Abstract

Emerging evidence suggests beneficial effects of sauna bathing on the cardiovascular system. However, the effects of sauna bathing on parameters of cardiovascular function and blood-based biomarkers are uncertain. We aimed to investigate whether sauna bathing induces changes in arterial stiffness, blood pressure (BP), and several blood-based biomarkers. We conducted an experimental study including 102 participants (mean age (SD): 51.9 (9.2) years, 56% male) who had at least one cardiovascular risk factor. Participants were exposed to a single sauna session (duration: 30 min; temperature: 73 °C; humidity: 10–20%). Cardiovascular as well as blood-based parameters were collected before, immediately after, and after 30-min recovery. Mean carotid–femoral pulse wave velocity was 9.8 (2.4) m/s before sauna and decreased to 8.6 (1.6) m/s immediately after sauna (p < 0.0001). Mean systolic BP decreased after sauna exposure from 137 (16) to 130 (14) mmHg (p < 0.0001) and diastolic BP from 82 (10) to 75 (9) mmHg (p < 0.0001). Systolic BP after 30 min recovery remained lower compared to pre-sauna levels. There were significant changes in hematological variables during sauna bathing. Plasma creatinine levels increased slightly from sauna until recovery period, whereas sodium and potassium levels remained constant. This study demonstrates that sauna bathing for 30 min has beneficial effects on arterial stiffness, BP, and some blood-based biomarkers. These findings may provide new insights underlying the emerging associations between sauna bathing and reduced risk of cardiovascular outcomes.

Introduction

Sauna bathing, a form of passive heat therapy, is commonly used for relaxation and pleasure purposes [1, 2]. Repeated sauna therapy has been shown to increase left ventricular ejection fraction and reduce plasma levels of norepinephrine and brain natriuretic peptide and increase the 6-min walk distance [3]. After 1 week of repeated sauna exposure (twice a day) in 10 healthy male volunteers, diastolic blood pressure (DBP) was shown to decrease substantially [4]. Warm water immersion, which is also a form of passive heat therapy, is associated with health benefits that include improved endothelial and microvascular function as well as reduced arterial stiffness (AS) and BP [5, 6]. Passive heat therapy (hot tub) improves cutaneous microvascular function by enhancing nitric oxide-dependent dilation in sedentary humans [5]. It has been demonstrated that sauna exposure results elevations in core temperature and changes in cardiovascular hemodynamics, such as cardiac output and vascular shear stress, which are similar to the effects of exercise, and thus may provide an alternative means of improving health [6]. In a 2-week trial of once-a-day infrared-sauna exposure for patients with cardiovascular risk factors, flow-mediated endothelium-dependent dilation was significantly improved [7].

However, there is still lack of evidence showing the positive effects of typical Finnish sauna bathing on cardiovascular function, which might potentially reduce cardiovascular disease (CVD) risk. Sauna exposure may improve vascular compliance, which has previously been demonstrated in subjects with cardiovascular risk factors, indicating a protective role of heat therapy on arterial stiffening [7]. However, although sauna bathing is well tolerated, there is evidence that sauna use might induce myocardial ischemia in patients with coronary artery disease [8]. Consistent with the positive effects of passive heat therapy, there is some evidence showing that BP may be decreased as a result of increased ambient temperature [9,10,11]. Using a long-term general population-based prospective study, our group has recently shown that frequent Finnish sauna exposure has multiple beneficial effects, which include reduced risk of hypertension, dementia, fatal cardiovascular outcomes, and all-cause mortality [12,13,14].

Sauna bathing leads to certain changes in the cardiovascular system such as vasodilation of circulatory system, blood re-distribution, and increase in sweating in an attempt to maintain body homeostasis due to heat stress. The acute physiological responses to the hot temperatures during sauna bathing induce fluid loss with an increase in heart rate [15, 16]. Some previous studies have shown an association between passive heat therapy and augmented cardiovascular function, with positive adaptations in arterial compliance and peripheral microvascular function [5,17,18,19,20].

The aim of this study was to investigate acute hemodynamic and physiological vascular responses and their respective recovery profiles 30 min after sauna bathing. This study setting will further clarify whether sauna bathing leads to beneficial effects on cardiovascular function, including changes in BP and AS as well as blood biomarkers among participants with cardiovascular risk factors. The main focus of this study is to evaluate the most immediate physiological and cardiovascular effects of a single Finnish sauna exposure in a large sample of both men and women in an experimental setting to confirm its protective effects on cardiovascular health and safety.

Materials and methods

Participants

Participants (n = 102) were recruited from the city of Jyväskylä, Central Finland region, through the local out-of-hospital healthcare center. The final study group consisted of asymptomatic participants (no cardiovascular symptoms) with at least one conventional risk factor, such as a history of smoking, hypertension, dyslipidemia, obesity, or family history of CHD. Hypertension was defined as SBP > 140 mmHg, DBP > 90 mmHg, or use of antihypertensive therapy. Dyslipidemia was defined as the use of cholesterol drugs or serum low-density lipoprotein (LDL) cholesterol over 3.5 mmol/L and obesity as body mass index (BMI) over 30 kg/m2. Family history of CHD was positive if father (< 55 years) or mother (< 65 years) had premature CHD.

Participants with diagnosed CVD were not included in the study. Prior to the participation of the study, all participants were informed about the research purposes and measurement procedures, and were screened by a cardiac specialist. The research protocol and study design were reviewed and approved by the institutional review board of the Central Finland Hospital District ethical committee, Jyväskylä, Finland (Dnro 5U/2016). All study participants provided written informed consent.


Clinical examination

A clinical evaluation with baseline data collection was conducted on a separate screening day prior to the experiment. During the screening visit, medical history, physical examination, and resting electrocardiogram (ECG) were assessed. All baseline and sauna exposure measurements were performed from May to June 2016. Resting BP was measured on the screening day as well as on the day of sauna exposure, using the same standard operating protocol; it was recorded as the mean of two measurements obtained while the participant was in supine with a standardized measurement protocol. BMI was calculated by dividing measured weight in kilograms by the square of height in meters. Assessment of baseline characteristics and diseases was based on a self-reported questionnaire [21], which was checked by a cardiologist during the screening visit. The regular use of medication was assessed by a detailed questionnaire. All questionnaires have been previously validated in a Finnish population-based cohort study [22, 23].


Assessment of self-reported physical activity and sauna bathing habits

Physical activity was assessed using the baseline questionnaire and was classified as endurance training, resistance training, or any leisure-time physical activity. Assessment of duration and frequency of physical activity was based on a self-reported questionnaire [23]. Previous regular sauna bathing habits were assessed by the questionnaires and collected data was based on frequency (weekly sauna sessions), duration of sauna exposure, and temperature in the sauna room. The questionnaires were checked at the time of baseline data collection.


Sauna exposure

Sauna exposure was based on a traditional Finnish sauna, which is characterized by air with a relative humidity of 10–20% and high temperature [12]. The total duration of a sauna session was 30 min, and it was interspersed at 15 min with a short, 2-min warm shower. There were separate sauna rooms for women and men; the sauna rooms were similar in the terms of space, humidity, temperature, and air conditioning. The sauna temperature was controlled and monitored by internal temperature sensors designed by Harvia Oy, Finland. The temperature was measured continuously by using a two-channel thermometer in the sauna room and the respective data were collected during experiment. Data obtained via the temperature-tracking device showed that the mean temperature was 73 (SD 2) °C with a relative humidity of 10–20%.

Participants were supervised by a physician and were allowed to leave the sauna at any time they felt uncomfortable. All participants underwent the recommended sauna protocol successfully. To make up for fluid loss due to increased sweating, participants were given 500 ml of room temperature still water for drinking during the entire sauna session, including the recovery period after sauna. Immediately after sauna exposure, participants were instructed to rest in a designated relaxing waiting lounge (mean temperature 21 °C) for 30 min recovery. Body temperature was measured for each participant by the tympanic method.


Exercise testing

A maximal exercise test was conducted on a cycle ergometer utilizing a graded exercise test protocol with ECG to assess the level of aerobic exercise capacity. The exercise test with continuous ECG (CardioSoft software V.1.84, GE Healthcare, Freiburg, Germany) recordings was performed at baseline between using an electrically braked cycle ergometer (Monark Exercise AB, Sweden). The symptom-limited exercise test was started with 3 min warm-up without workload for each participant and continued with 20 Watts (W) increments applied every 1 min until volitional exhaustion. Exercise capacity was expressed in metabolic equivalents (METs) and maximal exercise workload (W). All exercise tests were supervised by an experienced physician with the assistance of a trained nurse and were not performed on the same day of sauna session.


Arterial stiffness

The measurement of AS followed established guidelines [24, 25], with written and verbal instructions given to all participants informing them to avoid meals, caffeine and smoking within 3 h of the measurement. All measurements were taken on the right side of the body in the supine position in a quiet room with a stable temperature (21 °C). All AS-related measurements before, after, and at 30 min recovery from sauna were taken by a single trained tonometer operator and the same transit distances measured during baseline clinical evaluation were used throughout the experiment for consistency and reliability. Supine brachial systolic and DBPs were obtained using Microlife BP A200 (Microlife Corp., Taipei, Taiwan) [26]. Two sequential readings were measured and the mean values were used. Pulse pressure was calculated as the difference between SBP and DBP. Participants rested in the supine position for 10 min before AS was measured at baseline, and due to the nature of the study on acute effects of sauna, AS was measured immediately after and after 30 min of recovery from sauna following BP measurements. Heart rate was recorded with the assessment of AS.

Pulse wave velocity (PWV) data were collected by the software at a sample rate of 1000 Hz (PulsePen, DiaTecne s.r.l., Milan, Italy). PWV was defined as the distance between the measuring sites divided by the time delay between the distal pulse wave from the proximal pulse wave, using the ECG trace as reference [27]. The software is able to define augmentation index in relation to the level and early rise time of the reflected wave with other indexes of AS. Augmentation index is a parameter that provides an indication of the contribution of reflected waves to the total pulse pressure and was defined as the difference between the second and the first systolic peak on arterial pulse waveform and was expressed as a percentage of central pulse pressure. Arterial tonometry with simultaneous ECG was obtained from carotid and femoral arteries with the use of a commercially available tonometer that has been well validated previously [25, 27, 28]. Transit distances were assessed by body surface measurements using a tape measure from the suprasternal notch to each pulse recording site (carotid and femoral). Direct carotid to femoral measurement was adjusted to 80% (common carotid artery − common femoral artery × 0.8) for the calculation of PWV as recommended by current guidelines [25]. Left ventricular ejection time (LVET), diastolic time (DT), and augmentation index were obtained from the carotid pressure waveform analysis. This measurement relies on the R–R interval on an ECG. The point corresponding to the end of LVET and the beginning of DT is identified by the dicrotic notch in the carotid pulse waveform. This point is automatically estimated by the PulsePen software [29].


Laboratory analyses

Venous blood samples for the determination of plasma total cholesterol, high-density lipoprotein (HDL), LDL, Apolipoprotein A1 (Apo A1), Apolipoprotein B (Apo B), triglycerides (TG), and plasma glucose concentrations were collected by a qualified laboratory technician from the antecubital vein, into serum and plasma tubes (BD Vacutainer, Plymouth, UK). Participants were instructed to abstain from strenuous physical activity 24 h before the blood samples were taken. Whole blood samples were stored for 10 min before being centrifuged at 3500 r.p.m. (Megafuge, Heraeus, Germany), and serum and plasma samples stored at −80 °C until analysis using a spectrophotometry analyzer (Konelab 20XTi, Thermo Fisher Scientific, Vantaa, Finland). Basic hematological parameters (hemoglobin concentration, leucocyte, and thrombocyte count) were analyzed on site by Sysmex KX 21 (Sysmex Co., Kobe, Japan) analyzer. Venous blood samples for the determination of plasma biomarkers were analyzed using chemiluminescent immunoassay by Siemens Immulite 2000 XPi analyzer (Siemens Healthcare Diagnostics Products Ltd., Llanberies, UK). Serum sodium and potassium were measured using Gem Premier 3000 (IL laboratories, Barcelona, Spain) and were assessed before and after sauna.


Statistical analyses

Data are presented as means ± SDs or median (interquartile range, IQR) for continuous variables based on their distribution and as proportions for categorical variables. Normality was checked using the Shapiro–Wilk test as well as through observing the Q–Q plots. Absolute values (means) of physiological, AS, and laboratory variables before and after sauna were firstly analyzed for any within-group (time) changes with an analysis of variance (ANOVA) test. Normally distributed and log-transformed non-normally distributed data were further analyzed for within-group changes with a paired t-test to compare immediately after sauna values and post 30 min sauna values to pre-sauna values. Supplementary analyses were performed to analyze respective relative changes in physiological, cardiovascular, and laboratory variables. The level for significance was set at p < 0.05. All statistical analyses were carried out with Stata version 14.1 (Stata Corp, College Station, TX, USA).

Results

Characteristics of population

Overall, there were 56 male and 46 female participants; their characteristics are shown in Table 1. The mean age was 51.9 (SD 9.2) years and BMI of overall participants was 27.2 (IQR: 24.5–30.7 kg/m2). The proportion of current smokers was 14.4% and the mean resting SBP and DBP were 136 (16) and 84 (10) mm Hg, respectively. Biochemical parameters were slightly different between males and females and are reported in Table 1.

Table 1 Baseline characteristics

Underlying clinical conditions or cardiovascular risk factors of participants included hypertension (14.3%), dyslipidemia (63.0%), type 1 diabetes (2.0%), type 2 diabetes (1.0%), respiratory diseases (5.1%), thyroid disease (3.1%), skin disease (4.0%), and rheumatoid arthritis (1.0%). Family history of CHD was a common risk factor (34.0%) in this study population (Table 1).

Cardiorespiratory fitness level as assessed by median exercise capacity was 8.8 METs (7.8–10.4), being 9.7 (8.5–10.9) and 8.3 (6.7–9.3) in male and female participants, respectively. Most of participants achieved age-adjusted target maximal heart rate level during exercise test. The highest mean SBP during exercise test was 213 (24) mm Hg for men and 196 (24) mm Hg for women, while exercise-induced ST-segment changes of over 1 mm, indicating that minor ischemic changes were not common (6.5%). Detailed exercise testing results are shown in Table 1.

Participants bathed in their own sauna from one to four times per week based on the baseline questionnaires (Table 1). Most participants preferred to use sauna three times per week (43.9%), whereas 16.3% of participants used sauna one or two times per week, respectively. A sauna session lasted between 20 and 40 min for most participants (56.7%) and the average self-reported temperature was 72 °C.

Reported frequency of total leisure-time physical activity was distributed as follows: the proportion of those with one physical activity session per week was 25.8%, one to three sessions was 32.3%, three to five sessions was 30.6%, and more than five sessions was 9.7%. The distributions of duration of total physical activity in groups of < 20, 20–39, 40–60, and > 60 min per session are reported in Table 1.

Sauna and body temperature, heart rate, and BP

There were statistically significant effects of sauna heat exposure on body temperature, heart rate, and BP values. The directions of change in parameters evaluated were similar in both genders (Table 2 and Fig. 1). Body temperature, heart rate, and BP changed immediately after sauna and at 30 min recovery from sauna bathing. Mean body temperature was 36.4 °C before sauna, 38.4 °C immediately after sauna, and 36.6 °C at the end of recovery period (Table 2 and Fig. 1). Participants had no any abnormal cardiovascular symptoms after 30 min sauna bathing session. SBP was 137 (16) mmHg before sauna, 130 (14) mmHg immediately after sauna, and 130 (14) mmHg after 30 min recovery. The corresponding values for DBP were 82 (10), 75 (9), and 81 (9) mmHg (Table 2). The respective heart rate values at the time of BP and AS measurements were 64 (59–70), 79 (70–90), and 65 (59–71) beats per minute.

Table 2 Physiological parameters and blood pressure before and after sauna
Fig. 1
Fig. 1

Physiological, cardiovascular, and laboratory parameters before and after sauna. (Color figure online)

The mean relative changes in SBP and DBP were −4.3% (p < 0.0001) and −8.7% (p < 0.0001), respectively, comparing post-sauna to pre-sauna BP. BP remained lower until the end of recovery period compared to pre-sauna BP. The respective relative changes from pre-sauna to post-sauna values are presented in Supplementary Table 1. Supplementary Fig. 1 shows relative changes in temperature, heart rate, and BP.

Sauna and AS

Table 3 and Fig. 1 show changes in AS parameters after sauna. Mean carotid–femoral PWV before sauna was 9.8 (2.4) m/s and decreased to 8.6 (1.6) m/s immediately after sauna, being 9.0 (1.7) m/s after 30 min recovery period. Values for augmentation index were 9.6 (15.8) pre-sauna, 4.1 (15.7) immediately after sauna, and 7.5 (15.6) 30 min after sauna. LVET and DT were lower immediately after sauna (Table 3). From pre-sauna to immediate post-sauna assessment time points, LVET decreased from 306.7 (26.2) to 275.1 (31.8) ms and DT from 633.2 (116.0) to 493.3 (113.8) ms. The relative changes in PWV, LVET, and DT post-sauna were significant as shown in Supplementary Table 2. All indices of AS including PWV, augmentation index, LVET, and DT changed in the same direction for both genders after sauna exposure, and relative changes of AS parameters were statistically significant in the study group immediately after sauna (Supplementary Table 2 and Supplementary Fig. 1).

Table 3 Arterial stiffness parameters before and after sauna bathing

Sauna and laboratory parameters

There were significant changes in hemoglobin level, leucocyte and thrombocyte count during sauna exposure as presented in Table 4 and Fig. 1. Hemoglobin levels increased from pre-sauna level of 141 (11) to 144 (13) g/l immediately after sauna. Blood leucocytes count increased from 6.2 (1.6) to 6.8 (1.6) × 109/l and the leucocyte count was at the highest level immediately after sauna and thrombocyte levels were significantly higher immediately after sauna compared with pre-sauna values (Table 4, Supplementary Table 3). Although changes in hemoglobin, leucocyte, and thrombocyte over-time were statistically significant, hemoglobin and thrombocyte levels returned to the pre-sauna level after 30 min recovery.

Table 4 Laboratory parameters before and after sauna bathing

Changes in plasma creatinine, sodium, and potassium are presented in Table 4 and Fig. 1. Mean plasma creatinine levels increased from 76 to 79 µmol/L (p < 0.0001). Minimal changes were observed for sodium and potassium levels from pre-sauna levels until 30 min recovery, and the respective percentage changes are presented in Supplementary Table 3. Hematological and biochemical parameters are also shown as relative changes in Supplementary Fig. 1.

Discussion

This study was conducted to demonstrate effects of a single sauna bathing session on cardiovascular function in participants with at least one conventional cardiovascular risk factor. The main objective of the study was to measure the acute effects of sauna bathing on systemic BP and AS as well as common laboratory parameters, immediately before and after heat exposure and at 30-min recovery phase. BP levels and AS were modulated positively because of sauna exposure, while the sauna bathing-induced reduction in BP remained constant when comparing baseline values to recovery phase data. Hemoglobin levels, leucocyte, and thrombocyte counts increased significantly because of sauna exposure; with the exception of leucocyte, they all returned to pre-sauna levels after recovery time. The increase in creatinine levels was sustained at the time of recovery, whereas the changes in levels of sodium and potassium as a result of sauna exposure were very minimal. On the basis of measured basic laboratory values, it seems that 30-min sauna exposure is safe in terms of electrolyte (sodium/potassium) balance, and it was also well tolerated. Rise of hemoglobin concentration could be attributed to sauna-induced fluid loss, although 500 ml water was available to cover increased sweating.

This study showed that sauna bathing leads to significant decrease in BP, which is a clinically important finding among participants with cardiovascular risk factors. As sauna bathing produces acute vasodilation, which causes a significant drop in BP, it can be postulated that regular sauna bathing could potentially result in longer-term reduction of BP [16]. Systolic BP remained lower compared to pre-sauna levels during the whole 30-min recovery period. It is suggested that a short sauna session may reduce BP in patients with hypertension [3, 9, 30]. In patients with slightly elevated BP, sauna therapy produced positive effects on systemic BP, including 24-h BP levels [3, 9]. Increased sweating during sauna bathing is accompanied by reduction in BP and a higher heart rate, while cardiac stroke volume is largely maintained, although a part of blood volume is diverted from the internal organs to body peripheral parts with decreasing venous return, which is not facilitated by active skeletal muscle work. Indeed, comparable with exercise-induced adaptations, repetitive heat stress could improve endothelial function and AS and may lower resting BP in sedentary humans [6, 31]. Because of the increased skin blood flow under heat stress conditions, cutaneous microvascular function is improved by passive repeated heat therapy [5].

Our study suggested that hot sauna bathing leads to changes in cardiovascular function, which include beneficial effects on AS with decrease in BP. We found for the first time that PWV was decreased significantly after sauna bathing. Consistently, LVET and DT decreased because of sauna exposure. Enhanced AS is a possible protective link between heat exposure and postive changes in vascular function. All indicators of cardiovascular compliance were improved after a single session of sauna bathing. We have also shown that heat exposure of sauna has positive effects on arterial compliance, providing a possible protective pathway against arterial stiffening, which is a progressive pathology of the arterial wall [5, 6, 17]. Although resting BP levels are correlated with AS, studies have shown that AS is an additional indicator of both compliance of arteries and an independent marker of predicting CVD outcomes [32]. These beneficial effects of sauna bathing on indices of cardiovascular function may underpin the long-term protective effects of sauna bathing on cardiovascular and mortality risk, as recently demonstrated [12]. The proposed positive effects on vascular function in the current study were based on traditional hot and dry Finnish sauna bathing, which is not comparable to saunas operating at lower temperatures and heated water immersion [5, 6, 30].

We also assessed changes in hematological indices and their profile; hemoglobin levels were observed to be increased after sauna, which may be an indicator of increased hemoconcentration. This is consistent with findings showing that hemoglobin levels were significantly increased after sauna [4, 33]. Our study also showed that leucocytes and thrombocytes increased slightly after sauna bathing and electrolyte levels remained stable. The levels of plasma creatinine tended to increase slightly because of sauna bathing, although the changes were within normal range and unlikely to lead to long-lasting changes in kidney function. There are no previous comparable studies showing changes in basic laboratory parameters after sauna bathing.

Participants’ body temperature increased from the mean level of 36.4 °C until 38.4 °C immediately after sauna; however, all participants underwent sauna session successfully. Body temperature tended to decrease during the recovery period at an average room temperature back to individual pre-sauna levels. In general, a temperature for a typical Finnish sauna is usually adjusted around 80 °C. In this study, the temperature of sauna was stabilized and controlled for every participant, and measured at 10 s intervals during the sauna sessions. Body weight increased significantly during sauna session, which might be due to water consumption. In this study, participants were each allowed to drink 500 ml still water during the sauna session and recovery period (total amount 500 ml). All consumed water was accurately controlled. The wet swimming suits after the sauna sessions could also explain the increased body weight.

The current study presents the acute effects of 30-min sauna exposure on body physiology and cardiovascular function in a large study sample. Our study employed a large number of participants, which provided adequate pre-defined power to assess meaningful clinical changes in indices evaluated. The assessment of cardiovascular parameters such as BP and AS was performed using standard measurement protocols. Currently, PWV is considered the most reliable non-invasive measurement of AS. Conditions in the sauna including the duration of use simulated a typical dry and hot Finnish sauna session, and there were no any adverse events during the sauna. Study participants were allowed to drink water during sauna and recovery period according to the guidance of the local ethical committee. Limitations included the before and after exposure design with the short-term nature of the intervention without serial repeated post-sauna measurements during the recovery period and lack of a control group. However, the study setting is novel in this research context focusing on most immediate effects of sauna bathing on cardiovascular function and biological variables. Our previous epidemiological study suggests that, to reduce CVD risk, frequent sauna sessions at 19 min per single sauna session may be required to have beneficial effects on the cardiovascular system [12]. Consistently with our previous findings, we have recently shown that sauna bathing is associated with a lowered risk of future hypertension. [13] In the current study, we demonstrated acute cardiovascular adaptations of 30-min sauna session. However, the most beneficial duration of sauna for cardiovascular health has to be defined and as to whether combining a sauna bathing session with physical activity may be more beneficial needs exploration. In addition, a similar intervention using a long-term randomized controlled trial is needed in order to gain a better perspective of the benefits of sauna (heat stress) and to investigate long-term health effects in different populations since short-term findings have been currently documented.

In conclusion, this study demonstrated the effects of a typical Finnish sauna on short-term cardiovascular outcomes. Our study indicated that 30-min heat exposure of sauna leads to short-term decrease in BP and positive alterations in AS parameters. Sauna bathing with its beneficial effects on cardiovascular function is a recommendable activity in a population with cardiovascular risk factors. Further studies are warranted to establish the potential mid-term and longer-term effects of sauna bathing on cardiovascular adaptation.

Summary

What is known about topic

  • Frequent sauna bathing is associated with a reduced risk of fatal cardiovascular and all-cause mortality events

  • Increased sweating during sauna bathing is accompanied by increase in circulation and body temperature

  • Passive heat therapy may improve vascular function

What this study adds

  • This is the largest experimental study showing acute effects of sauna exposure on body physiology, hemodynamics and cardiovascular function.

  • Sauna bathing improved arterial compliance and lowered systemic blood pressure

  • Sauna bathing is a safe and recommendable health activity in a population with cardiovascular risk factors

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Acknowledgments

We sincerely thank Timo Harvia and the staff of Harvia Oy for sauna test facilities of the research and the subjects for their dedicated participation in the study.

Fundings

This study was supported by the Tekes, the Finnish Funding Agency for Technology and Innovation, Helsinki, Finland. Collaborators of the study project were Harvia Oy, Velha Oy, Pihlajalinna Clinic, Fintravel Oy, Finnish Sauna Culture Society and University of Eastern Finland.

Author information

Affiliations

  1. Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland

    • Tanjaniina Laukkanen
    •  & Jari A. Laukkanen
  2. Translational Health Sciences, Bristol Medical School, University of Bristol, Learning and Research 11 Building (Level 1), Southmead Hospital, Bristol, UK

    • Setor K. Kunutsor
  3. Diabetes Research Centre, Leicester General Hospital, University of Leicester, Leicester, UK

    • Francesco Zaccardi
  4. Department of Biology of Physical Activity, University of Jyväskylä, Jyväskylä, Finland

    • Earric Lee
  5. Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK

    • Peter Willeit
  6. Department of Neurology, Medical University Innsbruck, Innsbruck, Austria

    • Peter Willeit
  7. Emory University, Atlanta, GA, USA

    • Hassan Khan
  8. Central Finland Health Care District, Department of Internal Medicine, Jyväskylä, Finland

    • Jari A. Laukkanen

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Conflict of interest

The authors declare that they have no competing interests.

Corresponding author

Correspondence to Jari A. Laukkanen.

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DOI

https://doi.org/10.1038/s41371-017-0008-z

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