The autonomic nervous system controls the smooth muscles of the internal organs, the cardiovascular system and the secretory function of the glands and plays a major role in the processes of adaptation. Heart rate variability is a non-invasive and easily applicable method for the assessment of its activity. The following review describes the origin, parameters and characteristics of this method and its potential for evaluation of the changes of the autonomic nervous system activity in different physiological and pathological conditions such as exogenous hypoxia, physical exercise and sleep. The application of heart rate variability in daily clinical practice would be beneficial for the diagnostics, the outcome prognosis and the assessment of the effect of treatment in various diseases.

1. The impact of ventilatory efficiency on reduced exercise capacity and recovery oxygen kinetics has not been addressed in cirrhotic patients. The aim of the present study was to investigate exercise performance and ventilatory efficiency in patients with mild and moderate liver cirrhosis (LC). 2. Nineteen male non-hypoxic patients with LC (age 51.3 +/- 9.1 years; body mass index (BMI) 25.6 +/- 3.6 kg/m(2)) classified by the Child-Pugh score as class A (n = 7) and class B (n = 12) and 19 age- and BMI-matched controls participated in the study. Subjects undertook maximal incremental exercise testing on a treadmill using the Bruce protocol. 3. Patients with LC showed a reduced diffusion capacity (D(L,CO)%) compared with controls (74.6 +/- 15.2 vs 95.6 +/- 12.9%, respectively; P < 0.001), but a comparable volume standardized diffusion coefficient (1.33 +/- 0.22 vs 1.45 +/- 0.18 mmol/min per kPa per L, respectively; P = 0.74). Patients with LC had a significantly lower exercise capacity compared with controls (VO(2 max) 23.8 +/- 3.8 vs 30.6 +/- 4.4 mL/min per kg, respectively; P < 0.001). Recovery oxygen kinetics were also impaired in LC patients compared with controls (104.6 +/- 19.3 vs 84.4 +/- 22.7 s, respectively; P = 0.012). The chronotropic index was significantly lower in the LC group compared with controls (0.67 +/- 0.19 vs 0.82 +/- 0.17, respectively; P = 0.030) and LC patients showed higher ventilatory equivalents (30.4 +/- 3.8 vs 26.3 +/- 2.3, respectively; P < 0.001) and lower oxygen uptake efficiency slope values (2187 +/- 445 vs 2745 +/- 473 mL/min per log(10)L, respectively; P < 0.001) compared with controls, which is indicative of decreased ventilatory efficiency. Patients with LC also had a higher standardized maximal exercise perception score (SMEPS) compared with controls (0.62 +/- 0.18 vs 0.46 +/- 0.15, respectively; P = 0.011). Moderate negative correlations were found between Child-Pugh score and VO(2 max)% (r = -0.496; P = 0.031). 4. In conclusion, patients with mild and moderate LC have reduced exercise capacity, which correlates with Child-Pugh score, as well as reduced chronotropic index and prolonged recovery oxygen uptake kinetics. The results suggest worsened ventilatory efficiency during exercise and cardiopulmonary reasons for the higher SMEPS in these patients.

Characterized by periodic crescendo-decrescendo pattern of breathing alternating with central apneas, Central sleep apnea (CSA) with Cheyne-Stokes Breathing represents a highly prevalent, yet underdiagnosed comorbidity in chronic heart failure (CHF). A diverse body of evidence demonstrates increased morbidity and mortality in the presence of CSB. CSB has been described in both CHF patients with preserved and reduced ejection fraction, regardless of drug treatment. Risk factors for CSB are older age, male gender, high BMI, atrial fibrillation and hypocapnia.The pathophysiology of CSB has been explained by the loop gain theory, where a controller (the respiratory center) and a plant (the lungs) are operating in a reciprocal relationship (negative feedback) to regulate a key parameter (partial pressure of carbon dioxide (pCO)). The temporal interaction between these elements is dependent on the circulatory delay. Increased chemosensitivity/chemoresponsiveness of the respiratory center and/or augmented ascending non- CO stimuli from the C-fibers in the lungs (interstitial pulmonary edema), overly efficient ventilation when breathing at low volumes and prolonged circulation time are involved. An alternative hypothesis of CSB being an adaptive response of the failing heart has its merits as well. The clinical manifestation of CSB is usually poor, lacking striking symptoms and complaints. Witnessed apneas and snoring are infrequently reported by the sleep partner. Sometimes patients may report poor sleep quality with frequent awakenings, paroxysmal nocturnal dyspnea and frequent urination at night. Standard instrumental and laboratory studies, performed in CHF patients, may present clues to the presence of CSB. Concentric remodeling of the left ventricle and dilated left atrium (echocardiography), high BNP and C-reactive protein levels, increased ventilation-carbon dioxide output (VEVCO) and lower end-tidal CO (cardiopulmonary exercise testing), reduced diffusion capacity (pulmonary function testing) and hypocapnia (blood-gas analysis) may indicate the presence of CSB.CSB and cardiovascular disease are probably linked through bidirectional causality. Cyclic variations in heart rate, blood pressure, respiratory volume, partial pressure of arterial oxygen (pO) and pCO lead to sympathetic-adrenal activation. The latter worsens ventricular energetism and survival of cardiomyocytes and exerts antiarhythmogenic effects. It causes cardiac remodeling, potentiating the progression and the lethal outcome in CHF patients. Several treatment modalities have been proposed in CSB. The most commonly used are continuous positive airway pressure (CPAP), adaptive servoventilation (ASV) and nocturnal home oxygen therapy (HOT). Novel therapies like nocturnal supplemental CO and phrenic nerve stimulation are being tested recently. The current treatment recommendations (by the American Academy of Sleep Medicine) are for CPAP and HOT as standard therapies, while ASV is an option only in patients with EF > 45%. BPAP (bilevel device) remains an ...

The correlation between fatigue and cognitive performance in multiple sclerosis (MS) is well reported, but the intimate mechanisms of the fatigue impact on cognition are not fully defined yet. The aim of this study is to investigate blood oxygen level–dependent (BOLD) activations in relapsing remitting MS (RRMS) patients with and without cognitive dysfunction and the impact of fatigue on cortical activations. Forty-two patients with RRMS were enrolled in the study. Cognitive functioning was assessed by the Symbol Digit Modalities Test (SDMT) and Paced Serial Addition Test (PASAT). A cutoff point of a total score of 55 on the SDMT was used to divide the patients into two groups: cognitively impaired (CI), SDMT score equal to or below 55 points, and cognitively preserved (CP), SMDT score above 55 points. Fatigue was assessed by the Modified Fatigue Impact Scale (MFIS). Participants were assessed with the Beck Depression Inventory (BDI) prior to inclusion in order to exclude major depressive episode. Functional Magnetic Resonance Imaging (fMRI) scanning was performed on a 3T MRI. The PVSAT (Paced Visual Serial Addition Test) paradigm was applied as a cognitive task. All functional data were analyzed with SPM12 and statistical analysis with SPSS 19.0. No statistically significant differences between CI and CP patients were found (p=0.953, p=0.322) in the MFIS and BDI score. Performance on the PASAT in CI patients was 34.07±13.721, for CP patients 46.42±11.453, and the SDMT performance in the CI patient group was 42.40±9.179, in the CP group 57.83±2.552. Between-group analysis revealed increased activations in left Brodmann area (BA) 40 in CP patients with several clusters located in the left supramarginal gyrus. Regression analysis showed increased BOLD signal in left BA 40, right BA 40, and left BA 6, associated with a higher score on MFIS. Stronger BOLD signal in left BA 31 was associated with a lower score on MFIS. Significance level was set to p<0.05, FWE (family-wise error) corrected. The differences in BOLD activations suggest the presence of cortical reorganization in our CP patients. The impact of fatigue on cortical activation during a cognitive task is demonstrated by inconformity of activated areas depending on the MFIS score. Our results suggest that activation in BA 40 may represent a mechanism for diminishing fatigue impact on cognitive functioning in CP patients.

Zjistit dynamiku autonomního nervového systému (ANS) pomocí variability srdeční frekvence (heart rate variability, HRV) během akutní expozice normobarické hypoxii a po ní, k níž dochází během jednoho sezení podle protokolu intermitentního hypoxického tréninku. Materiál a metody: Čtyřiadvacet zdravých mužů ve věku 28,0 ± 7,2 (průměr ± SD) vdechovalo po dobu jedné hodiny hypoxický vzduch (inspirační koncentrace kyslíku [FiO 2 ] 12,3 ± 1,5 %) z hypoxického generátoru (Al-tiPro 8850 Summit+, Altitude Tech, Kanada). Před expozicí hypoxii, během ní a po ní se provádělo vyšetření pulsní oxymetrií a měřila se variabilita HRV. Výsledky: Na konci hypoxického sezení vykazovali všichni hodnocení jedinci vyšší nízkou frekvenci (lnLF) (6,9 ± 1,1 ms² vs. 7,5 ± 1,1 ms²; p = 0,042), LF/HF (1,5 ± 0,8 vs. 3,3 ± 2,8; p = 0,007) a směrodatnou odchylku 2 na Poincarého mapě (SD2) (92,8 ± 140,0 ms vs. 120,2 ± 54,2 ms; p = 0,005) i nárůst celkové síly (7,7 ± 1,1 ms² vs. 8,1 ± 1,2 ms²; p = 0,032) a směrodatné odchylky intervalu mezi dvěma normálními tepy (SDNN) (57,3 ± 31,0 ms vs. 72,3 ± 41,1 ms; p = 0,024), avšak nižší entropii vzorku (SampEn) (1,6 ± 0,2 vs. 1,4 ± 0,2; p = 0,010). Bezprostředně po expozici hypoxii se snížila hodnota LF/HF (3,3 ± 2,8 vs. 2,2 ± 1,8; p = 0,001) při současném významném zvýšení lnHF (6,6 ± 1,4 ms² vs. 7,1 ± 1,3 ms²; p = 0,020). Závěr: Akutní normobarická hypoxie jako součást jednoho sezení v rámci tréninkového protokolu intermitentní hypoxie vede ke změnám aktivity ANS. Během expozice hypoxii převažuje tonus sympatiku a okamžitě po zrušení účinku hypoxií indukovaného faktoru dochází k nárůstu tonu parasympatiku.