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.
Objective: To conduct a systematic review about the possible effects of passive heating protocols on cardiovascular autonomic control in healthy individuals. Approach: The studies were obtained from MEDLINE (PubMed), LILACS (BVS), EUROPE PMC (PMC) and SCOPUS databases, simultaneously. Studies were considered eligible if they employed passive heating protocols and investigated the cardiovascular autonomic control by spontaneous methods, such as heart rate variability (HRV), systolic blood pressure variability (SBPV) and baroreflex sensitivity (BRS), in healthy adults. The revised Cochrane risk-of-bias tool (RoB-2) was used to assess the risk of bias in each study. Main results: Twenty-seven studies were included in the qualitative synthesis. Whole-body heating protocols caused a reduction in cardiac vagal modulation in fourteen studies, and two studies reported both increased sympathetic modulation and vagal withdrawal. Contrariwise, local heating protocols and sauna bathing seem to increase cardiac vagal modulation. A reduction of BRS was reported in most of the studies that used whole-body heating protocols. However, heating effects on BRS remain controversial due to methodological differences among baroreflex analysis and heating protocols. Significance: Whole-body heat stress may increase sympathetic and reduce vagal modulation to the heart in healthy adults. On the other hand, local heating therapy and sauna bathing seem to increase cardiac vagal modulation, opposing sympathetic modulation. Nonetheless, further studies should investigate acute and chronic effects of thermal therapy on cardiovascular autonomic control.
last minute of handgrip under HOT through augmented HR, because stroke volume was unchanged. In conclusion, the main effect of HOT was to shift downwards BP and total peripheral resistance at rest and during isometric exercise in females. In males, the combination of handgrip and HOT increased cardiac output by augmented HR, whereas BP presented similar responses between thermal conditions during handgrip.
Third International Symposium on Intensive Care and Emergency Medicine for Latin America plays a critical role in the inflammatory response and, potentially, a polymorphism in IRAK1 may alter the immune response impacting clinical outcome. P2 Gene expression and intracellular NF-κ κB activation after HMGB1 and LPS stimuli in neutrophils from septic patients
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