S; 308+30, T vs. 344+30, S; 316+31, T vs. 348+31, S. Não houve diferença na atividade vagal entre T e S, tanto considerando o EV, como o TV, em nenhuma das condições estudadas. A influência simpática para o coração se mostrou semelhante entre T e S, tanto se considerando o ES quanto o TS, em todas as condições estudadas. T e S responderam de forma semelhante aos agonistas muscarínico e adrenérgico. Tanto a FC, quanto a FCI aumentaram do repouso para o exercício, e com o aumento da intensidade do mesmo. A atividade vagal diminuiu do repouso para o exercício, mas apenas em intensidade elevada. A atividade simpática aumentou na passagem do repouso para o exercício, e com o aumento da intensidade do mesmo. Concluiu-se que, em ratos idosos: a) o treinamento físico de moderada intensidade promoveu bradicardia de repouso e atenuação da taquicardia induzida pelo exercício essencialmente à custa de redução da FCI; e b) independentemente da condição de treinamento físico, a estimulação simpática contribuiu para o aumento da FC, em resposta ao exercício, de leve à alta intensidade, enquanto a retirada vagal o fez, apenas em alta intensidade. / We studied the effect of exercise training on heart rate (HR), on intrinsic heart rate (IHR), on vagal effect (VE), on vagal tone (VT), on sympathetic effect (SE) and on sympathetic tone (ST) during both treadmill resting and exercise of progressive intensity (four 5-min stages at 5, 7.5, 10 and 15 m.min-1) in old rats. HR responses to crescent doses of ?-adrenergic (isoproterenol) and muscarinic (metacholine) agonists were also verified. We used 20 male Wistar rats randomly assigned to two groups: trained (T, 28+2 months, 460+36 g) and sedentary control (S, 28+2 months, 461+43 g) rats. T was submitted to a ten-week moderate intensity exercise training program, while S was just handled, three to five times a week, for nine weeks and submitted to five-min bouts of daily exercise during the tenth week for taming and to become accustomed to experimental environment. Double pharmacological blockades (propranolol/ methylatropine and methylatropine/propranolol) were performed in order to determine IHR. Autonomic influences on heart rate were evaluated using also unilateral autonomic pharmacological blockade, which allowed us to measure VE and VT as well as SE and ST. Definitions: VE = HR after atropine - control HR, SE = control HR - HR after propranolol, VT = IHR - HR after propranolol, ST = HR after atropine - IHR. HR was recorded on a beat-to-beat basis with a 500 Hz acquisition frequency (AT/CODAS). For statistical analysis we used two-way ANOVA for repeated measurements with contrast, considering a P<0.05 as statistically significant. T rats had lower HR as well as IHR than their sedentary counterparts both at rest and during all progressive exercise stages: HR = 296+6,T vs. 325+16,S; 374+33,T vs. 420+29,S; 380+39,T vs. 423+29,S; 407+46,T vs. 434+25,S; 441+48,T vs. 455+30,S, respectively; and IHR = 288+28,T vs. 312+18,S; 302+27,T vs. 332+24,S; 301+30,T vs. 339+26,S; 308+30,T vs. 344+30,S; 316+31,T vs. 348+31,S, respectively. Vagal activity was not significantly different between groups, either considering VE or VT. Sympathetic influence was also similar between S and T considering both SE and ST in all of the studied conditions. T and S responded similarly to both muscarinic and ?-adrenergic agonists. Both HR and IHR increased from rest to exercise and with increasing exercise intensity. Vagal activity decreased from rest to exercise but only in high intensity exercise. Sympathetic activity increased from rest to exercise and also with increasing exercise intensity. We concluded that in old rats: a) exercise training of moderate intensity led to resting bradycardia and attenuation of exercise tachycardia essentially due to the decrease in IHR; and b) independently from exercise training status, sympathetic stimulation contributed to HR increase from light to high intensity exercise while vagal withdrawal became important only at high intensity exercise

Estudou-se o efeito do treinamento físico sobre a freqüência cardíaca (FC), a freqüência cardíaca intrínseca (FCI), o efeito vagal (EV), o tônus vagal (TV), o efeito simpático (ES) e o tônus simpático (TS), de ratos idosos em repouso volitivo, na esteira, e durante o exercício de intensidade progressiva (4 estágios de 5 min à 5; 7,5; 10 e 15 m.min-1). Verificaram-se, também, as respostas da FC à doses crescentes de agonistas ?-adrenérgico (isoproterenol) e muscarínico (metacolina). Utilizaram-se 20 ratos Wistar machos, aleatoriamente divididos em dois grupos: Treinado (T, 28+2 meses, 460+36 g), submetido a 10 semanas de treinamento físico de moderada intensidade; e Sedentário-controle (S, 28+2 meses, 461+43 g), apenas manipulado, três a cinco vezes por semana, durante nove semanas, e submetido a cinco minutos de exercício diário, na décima semana, para habituação ao pesquisador e ao ambiente experimental. Utilizaram-se duplos bloqueios farmacológicos (propranolol/atropina e atropina/propranolol) para determinação da FCI, bem como bloqueios farmacológicos autonômicos unilaterais que permitiram a medida do EV, do TV, do ES e do TS. Definições: EV = FC após atropina - FC controle, ES = FC controle - FC após propranolol, TV = FCI - FC após propranolol, TS = FC após atropina - FCI. Registros: batimento-a-batimento, 500Hz (AT/CODAS). Para comparação realizou-se análise de variância de dois caminhos para medidas repetidas, com contraste. Significância estatística, P<0,05. FC e FCI foram menores em T que S, em repouso e nos quatro estágios estudados: FC = 296+6, T vs. 325+16, S; 374+33, T vs. 420+29, S; 380+ 39, T vs. 423+29, S; 407+46, T vs. 434+25, S; 441+48, T vs. 455+30, S; e FCI = 288+28, T vs. 312+18, S; 302+27, T vs. 332+24, S; 301+30, T vs. 339+26, S; 308+30, T vs. 344+30, S; 316+31, T vs. 348+31, S. Não houve diferença na atividade vagal entre T e S, tanto considerando o EV, como o TV, em nenhuma das condições estudadas. A influência simpática para o coração se mostrou semelhante entre T e S, tanto se considerando o ES quanto o TS, em todas as condições estudadas. T e S responderam de forma semelhante aos agonistas muscarínico e adrenérgico. Tanto a FC, quanto a FCI aumentaram do repouso para o exercício, e com o aumento da intensidade do mesmo. A atividade vagal diminuiu do repouso para o exercício, mas apenas em intensidade elevada. A atividade simpática aumentou na passagem do repouso para o exercício, e com o aumento da intensidade do mesmo. Concluiu-se que, em ratos idosos: a) o treinamento físico de moderada intensidade promoveu bradicardia de repouso e atenuação da taquicardia induzida pelo exercício essencialmente à custa de redução da FCI; e b) independentemente da condição de treinamento físico, a estimulação simpática contribuiu para o aumento da FC, em resposta ao exercício, de leve à alta intensidade, enquanto a retirada vagal o fez, apenas em alta intensidade. / We studied the effect of exercise training on heart rate (HR), on intrinsic heart rate (IHR), on vagal effect (VE), on vagal tone (VT), on sympathetic effect (SE) and on sympathetic tone (ST) during both treadmill resting and exercise of progressive intensity (four 5-min stages at 5, 7.5, 10 and 15 m.min-1) in old rats. HR responses to crescent doses of ?-adrenergic (isoproterenol) and muscarinic (metacholine) agonists were also verified. We used 20 male Wistar rats randomly assigned to two groups: trained (T, 28+2 months, 460+36 g) and sedentary control (S, 28+2 months, 461+43 g) rats. T was submitted to a ten-week moderate intensity exercise training program, while S was just handled, three to five times a week, for nine weeks and submitted to five-min bouts of daily exercise during the tenth week for taming and to become accustomed to experimental environment. Double pharmacological blockades (propranolol/ methylatropine and methylatropine/propranolol) were performed in order to determine IHR. Autonomic influences on heart rate were evaluated using also unilateral autonomic pharmacological blockade, which allowed us to measure VE and VT as well as SE and ST. Definitions: VE = HR after atropine - control HR, SE = control HR - HR after propranolol, VT = IHR - HR after propranolol, ST = HR after atropine - IHR. HR was recorded on a beat-to-beat basis with a 500 Hz acquisition frequency (AT/CODAS). For statistical analysis we used two-way ANOVA for repeated measurements with contrast, considering a P<0.05 as statistically significant. T rats had lower HR as well as IHR than their sedentary counterparts both at rest and during all progressive exercise stages: HR = 296+6,T vs. 325+16,S; 374+33,T vs. 420+29,S; 380+39,T vs. 423+29,S; 407+46,T vs. 434+25,S; 441+48,T vs. 455+30,S, respectively; and IHR = 288+28,T vs. 312+18,S; 302+27,T vs. 332+24,S; 301+30,T vs. 339+26,S; 308+30,T vs. 344+30,S; 316+31,T vs. 348+31,S, respectively. Vagal activity was not significantly different between groups, either considering VE or VT. Sympathetic influence was also similar between S and T considering both SE and ST in all of the studied conditions. T and S responded similarly to both muscarinic and ?-adrenergic agonists. Both HR and IHR increased from rest to exercise and with increasing exercise intensity. Vagal activity decreased from rest to exercise but only in high intensity exercise. Sympathetic activity increased from rest to exercise and also with increasing exercise intensity. We concluded that in old rats: a) exercise training of moderate intensity led to resting bradycardia and attenuation of exercise tachycardia essentially due to the decrease in IHR; and b) independently from exercise training status, sympathetic stimulation contributed to HR increase from light to high intensity exercise while vagal withdrawal became important only at high intensity exercise

<p>Izvod: UVOD: Metabolički zdrave gojazne osobe su okarakterisane odsustvom metaboličkog sindroma i/ili insulinske rezistencije i sistemske inflamacije. Mali je broj podataka o ulozi aktivnosti autonomnog nervnog sistema u razvoju kardiometaboličkih komplikacija kod gojaznih osoba, kao i o njegovoj vezi sa specifičnom distribucijom masnog tkiva. CILJ: Analiza varijabilnost srčane frekvencije (HRV) kod metabolički zdravih (MHO) i gojaznih osoba sa metaboličkim rizikom (MUO), analiza povezanosti HRV sa metaboličkim faktorima i distribucijom masnog tkiva, kao i analiza uzrasne dinamike HRV kod gojaznih osoba različitih kardiometaboličkih profila. MATERIJAL I METODE: Ukupno 125 gojaznih ispitanika oba pola podvrgnuto je antropometrijskim merenjima u cilju procene mase i distribucije masnog tkiva, izvr&scaron;ena je analiza telesne kompozicije, uzeti su uzorci krvi u cilju određivanja lipidskog i lipoproteinskog statusa, stanja glikoregulacije i nivoa inflamatornih markera, meren je krvni pritisak i procenjena je HRV tokom petominutne digitalne elektrokardiografije. Podaci su statistički obrađeni kori&scaron;ćenjem paketa SPSS 11.5. REZULTATI: HRV mere se nisu razlikovale statistički značajno među MHO i MUO mu&scaron;karcima. MHO žene su imale vi&scaron;e vrednosti RRNN, SDNN, RMSSD, pNN50, LF, HF i TP u odnosu na MUO žene, na čega metabolički profil utiče sa 6,6-11,2%(p˂0,01), predstavljeno kroz parcijalnu deljenu varijansu. Nakon antropometrijskih faktora uzetih u obzir, perzistirale su vi&scaron;e vrednosti HF kod MHO žena. Razlika u RRNN, pNN50 i TP između MHO i MUO premenopauzalnih žena (vi&scaron;e vrednosti za MHO, p˂0,05) se izgubila nakon kontrole za krvni pritisak. Insulinemija je uticala na pojave razlika u RRNN između MHO i MUO premenopauzalnih žena, parcijalna deljena varijansa 7,6%. SAD kod žena se negativno povezivao sa LF/HF i LFnorm, a pozitivno sa HFnorm, parcijalne deljene varijanse 8,4-11,9% (p˂0,05). Prednji nabor podlaktice kod žena se pozitivno povezivao sa LF i LF/HF, a negativno sa HFnorm (p˂0,01). Visceralna masna masa je predviđala značajno HRV mere mu&scaron;karaca, parcijalna deljena varijansa 13-34% (p˂0,01). U okviru gornjeg tercila HRV mera RMSSD, pNN50 i LF MUO osoba, HOMA indeks je statistički značajno niži (p˂0,05). Kod MUO osoba SDNN, RMSSD, lnpNN50, lnLF, lnHF i TP značajno su se smanjivali u uzrastu od 19-29 do 40-49 godina. Kod MHO osoba primetna je uzrasna promena HF mere u četvrtoj deceniji života. ZAKLJUČAK: MHO osobe ženskog pola imaju značajno vi&scaron;e vrednosti markera varijabilnosti srčane frekvencije u odnosu na MUO. Razlike u HRV merama su uslovljene kriterijumima metaboličke podele, predominantno insulinemijom, vrednostima krvnog pritiska i centralnom masnom masom. Kod žena centralna distribucija masnog tkiva korelira sa smanjenom srčanom simpatičkom aktivno&scaron;ću dok se periferna distribucija masnog tkiva povezuje obrnuto sa komponentama aktivnosti autonomnog nervnog sistema. Kod mu&scaron;karaca centralna masna masa, ali ne i periferna, je značajno povezana sa HRV. MUO osobe sa nižom HRV imaju veći stepen insulinske rezistencije, dok HRV ne utiče na insulinsku senzitivnost MHO osoba. Značajniji uzrasno zavisni pad HRV mera primetan je kod MUO osoba, pogađajući obe komponente autonomnog nervnog sistema za razliku od MHO osoba.</p> / <p>Abstract: INTRODUCTION: Metabolically healthy obese (MHO) individuals are characterized by absence of metabolic syndrome and/or insulin resistance and inflammation. Little is known about the role of autonomic nervous system in development of cardiometabolic complications in obese people and about its influence on the specific adipose tissue distribution. AIM: Analysis of the hearth rate variability (HRV) in metabolically healthy (MHO) and unhealthy (MUO) obese people, its connection with adipose tissue distribution, and age dependent dynamics of HRV. MATERIAL AND METHODS: A total of 125 obese patients of both sexes underwent anthropometric measurements in order to assess adipose tissue mass and distribution, body composition was assessed, blood samples were taken in order to analyze parameters of lipid and lipoprotein profile, condition of glycoregulation and inflammatory markers, blood pressure was measured and short term HRV was conducted. Data were statisticaly analyzed using SPSS 11.5. RESULTS: HRV measures did not differ significantly between MHO and MUO men. MHO women had higher values of RRNN, SDNN, RMSSD, pNN50, LF, HF and TP compared to the MUO women, influence of metabolic profile was 6,6-11,2% (p˂0,01), presented through partial shared variance. After controlling for anthropometric factors higher HF persisted in MHO women. Differences in RRNN, pNN50 and TP between MHO and MUO premenopausal women (higher values of MHO, p˂0,05) were lost after controlling for blood pressure. Insulinemia influenced the difference in RRNN between MHO and MUO premenopausal women, partial shared variance 7,6%. SAD in women was connected negatively with the LF/HF and LFnorm, and positively with HFnorm, partial shared variance 8,4-11,9% (p˂0,05). Anterior forearm skinfold in women correlated positively with LF and LF/HF, and negatively with HFnorm (p˂0,01). Visceral fat mass predicted significantly HRV in men, partial shared variance 13-34% (p˂0,01). Within the upper tertile of HRV measures RMSSD, pNN50 and LF in MUO people, HOMA was significantly lower (p˂0,05). In MUO SDNN, RMSSD, lnpNN50, lnLF,lnHF and TP significantly decreased in the period from 19-29 to 40-49 years. In MHO people the change in HF was noticeable in the fourth decade of life. CONCLUSION: MHO women have significantly higher levels of HRV markers comparing to the MUO. The differences in HRV measures are influenced by metabolic criteria used, predominantly by insulinemia, blood pressure and central fat mass. In women, central distribution of adipose tissue correlates with reduced cardiac sympathetic activity, while the connection of peripheral fat mass distribution with components of autonomic nervuos system activity is reverse. In men, central fat mass, but not peripheral, is significantly associated with HRV. MUO people with lower HRV have a higher degree of insulin resistance, while the level of HRV measures does not affect insulin sensitivity in MHO individuals. Significant age-dependent decrease in both ANS representatives of HRV measures was noticed in MUO people, unlike MHO individuals.</p>