Joanna Słomko

Whole-body cryostimulation increases parasympathetic outflow and decreases core body temperature

The cardiovascular, autonomic and thermal response to whole-body cryostimulation exposure are not completely known. Thus the aim of this study was to evaluate objectively and noninvasively autonomic and thermal reactions observed after short exposure to very low temperatures. We examined 25 healthy men with mean age 30.1 ± 3.7 years and comparable anthropomorphical characteristic. Each subject was exposed to cryotherapeutic temperatures in a cryogenic chamber for 3 min (approx. -120 °C). The cardiovascular and autonomic parameters were measured noninvasively with Task Force Monitor. The changes in core body temperature were determined with the Vital Sense telemetric measurement system. Results show that 3 min to cryotherapeutic temperatures causes significant changes in autonomic balance which are induced by peripheral and central blood volume changes. Cryostimulation also induced changes in core body temperature, maximum drop of core temperature was observed 50-60 min after the stimulation. Autonomic and thermal reactions to cryostimulation were observed up to 6 h after the exposure and were not harmful for examined subjects.

Cardiovascular and Thermal Response to Dry-Sauna Exposure in Healthy Subjects

Dry-sauna is a strong thermal stimulus and is commonly used all over the world. The aim of this experiment was to comprehensively analyse cardiovascular and autonomic changes that result from an increase in core body temperature during sauna bath. The study included 9 healthy men with mean age 26.7 ± 3.0 years and comparable anthropomorphical characteristics. Each subject was exposed to one 15-minute session of dry-sauna treatment at 100°C and 30–40% humidity. The autonomic and baseline cardiovascular (i.e., hemodynamic and contractility) parameters were measured noninvasively with Task Force Monitor. Cardiovascular autonomic functions were assessed using baroreceptor reflex sensitivity (BRS) and spectral analysis of heart rate (HRV) and blood pressure (BPV) variability. Measurements were performed four times, at the following stages “before sauna,” “after sauna,” “sauna

Hemodynamic, Autonomic, and Vascular Function Changes after Sleep Deprivation for 24, 28, and 32 Hours in Healthy Men

This study aimed to analyze the impact of sleep deprivation (SD) on cardiac, hemodynamic, and endothelial parameters and to determine whether these are sustained with increased periods of SD. The study included 60 healthy men (mean: age 31.2±6.3 years; body mass index 24.6±2.6 kg/m2). Hemodynamic parameters, parameters of myocardial contractility, spectral analysis of heart rate (HR) and blood pressure (BP) variability, and the sensitivity of arterial baroreflex function were evaluated. Biochemical tests were performed to assess L-arginine (L-Arg) and asymmetric dimethylarginine (ADMA) levels in reflection of endothelial nitric oxide synthase ability. Measurements of cardiovascular system parameters were obtained at 9 a.m. (baseline) on the first day of the study and 9 a.m. (24-h SD), 1 p.m. (28-h SD), and 5 p.m. (32-h SD) on the second day. Blood samples for evaluating biochemical parameters were obtained at baseline and after 24-h SD. ANOVA Friedmans test revealed a significant effect for time in relation to HR (χ2=26.04, df=5, p=0.000), systolic BP (χ2=35.98, df=5, p=0.000), diastolic BP (χ2=18.01, df=5, p=0.003), and mean BP (χ2=28.32, df=5, p=0.000). L-Arg and ADMA levels changed from 78.2±12.9 and 0.3±0.1 at baseline to 68.8±10.2 and 0.4±0.1 after 24-hr SD, respectively (p=0.001, p=0.004). SD in healthy men is associated with increases in BP, which appear to occur after 24 hours of SD and are maintained over increasing periods of SD. The observed hemodynamic changes may have resulted due to disordered vascular endothelial function, as reflected in alterations in L-Arg and ADMA levels.

Do Changes in Hemodynamic Parameters Depend Upon Length of Sleep Deprivation? Comparison Between Subjects With Normal Blood Pressure, Prehypertension, and Hypertension

The main objective of the study was to analyze the impact of sleep deprivation upon hemodynamic and autonomic parameters in subjects with normal blood pressure (BP) compared to prehypertension and hypertension at 24, 28, and 32 h of total sleep deprivation (TSD). Thirty volunteers, healthy men with current medical tests indicating the absence of disease took part in the study. After physical examination (basic neurological, clinical examination, echocardiography and doppler ultrasound of the renal arteries, evaluation of the autonomic nervous system) subjects were divided into three groups: I – normotensive, II – pre-hypertensive, III – hypertensive (age: 31.2 ± 2.1 vs. 33.5 ± 2.7 vs. 36.8 ± 2.7 years, p > 0.05; BMI: 25.2 ± 0.8 vs. 29.0 ± 1.5 vs. 26.4 ± 1.0 kg/m2, p > 0.05). Hemodynamic and autonomic parameters were automatically measured at rest and in a tilted position with a Task Force Monitor. The Task Force Monitor consists of electrocardiography, impedance cardiography, oscillometric, and continuous BP measurement. Mixed models with random effects was applied in order to analyze the parameters’ dependence on the time and the group of patients. One-way ANOVA or Kruskal–Wallis test were used to detect differences between normotensive, pre-hypertensive and hypertensive groups in each time point. In the pre-hypertensive group 28-h TSD resulted in increased vagal outflow [changes in high frequency heart rate (HR) variability, p = 0.0189], as evidenced by decreased HR (p = 0.0293). Moreover after 24-h TSD and 28-h TSD we observed changes in BP parameters. In hypertensive group, the most important changes in hemodynamic parameters: systolic blood pressure (sBP, p = 0.0031), diastolic blood pressure (dBP, p = 0.0136), cardiac output (CO, p = 0.0439) and changes in HR (p = 0.0063) after tilt test were observed after 32-h TSD. In conclusion, our results show that changes in hemodynamic parameters during sleep deprivation depend on the baseline BP and duration of TSD. What is important, both groups reported a decrease of sBP and dBP during the TSD (pre-hypertensive group after 24, 28-h TSD; hypertensive group after 32-h TSD. In our opinion, this is the first study which considers three homogenous groups in terms of gender: only men, during different points of acute TSD: 24, 28, and 32 h of TSD in laboratory condition.

Acute Biochemical, Cardiovascular, and Autonomic Response to Hyperbaric (4 atm) Exposure in Healthy Subjects

The aim of this study was to explore the effect of a hyperbaric environment alone on the cardiovascular system by ensuring elimination of factors that may mask the effect on hyperbaria. The research was performed in a hyperbaric chamber to eliminate the effect of physical activity and the temperature of the aquatic environment. Biochemical analysis and examination with the Task Force Monitor device were performed before and immediately after exposure. TFM was used for noninvasive examination of the cardiovascular system and the functional evaluation of the autonomic nervous system. Natriuretic peptides were measured as biochemical markers which were involved in the regulation of haemodynamic circulation vasoconstriction (urotensin II). L-arginine acted as a precursor of the level of the nitric oxide whereas angiotensin II and angiotensin (1–7) were involved in cardiac remodeling. The study group is comprised of 18 volunteers who were professional divers of similar age and experience. The results shown in our biochemical studies do not exceed reference ranges but a statistically significant increase indicates the hyperbaric environment is not without impact upon the human body. A decrease in HR, an increase in mBP, dBP, and TPR, and increase in parasympathetic heart nerves activity suggest an increase in heart afterload with a decrease in heart activity within almost one hour after hyperbaric exposure. Results confirm that exposure to a hyperbaric environment has significant impact on the cardiovascular system. This is confirmed both by changes in peptides associated with poorer cardiovascular outcomes, where a significant increase in the studied parameters was observed, and by noninvasive examination.

Cardiac and autonomic function in patients with Crohn’s disease during remission

PURPOSE The aim of the study was to assess cardiac and autonomic function in patients with Crohns disease and explore their relation to disease duration using cardiovascular reflex tests. MATERIALS AND METHODS Cardiovascular parameters, baroreflex sensitivity, spectral-indices of short-term heart rate variability and blood pressure variability were compared between patients with Crohns disease in remission (n = 30) and a control group (n = 29). Cardiac autonomic function was assessed during response to standing (tilt) and deep breathing test (expiration/inspiration ratio-E/I). Aortic pulse wave velocity, aortic augmentation index and central systolic blood pressure were measured oscillometrically. RESULTS At rest, Crohns disease patients had significantly higher systolic (p = 0.03) and diastolic (p = 0.03) blood pressure, total peripheral resistance index (p = 0.003), sympathetic-parasympathetic ratio (p = 0.033) and lower baroreceptor effectiveness (p = 0.047), myocardial variables (stroke index; p = 0.03, cardiac index; p = 0.025, Heather index; p = 0.039, left ventricular ejection time; p = 0.038), as compared to controls. Orthostatic response to the tilt test in the Crohns disease group and the control group was similar, no intergroup differences were observed for E/I ratio and autonomic parameters. In Crohns disease patients, disease duration was negatively associated with baroreflex sensitivity and positively correlated with normalised high frequency heart rate variability, sympathetic-parasympathetic ratio at rest and post-tilt changes in Δsystolic blood pressure, p < 0.05. The control group had significantly lower central systolic blood pressure (p = 0.043) compared to Crohns disease patients. CONCLUSIONS Crohns disease patients in remission have preserved cardiac and autonomic function in response to cardiovascular reflex tests with a shift in cardiovascular autonomic regulation towards sympathetic predominate in the rest position.

Effects of Hyperbaric Exposure on the Cardiovascular System. Role of the Autonomous Nervous System

Abstract Introduction Among experienced divers, dive adaptation is seen as a modified pattern of physiological changes. This is reflected, inter alia, in the change in cardiovascular responses, therefore there is need to examine the role of the autonomic nervous system in cardiovascular response modulation after hyperbaric exposure. Material and methods Ten experienced divers took part in the study. The effects of hyperbaric exposure at 30 and 60 meters and interaction (depth x time) were measured. Changes in HR, RRI, CI and HRV values have been taken into analysis. Results Hyperbaric exposure at 30 meters significantly affected HFnu-RRI elevation and decrease of LFnu-RRI (F = 42.92, p <0.00001), without significant affecting the HR, RRI and CI. Exposure to hyperbaric 60 m increased HR and CI (F = 7.64, p = 0.01 and F = 4.89, p = 0.04 respectively) and RRI (F = 7.69, p = 0.01), without significant impact on other variables. The influence of interaction (depth x time) was significant in all measured variables. Conclusions The results indicate that hyperbaric exposure at 60 meters affected HR, RRI, CI parameters, that were not significantly affected by hyperbaric exposure at 30 meters. On the other hand, the exposure at 30 meters showed a significant effect on the LFnu and HFnu HRV, which were not significantly affected by the exposure at 60 meters. Significant effect of time and depth interaction in each of the analyzed variables was observed.

The Effects of Hyperbaric Exposure on Immediate and Delayed Changes in Core Temperature and Its Circadian Fluctuations

Abstract Changes observed in the core body temperature of divers are the result of a multifaceted response from the body to the change of the external environment. In response to repeated activities, there may be a chronic, physiological adaptation of the body’s response system. This is observed in the physiology of experienced divers while diving. The purpose of this study is to determine the immediate and delayed effects of hyperbaric exposure on core temperature, as well as its circadian changes in a group of three experienced divers. During compression at 30 and 60 meters, deep body temperature values tended to increase. Subsequently, deep body temperature values showed a tendency to decrease during decompression. All differences in core temperature values obtained by the group of divers at individual time points in this study were not statistically significant.

Long-term high intensity sport practice modulates adaptative changes in athletes heart and in the autonomic nervous system profile.

BACKGROUND The purpose of this study was to compare cardiovascular and autonomic adaptation changes in athletes exposed to high intensity and uninterrupted training for extended periods of time. METHODS We assessed hemodynamic profile and cardiac function in 22 international master-level athletes free of cardiovascular disease who experienced particularly intensive and uninterrupted training over an 8- to 21-year-period. RESULTS One-way ANOVA revealed that in athletes, extreme and uninterrupted strength and endurance training over long periods of time (up to 21 years) causes an increase in resting heart rate (50.3±7.1 vs. 63.0±10.7, P=0.0429), diastolic (65.8±5.2 vs. 75.2±5.7, P=0.0222) and mean blood pressure (85.4±6.0 vs. 95.6±6.4, P=0.0166). On multiple regression, increasing training experience was related to decrease in RRI (R2=0.18, P=0.0481) and increase in dBP (R2=0.32, P=0.0064) and mBP (R2=0.31, P=0.0075) although the effect was small. A negative correlation was observed between the training age and the parameters describing parasympathetic function: HF-RRI (R=-0.54, P=0.0321), HF-dBP (R=-0.52, P=0.0401) and PSD-RRI (R=-0.51, P=0.0414). CONCLUSIONS Long-term sport practice at a world class level causes an increase in resting heart rate, diastolic and mean blood pressure, and decrease of the parasympathetic dominance and this may result from decreasing adjustment to large training loads.

Role of peripheral vascular resistance as an indicator of cardiovascular abnormalities in patients with Parkinson's disease

The aim of this study was to evaluate cardiovascular autonomic modulation in response to an orthostatic stress in healthy subjects and Parkinsons disease (PD). The study included 47 controls and 56 PD patients divided into groups (vasoconstrictor PD, vasodilator PD, control) according to vasodilation/vasoconstriction response during 70° head up tilt test. Using impedance cardiography (ICG) and electrocardiography (ECG) we measured stroke volume, cardiac output, left ventricular work index, left ventricular ejection time, acceleration index, index of contractility, Heather index, thoracic fluid content, total peripheral resistance, total arterial compliance. We also analyzed heart rate variability (HRV), using spectral analysis and continuous blood pressure (contBP). At rest, the vasodilator PD group showed significantly higher values of total peripheral resistance and lower values of stroke volume and cardiac output, compared to the vasoconstrictor PD and the control groups. A post‐tilt drop in ∆ (change rest – tilt) systolic blood pressure, ∆mean blood pressure, ∆total peripheral resistance and ∆Heather index, and a significantly lower increase in ∆diastolic blood pressure was observed in subjects from the vasodilator PD group compared to the vasoconstrictor PD and the control groups. No statistically significant differences were observed for HRV parameters between the vasoconstrictor and vasodilator PD groups, P > .05. Longer duration and higher disease stage of PD correlated with a reduction in post‐tilt systolic blood pressure changes in vasodilator group. Positive inotropy of the cardiac muscle represents a significant factor preventing orthostatic hypotension in PD subjects with a concurrent drop in peripheral vascular resistance during orthostatic stress.