Exercise thermoregulatory responses following a 28-day sleep-high train-low regimen

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European Journal of AppliedPhysiology ISSN 1439-6319 Eur J Appl PhysiolDOI 10.1007/s00421-012-2374-0

Exercise thermoregulatory responsesfollowing a 28-day sleep-high train-lowregimen

Stylianos N. Kounalakis, Ola Eiken &Igor B. Mekjavic

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ORIGINAL ARTICLE

Exercise thermoregulatory responses following a 28-daysleep-high train-low regimen

Stylianos N. Kounalakis • Ola Eiken •

Igor B. Mekjavic

Received: 3 November 2011 / Accepted: 27 February 2012

� Springer-Verlag 2012

Abstract The potentiated exercise-sweating rate observed

during acute hypoxia is diminished after a sleep-high train-

low (SH-TL) regimen. We tested the hypothesis that this

attenuation of the sweating response after SH-TL is com-

pensated for by an increase in heat loss via vasodilatation.

Nine male subjects participated in a 28-day SH-TL regimen.

Before (pre-), and after (post-) the SH-TL protocol, they

performed an _VO2peak test under normoxia and hypoxia.

Additionally, pre- and post-SH-TL they completed three

30-min constant-work rate trials on a cycle ergometer. In one

trial, the subjects inspired room air while exercising at 50 %

of normoxic _VO2peak (CT). In the remaining trials, subjects

exercised in hypoxia (FIO2 12.5 %), either at the same

absolute (HAT) or relative (50 % of hypoxic _VO2peak)

work rate (HRT) as in CT. Despite similar exercise core

temperature responses between pre- and post-SH-TL trials,

sweating rate was potentiated in HAT pre-SH-TL [CT:

1.97 (0.42); HRT: 1.86 (0.31); HAT: 2.55 (0.53) mg

cm-2 min-1; p \ 0.05]. Post-SH-TL exercise sweating rate

was increased for CT, and remained unchanged in HRT and

HAT [CT: 2.42 (0.76); HRT: 2.01 (0.33); HAT: 2.59

(0.30) mg cm-2 min-1]. Pre-SH-TL, the forearm-fingertip

skin temperature difference (Tskf-f) was higher in HAT than

in CT and HRT by *3.5�C (p \ 0.05). The inter-condition

differences in Tskf-f were diminished post-SH-TL. In con-

clusion, the decrease in sweating rate during hypoxic exer-

cise, following a SH-TL regimen, was countered by an

increase in vasodilatation (reduced Tskf-f), whereas SH-TL

enhanced the sweating response during normoxic exercise.

The mechanisms underlying these SH-TL-induced altera-

tions in thermoregulatory responses remain to be settled.

Keywords Near infrared spectroscopy � Sweating �Aerobic training � Altitude acclimatization �Relative work rate � Absolute work rate

Introduction

The exercise sweating response is initiated by thermal

factors, namely, the elevation in core (Tc) and/or skin (Tsk)

temperatures, and by non-thermal factors such as acute

hypoxia and muscle ischemia (Mekjavic and Eiken 2006).

For example, during steady-state cycling at a given exter-

nal workload and at similar Tc and Tsk, sweating rate

is potentiated by local ischemia in the working muscles

(Eiken and Mekjavic 2004; Kacin et al. 2005) and by

hypoxemia (Kacin et al. 2007). During exercise with local

ischemia, the reduction in blood flow to the working

muscles is accompanied by an attenuated cutaneous vaso-

dilatation, which is compensated for by an exaggerated

sweating response (Kacin et al. 2005); a phenomenon that

would appear to serve the whole-body heat balance.

Likewise, at the same absolute work rate, acute hypoxia

enhances evaporative over conductive heat loss despite no

alterations in Tc (Greenleaf et al. 1969).

Communicated by George Havenith.

S. N. Kounalakis � I. B. Mekjavic

Department of Automation, Biocybernetics and Robotics,

Jozef Stefan Institute, Ljubljana, Slovenia

S. N. Kounalakis (&)

Human Performance-Rehabilitation Laboratory,

Faculty of Physical and Cultural Education,

Evelpidon Hellenic Military University, Vari, Greece

e-mail: [email protected]

O. Eiken

Department of Environmental Physiology, School of Technology

and Health, Royal Institute of Technology, Stockholm, Sweden

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DOI 10.1007/s00421-012-2374-0

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Prolonged interventions, such as aerobic training (Rob-

erts et al. 1977) and altitude acclimatization also modify

the sweating response. When such interventions are con-

current, their effects may be conflicting. For example, the

popular intervention to enhance working capacity in ath-

letes is the sleep-high train-low (SH-TL) regimen. The two

components of the SH-TL regimen, which may influence

the exercise thermoregulatory responses, are hypoxic

acclimatization (SH) and aerobic training (TL). Acclima-

tization to hypoxia would presumably reduce the magni-

tude of the response observed during acute hypoxia,

namely potentiation of sweating at the expense of con-

ductive heat loss (Eiken and Mekjavic 2004; Shibasaki

et al. 2001). In contrast, the training component of SH-TL

enhances the magnitude and gain of the sweating response

(Nadel et al. 1974; Roberts et al. 1977) and shifts the core

temperature threshold for onset of sweating and vasodila-

tation toward lower Tc levels (Roberts et al. 1977). Pre-

viously, we reported that the augmented sweating response

during hypoxic compared to normoxic exercise conducted

at identical absolute workloads, was no longer evident after

SH-TL (Kacin et al. 2007).

The present study was designed to investigate the

combined role of hypoxic acclimatization and aerobic

training on the exercise sweating and vasomotor responses,

with the concomitant exploration of the oxygenation levels

and blood volume in the working muscles and cerebral

area. The primary aims were to confirm previous findings

(Kacin et al. 2007) of potentiation of the sweating rate

during acute hypoxia, and of an attenuation of the exag-

gerated sweating responses following a 28-day SH-TL

regimen. The secondary aims were to investigate whether

the SH-TL-induced attenuation of the sweating response

during hypoxic exercise would be accompanied by changes

in cutaneous vasomotor tone, and hence in the provisions

for convective heat loss, and also to shed some light on the

mechanisms underlying such SH-TL-induced changes in

thermoregulatory responses by investigating regional

changes in muscle blood volume and oxygenation during

exercise. Thus, both endurance training and hypoxic

acclimatization may alter the exercise responses for blood-

flow distribution and oxygenation of cerebral and con-

tracting muscle tissues (Ainslie et al. 2008; Wang et al.

2010), factors that, as mentioned, are known to affect heat-

dissipation mechanisms (Greenleaf et al. 1969; Eiken and

Mekjavic 2004; Kacin et al. 2005, 2007).

Methods

Nine healthy, male subjects with an average (SD) age of 24

(3) years and stature of 179 (5) cm participated in the

study. All subjects were aerobically fit, but none were

endurance athletes. They were all accustomed to cycle

exercise as well as exercise testing on cycle ergometer.

Before enrolling in the study, each subject was familiarized

with the _VO2peak test and abstained from altitude exposures

[500 m above sea level for at least 1 month before the

experiments. Subjects’ participation was approved by a

physician. Following familiarization with the protocol and

instrumentation, subjects gave their written consent to

participate in the study. The protocol was approved by the

National Committee for Medical Ethics at the Ministry of

Health (Republic of Slovenia).

Study outline

All subjects conducted a normoxic and a hypoxic _VO2peak

test, and three constant-workload exercise tests, before

(pre-) and after (post-) the 28-day SH-TL regimen, during

which the subjects were exposed to normobaric hypoxia for

at least 9 h every night; ambient partial pressure of oxygen

corresponded approximately to that of an altitude above sea

level of 2,800 m (1st week), 3,000 m (2nd week) and

3,200 m (last 2 weeks) (for details see below). During

daytime, all subjects underwent 1 h training sessions in

room air on a cycle ergometer, five times per week. The

SH-TL regimen was conducted at the Olympic Sport

Centre Planica (Ratece, Slovenia) situated at an altitude of

900 m above sea level. The daily training sessions were

thus conducted at an altitude of 900 m. During the evening

and night-time hours, subjects were sequestered on one

floor of the Olympic Centre in which the oxygen levels

were reduced to simulate the partial pressure of oxygen at

the desired altitude.

Peak work rate tests

Subjects’ pre- and post-SH-TL _VO2peak was determined on

an electrically braked cycle ergometer (ERG 900S, Schil-

ler, Switzerland) twice: on one occasion under normobaric

normoxic and the other under normobaric hypoxic [fraction

of inspired O2 (FIO2) 12.5 %] conditions. All tests were

conducted in a laboratory situated at sea level (Orthopaedic

Hospital Valdoltra, Ankaran, Slovenia). Subjects were

transported from the Olympic Sport Centre Planica to the

laboratory on the day of the test, and returned to the

Olympic Sport Centre upon completion of the tests. Each

subject performed an incremental work rate (30 W min-1)

protocol to exhaustion. Baseline values were measured

during a 5-min period of rest preceding the exercise bout.

The initial workload was 60 W and the target pedalling rate

70–80 rpm. The criteria to achieve maximal _VO2 were the

observation of a plateau in _VO2 during the last 15 s of the

trial and the subject’s inability to maintain the required

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cadence. Work rate was interpolated between stages with

the formula: W = work rate of last stage com-

pleted ? [(work rate increment) 9 (time into current

stage/duration of the stage in seconds)] in order to define

the 50 % of peak workload (Wpeak) that should be used for

the constant-work rate tests. Peak workload was calculated

with the same formula assuming that the first 15 s of the

stage were completed.

Constant work rate tests

The three 30-min constant-work rate tests were conducted

on a cycle ergometer (Monark 849-E, Sweden) at the same

time of the day in a counterbalanced order pre- and post-

SH-TL. In these tests, subjects breathed either normobaric

normoxic air or a normobaric hypoxic gas mixture

(inspired fraction of oxygen, FIO2 12.5 %). In the norm-

oxic trial [control test (CT)], the subjects inspired room air

while exercising at 50 % of Wpeak attained in the normoxic_VO2peak test. In the remaining two trials, subjects exercised

in hypoxia either at the same absolute work rate as in CT

[hypoxic absolute work rate test (HAT)] or at 50 % of that

attained in the hypoxic _VO2peak test [hypoxic relative work

rate test (HRT)].

Training

Exercise training was conducted once per day, for 1 h,

5 days per week on a cycle ergometer (Monark 849-E,

Sweden). During each training session, heart rate (HR) was

monitored and stored continuously with a telemetry system

(Hosant, Italy). The work rate was adjusted to maintain HR

at a level observed at a work rate equivalent to 50 % of

normoxic Wpeak before training. The training was con-

ducted under normoxia in the hypoxic facility (b-Cat B.V.,

The Netherlands) of the Olympic Sports Centre Planica.

Analytical methods and equipment

Cardiorespiratory responses during the _VO2peak tests were

obtained at 10-sec intervals with a metabolic cart (Schiller

A-T 104, Switzerland). Subjects breathed through a

respiratory valve that permitted the inhalation of either

atmospheric air, or a decompressed hypoxic mixture from a

200-litre Douglas bag reservoir. During the normoxic trials

subjects inspired ambient air, whereas in the hypoxic trials

they inspired a premixed hypoxic mixture (12.5 % O2,

87.5 % N2). The hypoxic mixture was decompressed and

humidified, by passing it through a small bath of water, and

then accumulated in the Douglas bag. The O2 and CO2

analyzers of the metabolic cart were calibrated with two

different gas mixtures and the volume measurement device

with a 3-litre syringe, before each test, and in accordance

with the manufacturer’s recommendations. In the constant

load trials, minute oxygen uptake and carbon dioxide

elimination were determined from analyses of mixed

expired gases and inspired minute ventilation ( _VE). _VE was

measured with a turbine ventilation module (K520, KL

Engineering Co., CA, USA). The expiratory side was

connected via respiratory hosing to a plexiglas mixing box,

from which a continuous 0.5 l min-1 sample of expired

gases was drawn and analyzed for O2 and CO2 content

using a gas analyzer (1.440D, Servomex Ltd., England).

Core temperature (Tc) was measured by telemetry using

a gastrointestinal pill (Minimitter, USA). Mean skin sur-

face temperature ( �Tsk) was calculated as an arithmetic

average of temperatures (unweighted) measured at four

sites (forearm, chest, thigh and calf) using skin thermistors

(MSR 12, Switzerland). �Tsk can be used as an index of

convective and/or conductive heat loss from the body core

to the skin surface. The ventral fingertip temperature was

also measured to allow the calculation of the difference in

skin temperature between forearm and fingertip (Tskf-f).

Forearm-fingertip skin temperature difference is considered

a valid index of cutaneous vasomotor tone; high values of

Tskf-f indicate vasoconstriction (House and Tipton 2002;

Rubinstein and Sessler 1990).

Local sweating rate ( _msw) was measured with a venti-

lated capsule placed on the forehead. Forced evaporation of

sweat under the capsule (surface area 4.8 cm2) was

achieved by a constant flow of air (1 l min-1) through the

capsule. _msw was estimated from continuous measurements

of the difference between the temperature and the humidity

of inflowing and outflowing air. Air temperature was

measured with thermistors (LM35, National Semiconduc-

tor Corp., Santa Clara, CA, USA) and the relative humidity

with capacitance hygrometers (Valvo air humidity sensor,

Valvo-Philips GmbH, Hamburg, Germany).

Heart rate was monitored with a telemetry system (Polar

Electro Inc., Lake Success NY, USA), and capillary oxy-

haemoglobin saturation (SpO2) using an oximeter (Nellcor

BCI 3110, USA) with the sensor placed on the left index or

middle finger. Subjects were instructed to relax their hands

during measurement of SpO2. The oximeter is accurate to

±2 units across the range of 70–100 % and demonstrates

acceptable resilience to motion artifacts (Langton and

Hanning 1990). Local and general ratings of perceived

exertion (RPEs) were obtained every 5 min using a Borg

scale (6–20).

Cerebral (Cox) and muscle (Mox) oxygenations were

monitored at rest and during exercise by a continuous-wave

near infrared spectroscopy (NIRS; Oxymon MKII Artinis,

The Netherlands). The theory, limitations and the reli-

ability of the measurements during incremental exercise

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with the specific NIRS device have been detailed previ-

ously (Subudhi et al. 2008). Briefly, the NIR light consisted

of two wavelengths (780 and 850 nm) and the micromolar

changes in tissue oxygenation (oxygenated D[HbO2] and

deoxygenated D[HHb] haemoglobin) can be calculated

with the known differential path length factors (DPF) of

4.95 and 5.93 for the muscle (Duncan et al. 1995) and

cerebral tissue (Van der zee et al. 1992), respectively.

Differential path length factors is given by the L/Lo, where

Lo is the distance (cm) between light entering and exiting

the tissue, and L is the average distance travelled by each

photon. In addition, total haemoglobin (D[HbT]), which is

the sum of D[HbO2] and D[HHb] can be used as an index

of regional blood volume (Van Beekvelt et al. 2001). Two

pairs of NIRS probes were used to detect micromolar

changes in the brain and muscle during rest and exercise.

The cerebral probe was positioned on the forehead, at the

level of the left frontal cortex, and the muscle probe above

the vastus lateralis, 15 cm above the proximal line of the

patella and 5 cm lateral to the midline of the thigh. Probes

were kept in place with a plastic spacer (adjusted optode

distance up to 5 cm), which was stabilized on the shaved

and cleaned skin with a double-sided adhesive tape.

Adhesive tape was also used to prevent external light from

entering the measuring area. Skinfolds were taken in the

sagittal plane between emitter and receiver to account for

skin and adipose thickness. Because the exact DPFs were

unknown, cerebral and muscle measurements were nor-

malized to reflect changes from the onset of the exercise

protocol (arbitrarily defined as 0 lL). Therefore, the direct

comparison between cerebral and muscle oxygenation with

the respective data from pulse oximetry was not possible.

Near infrared spectroscopy data were recorded at 50 Hz

and stored for further analysis. All technical considerations

(probe position and stabilization) outlined in reports from

previous studies using the same NIRS device (Subudhi

et al. 2007, 2008) were taken into account, ensuring high

reliability of the NIRS measurements (Subudhi et al. 2007).

Lastly, we used a sufficient optode distance (*4 cm) to

minimize the influence of skin blood flow (Owen-Reece

et al. 1996), a factor that could underestimate the relative

extent of tissue deoxygenation, but could not alter the final

conclusions.

Normobaric hypoxia in five bedrooms and one living

room (total area of *100 m2) was achieved with an oxy-

gen dilution system (b-cat, The Netherlands), based on the

Vacuum-Pressure Swing Adsorption (VPSA) principle.

The oxygen levels in each room were monitored and

recorded continuously with oxygen sensors (Rae PGM-

1100, USA). The hypoxic stimulus during the SH-TL

period was adjusted to maintain SpO2 values between 85

and 90 % during sleep. Each subject was requested to

either wear, or have in close proximity, a personal clip-on

type of oxygen analyzer with an audible alarm, that was

activated in the event that the oxygen level decreased

below the pre-set level. Heart rate and finger-pulse oxim-

etry (Nonin, 3100, USA) were recorded continuously every

night.

Fasted, resting blood samples were drawn in the morn-

ing hours pre- and post-SH-TL. Blood samples were

assayed for haemoglobin, haematocrit, and reticulocytes

using the cytochemical impedance method (Pentra120;

Horiba ABX Diagnostics).

The environmental conditions were kept similar

between pre- and post-SH-TL trials. Namely, environ-

mental temperature ranged from 21.0 (0.4) �C in HAT

before, to 21.9 (0.6) �C in CT after SH-TL, and the relative

humidity from 47 (3) % in HRT before, to 51 (5) % in

HAT after the SH-TL.

Data analysis

A 2-way ANOVA (Condition, Pre–Post) was used to define

the effects of hypoxic relative and absolute work rate and the

SH-TL intervention. A Tukey post-hoc test was employed to

assign the specific differences in the analysis of variance in

case of a significant main effect. Rating of perceived exertion

was analyzed using the non-parametric Friedman test. The

threshold core temperature for sweating and the slopes

relating sweating to the increase in core temperature during

constant-work rate exercise were determined with the least

squares linear regression analysis. The reported values are

means from the individual linear regression analysis, which

were calculated for the linear part of each individual plot.

Values were presented as means (SD) unless indicated

otherwise. Significance level was set at 0.05.

Results

Haematology

Blood haemoglobin [mean (SD) pre-SH-TL: 144 (14) g l-1;

post-SH-TL: 144 (7) g l-1] and haematocrit [pre-SH-TL: 42

(3) %; post-SH-TL: 44 (2) %] remained unchanged after the

SH-TL regimen, but there was a tendency, albeit not sig-

nificant, of an increase in erythrocytes [pre-SH-TL: 5.0 (0.4)

1012 l-1; post-SH-TL: 5.1 (0.4) 1012 l-1] during this period

(p = 0.09).

Resting HR and SpO2 levels

The 5-min resting HR (obtained with the subjects seated

idle on the bike) was significantly reduced after the SH-TL

regimen. Specifically, HR was 84 (8), 86 (13) and 83 (13)

for the pre-SH-TL, and 76 (10), 76 (11) and 78 (6) for the

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post-SH-TL control (CT), hypoxic relative (HRT), and

hypoxic absolute (HAT) trials, respectively. The 5-min

mean SpO2 resting values before each trial were 5 % units

higher in the post-SH-TL hypoxic conditions. Namely, pre-

SH-TL SpO2 values were 97 (2), 88 (3) and 88 (4) %,

whereas post-SH-TL values were 98 (2), 93 (2) and 93

(2) % for the CT, HRT, and HAT trials, respectively.

_VO2peak and Wpeak

Sleep-high train-low improved (p = 0.03) normoxic_VO2peak by 5.5 % from 60.1 (8.5) to 63.5 (8.6) ml kg-1

min-1, but did not significantly affect hypoxic _VO2peak.

Sleep-high train-low improved Wpeak by 11.9 % (p \ 0.01)

in normoxia and by 8.5 % in hypoxia (p = 0.02), with

Wpeak pre- and post-SH-TL amounting to 311 (31) and 348

(36) W, respectively, in normoxia and to 270 (26) and 293

(23) W, respectively, in hypoxia.

Constant work rate exercise

The constant-work rate exercise data were only analyzed

up to the 25th minute of cycling, due to a progressive drop-

out of the subjects after this time point. Each subject

exercised at the same relative intensity pre- and post-SH-

TL. This intensity was set at *50 % of the Wpeak for the

CT and HRT trials, and at *60 % in the HAT trial

(Table 1). The work rate applied during the post-SH-TL

trials was 25–30 W higher so that the same relative

intensity was achieved in each condition (Table 1).

_VO2 and _VE

The mean _VO2 during the trials was *200–300 ml min-1

higher post-SH-TL, however this increment was not sig-

nificant. Both pre- and post-SH-TL, _VO2 were lower

(p \ 0.05) in HRT than in CT and HAT whereas there was

no difference in _VO2 between CT and HAT (Table 1).

Minute ventilation was significantly increased post-SH-TL

for all conditions (Table 1). In both testing periods _VE was

higher in HAT compared with CT and HRT by *12 and

18 l min-1 pre- and post-SH-TL, respectively (Table 1).

HR, SpO2 and RPE

Heart rate was higher in HAT than in CT and HRT both

pre- and post-SH-TL, but no significant differences were

observed between CT and HRT (Table 1). The SpO2 levels

were always lower (p \ 0.05) in the hypoxic trials but SH-

TL elevated (p \ 0.05) SpO2 both in the HAT and HRT

trials (Table 1). Local and general RPEs were higher

(p \ 0.05) during HAT than in CT and HRT, but in any

given exercise condition RPEs were unchanged by SH-TL

(Table 1).

Tc, �Tsk and Tskf-f

The mean core temperature at rest and during exercise and

the relative increase in Tc above resting values, are pre-

sented in Table 2 and Fig. 1, respectively. Core tempera-

ture at rest (baseline) and during the last 5 min of exercise

Table 1 Mean (SD) cardiorespiratory responses and median (range)

local and general rate of perceived exertion (RPE) after 25 min of

steady-state cycling before and after the SH-TL for the control trial

(CT; exercise in normoxia at 50 % of normoxic Wpeak), the hypoxic

relative trial (HRT; exercise in hypoxia at 50 % of hypoxic Wpeak)

and the hypoxic absolute trial (HAT; exercise in hypoxia at the same

absolute WR as in CT) (n = 9)

Pre-SH-TL Post-SH-TL

CT HRT HAT CT HRT HAT

WR (Watts) 149 (7) 127 (6) 149 (7) 180 (9) 153 (8) 180 (9)

% of Wpeak 50 (1) 50 (1) 60 (1)b,c 51.8 (2) 52.0 (3) 61.4 (2)b,c

HR (b min-1) 156 (6) 161 (6) 171 (9)b,c 154 (9) 158 (5) 167 (9)b,c

_VO2 (l min-1) 2.18 (0.4) 1.68 (0.3)b 2.01 (0.4)c 2.39 (0.2) 2.03 (0.4)b 2.25 (0.3)c

_VE (l min-1) 45 (8) 49 (9) 60 (8)b,c 59 (9)a 61 (9)a 78 (11)a,b,c

SpO2 (%) 97.4 (1.1) 73.3 (4.9)b 72.9 (4.1)b 96.6 (1.0) 77.7 (4.1)a,b 77.3 (4.3)a,b

RPE local 12 (7–15) 14 (8–17) 16 (10–19)b 12 (7–15) 14 (10–18) 15 (10–18)b

RPE general 12 (6–14) 14 (9–16) 16 (10–19)b 12 (7–15) 13 (7–16) 15 (10–19)b

_VO2 oxygen consumption, _VE minute ventilation, HR heart rate, SpO2 blood oxygen saturationa Significant difference compared to values before SH-TLb Significant difference compared to CTc Significant difference compared to HRT, p \ 0.05

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was not significantly different between trials, or pre- and

post-SH-TL for the same trial. The inter-trial differences in

exercise Tc (approximately 0.3 �C) were not significant

(Fig. 1). Mean skin surface temperature (which can be

considered an index of the provisions for convective and/or

conductive heat loss from the body surface) tended to be

lower in HAT than in CT and HRT (p = 0.07; Table 2)

pre-SH-TL. During the 30-min cycling post-SH-TL, �Tsk

was similar in all three conditions, but in the HAT trial

values were higher (p \ 0.05) post- than pre-SH-TL

(Table 2). The Tskf-f (a greater positive difference indi-

cates greater vasoconstriction) was higher (p \ 0.05) in

HAT than in CT and HRT pre-SH-TL, but similar in all

trials post-SH-TL (Table 2; Fig. 2).

Table 2 Mean (SD) thermoregulatory responses at rest and after

25 min of constant-work rate cycling before and after the SH-TL for

the control trial (CT; exercise in normoxia at 50 % of normoxic

Wpeak), the hypoxic relative trial (HRT; exercise in hypoxia at 50 %

of hypoxic Wpeak) and the hypoxic absolute trial (HAT; exercise in

hypoxia at the same absolute WR as in CT) (n = 9)

Pre-SH-TL Post-SH-TL

CT HRT HAT CT HRT HAT

Tcrest (�C) 36.7 (0.4) 36.9 (0.3) 36.9 (0.4) 36.9 (0.3) 37.0 (0.4) 36.9 (0.2)

Tcexer (�C) 38.1 (0.3) 38.1 (0.3) 38.0 (0.5) 37.9 (0.2) 38.1 (0.3) 38.2 (0.2)

�Tsk (�C) 32.6 (0.7) 32.5 (0.7) 32.0 (0.4) 32.8 (0.8) 32.5 (0.6) 32.8 (0.4)a

Tskf-f (�C) 0.5 (0.2) 1.7 (0.5) 4.6 (0.4)b 0.9 (0.1) 0.9 (0.2) 2.0 (0.1)a

_msw gain (mg min-1 cm-2 �C-1) 1.54 (0.13) 1.76 (0.19) 2.56 (0.21)b 2.67 (0.23)a 2.09 (0.16) 2.19 (0.19)

Threshold DSc for sweating (�C) 0.45 (0.3) 0.31 (0.3) 0.33 (0.3) 0.29 (0.1)a 0.19 (0.2) 0.30 (0.3)

Tc core temperature, at rest and during the last 5 min of exercise (exer), �Tsk mean skin temperature from four sites, Tskf-f difference between

forearm and fingertip skin temperatures (Tskf-f considered as an index of vasomotor tone and higher values indicate higher vasoconstriction),

_msw sweating ratea Significant difference compared to values before SH-TLb Significant difference compared to CT, p \ 0.05

Fig. 1 Mean changes in core temperature (DTc) relative to pre-

exercise values during the control trial (CT; exercise in normoxia at

50 % of normoxic Wpeak), hypoxic relative trial (HRT; exercise in

hypoxia at 50 % of hypoxic Wpeak) and hypoxic absolute trial (HAT;

exercise in hypoxia at the same absolute WR as in CT), before (uppergraph) and after (lower graph) the 28-day SH-TL regimen (n = 9)

Fig. 2 Mean changes in the difference between forearm and

fingertip skin temperatures (Tskf-f) plotted as functions of changes

in Tc in the control trial (CT; exercise in normoxia at 50 % of

normoxic Wpeak), hypoxic relative trial (HRT; exercise in hypoxia at

50 % of hypoxic Wpeak) and hypoxic absolute trial (HAT; exercise in

hypoxia at the same absolute WR as in CT), before (upper graph) and

after (lower graph) the 28-day SH-TL regimen (n = 9)

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Forehead _msw

Exercise _msw (p \ 0.001) (and therefore presumably evap-

orative heat loss) increased in all conditions and attained

asymptotic values 10–15 min after the initiation of exercise.

Figure 3 present the _msw responses relative to the changes in

Tc. Pre sleep-high train-low, _msw values during the last

10 min of cycling were higher (p = 0.02) in HAT [2.55

(0.53) mg cm-2 min-1] than in CT [1.97 (0.42) mg cm-2

min-1] and HRT [1.86 (0.31) mg cm-2 min-1]. The SH-TL

period increased (p = 0.037) the _msw response in CT [2.42

(0.76) mg cm-2 min-1] and tended to increase it also in the

HRT [2.01 (0.33) mg cm-2 min-1, p = 0.093], whereas

SH-TL did not affect the _msw response in HAT [2.59

(0.30) mg cm-2 min-1]. At similar Tc, _msw was higher pre-

SH-TL in HAT than in CT and HRT, but these differences

abated post-SH-TL (Fig. 3). The rate of increase in _msw was

also higher in HAT than in CT and HRT pre-SH-TL, but

there were no differences between conditions for this vari-

able post-SH-TL (Table 2). In addition, SH-TL reduced the

core-temperature threshold for onset of sweating in CT, but

not in HRT or HAT (Table 2).

Cox and Mox

During the course of exercise, cerebral oxygenation

decreased by *25 lL [increase in D(HbO2)] in HRT and

HAT, both pre- and post-SH-TL, whereas no significant

D(HbO2) changes were observed during exercise pre- or

post-SH-TL in CT. Also, oxygenation in the vastus lateralis

muscle, decreased [increase in D(HbO2)] during the course

of exercise in HRT and HAT but not in CT, with similar

responses pre- and post-SH-TL (Table 3).

Cerebral D(Hb) increased significantly during exercise

and by similar magnitudes pre- and post-SH-TL, the

exercise-induced increments being more pronounced in

HRT and HAT than in CT. At the muscle level, exercise

increased D(Hb) only in HAT and HRT without differences

pre- and post-SH-TL.

Fig. 3 Mean changes in rate of forehead sweating ( _msw) plotted as

functions of changes in Tc, in the control trial (CT; exercise in

normoxia at 50 % of normoxic Wpeak), hypoxic relative trial (HRT;

exercise in hypoxia at 50 % of hypoxic Wpeak) and hypoxic absolute

trial (HAT; exercise in hypoxia at the same absolute WR as in CT),

before (upper graph) and after (lower graph) the 28-day SH-TL

regimen (n = 9)

Table 3 Mean (SE) NIRS cerebral and muscle micromolar changes

(D, lM) from resting condition after 25 min of constant-work rate

cycling for oxyhaemoglobin D(HbO2), deoxyhaemoglobin D(Hb) and

total haemoglobin D(HbT) for the control trial (CT; exercise in

normoxia at 50 % of normoxic Wpeak), the hypoxic relative trial

(HRT; exercise in hypoxia at 50 % of hypoxic Wpeak) and the hypoxic

absolute trial (HAT; exercise in hypoxia at the same absolute WR as

in CT), before and after the SH-TL regimen

Pre-SH-TL Post-SH-TL

CT HRT HAT CT HRT HAT

Cerebral

D(HbO2) -6.4 (1.0) -25.7 (1.0)b -23.4 (1.4)b -6.32 (1.1) -23.4 (1.3)b -26.7 (1.2)b

D(Hb) 13.8 (1.1) 38.6 (1.1)b 33.5 (1.7)b 14.41 (1.2) 37.6 (1.3)b 38.9 (1.1)b

D(HbT) 7.3 (0.8) 12.9 (0.8) 10.1 (1.0) 7.0 (1.0) 14.2 (0.9) 12.8 (1.0)

Muscle

D(HbO2) -2.2 (0.8) -16.6 (1.0)b -16.8 (0.9)b -2.2 (0.9) -12.9 (0.7)b -17.0 (0.9)b

D(Hb) 5.4 (0.9) 13.7 (1.3)b 16.2 (1.3)b 2.8 (1.3) 14.8 (0.9)b 23.5 (0.9)b

D(HbT) 3.1 (0.9) -3.1 (1.3) -0.4 (1.1) -0.5 (1.3) 1.8 (0.9) 6.6 (0.8)a,b,c

a Significant difference compared to values before SH-TLb Significant difference compared to CT, p \ 0.01c Significant difference compared to HRT, p \ 0.05

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There was a tendency (p = 0.07) for an exercise-

induced increase in cerebral D(HbT) in HRT and HAT

compared to in CT pre-, as well as post-SH-TL. Exercise

increased D(HbT) in the muscle (p = 0.04) only in one

condition: HAT post-SH-TL (Table 3).

Discussion

Sleep-high train-low is a training strategy to acclimatize

individuals to altitude. It has been demonstrated to enhance

aerobic performance not only at altitude, but also at sea

level. It is for the later reason that it is commonly incor-

porated in athletes’ training schedules. The present study

investigated the effect of a SH-TL regimen on exercise

temperature regulation. Prior to SH-TL, during exercise at

a given external (absolute) work rate, and for similar core

and skin temperatures, hypoxia potentiated the sweating

response. This acute hypoxia-induced potentiation of

sweating rate was diminished after the SH-TL period. In

acute hypoxia, the augmented sweating, and hence provi-

sions for evaporative heat loss, occurred in concert with a

reduced cutaneous vasodilatation. Thus, SH-TL reversed

the augmentation of the sweating response observed in

acute hypoxia but increased the provisions for conductive

heat loss. Sleep-high train-low improved the normoxic

exercise sweating response, possibly by increasing the

secretion capacity and sensitivity of the sweat glands, as a

consequence of the aerobic training (Nadel et al. 1974;

Roberts et al. 1977; Buono and Sjoholm 1988).

Effects of the SH-TL regimen on exercise heat

dissipation mechanisms

That the pre-SH-TL exercise sweating response was greater

in the hypoxic than the normoxic condition, at a given

absolute work rate, does not necessarily imply that the

physiological pathways responsible for this increase were

triggered by oxygen deficiency per se. Presumably, the

exaggerated sweating response was secondary to the

greater relative work rate imposed by hypoxia (Bocqueraz

et al. 2004; Eiken and Mekjavic 2004; Kacin et al. 2007).

This hypoxia-induced augmentation of sweating rate was

accompanied by higher exercise values for HR, _VE, RPE,

DCox, DMox, TSkf-f in HAT than in CT, suggesting

increased sympathetic response resulting from greater

influence of central command and muscle metabosensitive

drive in HAT. Indeed, central command and muscle me-

taboreflex drive have previously been implicated as causal

factors in the exacerbation of sweating during exercise

(Eiken and Mekjavic 2004; Kondo et al. 1999; Shibasaki

et al. 2003). Furthermore, in agreement with previous

findings (Kacin et al. 2007), the present pre-SH-TL exac-

erbation of the exercise sweating response in HAT was

abated after a SH-TL regimen, as evidenced by the similar

post-SH-TL values of _msw, in CT, HAT and HRT for

identical changes in Tc (Fig. 3). Even though our data does

not allow us to discern the mechanisms underlying this SH-

TL-induced abatement of the exercise sweating response in

hypoxia, it appears likely that it was associated with the

acclimatization to hypoxia rather than with the aerobic

training. Thus, it appears from cross-sectional studies

comparing trained and untrained individuals (Amano et al.

2011; Buono and Sjoholm 1988; Tankersley et al. 1991;

Yamazaki et al. 1994; Yanagimoto et al. 2002) and from

longitudinal training studies (Nadel et al. 1974; Roberts

et al. 1977) that endurance training augments the exercise

sweating response. This notion is compatible with our

finding that SH-TL increased the sweating response during

normoxic exercise, both by lowering the core temperature

threshold for onset of sweating and by increasing the gain

of the sweating response (Table 2 and Fig. 3). Considering

that SH-TL did not alter the normoxic exercise responses

for Cox, Mox, RPE, _VO2, _VE, HR, SpO2, �Tsk or Tc, it

appears likely that the augmentation of the sweating

response was a result of peripheral adaptation of the sweat

glands rather than of increased sympathetic drive. Like-

wise, Buono and Sjoholm (1988) attributed their finding

that the in vivo secretory activity of sweat glands is greater

in aerobically trained than in sedentary subjects, to train-

ing-induced peripheral adaptations.

The question arises then as to what mechanism might

underlie the SH-TL-induced reversal of the initial hypoxic

exaggeration of the exercise sweating response, occurring

presumably despite improved peripheral provisions for

sweat secretion. Possibly, a reduced sudomotor drive dur-

ing hypoxic exercise may have been a consequence of SH-

TL-induced improvement of blood flow in the working

muscles resulting in reduced intramuscular accumulation

of metabolic end products and hence in reduced activation

of muscle metabosensitive afferents (Kondo et al. 1999;

Eiken and Mekjavic 2004); SH-TL increased D(HbT) in

the vastus lateralis, and hence presumably leg muscle blood

flow (Van Beekvelt et al. 2001), during the HAT. Notably,

judging from the increase in �Tsk and decrease in TSkf-f

(indices of cutaneous vasodilatation) it appeared that SH-

TL also increased cutaneous blood flow during HAT. The

notion that both the subsided sweating response and

increased vasodilatory response during HAT after SH-TL

were secondary to the increased muscle blood flow is

supported by previous findings that graded ischemia in the

working leg muscles increases sweating and reduces

cutaneous vasodilatation (Kacin et al. 2005). Another fac-

tor that may have contributed to the SH-TL-induced

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reversation of the exaggerated exercise sweating response

observed during acute exposure to hypoxia is the con-

comitant increase in the exercise hyperpnea. In agreement

with previous studies (Townsend et al. 2005) present

results showed that a main acclimatization effect of SH-TL

is an increased hypoxic ventilatory drive resulting in

improved oxyhaemoglobin saturation, whereas the regimen

appears to have marginal effects on haematological vari-

ables (Ashenden et al. 1999; Gore and Hopkins 2005).

Thus, the SH-TL-dependent increase in arterial oxygen

content during HAT may have reduced the sympathetic

outflow induced by hypoxia in peripheral, carotid chemo-

receptors and in oxygen sensitive cells within the brain

stem (Saito et al. 1988; Stickland et al. 2008; Xie et al.

2001).

Regulation of core temperature

During exercise, the increase in core temperature is a result

of heat production and heat dissipation. The former is a

function of the external load, and the later presumably

modified by the relative work rate (Gonzalez-Alonso et al.

2008). Thus, in the present study, the CT and HAT trials

incorporate the same external work rate, but the HAT trial

induced a greater relative work rate. Similar Tc responses

would therefore be anticipated simply on the basis of the

heat produced. However, since the heat-dissipation

responses are predominantly related to factors associated

with the relative work rate, HAT exercise would be

expected to initiate a greater heat loss. The manner in

which heat is lost via different pathways appears not to be

uniform during hypoxic exercise. Namely, the expected

potentiation of heat loss is only evident in the sweating

response, whereas the decreased vasodilatation reflects a

reduction in the conductive and/or convective heat loss.

The overall heat loss was not determined in the present

study, but presumably it was maintained at similar levels.

This would, to a degree, explain the lack of any difference

in the exercise Tc response during exercise at different

absolute work rates. A novel finding of the present study is

therefore that the factors associated with the relative work

rate do not have the same effect on the heat-loss pathways,

and that the process of acclimatization to hypoxia reduces

this effect. It is unlikely, that central thermoregulatory

mechanisms regulate the magnitude of heat loss, such that

enhancement of heat loss in one pathway (i.e., evaporative)

is compensated by a reduction in another (i.e., conductive).

Nevertheless, in the present study the overall effect of the

balance in the evaporative and conductive heat loss resul-

ted in similar exercise-induced increment in Tc.

From a practical perspective, the reduced sweating rate

during exercise in hypoxia after a SH-TL regimen might be

beneficial for alpinists, reducing any problems with alti-

tude-induced dehydration. Moreover, it appears that ath-

letes who have undertaken a SH-TL regimen to improve

endurance performance at sea level will not risk suffering

from reduced sweating rate since the normal increase in

exercise sweating rate following aerobic training seems to

be preserved also after SH-TL, provided the exercise bout

is executed under normoxic conditions.

Methodological limitations

The design of the present study, allows for analyses of the

combined effects of hypoxic acclimatization and aerobic

training, but does not permit one to distinguish the indi-

vidual contributions from these two components of the SH-

TL regimen. Addition of another condition, for instance a

sleep-low train-low condition, would make it possible to

single out effects contributed by the aerobic training per se.

Other delimitations of the present study include the lack of

direct measurement of cutaneous blood flow and the single

site for determining sweating rate. Skin temperature

between forearm and fingertip was used as an index of

vasoconstriction; although it does not necessarily reflect

overall cutaneous blood flow it has been shown to provide

a robust and reliable qualitative index of cutaneous vaso-

motor responses (House and Tipton 2002, Rubinstein and

Sessler 1990). Sweat secretion was only measured on the

forehead. Considering the substantial regional differences

in sweating rate, more sites of measurements are warranted

to make general assumptions regarding sweating responses

(Havenith and van Middendorp 1990; Kondo et al. 1998;

Machado-Moreira et al. 2008). Finally, to make it possible

to generalize the present findings, it is necessary to also

perform experiments in female subjects.

Thus in summary it appears that, a 28-day SH-TL reg-

imen can reduce the hypoxic exacerbation of the exercise

sweating response via higher convective heat loss and

improve the sweating response during normoxic exercise.

As regards mechanisms underlying these SH-TL-induced

changes in exercise heat dissipation, the present data on

blood-volume distribution and oxygenation of the cerebral

and exercising muscle tissues do not permit firm conclu-

sions, but are compatible with the notion that improved

muscle blood flow may play a role. Whether these SH-TL

responses are attributable to the effect of hypoxic accli-

matization or the aerobic training remains to be settled.

Acknowledgments We would like to thank all the subjects for their

cooperation and patience. We are grateful to Bogomir Vrhovec and

Mojca Amon for their valuable assistance. This study was supported

by a grant from the Slovenian Research Agency (ARRS grant no. L7-

2413) to Igor B. Mekjavic, and from b-Cat B.V. (The Netherlands) to

Igor B. Mekjavic and Ola Eiken.

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Conflict of interest The authors state that there is no personal

conflict of interest in the present study.

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