Cerebral autoregulation (CA) refers to the control of cerebral tissue blood flow (CBF) in response to changes in perfusion pressure. Due to the challenges of measuring intracranial pressure, CA is often described as the relationship between mean arterial pressure (MAP) and CBF. Dynamic CA (dCA) can be assessed using multiple techniques, with transfer function analysis (TFA) being the most common. A 2016 white paper by members of an international Cerebrovascular Research Network (CARNet) that is focused on CA strove to improve TFA standardization by way of introducing data acquisition, analysis, and reporting guidelines. Since then, additional evidence has allowed for the improvement and refinement of the original recommendations, as well as for the inclusion of new guidelines to reflect recent advances in the field. This second edition of the white paper contains more robust, evidence-based recommendations, which have been expanded to address current streams of inquiry, including optimizing MAP variability, acquiring CBF estimates from alternative methods, estimating alternative dCA metrics, and incorporating dCA quantification into clinical trials. Implementation of these new and revised recommendations is important to improve the reliability and reproducibility of dCA studies, and to facilitate inter-institutional collaboration and the comparison of results between studies.

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IMT increases HRV, improves 6MWT distance and HRR.

The autonomic nervous system (ANS) and the immune system are deeply interrelated. The ANS regulates both innate and adaptive immunity through the sympathetic and parasympathetic branches, and an imbalance in this system can determine an altered inflammatory response as typically observed in chronic conditions such as systemic autoimmune diseases. Rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis all show a dysfunction of the ANS that is mutually related to the increase in inflammation and cardiovascular risk. Moreover, an interaction between ANS and the gut microbiota has direct effects on inflammation homeostasis. Recently vagal stimulation techniques have emerged as an unprecedented possibility to reduce ANS dysfunction, especially in chronic diseases characterized by pain and a decreased quality of life as well as in chronic inflammation.

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Although the literature demonstrates that cardiac autonomic control (CAC) might be impaired in patients with chronic pulmonary diseases, the interplay between CAC and disease severity in end-stage lung disease has not been studied yet. We investigated the effects of end-stage lung disease on CAC through the analysis of heart rate variability (HRV) among patients awaiting lung transplantation. Forty-nine patients on the waiting list for lung transplantation (LTx; 19 men, age 38 ± 15 years) and 49 healthy non-smoking controls (HC; 22 men, age 40 ± 16 years) were enrolled in a case–control study at Policlinico Hospital in Milan, Italy. LTx patients were divided into two groups, according to disease severity evaluated by the Lung Allocation Score (LAS). To assess CAC, electrocardiogram (ECG) and respiration were recorded at rest for 10 min in supine position and for 10 min during active standing. Spectral analysis identified low and high frequencies (LF, sympathetic, and HF, vagal). Symbolic analysis identified three patterns, i.e., 0V% (sympathetic) and 2UV% and 2LV% (vagal). Compared to HCs, LTx patients showed higher markers of sympathetic modulation and lower markers of vagal modulation. However, more severely affected LTx patients, compared to less severely affected ones, showed an autonomic profile characterized by loss of sympathetic modulation and predominant vagal modulation. This pattern can be due to a loss of sympathetic rhythmic oscillation and a subsequent prevalent respiratory modulation of heart rate in severely affected patients.

Objective. To investigate the interplay between active standing and heat stress on cardiovascular autonomic modulation in healthy individuals. Approach. Blood pressure (BP) and ECG were continuously recorded during 30 min in supine (SUP) and 6 min in orthostatic position (ORT) under thermal reference (TC; ∼24 °C) or heated environment (HOT; ∼36 °C) conditions, in a randomized order. All data collection was performed during the winter and spring seasons when typical outdoor temperatures are ∼23 °C. Spectral analysis was employed by the autoregressive model of R–R and systolic blood pressure (SBP) time series and defined, within each band, in low (LF, 0.04 to 0.15 Hz) and high (0.15–0.40 Hz) frequencies. The indices of cardiac sympathetic (LF) and cardiac parasympathetic (HF) were normalized (nu) dividing each band power by the total power subtracted the very-low component (<0.04 Hz), obtaining the cardiac autonomic balance (LF/HF) modulation. The gain of the relationship between SBP and R–R variabilities within the LF band was utilized for analysis of spontaneous baroreflex sensitivity (alpha index; αLF). Nonlinear analysis was employed through symbolic dynamics of R–R, which provided the percentage of sequences of three heart periods without changes in R–R interval (0V%; cardiac sympathetic modulation) and two significant variations (2UV% and 2LV%; cardiac vagal modulation). Main results. HOT increased 0V% and HR, and decreased αLF and 2UV% during SUP compared to TC. During ORT, HOT provokes a greater increment on HR, LF/HF and 0V%, indexes compared to ORT under TC. Significance. At rest, heat stress influences both autonomic branches, increasing sympathetic and decreasing vagal modulation and spontaneous baroreflex sensitivity. The augmented HR during active standing under heat stress seems to be mediated by a greater increment in cardiac sympathetic modulation, showing an interplay between gravitational and thermal stimulus.