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Heart rate variability (HRV) has shown potential as a tool for monitoring thermal strain, but there is limited data to support its efficacy in older adults during prolonged heat exposures. We compared HRV between young (19-31 years, n  = 20) and older (61-78 years, n  = 39) adults during 9 h of heat exposure (40 °C, 9% RH). We also explored whether heart rate (HR) and/or HRV could be used to distinguish older adults who achieved elevated thermal strain, defined as either (1) an increase in core temperature >1.0 °C (occurring in 39%, 15/39) or (2) a reduction in systolic blood pressure >10 mm Hg (occurring in 67%, 26/39). Percentage of age-predicted maximal HR and percentage of heart rate reserve (HRR) were higher, whereas standard deviation of normal RR intervals, the square root of the mean of squared differences between successive RR intervals (RMSSD), high frequency power (HF), and cardiac vagal index (CVI) were lower in older compared to young adults during heat exposure ( P  ≤ 0.004). In older adults, increases in core temperature were correlated with percentage of age-predicted maximal HR, percentage of HRR, RMSSD, and CVI ( P  ≤ 0.031), whereas changes in systolic blood pressure were not significantly associated with HR or HRV indices ( P  ≥ 0.327). Receiver operating characteristic curve analysis indicated that HR and HRV indices had generally poor ability to identify older adults with elevated thermal strain (area under the curve ≤0.65). Age-related differences in HRV, consistent with vagal withdrawal among older adults, remained during daylong heat exposure, but marked heterogeneity of response likely contributed to HRV providing limited discriminatory value in identifying changes in core temperature or blood pressure in older adults., Competing Interests: The authors declare there are no competing interests.

Background: The Threshold Limit Values (TLV) of the American Conference of Governmental and Industrial Hygienists indicate the levels of heat stress that all workers may be repeatedly exposed to without adverse health effects. In this study, we evaluated heart rate variability (HRV) during moderate-to-heavy work performed continuously or according to different TLV work-rest (WR) allocations in healthy physically active older workers., Methods: Nine healthy older (58 ± 5 years) males performed three different 120-minute conditions in accordance with TLV guidelines for moderate-to-heavy intensity work (360 W fixed rate of heat production) in different wet-bulb globe temperatures (WBGT): continuous cycling at 28°C WBGT (CON), as well as intermitted work performed at WR of 3:1 in 29°C WBGT (WR3:1), and at WR of 1:1 at 30°C (WR1:1). Rectal temperature and HRV (3-lead electrocardiogram [ECG]) were assessed throughout., Results: Coefficient of Variation, Poincaré SD2, and Shannon Entropy were decreased during the CON compared with the WR3:1 when core temperature exceeded 38°C and after 1 hour of continuous work (P < .05). Also, 4 of the 12 HRV indices studied were reduced at CON compared with WR1:1 after 2 hours of accumulated work time (P < .05). Participants worked longer before core temperature reached 38°C during the WR1:1 and the WR3:1, compared with CON (P < .05)., Conclusions: Incorporating breaks during moderate-to-heavy work in the heat for older adults can reduce autonomic stress and prolong the work performed at safe core temperature levels. The TLV WR1:1 provides increased cardiac protection for older workers, as compared with the CON and the WR3:1., (© 2020 Wiley Periodicals LLC.)

Susceptibility to heat illness during physically demanding work in hot environments is greater on the second of two consecutive workdays. While it has been demonstrated that heat storage is exacerbated on the second compared to first workday in older workers (50-65 yr), the effects on heart rate variability (HRV), an established surrogate of cardiac autonomic modulation, remain unclear. This study evaluated HRV in older workers on the day following prolonged work in the heat. Electrocardiogram was recorded in nine older (53-64 yr) males at rest, during three 30-min bouts of semi-recumbent cycling at fixed rates of metabolic heat production (150, 200, 250 W/m 2 ), each separated by 15-min recovery. Experiments were conducted in hot-dry conditions (40 °C, 20% relative humidity), immediately prior to (Day 1), and on the day following (Day 2), a prolonged work simulation (∼7.5 hr) involving moderate intensity intermittent exercise in hot-dry conditions (38 °C, 34% relative humidity). Core temperature, as well as time, frequency, and nonlinear HRV indices were derived for analysis during rest, the final 5-min of exercise at the highest heat production and recovery. The change in core temperature at the end of work (mean ±SD) was significantly greater on Day 2 (1.0 °C ±0.3) relative to Day 1 (0.8 °C ±0.2; p  < 0.01). Heart rate, however, did not significantly differ between days 1 and 2 at rest (Day 1, 59 ±11 bpm; Day 2, 62 ±13 bpm), during exercise (Day 1, 113 ±21 bpm; Day 2, 114 ±18 bpm ) and at the end of recovery (Day 1, 75 ±16 bpm; Day 2, 76 ±12 bpm). Likewise, there were no significant differences in any HRV indices derived from time, frequency, and nonlinear domains (all p  > 0.05). Prolonged work in the heat did not modulate next-day heart rhythms, as reflected by HRV, despite augmented core temperature. While HRV can reflect physiological aspects of cardiac autonomic stressors, these findings indicate it does not provide a means to identify exacerbated heat strain in older workers over consecutive work shifts in the heat.

Purpose: Sweat-induced fluid loss during prolonged exercise-heat stress can compromise cardiovascular and thermoregulatory function, although its effects on cardiac autonomic modulation remain unclear. We therefore examined heart rate variability (HRV) and recovery (HRRec), as surrogates of cardiac autonomic modulation, during and after prolonged exercise in the heat with and without fluid replacement., Methods: Eleven young and healthy men performed 90 min of semi-recumbent cycling in dry heat (40°C; 20% relative humidity) at a fixed rate of metabolic heat production (600 W; ~46% V˙O2peak) followed by 40-min resting recovery without fluid replacement (No-FR; ~3.4% reduction in body mass). On a separate day, participants completed the same protocol with fluid replacement (FR; 500-700 mL timed boluses) to offset sweat losses. Esophageal temperature and ECG were recorded throughout, with measurements analyzed over 10-min averaged epochs during baseline, each 30-min interval during exercise and 20-min interval during recovery., Results: Esophageal temperature and heart rate were elevated in No-FR relative to FR throughout exercise (all P ≤ 0.02). The HRV indices reflecting vagal influence of heart rate including the cardiac vagal index (CVI = log10[16 × SD1 × SD2]) and root-mean-square of successive differences were attenuated throughout exercise relative to baseline in both conditions (all P < 0.05), with the magnitude of the reduction greater in the No-FR condition (all P < 0.05). Further, sample entropy was reduced throughout all time points measured during exercise in the No-FR relative to FR condition (all P ≤ 0.03)., Conclusions: Our unique observations indicate that while prolonged exercise heat stress attenuates the vagal influence and complexity of cardiac rhythms, that reduction is further exacerbated by fluid loss, highlighting the importance of fluid replacement in such conditions.

New Findings: What is the central question of this study? Does a delay in cold water immersion treatment affect the cardiac autonomic control of exertionally heat-strained individuals? What is the main finding and its importance? Cold water immersion is effective for treating exertionally heat-strained individuals even when treatment is commenced with a significant delay. However, that treatment delay leads to only partial/transient restoration of cardiac autonomic control. Therefore, we recommend that exertional heatstroke patients are continuously monitored for several hours even after core temperature has returned to normal values., Abstract: Immediate cold water immersion (CWI) is the gold-standard treatment for exertional heatstroke. In the field, however, treatment is often delayed, primarily owing to a delayed paramedic response and/or inaccurate diagnosis. We examined the effect of treatment (reduction of rectal temperature to 37.5°C) delays of 5 (short), 20 (moderate) and 40 (prolonged) min on cardiac autonomic control [as assessed via heart rate variability (HRV)] in eight exertionally heat-strained (40.0°C rectal temperature) individuals. Eleven HRV indices were computed that have been described commonly in the literature and characterize almost all known domains of the variability and complexity of the cardiopulmonary system. We found that the cardiac autonomic control (as assessed via HRV) of exertionally heat-strained individuals was significantly affected by the amount of time it took for the CWI treatment to be applied. Six out of 11 HRV indices studied, from all variability domains, displayed strong (P ≤ 0.005) time × delay interaction effects. Moreover, the number of significantly (P ≤ 0.005) abnormal (i.e. different from the short delay) HRV indices more than doubled (seven versus 15) from the moderate delay to the prolonged delay. Finally, our results demonstrated that a CWI treatment applied with delays of 20 and, primarily, 40 min did not lead to a full restoration of cardiac autonomic control of exertionally heat-strained individuals. In conclusion, this study supports CWI for treating exertionally heat-strained individuals even when applied with prolonged delay, but it highlights the importance of continued cardiac monitoring of patients who have suffered exertional heatstroke for several hours after restoration of core temperature to normal., (© 2019 The Authors. Experimental Physiology © 2019 The Physiological Society.)

Background: Risk stratification of patients presenting to the emergency department (ED) with sepsis can be challenging. We derived and evaluated performance of a predictive model containing clinical, laboratory, and heart rate variability (HRV) measures to quantify risk of deterioration in this population., Methods: ED patients aged 21 and older satisfying the 1992 consensus conference criteria for sepsis and able to consent (directly or through a surrogate) were enrolled (n = 1,247). Patients had clinical, laboratory, and HRV data recorded within 1 h of ED presentation, and were followed to identify deterioration within 72 h., Results: Eight hundred thirty-two patients had complete data, of whom 68 (8%) reached at least one endpoint. Optimal predictive performance was derived from a combination of laboratory values and HRV metrics with an area under the receiver-operating curve (AUROC) of 0.80 (95% CI, 0.65-0.92). This combination of variables was superior to clinical (AUROC = 0.69, 95% CI, 0.54-0.83), laboratory (AUROC = 0.77, 95% CI, 0.63-0.90), and HRV measures (AUROC = 0.76, 95% CI, 0.61-0.90) alone. The HRV+LAB model identified a high-risk cohort of patients (14% of all patients) with a 4.3-fold (95% CI, 3.2-5.4) increased risk of deterioration (incidence of deterioration: 35%), as well as a low-risk group (61% of all patients) with 0.2-fold (95% CI 0.1-0.4) risk of deterioration (incidence of deterioration: 2%)., Conclusions: A model that combines HRV and laboratory values may help ED physicians evaluate risk of deterioration in patients with sepsis and merits validation and further evaluation.

The processing of ECG signal provides a wealth of information on cardiac function and overall cardiovascular health. While multi-lead ECG recordings are often necessary for a proper assessment of cardiac rhythms, they are not always available or practical, for example in fetal ECG applications. Moreover, a wide range of small non-obtrusive single-lead ECG ambulatory monitoring devices are now available, from which heart rate variability (HRV) and other health-related metrics are derived. Proper beat detection and classification of abnormal rhythms is important for reliable HRV assessment and can be challenging in single-lead ECG monitoring devices. In this manuscript, we modelled the heart rate signal as an adaptive non-harmonic model and used the newly developed synchrosqueezing transform (SST) to characterize ECG patterns. We show how the proposed model can be used to enhance heart beat detection and classification between normal and abnormal rhythms. In particular, using the Massachusetts Institute of Technology-Beth Israel Hospital (MIT-BIH) arrhythmia database and the Association for the Advancement of Medical Instrumentation (AAMI) beat classes, we trained and validated a support vector machine (SVM) classifier on a portion of the annotated beat database using the SST-derived instantaneous phase, the R-peak amplitudes and R-peak to R-peak interval durations, based on a single ECG lead. We obtained sentivities and positive predictive values comparable to other published algorithms using multiple leads and many more features.

We examined whether older individuals with and without Type 2 diabetes (T2D) experience differences in heart rate variability (HRV) during a 3-h exposure to high heat stress compared with young adults. Young (Young; n = 22; 23 ± 3 yr) and older individuals with (T2D; n = 11; 59 ± 9 yr) and without (Older; n = 25; 63 ± 5 yr) T2D were exposed to heat stress (44°C, 30% relative humidity) for 3 h. Fifty-five HRV measures were assessed for 15 min at baseline and at minutes 82.5-97.5 (Mid) and minutes 165-180 (End) during heat stress. When compared with Young, a similar number of HRV indices were significantly different (P < 0.05) in Older (Baseline: 35; Mid: 29; End: 32) and T2D (Baseline: 31; Mid: 30; End: 27). In contrast, the number of HRV indices significantly different (P < 0.05) between Older and T2D were far fewer (Baseline: 13, Mid: 1, End: 3). Within-group analyses demonstrated a greater change in the Young group's HRV during heat stress compared with Older and T2D; the number of significantly different (P < 0.05) HRV indices between baseline and End were 42, 29, and 20, for Young, Older, and T2D, respectively. Analysis of specific HRV domains suggest that the Young group experienced greater sympathetic activity during heat stress compared with Older and T2D. In conclusion, when compared with young, older individuals with and without T2D demonstrate low HRV at baseline and less change in HRV (including an attenuated sympathetic response) during 3 h high heat stress, potentially contributing to impaired thermoregulatory function., (Copyright © 2016 the American Physiological Society.)

Fetal inflammation is associated with increased risk for postnatal organ injuries. No means of early detection exist. We hypothesized that systemic fetal inflammation leads to distinct alterations of fetal heart rate variability (fHRV). We tested this hypothesis deploying a novel series of approaches from complex signals bioinformatics. In chronically instrumented near-term fetal sheep, we induced an inflammatory response with lipopolysaccharide (LPS) injected intravenously (n = 10) observing it over 54 hours; seven additional fetuses served as controls. Fifty-one fHRV measures were determined continuously every 5 minutes using Continuous Individualized Multi-organ Variability Analysis (CIMVA). CIMVA creates an fHRV measures matrix across five signal-analytical domains, thus describing complementary properties of fHRV. We implemented, validated and tested methodology to obtain a subset of CIMVA fHRV measures that matched best the temporal profile of the inflammatory cytokine IL-6. In the LPS group, IL-6 peaked at 3 hours. For the LPS, but not control group, a sharp increase in standardized difference in variability with respect to baseline levels was observed between 3 h and 6 h abating to baseline levels, thus tracking closely the IL-6 inflammatory profile. We derived fHRV inflammatory index (FII) consisting of 15 fHRV measures reflecting the fetal inflammatory response with prediction accuracy of 90%. Hierarchical clustering validated the selection of 14 out of 15 fHRV measures comprising FII. We developed methodology to identify a distinctive subset of fHRV measures that tracks inflammation over time. The broader potential of this bioinformatics approach is discussed to detect physiological responses encoded in HRV measures. [ABSTRACT FROM AUTHOR]