Keywords passive heating - glucose tolerance test - insulin sensitivity - glucose metabolism
- thermoregulation
Introduction
Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by poor
glycemic control. Prolonged postprandial hyperglycemia is a major risk factor for
the development of microvascular complications and cardiovascular disease [1 ]. Nearly 45% of individuals with T2DM
fail to achieve recommended blood glucose levels (HbA1c<53 mmol HbA1c/mol Hb)
[2 ]. Though lifestyle-based regimens
can effectively improve glycemic control in T2DM [3 ], adherence to such regimens is generally
low [4 ]
[5 ]. Therefore, additional strategies are
required to improve glycemic control in individuals with T2DM.
Passive heating has been proposed as a potential additional approach due to some
similarities with low-intensity exercise [6 ]. This is interesting in the context of T2DM, considering that exercise
is a well-established non-pharmacological intervention known to improve glycemic
control in this population [3 ]
[7 ]. Physiological changes induced by
physical exercise, such as increased heart rate, body temperature, sweat rates, and
peripheral blood flow, are also observed during heat stress [8 ]
[9 ]. These thermoregulatory responses are crucial for maintaining
physiological core temperatures in acute heat stress [8 ]
[10 ]. Despite previous assumptions that thermoregulatory vasodilation
exclusively occurs cutaneously [11 ], heat
stress also induces a concomitant elevation in skeletal muscle blood flow [9 ]
[12 ]
[13 ]. As this may promote
insulin-mediated glucose uptake in skeletal muscle tissue [14 ], passive heat treatment can potentially
enhance postprandial peripheral glucose uptake in individuals with T2DM.
Despite its theoretical benefits, studies using a single session of hot water
immersion as the passive heat modality have so far failed to observe any
improvements in postprandial glucose concentrations and insulin sensitivity in
individuals with T2DM [15 ]
[16 ]
[17 ]. Given that different heating modalities have shown distinct effects
on physiological outcomes (e. g., body temperature) [18 ]
[19 ] highlights the importance of evaluating different passive heat
modalities on health-related outcomes [20 ]. Unlike hot water immersion, in which heat is transferred through the
skin, an infrared sauna utilizes infrared waves that penetrate beyond the
superficial layers of the skin [21 ],
thereby facilitating a more targeted heating effect of deeper tissues. Hence, this
approach may augment the temperature of peripheral skeletal muscles and improve
muscle perfusion more effectively. As a result, an infrared sauna could be a
beneficial heat treatment modality to improve peripheral glucose uptake in
individuals with T2DM. To date, no studies have assessed how infrared sauna bathing
acutely affects postprandial glycemic excursions in individuals with T2DM.
This study investigated the impact of a single infrared sauna bathing session on
glycemic excursions during a subsequent oral glucose tolerance test (OGTT) in
individuals with T2DM. We hypothesized that, compared to a thermoneutral control
condition, infrared sauna bathing lowers postprandial glycemic excursions in
individuals with T2DM.
Methods
Participants
Twelve men and women with T2DM, aged 50 y or older and using at least one oral
hypoglycemic agent, were recruited to participate in the current study through
advertisements ([Table 1 ]). Exclusion
criteria included insulin usage, recent changes in diabetes medication, frequent
(≥1 time/week) use of sauna, participation in a structured exercise program in
the past 3 months,>5% weight change over the past 6 months, inability to
tolerate high temperatures, smoking, and diagnosis of medical condition(s) that
could jeopardize participant safety or hinder data interpretation.
Table 1 Participant characteristics.
Participants (n= 12)
Age (y)
69±7
Sex
Female
2
Male
10
Body mass (kg)
83.4±12.2
Height (m)
1.74±0.10
BMI (kg/m2 )
27.5±2.9
Fat free mass (kg)
33.0±5.4
Fat mass (kg)
23.8±5.9
Fat percentage (%)
28.5±4.9
Time since onset T2DM (y)
12±7
HbA1c (mmol HbA1c/mol Hb)
55.0±7.1
HOMA-IR
2.4±1.3
Number of hypoglycemic agents
2.0±0.6
Metformin
11
SGLT2-inhibitors
3
DPP4-inhibitors
3
Sulfonylureum derivates
7
Values are expressed as means±SDs. BMI: body mass index. HbA1c:
Hemoglobin A1c. T2DM: type 2 diabetes mellitus. HOMA-IR: Homeostatis
Model Assessment for Insulin Resistance; SGLT2: sodium-glucose
cotransporter-2; DPP4: dipeptidyl peptidase 4.
All participants were fully informed regarding the experimental procedures and
associated risks. The remaining queries were answered before written informed
consent was obtained. The study was conducted in accordance with the principles
outlined in the Declaration of Helsinki and was approved by the Medical Research
Ethics Committee Academic Hospital Maastricht/Maastricht University (METC
22–057). The study was registered on ClinicalTrials.gov (NCT05610046).
Study design
This counterbalanced randomized cross-over controlled trial was conducted at the
Department of Human Biology, Maastricht University, The Netherlands, between
February 2023 and April 2023 to minimize natural heat acclimatization.
Participants were randomly allocated to start with the HOT (infrared sauna at
60°C) or CON (thermoneutral) experimental condition by an independent researcher
according to a block randomization plan using an online block randomizer (http://www.randomization.com ).
Participants underwent the HOT and CON conditions in a counterbalanced order: at
rest in a seated position in an infrared sauna (HM-LSE-3 Professional edition,
Health Mate, Belgium) at 60°C (humidity is not controlled in an infrared sauna)
for 40 min (HOT) and in thermoneutral conditions at 21°C for 40 min (CON),
immediately followed by a 7-point OGTT to determine postprandial glycemic
excursions. Outcome parameters included plasma glucose and insulin
concentrations, tympanic and skin temperature, hematocrit, blood pressure, and
heart rate. Experimental trials were completed with a wash-out period of at
least 7 days between visits to limit acclimation effects. Humidity in the
laboratory was 64±2.7%.
Screening
All participants were invited to the laboratory for a screening visit to assess
eligibility for the study. Participants arrived in the laboratory in a fasted
state and without consumption of their morning hypoglycemic medication. Medical
history was assessed, and heart and lungs were auscultated by a qualified
physician. Subsequently, body mass and height, resting blood pressure, and
resting heart rate were measured. A multi-frequency bioelectrical impedance
analyzer (InBody-S10; Biospace, Cerritos, CA, USA) was used according to the
manufacturer’s guidelines for the estimation of body composition. Lastly, all
participants were familiarized with infrared sauna bathing at 60°C for
30 min.
Instructions prior to test days
Throughout the 2 days prior to the experimental procedures, participants were
instructed to maintain their habitual diet and activity levels, refrain from
strenuous physical activities, and avoid alcohol consumption. A standardized
meal (~3000 kJ, providing 54 energy percent (En%) carbohydrates, 27 En% fat, and
16 En% protein) was consumed before 10:00 PM prior to each test day, and
followed by an overnight fast. On the morning of each test day, participants
were asked not to consume any hypoglycemic medication. Food intake was recorded
in 2-day food diaries before both test days to allow replication and check for
differences between test days. Food intake records were summarized based on the
Dutch food composition table NEVO 2021 [22 ] and described as total energy intake (kJ), total carbohydrate,
total protein, and total fat intake (En%).
Experimental visits
An overview of the experimental protocol is depicted in [Fig. 1 ]. Participants reported to the
laboratory between 08:00 and 09:00 AM, after which resting blood pressure, body
mass, and tympanic temperature (as a measure for core temperature) were
measured. Subsequently, a heart rate monitor was adjusted around the chest and
skin thermometers (iButton, Maxim Integrated Products, San Jose, CA, USA) were
applied on both upper legs to continuously measure heart rate and skin
temperature, respectively, throughout the test day. Tympanic temperature was
measured using a tympanic thermometer (Braun ThermoScan IRT 6520, Kronberg,
Germany) with each blood collection. After baseline measurements, a cannula was
inserted into an antecubital vein. Following pre-sauna blood sampling (baseline,
t=− 40 min), participants entered the infrared sauna and remained seated for
40 min in the HOT or CON condition, wearing underwear only. Directly after
exiting the sauna, tympanic temperature and blood pressure were measured. After
removing all sweat from the body, body mass was determined. A blood sample
(t=0 min) was collected before consumption of the glucose beverage containing
75 g glucose dissolved in 200 mL water (LemonGluc, Novolab, Belgium), after
which participants were allowed to drink 100 mL of water. The 2-h OGTT commenced
within 10 min after exiting the sauna. During the OGTT, participants remained
seated (were allowed to read) and wore clothing of choice. Additional blood
samples were obtained at t=15, 30, 45, 60, 90, and 120 min. Blood pressure and
body mass were measured again following the final blood draw.
Fig. 1 Schematic representation of an experimental visit. CON,
control: 40 min at 21°C; HOT, infrared sauna: 40 min at 60°C; OGTT, oral
glucose tolerance test.
Blood analysis
On the first test day, one blood sample was collected at baseline in a
heparin-containing tube for HbA1c analysis, while all other blood samples were
collected in EDTA-containing tubes. Homogenized blood was collected into three
heparinized micro-hematocrit capillary tubes, centrifuged (5 min at
8500 g at 21°C) and subsequently, hematocrit values were determined.
Thereafter, the remaining blood was centrifuged (10 min at 1000 g at 4°C)
to obtain plasma. Aliquots of plasma were frozen in liquid nitrogen and stored
at − 80°C until analysis of plasma glucose, insulin, noradrenaline, and cortisol
concentrations using commercially available kits (glucose HK CP, ABX
Diagnostics, Montpellier, France; Human Insulin ELISA, Meso Scale Discovery,
Rockville, Maryland, USA; TECAN ELISA, IBL International GmbH, Hamburg, Germany,
respectively).
Insulin sensitivity indices
Plasma glucose and insulin concentrations throughout the 7-point OGTT were used
to calculate the whole-body composite insulin sensitivity index
(ISIcomposite ) as defined by Matsuda and DeFronzo [23 ], as shown in the formula below:
where G0 and I0 represent fasting post-sauna (t=0 min)
plasma glucose (mg/dL) and insulin (mUi/L) concentrations, respectively.
Gmean and Imean represent time-weighted means of
plasma glucose and insulin concentrations during the OGTT. Additionally,
tissue-specific insulin sensitivity indices including the hepatic insulin
resistance index (HIRI) and muscle insulin resistance index (MISI) [24 ] were calculated. HIRI and MISI were
calculated using the formulas as shown below:
The incremental area under the curve (iAUC) for plasma glucose and insulin
concentrations during the OGTT were calculated based on the trapezoid method,
using fasting post-sauna plasma glucose (mmol/L) and insulin (pmol/L)
concentrations as a baseline. The Homeostatis Model Assessment for Insulin
Resistance (HOMA-IR) [25 ] was
determined from fasting pre-sauna plasma glucose (mg/dL) and insulin (mUi/L)
concentrations.
Statistics
All data were tested for normality using the Shapiro-Wilk test
(P< 0.05). Wilcoxon Signed-Rank test was used for non-normally
distributed data of ISIcomposite, HIRI and MISI. A paired samples
T-test was used to analyze the iAUC of plasma glucose and insulin.
Time-dependent outcomes (i. e., plasma glucose and insulin concentrations,
noradrenaline, and cortisol concentrations, hematocrit, tympanic and skin
temperature, heart rate, and blood pressure) were analyzed using two-way
(time×condition) repeated measures analysis of variance (ANOVA). If a
significant time effect was observed, Bonferroni post-hoc corrections were
applied to localize differences between time-points. In case of a significant
interaction, separate one-way repeated measures ANOVA analyses were performed
for HOT and CON to locate significant differences between time-points and paired
samples T-tests were used to analyze differences between HOT and CON at all
time-points. T-tests were not corrected for multiple comparisons. Correlations
were explored between plasma noradrenaline and cortisol concentrations and iAUC
of plasma glucose and insulin during HOT and CON for time points t=− 40, t=0,
and t=60 min using Pearson’s correlation coefficients. Significance was set at
P <0.05. Normally distributed data are presented as means±SDs and
not normally distributed data as medians with [95% confidence intervals].
Statistical analyses were performed using the statistical software program IBM
SPSS (version 28.0, IBM Corp., Armonk, NY, USA).
Results
Participant characteristics
Participant characteristics are depicted in [Table 1 ]
. All participants completed both test days. No
adverse effects were reported.
Thermoregulatory response
Tympanic and skin temperature were not different at baseline in HOT
(P= 0.384) and CON (P= 0.157), [Fig. 2a–b ]. A significant time×condition interaction was observed for
tympanic and skin temperature (P< 0.001 for both). Between baseline and
t=0 min (pre- to post-sauna) in HOT, the tympanic temperature increased
(P <0.001). Likewise, skin temperature in HOT increased from
baseline to t=0 min (P< 0.001), while no changes in tympanic and skin
temperature were observed over time for CON (P >0.05). At t=0 min,
tympanic and skin temperature were higher in HOT compared to CON
(P <0.001 for both). Compared to CON, the tympanic temperature in HOT
remained elevated until t=60 min (P< 0.05 for all), while skin
temperature remained higher until t=90 min (P <0.05 for all).
Fig. 2 Tympanic temperature (a ), skin temperature
(b ), and heart rate (c ) throughout the experimental visit.
The glucose beverage was ingested at t=0 min (dotted line). Data are
presented as means±SDs, n=12. *HOT is significantly higher than CON
(P <0.05). Data were analysed using two-way
(time×condition) repeated measures ANOVAs. CON, control: 40 min at 21°C;
HOT, infrared sauna: 40 min at 60°C.
Plasma glucose and insulin concentrations
Plasma glucose concentrations at baseline were not different between HOT and CON
(P= 0.81, [Fig.
3a ]). Plasma glucose concentrations did not differ between
baseline and t=0 min in HOT (P =1.0) and CON (P =1.0). A significant
time×condition interaction was found for plasma glucose concentrations
throughout the test day (P <0.001). Plasma glucose concentrations
increased following glucose ingestion and remained elevated until the end of the
test day in both conditions (P <0.001 for all values after t=0 min).
From t=15 to t=120 min, plasma glucose concentrations were higher in HOT
compared to CON (P <0.05 for all). The iAUC of plasma glucose
concentrations (P <0.001) and peak plasma glucose concentrations
(P <0.001) were also higher in HOT when compared to CON. A
significant effect of time (P <0.001), but not condition
(P =0.92) was observed for plasma insulin concentrations throughout the
test days ([Fig. 3c ]). Compared to
t=0 min, plasma insulin concentrations were significantly higher at t=15, 45,
60, 90, and 120 min in HOT (P< 0.05 for all) and t=15, 60, 90, and
120 min in CON (P <0.05 for all), with no difference between the two
groups (time×condition interaction, P= 0.059). Insulin iAUC did not differ
between conditions (P =0.93). Hematocrit at baseline was 43.0±3.1 and
42.5±3.6% during HOT and CON, respectively, and did not differ between
conditions or over time (time: P= 0.60; condition: P= 0.60;
time×condition: P =0.15). Similar outcomes were observed when plasma
glucose and insulin values were corrected for hematocrit (Supplementary
Figure 1 ).
Fig. 3 Plasma glucose (a ) and insulin (c )
concentrations throughout the experimental visit and iAUC for glucose
(b ) and insulin (d ) dext-linkng the OGTT. The glucose
beverage was ingested at t=0 min (dotted line). Data are presented as
means±SDs including individuals data points for c and d ,
n=12. *HOT is significantly higher than CON (P <0.05). Data
were analysed using two-way (time×condition) repeated measures ANOVAs
for panel A and C and using paired T-tests for panel b and
d . CON, control: 40 min at 21°C; HOT, infrared sauna: 40 min
at 60°C; iAUC, incremental area under the curve; OGTT, oral glucose
tolerance test.
Insulin sensitivity indices
No differences were observed between HOT and CON for ISIcomposite
(P =0.67), HIRI (P =0.39), and MISI (P =0.73), as depicted
in [Fig. 4 ].
Fig. 4 Insulin sensitivity indices. Matsuda index, n=12 (a )
HIRI, n=12 (b ) MISI, n=8 (c ) for HOT and CON, derived from
plasma glucose and insulin concentrations dext-linkng the 2-h OGTT. Data
are presented as individuals data points. Data were analysed using
non-parametric Wilcoxon Signed-Rank test. HIRI: hepatic insulin
resistance index; Matsuda index: whole-body composite insulin
sensitivity index; MISI: muscle insulin sensitivity index.
Cardiovascular response
Heart rate was not recorded for n= 1 during CON due to technical
malfunctioning of the heart rate monitor. Heart rate did not differ at baseline
between conditions (P= 0.63, [Fig.
2c ]). A significant time×condition interaction was found for heart
rate (P< 0.001). Heart rate increased between baseline and t=0 min in
HOT (P= 0.04), while no changes over time were observed for CON
(P= 1.0). Heart rate was higher in HOT than in CON between t=− 30 and
t=15 min (P< 0.05 for all).
Systolic blood pressure (SBP) at baseline was not different in HOT and CON
(144±13 and 144±13 mmHg; P =1.0, Supplementary figure 2 ). A main
effect of time (P =0.005), but not condition (P =0.139) was observed
for SBP. SBP decreased from 144±13 at baseline to 133±19 mmHg at t=0 min during
both HOT and CON (P= 0.008), with no difference between the two groups
(time×condition interaction, P =0.222). Diastolic blood pressure (DBP) was
not different between HOT and CON at baseline (78±6 vs. 79±7 mmHg;
P= 0.61). DBP showed a significant time×condition interaction
(P =0.013). During HOT, DBP decreased from 78±6 to 63±11 mmHg between
baseline and t=0 (P <0.001) and did not return to baseline at t=120
(72±11 mmHg; P =0.011), while no changes over time occurred during CON.
DPB was lower in HOT compared to CON at t=0 min (63±11 vs. 77±12 mmHg;
P =0.005) and t=120 min (72±11 vs. 79±14 mmHg; P =0.021).
Catecholamines
Noradrenaline and cortisol concentrations did not differ between HOT and CON at
baseline (P >0.05, [Fig.
5 ]). A significant time×condition interaction was found for both
noradrenaline and cortisol concentrations (P <0.001). In HOT,
noradrenaline concentrations increased between baseline and t=0 min
(P <0.001) and returned to baseline at t=60 min (P =1.0), while
cortisol concentrations did not change over time (P =1.0). In CON,
noradrenaline concentrations remained unchanged between baseline and t=0 min
(P =0.378), whereas cortisol concentrations decreased
(P <0.001). Noradrenaline concentrations in CON increased from baseline
to t=60 (P =0.017), while cortisol concentrations returned to baseline
(P =1.0). At t=0 min, noradrenaline and cortisol concentrations were
higher in HOT compared to CON (P <0.05). At t=60 min, noradrenaline
concentrations were lower in HOT compared to CON (P =0.020), while
cortisol concentrations did not differ between HOT and CON (P =0.64).
During CON, a positive correlation was found between glucose iAUC and cortisol
concentrations at t=0 (Pearson’s r =0.617; P= 0.033). Furthermore,
during HOT, a tendency towards a positive correlation was observed between
glucose iAUC and noradrenaline concentrations at t=0 min (Pearson’s
r= 0.560; P =0.058, Supplementary Figure 3 ).
Fig. 5 Noradrenaline (a ) and cortisol (b )
concentrations throughout the experiment at t=− 40, 0, and 60 min. The
glucose beverage was ingested at t=0 min (dotted line). Data are
presented as means±SDs, n=12. *HOT is significantly higher than CON
(P <0.05). Data were analysed using two-way
(time×condition) repeated measures ANOVAs. CON, control: 40 min at 21°C;
HOT, infrared sauna: 40 min at 60°C.
Body mass
A significant time×condition interaction was observed for body mass
(P <0.001). During HOT, body mass decreased from 82.7±12.1 to
82.4±12.1 kg between baseline and t=0 min (P <0.001) and did not return
to baseline values at t=120 (82.5±12.1 kg; P =0.022). During CON, body
mass was 83.2±12.4 kg at baseline and did not change throughout the test
day.
Dietary intake
During the 2 days prior to HOT and CON, no differences were observed in average
daily intake of dietary energy (84±24 vs. 80±20 kJ/kg/d; P= 0.52),
carbohydrate (43±4 vs. 44±7 En%; P =0.58), protein (18±3 vs. 19±3 En%;
P =0.26) and fat (39±5 vs. 37±6 En%; P =0.28).
Discussion
The present study shows a greater postprandial rise in circulating plasma glucose
concentrations following glucose ingestion after a single session of infrared sauna
bathing compared to a thermoneutral condition in individuals with T2DM, with no
differences in circulating plasma insulin concentrations. In contrast to our
hypothesis, a single session of infrared sauna bathing did not result in lower blood
glucose excursions following glucose ingestion in individuals with T2DM.
In line with previous work on passive heat treatment [15 ]
[17 ]
[26 ]
[27 ]
[28 ]
[29 ]
[30 ]
[31 ], we showed that infrared sauna bathing increased tympanic
temperature, skin temperature, and heart rate ([Fig. 2a–c ]). These physiological changes, though varying in magnitude,
show some similarities to those elicited by low-intensity exercise [6 ]. It has been well established that
exercise increases skeletal muscle blood flow, which partly contributes to increased
glucose uptake in people with T2DM [3 ]
[7 ]. Given that infrared
sauna bathing may also potently stimulate skeletal muscle blood flow, we
hypothesized that a single session of infrared sauna bathing lowers glucose
excursions during a subsequent OGTT in adults with T2DM. However, we observed a more
(instead of less) pronounced postprandial rise in circulating plasma glucose
concentrations, with no changes in insulin concentrations and insulin sensitivity,
during the 2-h OGTT that was performed immediately following infrared sauna bathing
when compared to the same treatment in a thermoneutral condition ([Fig. 3 ]
a , [c and [4 ], respectively). Our data are in
contrast with previous studies showing no impact of a single session of passive heat
treatment (i. e., hot water immersion) on postprandial glucose concentrations and/or
insulin sensitivity in individuals with T2DM [15 ]
[16 ]
[17 ]. However, it is important to note that
previous studies in non-diabetic populations have also observed increased (rather
than reduced) postprandial glucose concentrations with acute passive heat treatment
compared to thermoneutral control settings [28 ]
[29 ]
[30 ]
[32 ]
[33 ]. Taken together, our
study adds to the existing literature suggesting that a single session of passive
heat treatment does not facilitate a reduction in postprandial glucose
concentrations or an improvement in insulin sensitivity [15 ]
[16 ]
[17 ]
[28 ]
[29 ]
[30 ]
[32 ]
[33 ].
Several mechanisms can be explored to elucidate the observed increase, instead of
a
decrease, in post-prandial rise in circulating plasma glucose concentrations. We
explored whether a decline in blood volume through sweating might explain the more
elevated post-prandial blood glucose concentrations following passive heat
treatment. Participants lost 300±100 mL of body mass following passive heating,
while no decline in body mass was observed in the thermoneutral condition. However,
no significant changes were observed in blood hematocrit levels over time or between
treatments. In line with previous work investigating the impact of hypohydration on
glycemic excursions [34 ], we did not
detect any differences in plasma glucose data when data were corrected for blood
sample hematocrit values. The initial elevation in plasma glucose concentrations may
also be (partly) attributed to arterialization of venous blood samples after heating
[35 ]
[36 ]. Nevertheless, the arterialization
effect of local hand heating has been shown to disappear within ~15 min after
removing the heat source [37 ]. How long
this effect persists after whole-body heating is not known, though it is unlikely
that arterialization explains the prolonged elevation in glucose concentrations
observed up until 2 h after exiting the sauna.
As skin and tympanic temperature and heart rate increased, we reasonably assumed that
peripheral blood flow increased following passive heat treatment [9 ]. However, enhanced peripheral blood flow
did not result in an increase in peripheral blood glucose uptake, or was
insufficient to attenuate post-prandial blood glucose excursions. Therefore, we
speculate that increased muscle perfusion during heat stress primarily facilitates
heat dissipation to the skin, rather than improving peripheral glucose uptake in
skeletal muscle. Furthermore, heat stress-induced release of stress hormones may
have stimulated hepatic glucose output, leading to an elevation in endogenous
glucose appearance [9 ]
[31 ]
[38 ]
[39 ]. In accordance, we
observed an elevation in plasma noradrenaline and cortisol concentrations measured
immediately following infrared sauna bathing and a tendency towards a positive
correlation between glucose iAUC and noradrenalin concentrations after infrared
sauna bathing. This finding implies that a systemic stress response may have
contributed to the observed elevation in postprandial blood glucose concentrations
in this study. Finally, during heat stress, blood may have been redirected from the
splanchnic region to accommodate increased skin perfusion [40 ], potentially slowing gastric emptying
and, as such, glucose absorption. Speculatively, this may also account for the
prolonged postprandial elevation of blood glucose concentration.
Although a relatively small sample size was included, the robust cross-over study
design allowed us to reliably detect relevant differences in body and skin
temperature between the two conditions. Unfortunately, we were not able to measure
rectal temperature and/or skin temperature at multiple body sites to provide a more
accurate assessment of body temperature during and following passive heat treatment.
Also, composite indicators of whole-body insulin sensitivity are not as reliable as
measurements using the gold standard hyperinsulinemic-euglycemic clamp and glucose
tracers. Therefore, to understand glucose fluxes and insulin action following heat
treatment, future work that directly measures glucose fluxes is warranted. The
present study should be regarded as a proof-of-principle, as the study design
applied in the present study does not apply to normal, daily life conditions.
Participants ingested 75 g glucose within 5 min for the OGTT following the passive
heat treatment and control condition. The administration of such high glucose loads
result in more rapid glucose absorption compared to the gradual absorption of
glucose following ingestion of a normal mixed meal [41 ]. The timing of heat treatment, however,
does not seem to impact subsequent post-prandial blood glucose responses. To
illustrate, no difference was observed between glycemic excursions when performing
the OGTT either during or 30 min after hot water immersion in individuals with T2DM
[17 ]. Moreover, glycemic excursions
did not differ 1 h [15 ] or 24 h [16 ] after hot water immersion in
individuals with T2DM.
Interestingly, in contrast to the outcomes of most studies addressing the acute
impact of heat treatment, prolonged passive heat treatment has consistently been
found to improve glycemic excursions in healthy [42 ], overweight [26 ]
[43 ], and individuals with T2DM [44 ]. It seems that the thermal stress
through repeated acute passive heating triggers adaptations that may improve
thermoregulation in challenging environments. At present, the effects of prolonged
application of frequent infrared sauna bathing on glycemic outcomes in T2DM remain
to be investigated.
In conclusion, a single session of infrared sauna bathing does not attenuate the
postprandial rise in circulating blood glucose concentrations during a subsequent
OGTT in individuals with T2DM. Future work should focus on identifying underlying
mechanisms by directly measuring glucose fluxes, investigating hormonal influences,
and analyzing blood flow distribution to further explore the effects of different
modalities of acute and more chronic passive heat treatment on glycemic excursions
and cardiovascular risk factors in individuals with T2DM.
