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We studied thermoregulatory responses of ten well-trained (V . O2max, 57 (7) mL min-1 kg-1) women taking a combined, mono-phasic oral contraceptive pill (OCP; ≥ 12 months) during exercise in dry and humid heat, across their active OCP cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), to assess autonomic regulation, then self-paced intensity (30- min work trial), to assess behavioural regulation. Trials were in quasi-follicular (qF) and quasi-luteal (qL) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT, 27°C). During rest and exercise at 125 W, rectal temperature was 0.15°C higher in qL than qF (p = 0.05) independent of environment (p = 0.17). The onset threshold and thermosensitivity of local sweat rate and forearm blood flow relative to mean body temperature was unaffected by the OCP cycle (both p > 0.30). Exercise performance did not differ between quasi-phases (qF: 268 (31), qL: This article is protected by copyright. All rights reserved. 263 (26) kJ, p = 0.31), but was 5 (7)% higher in DRY than HUM (273 (29), 258 (28) kJ; p = 0.03). When compared to our matched eumenorrhoeic athletes (Lei et al. 2017), chronic OCP use impaired the sweating onset threshold and thermosensitivity (both p < 0.01). In well-trained, OCP-using women exercising in the heat: i) a performance-thermoregulatory trade-off occurred that required behavioural adjustment, ii) humidity impaired performance due to reduced evaporative power despite matched WBGT, and iii) the sudomotor but not behavioural thermoregulatory responses were impaired compared to matched eumenorrhoeic athletes.
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J Physiol 597.1 (2019) pp 71–88 71
The Journal of Physiology
On exercise thermoregulation in females: interaction
of endogenous and exogenous ovarian hormones
Tze-Huan Lei1, James D. Cotter2, Zachary J. Schlader3, Stephen R. Stannard1,BlakeG.Perry
1,
Matthew J. Barnes1and Toby M¨
undel1
1School of Sport, Exercise and Nutrition, Massey University, Palmerston North, New Zealand
2School of Physical Education, Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand
3Center for Research and Education in Special Environments, Department of Exercise and Nutrition Sciences, University at Buffalo, Buffalo, NY, USA
Edited by: Scott Powers & Bettina Mittendorfer
Key points
rOne in two female athletes chronically take a combined, monophasic oral contraceptive pill
(OCP). Previous thermoregulatory investigations proposed that an endogenous rhythm of the
menstrual cycle still occurs with OCP usage.
rForthcoming large international sporting events will expose female athletes to hot environments
differing in their thermal profile, yet few data exist on how trained women will respond from
both a thermoregulatory and performance stand-point.
rIn the present study, we have demonstrated that a small endogenous rhythm of the menstrual
cycle still affects Tcore and also that chronic OCP use attenuates the sweating response, whereas
behavioural thermoregulation is maintained.
rFurthermore, humid heat affects both performance and thermoregulatory responses to a
greater extent than OCP usage and the menstrual cycle does.
Abstract We studied thermoregulatory responses of ten well-trained ( ˙
VO2max,57±
7mLmin
1kg1) women taking a combined, monophasic oral contraceptive pill (OCP)
(12 months) during exercise in dry and humid heat, across their active OCP cycle. They
completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), aiming
to assess autonomic regulation, and then a self-paced intensity (30-min work trial) to assess
behavioural regulation. Trials were conducted in quasi-follicular (qF) and quasi-luteal (qL) phases
in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT) (27°C).
During rest and exercise at 125 W, rectal temperature was 0.15°ChigherinqLthanqF(P=
0.05) independent of environment (P=0.17). The onset threshold and thermosensitivity of
local sweat rate and forearm blood flow relative to mean body temperature was unaffected by
the OCP cycle (both P>0.30). Exercise performance did not differ between quasi-phases (qF:
268 ±31 kJ, qL: 263 ±26 kJ, P=0.31) but was 5 ±7% higher during DRY than during
To by M ¨
undel is a tenured academic at Massey University in New Zealand, where he is teacher, supervisor and researcher of
human exercise physiology, particularly temperature regulation during heat stress. Tze -Hu an ( Joe) Lei is a doctoral candidate
under the supervision of Dr Toby M¨
undel at Massey University in New Zealand. His research has focussed on human exercise
thermoregulation, particularly with environmental heat stress. His work has determined the physiological, behavioural and
perceptual consequences of (i) the menstrual cycle and oral contraception and (ii) the thermal profile of the environment (i.e.
ambient temperature and humidity). Having previously been educated and trained in New Zealand and his native Taiwan, Joe
will be continuing his research apprenticeship via a prestigious JSPS International Fellowship for Research in Japan, aiming to
study the induction and decay of dry and humid heat acclimation on sweat gland function with Dr Narihiko Kondo at Kobe
Unive rsity.
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2018 The Authors. The Journal of Physiology C
2018 The Physiological Society DOI: 10.1113/JP276233
72 T.-H. Lei and others J Physiol 597.1
HUM (273 ±29 kJ, 258 ±28 kJ; P=0.03). Compared to matched eumenorrhoeic athletes,
chronic OCP use impaired the sweating onset threshold and thermosensitivity (both P<0.01).
In well-trained, OCP-using women exercising in the heat: (i) a performance-thermoregulatory
trade-off occurred that required behavioural adjustment; (ii) humidity impaired performance as
a result of reduced evaporative power despite matched WBGT; and (iii) the sudomotor but not
behavioural thermoregulatory responses were impaired compared to matched eumenorrhoeic
athletes.
(Received 28 March 2018; accepted after revision 1 October 2018; first published online 15 October 2018)
Corresponding author T. M ¨
undel: School of Sport, Exercise and Nutrition, Massey University, Private Bag 11-222,
Palmerston North, New Zealand. Email: t.mundel@massey.ac.nz
Introduction
The primary ovarian steroidal hormones influence
several non-reproductive organs and systems. Concerning
thermoregulation, oestrogens promote heat dissipation
and lower core body temperature (Tcore), whereas
progestogens are thermogenic (Israel & Schneller,
1950; Charkoudian & Stachenfeld, 2014). Studies have
investigated the impact of these hormones on thermo-
regulation during different phases of the menstrual
cycle. In eumenorrhoeic women, the thermoregulatory
balance-point shows Tcore to be regulated 0.4°Chigher
during the post-ovulatory (luteal) phase at rest and during
passive and active heat stress, as the rise in progesterone
exerts its dominant effect (Harvey & Crockett, 1932; Israel
& Schneller, 1950). This is accompanied by an increased
Tcore threshold for thermoregulatory effector responses
such as sweating and cutaneous vasodilatation (Hessemer
&Br
¨
uck, 1985; Stephenson & Kolka, 1985; Stachenfeld
et al. 2000). Therefore, several studies have suggested
that, when performing exercise under environmental heat
stress during their luteal phase, women should avoid
competition or face a thermoregulatory and performance
disadvantage (Stephenson & Kolka, 1993; Charkoudian &
Joyner, 2004; Janse de Jonge et al. 2012). However, for a
well-trained and competitive female athlete, this may not
be the case. First, trained females have a greater capacity to
deal with a heat load as a result of their enhanced thermo-
effector responses compared to less-trained counter-
parts (Kuwahara et al. 2005a,b). Second, trained women
show smaller biphasic effects on Tcore and thermo-
effector responses because of reduced ovarian hormone
concentrations and fluctuation between their menstrual
phases (Kuwahara et al. 2005a,b). Third, most pre-
vious investigations have utilised a fixed-intensity exercise
protocol that is less ecologically-valid (i.e. most athletes
use pacing) and does not examine the fundamental pre-
mise of heat balance: that heat loss needs only to equal
heat production (Gagnon et al. 2013). However, we
recently demonstrated that, when well-trained females can
use behavioural thermoregulation (self-pacing) during
exercise in heat stressful environments, exercise intensity,
and therefore, metabolic heat production is reduced (Lei
et al. 2017). This eases the required evaporation and
decreases thermoregulatory strain to the point where the
menstrual phase-related thermodynamic and autonomic
differences become nullified (Lei et al. 2017). Furthermore,
these menstrual phase-related effects were relatively small
in well-trained women.
The prevalence of oral contraceptive (OC) use is
high (42–83%) among athletically competitive and
elite females, three-quarters of whom reportedly use a
combined monophasic OC pill (OCP) (Rechichi et al.
2009). The combined monophasic OCP provides a
constant dose of synthetic oestrogen and progestogen
for 21 days followed by 7 days of a placebo. Previous
investigations on OCP users report that the phase-related
elevation in Tcore and concomitant increase in the Tcore
threshold for effector responses is maintained during
active and passive heating, and that this shift can be
regarded as a strong and residual effect of the phase
of the menstrual cycle (Grucza et al. 1993; Martin &
Buono, 1997; Rogers & Baker, 1997; Charkoudian &
Johnson, 1997a;Tenagliaet al. 1999; Sunderland & Nevill,
2003). However, although these investigations generally
describe their comparison between a quasi-follicular and
quasi-luteal phase, the comparison always occurred when
the females were taking active OC compared to their
placebo week (withdrawal). This raises several important
considerations. First, the variable tissue washout rates
mean that the exogenous hormones, or their metabolites,
probably remain elevated and able to exert an effect
(Israel & Schneller, 1950; Rothchild & Barnes, 1952;
Charkoudian & Stachenfeld, 2014). Second, towards the
end of the placebo week, the concentration of endogenous
oestrogens increases and, as such, this phase should be
viewed as a transitory hormonal phase and not a controlled
‘low’ hormonal phase (i.e. compare OC use as a ‘high’
hormonal phase: Rechichi et al. 2008; Charkoudian &
Stachenfeld, 2014). Third, the synthetic progestins found
in OCPs differ in some of their basic actions to those of
endogenous progesterone, probably influencing physio-
logical systems differently (Charkoudian & Stachenfeld,
2014). Thus, the supposition that an endogenous rhythm
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J Physiol 597.1 Exercise thermoregulation in trained women taking oral contraception 73
of the menstrual cycle is maintained during OC use has
not been investigated properly because, to our knowledge,
no data exist on variation within the active OCP cycle. This
was the principle objective of the present study. Moreover,
data exist indicating that chronic OCP use may alter
Tcore and thermoeffector responses to active and passive
heating in women, as indicated by greater resting Tcore
and attenuated changes in mean body temperature and
gain for local sweat rate (Grucza et al. 1993; Sunderland
& Nevill, 2003). Therefore, a secondary objective was to
compare the results of the current OCP cohort matched
in relevant physical and fitness characteristics with those
of our previous eumenorrhoeic cohort (Lei et al. 2017).
Forthcoming large international events [e.g. 2019 Inter-
national Association of Athletics Federations (IAAF)
World Championships in Doha; 2020 Summer Olympic
Games in Tokyo] will expose female athletes to high
environmental heat stress, and the number of women
participating at this elite level is ever increasing,
now approximating that of males. However, these
environments differ in their ambient thermal profile,
with arid environments usually permitting almost
full evaporation of sweat, whereas humid tropical
environments do not. In our previous investigation, the
performance of eumenorrhoeic athletes was impaired
in humid compared to dry ambient heat matched for
wet bulb globe temperature (WBGT) (27 °C) (Lei et al.
2017). To our knowledge, no previous study has compared
thermoregulatory and performance responses in women
taking OCP when exposed to humid vs. dry heat. This was
our final objective.
In the present study, we aimed to characterise
and compare the behavioural and autonomic thermo-
regulatory responses to exercise when exposed to
equivalent dry and humid heat stress in well-trained
women who had been chronically taking a combined,
monophasic OCP. Based on our previous study in
eumenorrhoeic women, as well as the literature described
above, we hypothesised that: (i) if an endogenous thermo-
regulatory rhythm persisted during their active OCP
cycle, it would be small and nullified by behavioural
adjustments; (ii) these differences in thermoregulatory
control across the OCP cycle would interact with
differences brought about by the thermal environment (i.e.
dry vs. evaporative heat transfer); and (iii) compared to a
matched cohort of eumenorrhoeic athletes, chronic OCP
users would display an attenuated autonomic response.
Methods
Ethical approval
The present study was approved by the Massey University
Human Ethics Committee: Southern A (14/99). The study
conformed to the standards set by the latest revision of
Table 1. Participant characteristics for the matched eummeno-
rrhoeic (EUM) (Lei et al. 2017) and OCP groups
Characteristic OCP EUM Pvalue
Age (years) 25 ±534±90.02
Height (cm) 167 ±5 165 ±50.30
Mass (kg) 68 ±10 62 ±40.10
AD(m2)1.76±0.13 1.67 ±0.06 0.10
AD: mass 0.026 ±0.002 0.027 ±0.001 0.14
% fat 24 ±524±50.85
˙
VO2max (L min1)3.7±0.5 3.5 ±0.5 0.42
˙
VO2max
(mL min1kg1)
55 ±957±70.69
Wmax (W) 278 ±25 261 ±30 0.19
Wmax (W kg1)4.2±0.7 4.2 ±0.4 0.82
Data are the mean ±SD. AD, Dubois body surface area. Both
EUM and OCP cohorts: n=10.
the Declaration of Helsinki, except for registration in a
database, with each participant providing their informed,
written consent.
Participants
Ten aerobically well-trained and competitive women
cyclists and triathletes volunteered for this study.
Table 1 displays the participants’ mean ±SD
physical characteristics alongside those of our matched
eumenorrhoeic group (Lei et al. 2017); this was considered
appropriate because all methods were identical between
this group and the OCP group. The data of the
eumenorrhoeic group have been reported previously
with respect to testing unique aims and hypotheses (Lei
et al. 2017). The training history for both OCP and
eumenorrhoeic groups was similar at 5 ±3years(range
2–12 years). All OCP participants were taking a mono-
phasic combination OCP (1 year) that provides a
constant level of hormones for 21 days followed by a
placebo pill for 7 days. Five were taking GinetR(REX
Medical Ltd, Auckland, New Zealand; containing 2 mg
of cyproterone acetate and 35 μg of ethinylestradiol),
four Ava 20 ED R(Teva Pharma Ltd, Auckland, New
Zealand; containing 0.1 mg of levonorgestrel and
20 μg of ethinylestradiol) and one Norimin R(Pfizer
Ltd, Auckland, New Zealand; containing 0.5 mg of
norethisterone and 35 μg of ethinylestradiol).
Experimental overview
The present study replicated all of the conditions used
for our matched eumenorrhoeic group (Lei et al. 2017).
All trials were conducted during autumn to spring in
Palmerston North, New Zealand, when temperatures
rarely exceed 22°C. No participant had spent time in
warmer climates or training environments within 1 month
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74 T.-H. Lei and others J Physiol 597.1
preceding testing. All participants attended the laboratory
on six occasions: (i) preliminary submaximal and maximal
tests; (ii) experimental familiarisation; and (iii) to (vi)
experimental trials. The four experimental trials were
a full cross-over of OCP phase (quasi-follicular: qF;
quasi-luteal: qL) and environment (dry and humid, at
matched WBGT). All trials were counterbalanced except
that the same order of dry or humid environment
was retained for each OCP phase within participants.
Experimental trials were conducted at the same time
of day (±1h)andfollowing>24 h of dietary and
exercise control. Each trial consisted of 12 min of
fixed-intensity cycling followed immediately by 30 min
of a self-paced cycling performance trial. All exercise
was performed on an electromagnetically-braked cycle
ergometer (Lode Excalibur, Groningen, The Netherlands)
with a participant-specific set up for the seat, handle bars
and pedals, which was maintained constant for each trial
with respect to a participant.
Preliminary testing and familiarisation
Submaximal and maximal capacity tests were under-
taken in the qF phase to minimise the potential
physiological effects of the menstrual/OCP cycle on
˙
VO2max performance. Following body mass and height
measurement, preliminary testing was conducted in a
temperate laboratory environment (18–22°C) with a
fan-generated airflow of 19 km h1facing participants.
The submaximal test consisted of four consecutive 6-min
power outputs: 100, 125, 150 and 175 W, at comfortable
but constant cadence. The rate of oxygen consumption
(˙
VO2) was measured during the last 2 min of each stage.
Following a 10-min rest, a maximal capacity test was
undertaken to measure ˙
VO2max. Work rate began at 100 W
and consisted of increments at 25 W min1until volitional
fatigue. The linear relationship between power output
and ˙
VO2was subsequently used to calculate workload
for experimental trials, as 75% ˙
VO2max (Jeukendrup et al.
1996).
At least 24 h following preliminary testing, the
familiarisation trial was undertaken to ensure that
participants were accustomed to the experimental
procedures and to minimise learning effects. These trials
replicated entirely the experimental trials outlined below.
Dietary and exercise control
The day of and prior to any experimental trial was
marked by abstinence from alcohol, exercise and only
habitual caffeine use (i.e. because abstinence would in
itself confound from withdrawal effects). Participants were
provided with a standardised dinner (2 ×Watti e s Snack
Meals; Heinz Watties, Hastings, New Zealand: 1363 ±
247 kJ providing 53 ±6gofcarbohydrate,12±4gof
protein and 8 ±0.3 g of fat) the night preceding the trial
and were asked to consume the same light meal (consisting
of toast or cereal) between 2 and 4 h prior to visiting
the laboratory for the trial. Fluid was encouraged and
a euhydrated state was further ensured by instructing the
participants to drink 500 mL of water 2 h prior to each trial.
OCP cycle phase and type of heat stress
Participants were tested during the qFandqLphases
to permit comparison with our eumenorrhoeic group.
Testing occurred on days 3–5 and 18–20 following the
start of OCP use, whereas testing of our eumenorrhoeic
group occurred on days 3–6 (early follicular) and 18–21
(mid-luteal) following the start of menses. This was
unavoidable as a result of the study hypothesis and
therefore design and, as such, this meant that the current
OCP users were being tested on days 10–12 (quasi mid-late
follicular) and 25–27 (quasi mid-late luteal) following the
start of menses.
In accordance with previous studies investigating the
influence of humid (HUM) vs. dry (DRY) environmental
heat in women (Morimoto et al. 1967; Shapiro et al.
1980; Frye & Kamon, 1983), heat stress was indexed using
WBGT because it is the most widely used empirical index
(Brotherhood, 2008; Budd, 2008). Our decision-making
was guided by the typical (or possible) extreme conditions
athletes would encounter at the 2018 Commonwealth
Games (humid) compared to the 2019 IAAF World
Championships (dry). Therefore, a WBGT equivalent to
27°C was chosen to elicit our HUM (29 ±0.3°C, 83 ±
2% relative humidity) and DRY (34 ±0.2°C, 42 ±3%
relative humidity) environments. Absolute humidity in
these two environments was 3.4 ±0.1 kPa and 2.2 ±
0.2 kPa, respectively. Within each OCP phase, exposure to
DRY and HUM environments was separated by 3 days.
Experimental procedures
The four experimental sessions were conducted in the
same environmental chamber with a 19 km h1airflow.
However, the fan was turned off for each 2 min data
collectionperiod(ofeach6minstageorinterval)to
minimise the interference of airflow on measurement. On
arrival at the laboratory, participants voided to produce a
urine sample to confirm a urine specific gravity <1.010
and hence euhydration, nude mass was recorded and they
then self-inserted a rectal thermistor. A blood sample
was obtained from the antecubital vein, following which
participants entered the environmental chamber wearing
only cycling shorts and top, shoes and socks. Participants
rested seated on the ergometer for 20 min during which
they were instrumented and baseline measurements were
recorded. Participants then completed 6 min of cycling
at each of 125 and 150 W to allow sufficient warm-up
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J Physiol 597.1 Exercise thermoregulation in trained women taking oral contraception 75
and fixed-intensity responses to be recorded. Physio-
logical measurements taken during the final 2 min of each
intensity included expired gas, heart rate (HR), blood
pressure (BP), forearm blood flow (FBF) and cardiac
output ( ˙
Q) responses, whereas rectal (Trec) and skin
(Tsk) temperatures, as well as local sweat rate (LSR), were
measured continuously. Immediately on completion of the
150 W bout, the ergometer was set to linear mode based on
the formula of Jeukendrup et al. (1996), and participants
were instructed to perform as much work as possible
over 30 min. During this 30 min of self-paced period,
work completed (kJ), HR and expired gas responses were
recorded every 6 min, whereas Trec,Tsk and LSR were
measured continuously. Total work completed was used
as the performance criterion, whereas the time profile
of power output was used as the behavioural criterion
(Lei et al. 2017). Immediately following the 30 min
self-paced exercise, FBF was measured when participants
began their 5 min cool-down (100 W) before the nude
mass of participants (towelled dry) was recorded to allow
estimation of whole-body sweat rate (WBSR). Tap water
at 20°C and in aliquots of 3 mL kg1bodyweight was
provided to drink ad libitum either at 15-min intervals
or when requested throughout each trial to minimise
dehydration.
Measurements
Anthropometric. Participant height and mass were
measured using a stadiometer (Seca, Hamburg, Germany;
accurate to 0.1 cm) and scale (Jadever, Taipei, Taiwan;
accurate to 0.01 kg), from which surface area was estimated
(Dubois & Dubois, 1916). Body composition was
measured using multifrequency bioelectrical impedance
analysis (InBody 230; InBody, Seoul, Korea) in accordance
with a standard procedure (Kyle et al. 2004).
Respiratory. Expired respiratory gases were collected
and analysed to then calculate ˙
VO2and carbon dioxide
elimination ( ˙
VCO2), ventilation ( ˙
VE) and respiratory
exchange ratio (RER), using an online, breath-by-breath
system (Vista Turbofit; VacuMed, Ventura, CA, USA)
using a 30-s average. The system was calibrated before
each trial using β-standard gas concentrations and a 3 L
syringe (VacuMed).
Cardiovascular. The HR was recorded from detection of
R-R intervals (Polar Vantage XL; Polar Electro, Kempele,
Finland), whereas BP was measured using a stethoscope
and a sphygmomanometer over the right brachial artery,
in duplicate and by the same experienced operator.
Mean arterial pressure (MAP) was calculated as diastolic
blood pressure +1/3 pulse pressure. The FBF was
measured in triplicate (mean values reported) using
venous occlusion plethysmography (Whitney, 1953) with
a mercury-in-silastic strain-gauge on the widest part of
the forearm supported at heart level. The voltage output
was acquired (PowerLab; ADInstruments, Dunedin, New
Zealand) and displayed (Labchart Pro; ADInstruments)
in real time, as well as for offline analysis. The venous
occlusion pressure was 50 mm Hg, cycle duration 10 s.
Forearm vascular resistance (FVR) was calculated as
MAP/FBF. The ˙
Qwas measured using CO2rebreathing
(Defares, 1958), as described previously (Schlader et al.
2010). Pressure of end-tidal CO2(PETCO2)duringthe
rebreathing procedure was measured (O2/CO2gas
analyser; ADInstruments), with data acquisition and
display as noted above (AD Instruments). Differences
between PETCO2and venous and arterial PCO2were
corrected in accordance with Paterson & Cunningham
(1976) and Jones et al. (1979). The CO2content
difference was calculated as described by McHardy
(1967). Stroke volume (SV) was calculated from the Fick
equation.
Body temperatures. The Tcore was indexed from
Trec, measured using a calibrated rectal thermistor
(Mon-a-Therm; Covidien, Medtronic, Minneapolis, MN,
USA; accurate to 0.1˚C) inserted 10 cm beyond the
anal sphincter. The Tsk was measured at four sites
using calibrated skin thermistors (Grant Instrument Ltd,
Cambridgeshire, UK; accurate to 0.2°C) fastened on the
calf, thigh, chest and forearm using surgical tape (3M
Healthcare, St Paul, MN, USA). Area-weighted mean
Tsk was calculated in accordance with the equation
of Ramanathan (1964). Core and skin temperatures
were recorded using TracerDAQ Rsoftware (Measurement
Computing Corporation, Norton, MA, USA). To account
for the relative influence of Tcore and Tsk on the activation
of heat loss responses (Hertzman et al. 1952), mean body
temperature (Tb) was calculated as: 0.8 ×Trec +0.2 ×Tsk
(Stolwijk & Hardy, 1966).
Sweat rates. The LSR was measured using a ventilated
capsule (Graichen et al. 1982). The capsule (3.5 cm2)
was attached to the neck dorsally and ventilated with
dry air at 0.4 L min1. The effluent gas was sensed for
humidity (Honeywell Ltd, Auckland, New Zealand) and
temperature (National Semiconductor, Santa Clara, CA,
USA). The neck was used because all limbs were used for
other measurements and it was not exposed directly to
the fan. The WBSR was estimated from body mass loss,
corrected for fluid consumed.
Thermodynamics. Heat stress compensability was
estimated using the heat strain index (HSI), with >1.0
indicating uncompensable heat stress (Cheung et al.
2000). The HSI was calculated as the ratio of the required
evaporative cooling for heat balance (Ereq;Wm
2)andthe
maximal evaporative capacity of the environment (Emax;
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76 T.-H. Lei and others J Physiol 597.1
Wm
2) (Belding & Hatch, 1955). Ereq was calculated as
Ereq =M-W ±(C+R)±(Cres Eres). MWrepresents
metabolic heat production, where Mis the metabolic
rate (W m2), calculated as (Kenney, 1998): M=[352 ×
(0.23 ×RER +0.77) ×˙
VO2]/body surface area, and
Wistherateofenergylostasexternalwork(Wm
2).
C+Ris the rate of heat transfer from convection (C;
Wm
2) and radiation (R;Wm
2), calculated as the sum
of: C=hc·(TSk TA) (Kerslake, 1972) and R=4.7 ×
(TSk TA) (Kenney, 1998), where hcis the convective
heat transfer coefficient (W m2°C) (Kerslake, 1972)
and TAis the ambient temperature (°C). Cres +Eres is
the rate of respiratory conductive (Cres) and evaporative
(Eres) heat transfer, and was calculated as (Kenney, 1998):
Cres +Eres =[0.0012 ×M×(34 TA)] +[0.0023 ×
M×(44 PA)], where PAis ambient vapour pressure
(kPa). Emax was calculated as Emax =LR ·hc
(PSk PA), where LR is the Lewis relationship (16.5°C
kPa) and PSk is the saturated vapour pressure at the skin
(kPa).
Hormonal. Blood was collected by venipuncture into
a vacutainer (Becton-Dickinson, Wokingham, UK)
containing clot activator. Following inversion and clotting,
the whole blood was centrifuged at 4 °C and 805 g
for 12 min and aliquots of serum were transferred
into Eppendorf tubes (Genuine Axygen Quality; Corning
Inc., Union City, CA, USA) and stored at 80 °C
until further analysis. Serum samples were analysed
using enzyme-linked immunoassays for 17β-oestradiol
(Demeditec Diagnostics, Kiel, Germany) and progesterone
(IBL International, Hamburg, Germany), with a sensitivity
of 22.7 pmol L1and 0.14 nmol L1, respectively, and an
intra-assay variation of 4% and 6%, respectively.
Statistical analysis
All statistical analyses were performed with SPSS, version
20 (IBM Corp., Armonk, NY, USA). Descriptive values
were obtained and reported as the means ±SD, unless
stated otherwise. Levene’s test was used to ensure the data
did not differ substantially from a normal distribution.
Data were analysed using a three-way (OCP phase ×
environment ×time) ANOVA for repeated measures.
Resting and fixed-intensity exercise data were analysed
separately from self-paced exercise data. Sphericity was
assessed and, where the assumption of sphericity could
not be assumed, adjustments to the degrees of freedom
were made (ε>0.75 =Huynh–Feldt; ε<0.75 =
Greenhouse–Geisser). Where main or interaction effects
occurred, post hoc pairwise analyses were performed using
a paired samples ttest (Bonferroni correction where
relevant), with statistical significance set at P0.05.
Partial eta-squared (ηp2)isreportedasameasureofeffect
size, with demarcations of small (<0.09), medium (>0.09
and <0.25) and large (>0.25) effects, respectively (Cohen,
1988). This combination of statistical significance and
effect size provides an indication of the likelihood of
committing a Type I (i.e. P0.05 but ηp2<0.09) or II
(i.e. P<0.10 but ηp2>0.25) error. To examine how OCP
phase and type of heat stress affected the thermal control
of the effector responses (LSR and FBF), the visually
determined linear portion of each response against Tbwas
analysed by the same experienced researcher using simple
linear regression (y=y0+ax) and compared using
two-way (menstrual phase ×heat stress) ANOVA. We
used linear regression, as opposed to segmental regression,
to allow direct comparison with our previous cohort
(Lei et al. 2017). The onset threshold was defined as the
y-intercept (y0) of the regression line with values at base-
line once instrumented in the environmental chamber,
whereas the thermosensitivity was defined as the slope
(a) of the regression line. Notably, although the absolute
values determined for the onset threshold may not be
physiologically plausible using linear regression, shifts or
differences in the thresholds between groups are inter-
preted as physiologically meaningful. To allow comparison
between our OCP and previous eumenorrhoeic group
(Lei et al. 2017), a fourth (between-group) factor was
introduced using a mixed-model (group ×OCP phase ×
environment ×time) ANOVA, with the group effect
reported.
Results
Ovarian hormone concentrations (Table 2)
OCP use maintained constant endogenous concentrations
of both progesterone and 17β-oestradiol between qF
and qL(P=0.93, ηp2<0.01 and P=0.62, ηp2=
0.02, respectively) and concentrations were also not
different between days of testing within a quasi-phase
(P=0.24, ηp2=0.17 and P=0.22, ηp2=0.19,
respectively). Between-group analysis revealed that end-
ogenous concentrations of progesterone (P<0.01, ηp2=
0.41) but not 17β-oestradiol (P=0.07, ηp2=0.09, possible
type I error) were significantly lower in the current OCP
than in the previous eumenorrhoeic group.
Exercise performance and behaviour (Figure 1)
Work capacity was similar between OCP phases (qF:
268 ±31 kJ vs. qL: 263 ±26 kJ, P=0.31, ηp2=0.12) but
was 5 ±7% higher during DRY than during HUM (273 ±
29 kJ vs. 258 ±28 kJ; P=0.03, ηp2=0.45). Accordingly,
mean power output was unaffected by OCP phase (P=
0.44, ηp2=0.07) but was 5 ±7% higher during DRY than
during HUM (152 ±16 W vs. 143 ±16 W; P=0.03, ηp2=
0.43). When viewing behaviour as the self-paced exercise
profile, behaviour was similar between OCP phases
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Table 2. Individual and group progesterone and 17β-oestradiol concentrations during the qFandqL phase for the matched
eummenorrheic (EUM) (Lei et al. 2017) and OCP groups
Progesterone (nmol L1)17β-Oestradiol (pmol L1)
FLFL
Participant EUM OCP EUM OCP EUM OCP EUM OCP
1 0.3, 0.3 0.4, 0.4 30, 42 0.5, 0.5 195, 202 79, 75 290, 264 89, 102
2 0.6, 3.8 49, 43 33, 7 330, 301
3 2.2, 2.9 0.0, 0.1 219, 168 0.0, 0.1 503, 602 8, 4 1057, 833 3, 0
4 0.3, 0.3 0.2, 0.3 4.1, 11 0.4, 0.5 88, 132 96, 95 176, 723 90, 77
5 2.9, 1.0 0.2, 0.1 39, 21 0.5, 0.2 92, 103 56, 57 162, 165 71, 62
6 2.9, 1.9 0.3, 0.2 18, 39 0.2, 0.3 117, 44 24, 67 198, 198 36, 29
7 1.3, 0.6 0.5, 0.4 61, 60 0.5, 0.8 40, 62 60, 66 139, 261 64, 72
8 1.3, 2.2 0.9, 1.4 19, 61 0.5, 1.1 147, 136 28, 64 242, 169 76, 46
9 3.5, 3.2 0.1, 1.0 35, 59 0.2, 0.2 396, 430 1, 9 426, 716 0, 12
10 1.0, 1.3 0.2, 0.1 27, 65 0.2, 0.2 176, 195 10, 2 272, 363 4, 7
Mean ±SD 1.7 ±1.2 0.4 ±0.4 54 ±52 0.4 ±0.3 185 ±166 44 ±33 364 ±259 47 ±36
–, Blood sample not obtained. Significant difference between EUM and OCP. Both EUM and OCP cohorts: n=10.
(P=0.44, ηp2=0.07) but was 8 ±10 W higher during
DRY than during HUM (P=0.03, ηp2=0.43) and
changed over time (P<0.01, ηp2=0.61). Between-group
analysis revealed no differences between the OCP
and eumenorrhoeic groups for work capacity (P=
0.50, ηp2=0.03) or power output profile (P=0.52,
ηp2=0.02).
Physiological measures
Body temperatures (Figure 2). The Trec when resting was
0.15 ±0.21°ChigherinqLthaninqF(P=0.05, ηp2=
0.35) and was 0.12 ±0.12°C higher during HUM than
during DRY (P=0.01, ηp2=0.52). The rise in Trec during
fixed-intensity exercise differed between OCP phases as a
200
180
160
140
120
100
200
180
160
140
120
100
350
300
250
200
150
350
300
250
200
150
DRY HUM
Power Output (W)
Power Output (W)
Work Completed (kJ)
Work Completed (kJ)
0 6 12 18 24 30 0 6 12 18 24 30
Stage / Time (min) Stage / Time (min)
qF
qFqLqFqL
qLEFML qFqLEFML
Figure 1. Mean (SD) power output (n=10) and individual and mean ±SD work capacity (n=10) during
exercise in dry (DRY) and humid (HUM) heat during the qFandqL phase
Significant difference between qFqL within environment. Significant difference between corresponding
qFHUM value. Significant difference between corresponding qLHUM value. Mean early follicular (EF) and
mid-luteal (ML) values are provided for our previous eumenorrhoeic cohort (Lei et al. 2017).
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function of work-rate (OCP phase ×time: P=0.05, ηp2=
0.35) but was not dependent on environment (interaction:
P=0.17, ηp2=0.20), with the between-phase difference
seen at rest still being evident at 125 W (0.12 ±0.19°C) but
not at 150 W (0.06 ±0.21°C). During self-paced exercise,
Trec was similar between OCP phases (P=0.74, ηp2=0.05)
and environments (P=0.54, ηp2=0.08) but continued
to increase with time (P<0.01, ηp2=0.94) until the end
of exercise.
Resting Tsk was similar between OCP phases (P=
0.78, ηp2=0.01) but was 1.2 ±0.7°C higher during DRY
than during HUM (P<0.01, ηp2=0.76). During fixed-
intensity exercise, Tsk was similar between OCP phases
(P=0.85, ηp2<0.01) but differed between environments
as a function of work-rate (environment ×work-rate:
P<0.01, ηp2=0.61) such that the difference between
work rates was greater during HUM (0.79 ±0.42°C) than
during DRY (0.19 ±0.52°C). During self-paced exercise,
Tsk differed between environments as a function of time
(environment ×time: P=0.01, ηp2=0.31). Specifically,
Tsk values were maintained constant during DRY but
continued to increase by 0.7°CduringHUM.
Between-group analysis revealed no differences between
the OCP and eumenorrhoeic groups for Trec (all P>0.47,
ηp2<0.03) or Tsk (all P>0.58, ηp2<0.03) during any
stage of the protocol.
Cardiovascular and thermoeffectors (Table 3 and
Figures 3–5). Resting SV, ˙
Qand MAP were similar
between OCP phases and environments (all P>0.22,
ηp2<0.20), whereas resting HR was 2 ±2 beats min1
higher in DRY, with this being more evident in qFthan
in qL (environment ×OCP phase: P=0.08, ηp2=
0.30, possible type II error), and resting FVR was 2.9 ±
2.6 mm Hg min dL1higher during DRY than during
HUM (P=0.02, ηp2=0.59), although this may have
been more evident in qFthaninqL (environment ×
OCP phase: P=0.08, ηp2=0.37, possible type II error).
During fixed-intensity exercise, ˙
Qand possibly also SV
differed between environments as a function of OCP
phase and work-rate (environment ×phase ×time: P=
0.01, ηp2=0.75 and P=0.09, ηp2=0.47, possible type II
error, respectively), such that values were highest at 150 W
during qL-HUM. MAP and HR were similar between
OCP phases and environments (all P>0.16, ηp2<0.20)
but increased with work rate (both P<0.01, ηp2>0.86).
Thus, during fixed-intensity exercise, FVR was 1.5 ±
1.0 mm Hg min dL1higher during DRY than during
HUM (P<0.01, ηp2=0.74) and differed between OCP
phase as a function of work-rate (OCP phase ×time: P<
0.01, ηp2=0.82) such that FVR was lower during qLthan
qF at 125 W (by 1.6 ±2.2mLdLminmmHg
1)but
not at 150 W (0.2 ±1.8mLdLminmmHg
1). During
self-paced exercise, HR changed over time (P<0.01,
ηp2=0.71) independent of OCP phase and environment
(both P>0.24, ηp2<0.14), with a characteristic
end-spurt higher than all previous time-points by
>10 beats min1.
39.5
39.0
38.5
38.0
37.5
37.0
36.0
35.0
34.0
33.0
32.0
31.0
36.0
35.0
34.0
33.0
32.0
31.0
36.5
39.5
39.0
38.5
38.0
37.5
37.0
36.5
Rest 125W 150W 6 12 18 24 30 Rest 125W 150W 6 12 18 24 30
Stage / Time (min) Stage / Time (min)
*
*
qFqLEF ML qFqLEF ML
DRY HUM
Tsk (°C)
Tsk (°C) Trec (°C)
Trec (°C)
Figure 2. Mean ±SD rectal temperature (Trec,n=10) and weighted mean skin temperature (Tsk ,
n=10) during exercise in dry (DRY) and humid (HUM) heat during the qFandqL phase
Significant difference between qFqL within environment. Significant difference between corresponding
qFHUM value. Significant difference between corresponding qLHUM value. Mean early follicular (EF) and
mid-luteal (ML) values are provided for our previous eumenorrhoeic cohort (Lei et al. 2017).
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Tabl e 3 . MA P ( n=8), ˙
Q(n=6), FVR (n=8) and SV (n=6) at rest and during fixed-intensity exercise in dry (DRY) and humid (HUM) heat during the qFandqL phase
DRY HUM
qF qL qF qL
Rest 125 W 150 W Rest 125 W 150 W Rest 125 W 150 W Rest 125 W 150 W
MAP (mmHg) 90 ±698±5 103 ±784±595±7 100 ±787±798±6 103 ±684±695±8 100 ±9
˙
Q(L min1)8±220±321±47±222±720±37±220±221±38±420±323±3a
FVR (mm Hg min dL1) 11.9 ±5.8 7.4 ±2.3 5.6 ±1.9 7.7 ±1.5b5.3 ±1.7 4.9 ±1.5 7.2 ±1.4b5.2 ±0.9 3.8 ±0.5 6.6 ±1.6 4.2 ±1.8 4.0 ±1.6
SV (mL) 109 ±33 138 ±24 133 ±25 94 ±33 160 ±59 128 ±28 91 ±20 140 ±18 132 ±21 122 ±72 149 ±31 154 ±23cd
Data are the mean ±SD.
aSignificant difference from the preceding time-point.
bSignificant difference from the corresponding qFDRY time-point.
cSignificant difference from the corresponding qLDRY time-point.
dSignificant difference from the corresponding qFHUM time-point.
Between-group analysis revealed no effect of OCP usage
for SV, HR, ˙
Qand MAP (all P>0.23, ηp2<0.10); however,
FVR was 2.7 ±2.3 mm Hg min dL1(P<0.01, ηp2=
0.45) and 1.1 ±1.1 mm Hg min dL1(P=0.01, ηp2=
0.37) higher at rest and during fixed-intensity exercise,
respectively, in the current OCP than in the previous
eumenorrhoeic group.
Resting LSR was similar between OCP phases and
environments (both P>0.21, ηp2<0.17), whereas resting
FBF differed between environments as a function of OCP
phase (environment ×OCP phase: P=0.05, ηp2=
0.46), such that values were higher during HUM than
during DRY at both quasi-phases and higher in qLthan
in qF during DRY. During fixed-intensity exercise, LSR
was 0.07 ±0.06 mg cm2min1lower in qLthanin
qF(P<0.01, ηp2=0.60), 0.08 ±0.10 mg cm2min1
lower during DRY than during HUM (P=0.04, ηp2=
0.40) and increased with work-rate (P<0.01, ηp2=0.86).
Whereas FBF differed between OCP phases as a function
of environment (environment ×OCP phase: P=0.05,
ηp2=0.45) and work-rate (time ×OCP phase: P<0.01,
ηp2=0.53), such that FBF was higher during DRY in
qF(by7±3mLdL
1min1)butnotinqL(by4±
6mLdLmin
1) and increased from 125 to 150 W (by
6±4mLdL
1min1)inqFbutnotinqL. During
self-paced exercise, LSR was 0.13 ±0.10 mg cm2min1
higher during HUM than during DRY (P<0.01, ηp2=
0.64) and continued to increase with time (P<0.01, ηp2=
0.79) until the end of exercise, although this tended to be
more pronounced during HUM (environment ×time:
P=0.06, ηp2=0.22, possible type II error), regardless of
OCP phase (interaction: P=0.43, ηp2=0.10). Neither
onset thresholds, nor thermosensitivities of the effector
responses were affected by OCP phase or environment (all
P>0.19, ηp2<0.23). Water consumption was similar
between OCP phases and environments (597 ±193 mL;
both P>0.46, ηp2<0.06), as was WBSR (843 ±218 g h1;
both P>0.28, ηp2<0.13), resulting in a 1.3 ±0.6% loss
of body mass that was similar between OCP phases and
environments (both P>0.47, ηp2<0.06).
Between-group analysis revealed no differences between
the OCP and eumenorrhoeic groups for LSR at rest or
during fixed-intensity exercise (both P>0.19, ηp2<0.11);
however, LSR was 0.23 ±0.21 mg cm2min1lower (P<
0.01, ηp2=0.43) during the self-paced time trial in the
current OCP than in the previous eumenorrhoeic group.
FBF was 4 ±3mLdL
1min1(P<0.01, ηp2=0.54)
and 6 ±6mLdL
1min1(P=0.01, ηp2=0.38) lower
at rest and during fixed-intensity exercise, respectively,
in the current OCP than in the previous eumenorrhoeic
group. The onset threshold and thermosensitivity for LSR
(both P<0.01, ηp2=0.54) but not FBF (both P>
0.54, ηp2<0.03) revealed differences between the OCP
and eumenorrhoeic groups, such that LSR occurred at
ahigherTband its sensitivity was lower in the current
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80 T.-H. Lei and others J Physiol 597.1
OCP users. Water consumption and percentage loss of
body mass were similar between groups (both P>0.11,
ηp2<0.04); however, WBSR was 200 ±265 g (P=0.03,
ηp2=0.24) lower in the current OCP than in the previous
eumenorrhoeic group.
Respiratory (data not shown). Hyperventilation was
evidentatrest(1416Lmin
1), although similar
between OCP phases and environments (both P>0.27,
ηp2<0.13) and therefore data derived from this (e.g.
thermodynamic) were not analysed further or displayed.
During fixed-intensity exercise, ventilation was 2.5 ±3.1 L
min1higher in qLthaninqF(P=0.03, ηp2=0.41) and
increased with work-rate (P<0.01, ηp2=0.95). PETCO2
was similar between OCP phases and environments (both
P>0.56, ηp2<0.06) during fixed-intensity exercise.
Participants were exercising at 61 ±11%, 72 ±12% and
75 ±8% of their ˙
VO2max at 125 W, 150 W and during the
self-paced time-trial, respectively, and similar between
OCP phases and environments (both P>0.57, ηp2<0.04)
but increased with work-rate (P<0.01, ηp2=0.78) from
125 W to 150 W only. Between-group analysis revealed
no differences between the OCP and eumenorrhoeic
1.4
1.2
1.0
0.8
0.6
0.4
0.2
0.0
1.4
1.2
1.0
0.8
0.6
0.4
0.2
0.0
50
40
30
20
10
0
50
40
30
20
10
0
1.4
1.2
1.0
0.8
0.6
0.4
0.2
0.0
1.4
1.2
1.0
0.8
0.6
0.4
0.2
0.0
50
40
30
20
10
0
50
40
30
20
10
0
LSR (mg cm-2 min-1)
LSR (mg cm-2 min-1)
LSR (mg cm2 min-1)
LSR (mg cm-2 min-1) FBF (mL dL-1 min-1)
FBF (mL dL min-1)
FBF (mL dL-1 min-1)
FBF (mL dL min-1)
Rest
36.0 36.5 37.0
37.5 38.0 38.5 36 36.5 37 37.5 38 38.5
125W 150W
Stage / Time (min) Stage / Time (min)
6 12 18 24 30 Rest 125W 150W 6 12 18 24 30
Tb (oC)
Tb (oC)
DRY
qFqLEFML MLEFqFqL
HUM
*
*
Figure 3. Mean ±SD LSR (n=9) and FBF (n=8) against time and mean body temperature (Tb) during
exercise in dry (DRY) and humid (HUM) heat during the qFandqL phase
Significant difference between qFqL within environment. Significant difference between corresponding
qFHUM value. Significant difference between corresponding qLHUM value. Mean early follicular (EF) and
mid-luteal (ML) values are provided for our previous eumenorrhoeic cohort (Lei et al. 2017).
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J Physiol 597.1 Exercise thermoregulation in trained women taking oral contraception 81
groups for ventilation, PETCO2or percentage ˙
VO2max
during fixed-intensity or self-paced exercise (all P>0.47,
ηp2<0.05).
Thermodynamics (Figure 6). During fixed-intensity
exercise MWwas similar between OCP phases and
environments (both P>0.50, ηp2<0.06) but increased
with work-rate (P<0.01, ηp2=0.94). Emax was 44 ±
14 W m2higher during DRY than during HUM (P<0.01,
ηp2=0.92) and increased with work-rate (P<0.01, ηp2=
0.80), whereas Ereq was similar between OCP phases and
environments (both P>0.57, ηp2<0.04) but increased
with work-rate (P<0.01, ηp2=0.94). Consequently, the
HSIwassimilarbetweenOCPphases(P=0.71, ηp2<0.02)
but was 0.09 ±0.06 a.u. lower during DRY than during
HUM (P<0.01, ηp2=0.71) and increased with work-rate
(P<0.01, ηp2=0.82). During self-paced exercise, MW
was similar between OCP phases (P=0.48, ηp2=0.07)
but increased with time (P<0.01, ηp2=0.75). Emax was
26 ±15 W m2higher during DRY than during HUM
(P<0.01, ηp2=0.75) and increased with time (P<0.01,
ηp2=0.54). Ereq was similar between OCP phases and
environments (both P>0.18, ηp2<0.19) but increased
with time (P<0.01, ηp2=0.70). Consequently, the HSI
was similar between OCP phases and environments (both
P>0.47, ηp2<0.06) but increased with time (P<0.01,
ηp2=0.66).
Between-group analysis revealed no differences between
the OCP and eumenorrhoeic groups for MWduring
fixed-intensity or self-paced exercise (both P>0.25, ηp2<
0.08). Emax,Ereq and HSI were similar between groups at
all time-points (all P>0.12, ηp2<0.15).
Discussion
We tested the hypotheses that, in female athletes who are
chronic users of the combined monophasic OCP: (i) a
small endogenous thermoregulatory rhythm would persist
during their active OCP cycle, and would be nullified by
behavioural adjustments when faced with the heat stress
of exercise in warm environments; (ii) there would be an
interplay with the different thermal environments; and
(iii) autonomic responses would be attenuated compared
to our matched cohort of eumenorrhoeic athletes. In
support of our hypotheses, (i) a small increase in Tcore
occurs during qL at rest and fixed-intensity exercise,
1. 8
1. 6
1. 4
1. 2
1. 0
0.8
0.6
0.4
0.2
0.0
1. 8
1. 6
1. 4
1. 2
1. 0
0.8
0.6
0.4
0.2
0.0
DRY HUM
35.5 36.5 37.5 38.5 35.5 36.5 37.5 38.5
1. 8
FqF
qL qL
qF
LL
F
1. 6
1. 4
1. 2
1. 0
0.8
0.6
0.4
0.2
0.0
1. 8
1. 6
1. 4
1. 2
1. 0
0.8
0.6
0.4
0.2
0.0
LSR (mg cm-2 min-1)LSR (mg cm-2 min-1)
LSR (mg cm-2 min-1)LSR (mg cm-2 min-1)
Tb (oC) Tb (oC)
DRY
-24.5 (6.8)
-10.9 (6.0)
0.67 (0.18)
0.30 (0.16)
0.93 (0.03)
0.89 (0.10)
-22.4 (10.3)
-15.2 (8.5)
0.62 (0.28)
0.42 (0.23)
0.87 (0.08)
0.82 (0.14)
-22.2 (5.5)
-14.6 (6.8)
0.62 (0.15)
0.41 (0.19)
0.94 (0.05)
0.88 (0.14)
-23.6 (9.6)
-12.6 (3.5)
0.65 (0.26)
0.35 (0.10)
0.93 (0.05)
0.86 (0.20)
aaaa
HUM
LFF
yo yo yo yo
L
R2R2R2R2
EUM
OCP$
Figure 4. Individual traces, and group onset threshold and thermosensitivity for LSR
Upper: individual traces for LSR (n=9) against mean body temperature (Tb) during exercise in dry (DRY) and
humid (HUM) heat during the qFandqL phase. Early follicular (EF) and mid-luteal (ML) traces are provided for
our previous eumenorrhoeic cohort (Lei et al. 2017). Lower: mean ±SD values for onset threshold (y0,i.e.Tb
in °C) and thermosensitivity (a) of LSR (in mg cm2min1°C1) responses using simple linear regression (y=
y0+ax) during the qFandqL phase for the matched eummenorrhoeic (EUM) (Lei et al. 2017) and OCP groups.
$Significantly different from EUM. The values give an indication of the central modification of the thermoeffector
(sweating), thus demonstrating that chronic consumption of an OCP, but not (quasi-) phase, nor environment,
causes a meaningful shift in sweating control.
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82 T.-H. Lei and others J Physiol 597.1
although this disappears before behavioural adjustments
are utilised; (ii) autonomic heat loss mechanisms were
activated to a greater extent during HUM, whereas
behavioural thermoregulation was effective in minimising
further strain and did not differ between environments;
and (iii) chronic OCP use impairs the sweating response,
although this impairment was not sufficient to affect Tcore
during exercise. These results indicate that, under the
conditions of this investigation, the evaporative capacity
of the environment determines endurance performance
and, although the sudomotor response is attenuated by
chronic OCP use, behavioural adjustments by female
athletes are influenced by the environmental conditions
but not chronic OCP use.
A quasi-phase related shift in Tcore and, to a lesser
extent, heat loss mechanisms occurs despite OCP use
We observed a consistent and significant but small
quasi-phase increase in resting Tcore, by 0.15°CfromqFto
qL that persisted into the fixed-intensity exercise (Fig. 2).
To our knowledge, this finding during active OC use is
unique. Previous investigations suggested that this shift
be regarded as a strong and residual effect of the end-
ogenous menstrual cycle (Grucza et al. 1993; Martin
& Buono, 1997; Rogers & Baker, 1997; Charkoudian
& Johnson, 1997a;Tenagliaet al. 1999; Sunderland &
Nevill, 2003), yet, in these studies, the comparison always
occurred when the females were actively taking OC
compared to their placebo week. However, this finding
is difficult to explain because, in the present study, both
endogenous (Table 2) and exogenous (by design, not
measured) concentrations of progestogens and oestrogens
remained unchanged between qFandqL. This is probably
not an estrogenic effect because it is known that,
when progestogens and oestrogens are naturally elevated
or administered, a progestogen-dominant thermogenic
response ensues (Israel & Schneller, 1950; Rothchild &
Barnes, 1952). However, the current design of maintained
OC use is sub-optimal for determining causal mechanisms
for the apparent ‘lack of an OC effect in resetting
the thermoregulatory balance point’ (Tenaglia et al.
1999). For this, other study designs (i.e. gonadotrophin-
releasing hormone suppression) would be required
50
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FBF (mL dL-1 min-1) FBF (mL dL-1 min-1)
FBF (mL dL-1 min-1)FBF (mL dL-1 min-1)
DRY HUM
FqFFqF
LqL
LqL
Tb (°C)
_
Tb (°C)
_
DRY HUM
FLF L
y0 y0aay0ay0a
EUM
OCP
-734 (394)
-672 (266)
-680 (297)
-817 (554)
20.4 (10.7) 0.94 (0.06)
0.92 (0.12)18.6 (7.2) 22.6 (15.1) 0.91 (0.08)
0.85 (0.18)
-1191 (1284)
-846 (354)
33.0 (34.9)
23.8 (9.7)
0.91 (0.08)
0.87 (0.12)
-988 (755)
-793 (419)
27.5 (20.6)
22.2 (11.5)
0.73 (0.20)
0.87 (0.16)18.9 (8.1)
R2
R2
R2
R2
35.5 36.5 37.5 38.5 35.5 36.5 37.5 38.5
Figure 5. Individual traces, and group onset threshold and thermosensitivity for FBF
Upper: individual traces for FBF (n=8) against mean body temperature (Tb) during exercise in dry (DRY) and
humid (HUM) heat during the qFandqL phase. Early follicular (EF) and mid-luteal (ML) traces are provided for
our previous eumenorrhoeic cohort (Lei et al. 2017). Lower: mean ±SD values for onset threshold (y0,i.e.Tbin
°C) and thermosensitivity (a)ofFBF(inmLdL
1min1°C1) responses using simple linear regression (y=y0+
ax) during the qFandqL phase for the matched eummenorrhoeic (EUM) (Lei et al. 2017) and OCP groups. The
values give an indication of the central modification of the thermoeffector (skin blood flow), thus demonstrating
that chronic consumption of an OCP, (quasi-) phase and environment, causes no meaningful shift in vasodilatatory
control.
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J Physiol 597.1 Exercise thermoregulation in trained women taking oral contraception 83
(Stachenfeld & Taylor, 2014), although we are unaware
of any such published data on measures of regulated Tcore.
Furthermore, hormone exposure does not necessarily
determine its effect, and both central and peri-
pheral thermoregulatory receptors respond differently
to synthetic progestin compared to progesterone
(Charkoudian & Stachenfeld, 2014).
The quasi-phase related difference in Tcore had
disappeared by 12 min of fixed-intensity exercise. This
could be the result of a sufficient reserve in the capacity
of the thermoregulatory system. This ‘disappearance’
has been observed by some (Tenaglia et al. 1999;
Sunderland & Nevill, 2003) but not all investigators
(Grucza et al. 1993; Rogers & Baker, 1997), whereas the
reverse has also been reported (Martin & Buono, 1997).
Notably, this quasi-phase related difference in Tcore is
similar in magnitude to that observed in our matched
eumenorrhoeic cohort (Lei et al. 2017) and supports
700
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600
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1.6
1.4
1.2
1.0
0.8
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0.0
125W 150W 612 18 24 30 125W 150W 612 18 24 30
Stage / Time (min) Stage / Time (min)
Emax (W m-2)
Emax (W m-2)HSI (Ereq : Emax)
HSI (Ereq : Emax)E
req (W m-2)
Ereq (W m-2)
M-W (W m-2)
M-W (W m-2)
qFqLEFML qFqLEFML
DRY HUM
Figure 6. Mean ±SD rate of metabolic heat production (MW,n=10), required evaporative cooling
for heat balance (Ereq,n=10), maximal evaporative capacity of the environment (Emax,n=10) and HSI
(n=10) during exercise in dry (DRY) and humid (HUM) heat during the qFandqL phase
Significant difference between corresponding qFHUM value. Significant difference between corresponding
qLHUM value. Mean early follicular (EF) and mid-luteal (ML) values are provided for our previous eumenorrhoeic
cohort (Lei et al. 2017).
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84 T.-H. Lei and others J Physiol 597.1
previous observations at rest and during heat stress of
a smaller difference in the biphasic Tcore in trained women
(Kuwahara et al. 2005a,b;Leiet al. 2017).
Concurrent to the quasi-phase difference observed
for Tcore, LSR during fixed-intensity exercise was lower
during qL, whereas FBF was indistinguishable between
environments and intensity during qLyetduringqF
was increased during DRY (vs. HUM) and at 150 W
(vs. 125 W), indicating a differential response between
quasi-phases (Fig. 3). However, the activation of heat
loss responses relative to Tb(onset threshold, thermo-
sensitivity) was unaffected by OCP phase. Therefore, the
physiological significance of a shift in resting Tcore <
0.2°C that effectively disappears during exercise should
be considered closely.
The evaporative capacity of the environment infers
greater performance and thermoregulatory strain
than does an OCP cycle
Exercise performance was unaffected by the quasi-phase
of the OCP cycle but was impaired by the humid tropical
environment despite it being WBGT-matched to the dry
heat (Fig. 1). This result confirms our observations in
eumenorrhoeic athletes (Lei et al. 2017) and indicates that
a reduction in the evaporative power of the environment
is of greater performance consequence to a female athlete
than is her menstrual/OCP cycle. Evaporative cooling
rates decrease when the vapour pressure gradient between
skin and environment is reduced (Morimoto et al. 1967;
Shapiro et al. 1980; Frye & Kamon, 1983). Therefore, our
females demonstrated a performance–thermoregulatory
trade-off, where their reduction in (self-paced) work
completed during HUM (Fig. 1) maintained a similar
thermoregulatory strain (Fig. 2). These results are also in
agreement with those of the study by Tenaglia et al. (1999)
but are in contrast to those of Sunderland & Nevill (2003)
who observed an improved running distance during qLin
their OCP users. However, both studies compared their
females in the active pill vs. placebo phases.
Chronic OCP use impairs sudomotor but not
behavioural thermoregulatory responses
The careful matching of groups and experimental
procedures of this and our previous study on
eumenorrhoeic females (Lei et al. 2017) permits us to
isolate the effects of chronic OCP use on autonomic
and behavioural thermoregulation during heat stress.
Namely, we used the same exercise protocols, ambient
conditions and phases of the endogenous menstrual cycle,
and matched our OCP and eumenorrhoeic cohorts for all
appropriate physical and functional characteristics. This
matching was so successful in as much as comparable
self-paced mean power output and work were completed
between the groups, which lead to MWbeing similar
(Figs. 1 and 6). Thus, the between-group differences
evident for the onset threshold and thermosensitivity of
the sweating response (Figs. 3 and 4) demonstrate that
long-term combined, monophasic OCP use in endurance
athletes affects an autonomic thermoregulatory response.
However, behavioural thermoregulation was maintained
(in that self-pacing was evident) with no differential
effect on regulated body temperature(s), which indicates
that overall thermoregulation and performance were not
compromised. Thus, although both LSR and WBSR were
higher in our previous cohort, this sweat was either not
evaporated (dripped) or too small to affect evaporative
heat loss.
The potential mechanism(s) through which chronic
OCP use affects an autonomic heat loss mechanism is not
well understood, although this probably concerns a direct
central action given the upward (i.e. rightward) shift in
Tcore fortheonsetofsweating(Figs.3and4).Oestrogens
and progestogens both readily cross the blood–brain
barrier and can inhibit temperature-sensitive neurons
in the preoptic/anterior hypothalamus (Lincoln, 1967;
Nakayama, 1975). The direction of this shift implies that
this constraint of heat dissipation is a result of progestin
inhibiting warm-sensitive neuronal activity (Nakayama,
1975). Mediation by a pyrogen or heat shock proteins
(Rogers & Baker, 1997; Charkoudian & Johnson, 1997b;
Chang et al. 1998) is probably not possible. Equally, our
results are probably not the result of an interaction with
the system(s) that regulate volume of the extracellular fluid
(Fortney et al. 1981; Fortney et al. 1983) because, although
we did not quantify plasma volume, SV and ˙
Qwere
similar at rest and during exercise between our OCP and
eumenorrhoeic cohorts. However, our findings could be a
result of changes in osmotic pressure (Fortney et al. 1984)
because some studies (Stachenfeld et al. 1999; Stachenfeld
et al. 2000) but not others (Rogers & Baker, 1997) have
reported a reduction in plasma osmolality with 1month
of OCP use. Interestingly, Rogers & Baker (1997) still
observed a delay in the sweating onset despite no reduction
in osmolality, whereas Stachenfeld et al. (2000) observed
no delay with OCP use, indicating that the effect of plasma
osmolality may be small.
Acute and chronic OCP use has different effects
on thermoregulation (Charkoudian & Johnson, 1997a;
Stachenfeld et al. 2000). Previous investigations have
compared women when actively taking OC compared
to their placebo week, even when separate groups of
chronic OCP- and non-users were compared (Grucza
et al. 1993; Tenaglia et al. 1999; Sunderland & Nevill,
2003). Nevertheless, data comparing our OCP and
eumenorrhoeic females support the findings of several
previous observations, such as a higher onset threshold
for sweating (Rogers & Baker, 1997; Charkoudian &
Johnson, 1997a) and an attenuated gain for local sweat rate
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J Physiol 597.1 Exercise thermoregulation in trained women taking oral contraception 85
(Grucza et al. 1993). However, our result of resting
(and exercising) Tcore being similar between groups is in
contrast to the upward-shift reported as a result of OCP
use (Grucza et al. 1993; Sunderland & Nevill, 2003).
The OCP and quasi-phase exert haemodynamic
effects
A combined OCP affects both central (Walters & Lim,
1970; Lehtovirta, 1974a) and peripheral (Lehtovirta,
1974b) haemodynamics at rest and during exercise
(Lehtovirta et al. 1977), which is probably caused by
the oestrogen component (Lehtovirta, 1974a,b)and
requires longer than 1 month of OC consumption
(Walters & Lim, 1970; Lehtovirta, 1974a,b;Stachenfeld
et al. 2000). We observed no differences in the central
cardiovascular response (SV and ˙
Q)betweentheOCP
and eumenorrhoeic groups. However, FVR was higher
in our current OCP compared to the eumenorrhoeic
cohort, a finding that contrasts with the lower peripheral
resistance found following 2 months of combined OCP
use (Lehtovirta, 1974a,b). Methodological differences
probably account for these discrepant results because
(i) vascular effects of the synthetic and endogenous
hormones may be a confounding factor and our OCP
had a lower concentration of 17β-oestradiol (Table 2)
and(ii)ourOCPusershadbeentakingtheOCP
12 months, whereas Lehtovirta (1974a,b) used a
within-subject design (pre-post) following 2 months of
OCP use.
The central cardiovascular response was similar
between quasi-phases of the OCP cycle at rest but
showed augmentation of SV (20-30 mL) and ˙
Q
(2-4 L min1)duringqLcomparedtoqF at matched
workloads (70% ˙
VO2max)andreducedsweatingpower
(during HUM) (Table3). The p eripheral vascular response
was correspondingly affected by the OCP cycle, such
that FVR was lower at rest during qLduringHUMand
during exercise at 60% ˙
VO2max qL(Table3).Mostpre-
vious investigations (Walters & Lim, 1970; Lehtovirta,
1974a,b;Stachenfeldet al. 2000) did not compare across
an OCP cycle, such as in the current study. Moreover,
the observed qLreductioninFVRatrestandduring
fixed-intensity exercise is similar in magnitude to that of
our eumenorrhoeic cohort (Lei et al. 2017), indicating that
the menstrual cycle could be exerting a peripheral cardio-
vascular effect beyond the regulated Tcore in these OCP
users. In support of this, the menstrual cycle phase has
been shown to modulate vessel conductance and resistance
that parallel changes in oestrogen (Williams et al. 2001),
nitric oxide production (Kharitonov et al. 1994) and end-
othelial nitric oxide synthase expression (Taguchi et al.
2000), the most probable cause(s) of vascular smooth
muscle relaxation (Charkoudian & Stachenfeld, 2016).
Our aprioristudy design does not allow for further
insight; this would require, for example, cutaneous micro-
dialysis with concurrent pharmacological administration
to determine endothelium-dependent and independent
factors.
Considerations
By design, the present study tested whether any
quasi-phase related endogenous thermoregulatory
rhythms persist during the active pill phase in chronic
OCP users, therefore capturing 75% of their OCP
cycle and mimicking real-world use in athletes (i.e.
competition/performance occurring during active pill
use). Therefore, it would simply be speculation and
beyond the scope of the data obtained in the present study
to determine how these responses compare to the 25%
of the OCP cycle in which athletes consume a placebo
pill; nevertheless, this warrants further investigation.
Furthermore, we tested women taking the combined,
monophasic OCP because this reflects most athlete use,
yet there is evidence that these responses could differ in
those taking a progestin-only OCP (Stachenfeld et al.
2000).
The same de-limitations are present in the present study
as in our previous study on eumenorrhoeic females (Lei
et al. 2017) and were unavoidable in the protocol and
design as a result of a direct comparison between these
cohorts; namely, the lack of an untrained cohort, peri-
ods of fixed-intensity and a variable-intensity exercise
that were unequal (and limited) in duration, as well
as a lack of other physiological measures such as leg
blood flow and arterial oxygenation. Similarly, it is
worth noting that the current data are derived from an
index of Tcore known to exhibit a lag-time (compared
to oesophageal temperature; M¨
undel et al. 2016) and
from limited data points for effector responses. Equally,
and as noted above, several of the statistical differences
between quasi-phases probably have little physiological
consequence and are within the biological variability
or measurement error, such as the onset threshold for
sweating (0.1 °C; Brengelmann et al. 1994) and local
sweat rate (0.05–0.2 mg cm2min1;Kenecket al.
2012; Morriss et al. 2013), albeit these investigations yield
data predominantly from male not female participants.
Nevertheless, the above is probably not the case for the
between-group (OCP vs. eumenorrhoeic) results, which
demonstrate clear differences in the onset threshold for
sweating (Figure 4). However, verification of these results
iswarrantedprobablyasaresultofourlessconventional
method of determining onset thresholds. The sensitivity
of our partitional calorimetry-derived data could be
improved by the use of a direct calorimeter, especially
because we were unable to accurately estimate the rate of
evaporative heat loss. However, such a facility has very
limited access at much greater expense, exhibits a greater
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2018 The Authors. The Journal of Physiology C
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86 T.-H. Lei and others J Physiol 597.1
lag and the conditions used during HUM are probably
beyond the reported operating range of such a calorimeter
(Reardon et al. 2006; Kenny et al. 2008; Kenny & Jay, 2013).
We also recognise that homeostatic systems interact, such
that the regulation of body temperature is not separate
and distinct from, for example, that of fluid, energy sub-
strate and metabolite balance (Boulant & Silva, 1988).
Therefore, representative measures, particularly of plasma
osmolality and volume, would have further strengthened
our conclusions. Despite careful matching of the groups,
our current OCP cohort were an average of 9 years younger
than our previous eumenorrhoeic females (Lei et al. 2017).
Nevertheless, all other relevant physical and functional
characteristics were similar (Table 1) and we are unaware
of any research indicating that, in such pre-menopausal
women, this magnitude of an age difference should
confound the results.
Finally, the results of the present study should be of
interest to those (thermoregulation) researchers whose
participants include OC users because there is now
evidence to question the validity of treating the active OCP
cycle as a way of controlling for menstrual cycle hormones
that are known to affect thermoregulation.
Conclusions
The present study demonstrates that, when well-trained
women chronically using the combined, monophasic OCP
exercise in heat-stressful environments, a performance-
thermoregulatory trade-off occurs to ensure over-
all thermoregulation is not impaired. The biggest
determinant of this trade-off is the evaporative capacity
of the environment. Finally, an endogenous thermo-
regulatory rhythm persists despite chronic OCP use.
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Additional information
Competing interests
The authors declare that they have no competing interests.
Author contributions
TM was responsible for the conception of the study. THL, JDC,
ZJS, SRS, BGP, MJB and TM were responsible for the design
of the work. THL, SRS, BGP, MJB and TM were responsible for
data acquisition. THL and TM were responsible for data analysis.
THL, JDC, ZJS and TM were responsible for data interpretation.
THL and TM were responsible for drafting intellectual content.
THL, JDC, ZJS, SRS, BGP, MJB and TM were responsible for
critically revising intellectual content. All authors approved the
final version of the manuscript submitted for publication. All
experimental procedures were performed in the School of Sport,
Exercise and Nutrition, Massey University, Palmerston North.
Funding
No funding was received for the present study.
Acknowledgements
We would like to specifically thank the very dedicated group of
women that participated in this study.
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2018 The Authors. The Journal of Physiology C
2018 The Physiological Society
... Firstly, metabolic heat production in trained women at these higher intensities is likely double the values previously examined in the literature, i.e., metabolic rates of 148-389 vs. 464-716 W·m −2 (Lei et al. 2019;Notley et al. 2019), while trained women have a greater capacity to deal with a heat load on account of their enhanced heat loss effectors (Kuwahara et al. 2005). Next, these previous studies have not reported or accounted for differences in thermoregulation secondary to fluctuations in the primary ovarian steroids (E 2 and P 4 ), whereby generally speaking E 2 promotes heat dissipation and lowers T core , while P 4 has the opposite effect (Charkoudian and Stachenfeld 2014). ...
... This paper combines data from three separate experiments (Lei et al. 2017(Lei et al. , 2019Zheng et al. 2021a), which included n = 28 ovulatory and OCP-user female cyclists/triathletes and adds to this new data of the n = 8 participants that did not complete all trials or were excluded from the final analyses on account of being deemed anovulatory (Lei et al. 2017;Zheng et al. 2021a). Interested readers are directed to these studies for further methodological details and results. ...
... All original studies (Lei et al. 2017(Lei et al. , 2019Zheng et al. 2021a) had received approval by the Massey University Human Ethics Committee (Southern A) and were performed in accordance with the latest revision of the Declaration of Helsinki, except for registration in a database. Informed, written consent was obtained from all participants prior to their participation. ...
Article
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Purpose Women remain underrepresented in the exercise thermoregulation literature despite their participation in leisure-time and occupational physical activity in heat-stressful environments continuing to increase. Here, we determined the relative contribution of the primary ovarian hormones (estrogen [E 2 ] and progesterone [P 4 ]) alongside other morphological (e.g., body mass), physiological (e.g., sweat rates), functional (e.g., aerobic fitness) and environmental (e.g., vapor pressure) factors in explaining the individual variation in core temperature responses for trained women working at very high metabolic rates, specifically peak core temperature ( T peak ) and work output (mean power output). Methods Thirty-six trained women (32 ± 9 year, 53 ± 9 ml·kg ⁻¹ ·min ⁻¹ ), distinguished by intra-participant (early follicular and mid-luteal phases) or inter-participant (ovulatory vs. anovulatory vs. oral contraceptive pill user) differences in their endogenous E 2 and P 4 concentrations, completed a self-paced 30-min cycling work trial in warm–dry (2.2 ± 0.2 kPa, 34.1 ± 0.2 °C, 41.4 ± 3.4% RH) and/or warm–humid (3.4 ± 0.1 kPa, 30.2 ± 1.2 °C, 79.8 ± 3.7% RH) conditions that yielded 115 separate trials. Stepwise linear regression was used to explain the variance of the dependent variables. Results Models were able to account for 60% of the variance in T peak ( $$\overline{R }$$ R ¯ ² : 41% core temperature at the start of work trial, $$\overline{R }$$ R ¯ ² : 15% power output, $$\overline{R }$$ R ¯ ² : 4% [E 2 ]) and 44% of the variance in mean power output ( $$\overline{R }$$ R ¯ ² : 35% peak aerobic power, $$\overline{R }$$ R ¯ ² : 9% perceived exertion). Conclusion E 2 contributes a small amount toward the core temperature response in trained women, whereby starting core temperature and peak aerobic power explain the greatest variance in T peak and work output, respectively.
... Indeed, studies have demonstrated that whole body heat exchange is unaffected by menstrual cycle phase during passive heat stress (420) and exercise in the heat (421). Furthermore, Lei et al. demonstrated that thermoeffector (forearm blood flow and sweating) to mean body temperature relations are unaffected by menstrual cycle phase (422) or oral contraceptive use (423) in trained females during fixed-intensity exercise in warm/ humid and warm/dry environments. They also demonstrated that exercise performance was unaffected by menstrual cycle phase or oral contraceptive use in both environments (422,423). ...
... Furthermore, Lei et al. demonstrated that thermoeffector (forearm blood flow and sweating) to mean body temperature relations are unaffected by menstrual cycle phase (422) or oral contraceptive use (423) in trained females during fixed-intensity exercise in warm/ humid and warm/dry environments. They also demonstrated that exercise performance was unaffected by menstrual cycle phase or oral contraceptive use in both environments (422,423). Taken together, the fluctuations in female sex hormones that occur over the course of the menstrual cycle do not appear to alter thermoregulatory control, even though they are associated with a shift in basal deep body temperature. were compared during two exercise bouts; one performed at a fixed rate of metabolic heat production and a second performed at a rate of metabolic heat production normalized to body mass to account for the greater body mass associated with pregnancy. ...
Article
The human body constantly exchanges heat with the environment. Temperature regulation is a homeostatic feedback control system that ensures deep body temperature is maintained within narrow limits despite wide variations in environmental conditions and activity-related elevations in metabolic heat production. Extensive research has been performed to study the physiological regulation of deep body temperature. This review focuses on healthy and disordered human temperature regulation during heat stress. Central to this discussion is the notion that various morphological features, intrinsic factors, diseases, and injuries independently and interactively influence deep body temperature during exercise and/or exposure to hot ambient temperatures. The first sections review fundamental aspects of the human heat stress response, including the biophysical principles governing heat balance and the autonomic control of heat loss thermoeffectors. Next, we discuss the effects of different intrinsic factors (morphology, heat adaptation, biological sex, and age), diseases (neurological, cardiovascular, metabolic, genetic), and injuries (spinal cord injury, deep burns, heat stroke), with emphasis on the mechanisms by which these factors enhance or disturb the regulation of deep body temperature during heat stress. We conclude with key unanswered questions in this field of research.
... In addition to differences observed in the blood biomarkers, the ventilatory response to fixed-intensity cycling was different between groups (i.e., ventilation was 2.8 L·min −1 higher in WomenOC compared to WomenNC at Ex 40 ), and the magnitude of difference was dependant on exercise duration. This finding has been noted during some studies (Assadpour et al. 2020;Quinn et al. 2018), but not all (Lei et al. 2019). Since there has been limited research to support OC-induced changes in ventilation, this study provides an important contribution to the literature. ...
... Future research could include measurements of pH and bicarbonate to interrogate any potential implications to acid-base balance in OC users. While ventilation was different between groups during fixed-intensity cycling, there were no differences observed in lactate, heart rate or perceived exertion between WomenNC and WomenOC during our exercise conditions, which is consistent with previous literature of exercise in similar temperature and humidity (Lei et al. 2019;Quinn et al. 2018). ...
Article
Full-text available
Purpose To compare physiological responses to submaximal cycling and sprint cycling performance in women using oral contraceptives (WomenOC) and naturally cycling women (WomenNC) and to determine whether N-acetylcysteine (NAC) supplementation mediates these responses. Methods Twenty recreationally trained women completed five exercise trials (i.e., an incremental cycling test, a familiarisation trial, a baseline performance trial and two double-blind crossover intervention trials). During the intervention trials participants supplemented with NAC or a placebo 1 h before exercise. Cardiopulmonary parameters and blood biochemistry were assessed during 40 min of fixed-intensity cycling at 105% of gas-exchange threshold and after 1-km cycling time-trial. Results WomenOC had higher ventilation (β [95% CI] = 0.07 L·min⁻¹ [0.01, 0.14]), malondialdehydes (β = 12.00 mmol·L⁻¹ [6.82, 17.17]) and C-reactive protein (1.53 mg·L⁻¹ [0.76, 2.30]), whereas glutathione peroxidase was lower (β = 22.62 mU·mL⁻¹ [− 41.32, − 3.91]) compared to WomenNC during fixed-intensity cycling. Plasma thiols were higher at all timepoints after NAC ingestion compared to placebo, irrespective of group (all p < 0.001; d = 1.45 to 2.34). For WomenNC but not WomenOC, the exercise-induced increase in malondialdehyde observed in the placebo trial was blunted after NAC ingestion, with lower values at 40 min (p = 0.018; d = 0.73). NAC did not affect cycling time-trial performance. Conclusions Blood biomarkers relating to oxidative stress and inflammation are elevated in WomenOC during exercise. There may be an increased strain on the endogenous antioxidant system during exercise, since NAC supplementation in WomenOC did not dampen the exercise-induced increase in malondialdehyde. Future investigations should explore the impact of elevated oxidative stress on exercise adaptations or recovery from exercise in WomenOC.
... These observations are valid only for the current sample, protocol, and conditions. Our decision to use only men was guided by the fact that i) even in trained women hormonal differences brought about by menstrual phase and oral contraceptive pill use cause differences in T core , a criterion measure in the current study, of ~0.2°C that interact with exercise intensity and duration [25,26]; ii) data collection was conducted during a period of national lockdowns due to COVID-19 meaning we were unable to control for the above factor(s) in women. Small data sets (e.g. ...
Article
Full-text available
We determined the reliability of a 60-min treadmill protocol in the heat when spaced >4 weeks apart, longer than the test–retest duration of 1 week found in the literature. Nine unacclimated, trained males (age: 31 ± 8 y; VO2peak: 60 ± 6 ml∙kg⁻¹∙min⁻¹) undertook a 15 min self-paced time-trial pre-loaded with 45 min of running at 70% of individual ventilatory threshold (11.2 ± 0.3 km∙h⁻¹) in 30 ± 1°C (53 ± 5% relative humidity). They repeated this following 40 ± 14 and 76 ± 26 days, with pre-trial standardization of diet and exercise for 48 h. When considering trial 1 as a familiarization, change in core temperature (∆Tcore) during the first 45 min (∆2.0 ± 0.2°C) between trials 2 and 3 yielded bias and 95% limits of agreement (LoA) of −0.10 ± 0.43°C, standard error of measurement (SEM) of 0.13°C and intraclass correlation coefficient (ICC) of 0.75, more reliable than measures of baseline Tcore (36.9 ± 0.2°C; LoA: −0.23 ± 0.90°C; SEM: 0.22°C; ICC: 0.03) and Tcore at 45 min during exercise (38.9 ± 0.4°C; LoA: 0.32 ± 1.12°C; SEM: 0.28°C; ICC: 0.15). The coefficient of variation (CV) between trials 2 and 3 for distance run during the 15 min time-trial was 2.1 ± 2.0% with LoA of 0.001 ± 0.253 km and SEM of 0.037 km. This protocol is reliable spaced ~5 weeks apart when considering the most commonly accepted limit of <5% CV for performance, reinforced by reliability of the ΔTcore being 0.1 ± 0.4°C.
... (3) Research in female athletes is scarce. Given the effect of the menstrual cycle on thermoregulatory controls [72], there is a need to examine caffeine's impact on EP and C T during the different phases of the menstrual cycle. (4) Recent work has demonstrated that untrained habituated caffeine consumers show a greater rise in C T with caffeine than a placebo during exercise, which is not the case in non-habituated consumers for whom the increase in C T with or without caffeine is similar. ...
Article
Full-text available
Background Heat is associated with physiological strain and endurance performance (EP) impairments. Studies have investigated the impact of caffeine intake upon EP and core temperature (CT) in the heat, but results are conflicting. There is a need to systematically determine the impact of pre-exercise caffeine intake in the heat. Objective To use a meta-analytical approach to determine the effect of pre-exercise caffeine intake on EP and CT in the heat. Design Systematic review with meta-analysis. Data Sources Four databases and cross-referencing. Data Analysis Weighted mean effect summaries using robust variance random-effects models for EP and CT, as well as robust variance meta-regressions to explore confounders. Study Selection Placebo-controlled, randomized studies in adults (≥ 18 years old) with caffeine intake at least 30 min before endurance exercise ≥ 30 min, performed in ambient conditions ≥ 27 °C. Results Respectively six and 12 studies examined caffeine’s impact on EP and CT, representing 52 and 205 endurance-trained individuals. On average, 6 mg/kg body mass of caffeine were taken 1 h before exercises of ~ 70 min conducted at 34 °C and 47% relative humidity. Caffeine supplementation non-significantly improved EP by 2.1 ± 0.8% (95% CI − 0.7 to 4.8) and significantly increased the rate of change in CT by 0.10 ± 0.03 °C/h (95% CI 0.02 to 0.19), compared with the ingestion of a placebo. Conclusion Caffeine ingestion of 6 mg/kg body mass ~ 1 h before exercise in the heat may provide a worthwhile improvement in EP, is unlikely to be deleterious to EP, and trivially increases the rate of change in CT.
... Stachenfeld (2008) further reported that >90% of European and U.S. females are currently taking or previously have taken OCPs. In athletes, the prevalence of females taking combined, monophasic OCPs is one in two (50%) (Lei et al., 2019). Fluid balance studies have suggested that OCPs containing estrogen (combined hormone OCPs) increased osmotically induced AVP and thirst during dehydration and ad libitum rehydration even though there were no changes in water retention (Stachenfeld et al., 1999); confirming that estrogen decreases the plasma osmotic threshold. ...
Article
Full-text available
The purpose of our study was to determine the responses to an acute water bolus in long-term oral contraception (OCP) users. Seventeen female volunteers (27 ± 5 y, 64.1 ± 13.7 kg, 39.6 ± 5.9 kg/LBM) provided consent and enrolled in our study. All were long-term OCP users and participated in two trials, one during the active pill (High Hormone, HH) dose of their prescribed OCP and one during the sham pill (Low Hormone, LH) dose. Participants reported to the laboratory euhydrated, were fed breakfast, remained seated for 60 min and were provided a bolus of room temperature water in the amount of 12 mL/kg/LBM. Urine output over 180 min was measured. Nude body mass was measured pre- and post-trial. Urine specific gravity (USG) and urine osmolality were analyzed. Between trials, there were no differences in 3-h total urine volume (P = 0.296), 3-h USG (P = 0.225), 3-h urine osmolality (P = 0.088), or 3-h urine frequency (P = 0.367). Heart rate was not different between trials (P = 0.792) nor over time (P = 0.731). Mean arterial pressure was not different between trials (P = 0.099) nor over time (P = 0.262). Perceived thirst demonstrated a significant main effect for increasing over time regardless of trial (P < 0.001) but there was no difference between trials (P = 0.731). The urgency to void was not different between trials (P = 0.149) nor over time (P = 0.615). Plasma volume change was not different between trials (P = 0.847) (HH: −3.4 ± 5.0, LH post: −3.8 ± 4.5%) and plasma osmolality did not differ between trials (P = 0.290) nor over time (P = 0.967) (HH pre: 290 ± 4, HH post: 289 ± 4, LH pre: 291 ± 4, LH post: 291 ± 4 mosm/L). Blood glucose significantly decreased over time (P < 0.001) but there was no difference between trials (P = 0.780) (HH pre: 95.9 ± 113.9, HH post: 86.8 ± 6.5, LH pre: 95.9 ± 13.5, LH post: 84.6 ± 9.4 mmol/L). Copeptin concentration did not differ between phases of OCP use (P = 0.645) nor from pre- to post-trial (P = 0.787) Despite fluctuations in hormone concentrations, responses to a water bolus seem to be unaffected in OCP users in euhydrated, resting conditions.
... Eumenorrhoeic female participants were asked to self-report the date of last menses to restrict collection of thermoregulatory data only within the early follicular phase (cycle days 3-6). Those that reported using a biphasic oral contraceptive (n = 1) were tested within the first 3-6 days of active pills following the withdrawal week, in an attempt to minimize the day-to-day variability in thermoregulatory variables, especially rectal temperature (Lei et al., 2019). Notably, pre-exercise rectal temperature did not significantly differ between conditions (control: 37.13 ± 0.30, ice vest: 37.23 ± 0.28, single-hand cooling: 37.17 ± 0.30, p = 0.734). ...
... Eumenorrhoeic female participants were asked to self-report the date of last menses to restrict collection of thermoregulatory data only within the early follicular phase (cycle days 3-6). Those that reported using a biphasic oral contraceptive (n = 1) were tested within the first 3-6 days of active pills following the withdrawal week, in an attempt to minimize the day-to-day variability in thermoregulatory variables, especially rectal temperature (Lei et al., 2019). Notably, pre-exercise rectal temperature did not significantly differ between conditions (control: 37.13 ± 0.30, ice vest: 37.23 ± 0.28, single-hand cooling: 37.17 ± 0.30, p = 0.734). ...
Article
Both adult females and children have been reported to have a lower sweating capacity and thus reduced evaporative heat loss potential which may increase their susceptibility to exertional hyperthermia in the heat. Compared to males, females have a lower maximal sweat rate and thus a theoretically lower maximum skin wettedness, due to a lower sweat output per gland. Similarly, children have been suggested to be disadvantaged in high ambient temperatures due to a lower sweat production and therefore reduced evaporative capacity, despite modifications of heat transfer due to physical attributes and possible evaporative efficiency. The reported reductions in sudomotor activity of females and children suggests a lower sweating capacity in girls. However, due to the complexities of isolating sex and maturation from the confounding effects of morphological differences (e.g., body surface area-to-mass ratio) and metabolic heat production, limited evidence exists supporting whether children and, more specifically, girls are at a thermoregulatory disadvantage. Furthermore, a limited number of child-adult comparison studies involve females and very few studies have directly compared regional and whole-body sudomotor activity between boys and girls. This mini review highlights the exercise-induced sudomotor response of females and children, summarises previous research investigating the sudomotor response to exercise in girls and suggests important areas for further research.
Article
Objectives Due to the nature of firefighting, most effective cooling interventions to reduce heat strain and optimise performance are not practically viable. This study quantified the effects of two practical cooling strategies, co-designed with subject-matter experts, on physiological strain and physical, perceptual, and visuo-motor performance during simulated firefighting in the heat. Design Randomised cross-over. Methods On three occasions 14 firefighters completed an 80-min simulation in a hot-humid environment (32.0[0.9]°C, 59[3]%RH) including two 20-minute firefighting tasks in full protective clothing, each followed by 20-minutes seated recovery. Recovery involved removal of protective clothing and one of three interventions – control (CON; ambient-temperature water consumption), basic (BASIC; cool-water consumption, ambient-forearm immersion/towels, fan), and advanced (ADV; ice-slushy consumption, cool-forearm immersion/ice packs, misting-fan). Thermal (core temperature) and cardiovascular (heart rate, arterial pressure) responses were measured throughout, whilst physical (handgrip/balance), visuo-motor (reaction time/memory recall) and perceptual (fatigue/thermal sensation/comfort) measures were assessed pre- and post-trial. Results Compared to CON, core temperature was lower in BASIC and ADV following the second task (ADV: 37.7[0.4]; BASIC: 38.0[0.4]; CON: 38.3[0.4]°C) and recovery protocol (ADV: 37.5[0.3]; BASIC: 37.7 [0.3] CON: 38.3[0.4]°C). This was paralleled by lowered heart rate, rate pressure product, and thermal sensation following the recovery protocols, in the ADV and BASIC condition compared to CON (p < .05). No physical or visuo-motor outcomes differed significantly between conditions. Conclusion Whilst these observations need to be extended to field conditions, our findings demonstrate that two novel cooling interventions developed in collaboration with subject-matter experts offered benefits for reducing thermal strain and optimising firefighter safety.
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Key points: Despite an attenuated fluctuation in ovarian hormone concentrations in well-trained women, one in two of such women believe their menstrual cycle negatively impacts training and performance. Forthcoming large international events will expose female athletes to hot environments, and studies evaluating aerobic exercise performance in such environments across the menstrual cycle are sparse, with mixed findings. We have identified that autonomic heat loss responses at rest and during fixed-intensity exercise in well-trained women are not affected by menstrual cycle phase, but differ between dry and humid heat. Furthermore, exercise performance is not different across the menstrual cycle, yet is lower in humid heat, in conjunction with reduced evaporative cooling. Menstrual cycle phase does not appear to affect exercise performance in the heat in well-trained women, but humidity impairs performance, probably due to reduced evaporative power. Abstract: We studied thermoregulatory responses of ten well-trained [V̇O2 max , 57 (7) ml min-1 kg-1 ] eumenorrheic women exercising in dry and humid heat, across their menstrual cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), to assess autonomic regulation, then self-paced intensity (30 min work trial), to assess behavioural regulation. Trials were in early-follicular (EF) and mid-luteal (ML) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT, 27°C). During rest and fixed-intensity exercise, rectal temperature was ∼0.2°C higher in ML than EF (P < 0.01) independent of environment (P = 0.66). Mean skin temperature did not differ between menstrual phases (P ≥ 0.13) but was higher in DRY than HUM (P < 0.01). Local sweat rate and/or forearm blood flow differed as a function of menstrual phase and environment (interaction: P ≤ 0.01). Exercise performance did not differ between phases [EF: 257 (37), ML: 255 (43) kJ, P = 0.62], but was 7 (9)% higher in DRY than HUM [263 (39), 248 (40) kJ; P < 0.01] in conjunction with equivalent autonomic regulation and thermal strain but higher evaporative cooling [16 (6) W m2 ; P < 0.01]. In well-trained women exercising in the heat: (1) menstrual phase did not affect performance, (2) humidity impaired performance due to reduced evaporative cooling despite matched WBGT and (3) behavioural responses nullified thermodynamic and autonomic differences associated with menstrual phase and dry vs. humid heat.
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The use of bioelectrical impedance analysis (BIA) is widespread both in healthy subjects and patients, but suffers from a lack of standardized method and quality control procedures. BIA allows the determination of the fat-free mass (FFM) and total body water (TBW) in subjects without significant fluid and electrolyte abnormalities, when using appropriate population, age or pathology-specific BIA equations and established procedures. Published BIA equations validated against a reference method in a sufficiently large number of subjects are presented and ranked according to the standard error of the estimate. The determination of changes in body cell mass (BCM), extra cellular (ECW) and intra cellular water (ICW) requires further research using a valid model that guarantees that ECW changes do not corrupt the ICW. The use of segmental-BIA, multifrequency BIA, or bioelectrical spectroscopy in altered hydration states also requires further research.
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The present discussion reviews current knowledge regarding influences of the primary reproductive hormones on mechanisms of thermoregulatory control in women. The human body is remarkably capable of maintaining body temperature within a few tenths of a degree of normal (37°C) over a wide range of activity and environmental exposures; this regulation is accomplished via integration of central and peripheral thermal information at the preoptic area of the anterior hypothalamus (PO/AH). We describe both central and peripheral mechanisms involved in controlling thermoregulation in humans, and how these mechanisms are affected by sex and hormone exposure. Estrogens generally promote vasodilation, heat dissipation, and lower body temperature and progesterone or progestins generally have the opposite effect. Estrogens and progesterone/progestins can also interact with androgens; this is an important point because androgens in the body can increase in both older and younger women. The study of reproductive hormone (estrogens, progesterone, luteinizing, and follicle stimulating hormones) effects on body systems is challenging because of the complex and multifaceted influences of these hormones, both individually and in combination. Thus, a number of methods to alter hormone exposure are explained in this article. We conclude that men and women do not exhibit major quantitative differences in physiological thermoregulatory responses to exercise and/or body heating when factors such as fitness and body size are taken into account. However, female and male reproductive hormones have important influences that can significantly alter individual thermoregulatory responses at various points throughout the lifespan. © 2014 American Physiological Society. Compr Physiol 4:793-804, 2014.
Article
Previous observations support the belief that the midcycle thermal shift occurs immediately after ovulation. The biphasic character of the basal body temperature during an ovarian cycle should be related to the 2 phases of secretory activity in the ovary. The opposed thermic effects of the ovarian steroids was studied in female castrates. Observations were correlated with the temperature-altering effects of estrogen and progesterone when administered during each phase of the cycle in regularly menstruating women. 26 surgically castrated and 6 intact regularly menstruating women aged 22-54 were selected for study. The bilateral oophorectomy of each of the 26 castrates had been performed by a member of the Department of Gynecology of the Graduate Hospital University of Pennsylvania. The 6 regularly menstruating women were hospital patients. The experimental facts comprised the daily waking temperature taken rectally. Ethinyl estradiol was the estrogen and pregneninolone the progesterone employed in all of the castrated subjects. 4 types of experiments were performed in the 12 castrates who took and recorded their rectal temperature daily for 2-4 months: 1) estrogen alone as administered 2) progestogen alone 3) estrogen followed by progestogen and 4) estrogen and progestogen simultaneously. Ethinyl estradiol lowered the waking temperature from .2 to .4 degrees Farenheit in 18 of 27 tests. 60 mg of pregneninolone daily raised by body temperature from .4 to .6 degrees Farenheit in 20 of 30 trials but 80 mg daily caused a slightly higher thermogenic response in 19 of 22 experiments. Successively administered ethinyl estradiol and pregneninolone resulted in an estrogen-evoked depression followed by a progestogen stimulated elevation of temperatuure in 11 of 15 attempts. The simultaneous administration of .15 mg of ethinyl estradiol and 60 mg of pregneninolone daily resulted in a slight rise of the basal body temperature in 12 of 17 trials. The temperature-depressing effect of estrogen and the thermogenic property of progestogen were demonstrated in the 6 menstruating women.