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Testicular Heat Stress and Sperm Quality


Abstract and Figures

Testicular temperature is reflected by the temperature of the overlying scrotum. The scrotum is well placed anatomically and is capable of physiologically maintaining a hypothermic testis. However, when normal thermoregulation of the testis is impaired, heat stress can occur, negatively effecting semen quality and sperm concentration, motility, and morphology. A number of factors can disturb thermoregulation and increase testicular temperature including pathological conditions such as varicocele and cryptorchidism, posture, clothing, common lifestyle choices such as use of saunas and warm baths, certain exercises such as cycling, laptop usage and occupations that involve or generate heat, and raised ambient temperature. Often, these factors do not occur alone but in combination with one another, which compounds the negative effect of high testicular heat levels on semen parameters. This chapter discusses physiological thermoregulation in the testis, the impact of its failure on semen quality and enumerates factors that could simultaneously and cumulatively contribute to testicular heat stress. Awareness of the potential risks involved and methods to alleviate prolonged scrotal warming are important in the preservation of male fertility. Simple changes to daily habits could help lessen the impact of increased testicular temperatures on male fertility.
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S.S. du Plessis et al. (eds.), Male Infertility: A Complete Guide to Lifestyle and Environmental Factors,
DOI 10.1007/978-1-4939-1040-3_8, © Springer Science+Business Media New York 2014
In the male, exposure to heat has a deleterious
effect on fertility and is considered a signifi cant
risk factor for male infertility [ 1 ]. Testicular tem-
peratures should ideally be hypothermic compared
to the core body temperature of 36.9 °C. This is
essential for maintaining normal spermatogenesis
and ideal sperm characteristics. A crucial feature
that contributes towards this is the anatomical posi-
tion of the human testes, which is located outside
the body. Homeothermic animals have the ability
to maintain a stable core body temperature despite
uctuating environmental temperatures. This is
achieved by regulating heat production and loss by
means of adjusting the body’s metabolism.
In most homeothermic birds and mammals,
including humans, testicular function depends on
temperature. Temperatures that either fall below
or above the physiological range required for
optimal testicular function could potentially dis-
rupt spermatogenesis. Certain land mammals
(such as elephants and rhinoceroses) and aquatic
mammals (such as whales and dolphins) have
intra-abdominal testes throughout their lifespan.
The abdomen is metabolically active and it
therefore generates a lot of heat. However,
spermatogenesis functions optimally in these
mammals despite the proximity of their testes to
the abdomen.
Humans, on the other hand, have intra-scrotal
testes that develop within the abdomen and,
towards the end of the gestation period, begins its
descent through the inguinal canals into the scro-
tum. In humans, normal testicular function is
temperature dependent and the extra-abdominal
testes are maintained at temperatures below that
of core body temperature [ 2 ]. Under normal
healthy environmental conditions, testicular ther-
moregulation maintains scrotal hypothermy to
ensure optimal testicular function [ 1 ].
Testicular Thermoregulation
The normal physiological temperature of the
human testis ranges between 32 and 35 °C [
3 ].
Thermoregulation in the testis occurs via two
mechanisms: the physiological properties of the
scrotum and the counter-current mechanism.
The scrotum is a loose sac-like structure that
houses each testicle. The main function of the
scrotum in most mammals is to prevent heat from
reaching at the testis by means of adjusting to
heat stress [ 4 ]. The scrotum has features that
allow free dissipation of heat through passive
D. Durairajanayagam , PhD R. K. Sharma , PhD
A. Agarwal , PhD (*)
Center for Reproductive Medicine, Cleveland Clinic ,
Cleveland , OH , USA
S. S. du Plessis , BSc (Hons), MSc, MBA, PhD (Stell)
Division of Medical Physiology, Department of
Biomedical Sciences , Faculty of Medicine and Health
Sciences, Stellenbosch University ,
Tygerberg , Western Cape , South Africa
Testicular Heat Stress and Sperm
Damayanthi Durairajanayagam , Rakesh K. Sharma ,
Stefan S. du Plessis , and Ashok Agarwal
convection and radiation. These include a large
total skin surface area that changes according to
the surrounding temperature, a large number of
sweat glands, minimal subcutaneous fat, and
sparse hair. When external temperatures rise and
cause the scrotal temperature to increase beyond
a threshold value, cutaneous receptors on the
scrotal skin are activated, initiating secretions of
the scrotal sweat glands and active heat loss
occurs through the evaporation of sweat [ 4 , 5 ].
Vasodilation of the scrotal vessels, the very thin
scrotal skin and the near-absence of surface hair
further contribute to heat dissipation.
The spermatic cord is made up of the testicu-
lar artery, veins, cremaster muscle, and vas defer-
ens. The testicular artery is greatly coiled while
the veins have thin walls and poor musculariza-
tion. The bulk of the spermatic cord is composed
of numerous testicular veins that anastomose and
drain into the convoluted pampiniform plexus
[ 6 ]. The testicular arterial and venous blood ves-
sels are intimately associated with each other,
facilitating the transfer of heat between the
infl owing arterial blood to the outfl owing venous
blood in the spermatic cord. Thus, the arterial
blood arriving at the testis is effectively cooled
while the venous blood disperses this heat
through the scrotal skin [ 7 ]. In a normal individ-
ual, this counter-current heat exchange regulates
the temperature of the arterial blood supply to the
testis and epididymis at 2–4 °C below rectal tem-
perature [ 7 ].
Thermoregulation of the testis is further aided
by two muscles: the cremasteric and dartos mus-
cles. The cremaster muscle is skeletal-type mus-
cle that is associated with the spermatic cord and
testis. A refl ex contraction of the cremasteric
muscle can be produced by gently stroking the
skin on the medial side of the thigh (cremasteric
refl ex). The dartos muscle is a layer of smooth
muscle fi bers that surround the testis subcutane-
ously. When the ambient temperature falls, both
the cremaster and the dartos muscles contract
involuntarily, raising the testes and bringing them
closer to the warmer body. The scrotal skin wrin-
kles with the contraction of these muscles, reduc-
ing the exposed surface area to avoid further heat
loss. Conversely, when ambient temperatures
increase, the dartos and cremasteric muscles
relax causing the testes to lower away from the
body and the scrotal skin to become looser around
the testes, aiding heat loss.
Mechanism of Heat Stress:
Testicular and Germ Cell Changes
Germ cells have high mitotic activity, which
makes them more susceptible to heat stress [ 8 ].
The type of germ cells that is most sensitive to
heat is the pachytene and diplotene spermatocytes
and early round spermatids in both the rat [ 9 , 10 ]
and in humans [ 11 ]. In fact, the spermatogenic
process, particularly the differentiation and matu-
ration of spermatocytes and spermatids, is tem-
perature dependent and occurs ideally at a
temperature of at least 1–2 °C below core body
temperature [ 1 , 10 ]. As such, raising the scrotal
temperature causes testicular germinal epithelial
atrophy and spermatogenic arrest [ 12 ], leading to
lower sperm counts. The supportive role of Sertoli
[ 13 ] and Leydig [ 14 ] cells towards germ cell
development are also impacted by heat stress.
Levels of a biochemical marker of spermatogene-
sis, inhibin B [ 15 ], decrease along with sperm
concentration when scrotal temperatures are high
[ 16 ]. Irreversible testicular weight loss follows
shortly after heat exposure [ 17 ]. Histopathological
changes in the testis following heat exposure
include degeneration of the mitochondria, dilata-
tion of the smooth endoplasmic reticulum, and
wider intercellular spaces in both Sertoli and sper-
matid cells [ 18 ].
The fundamental mechanism by which loss of
germ cells occurs in response to heat stress is due
to apoptosis [ 9 , 19 ]. The intensity of heat stress
and duration of heat exposure infl uence germ cell
apoptosis. For example, 2 days after a single
exposure to heat (43 °C for 15 min), late pachy-
tene and early spermatids degenerate [ 20 ].
However, shorter heat exposure of the rat testes
(43 °C for 10 min) does not result in apoptotic
germ cells whereas a longer heat exposure (43 °C
for 30 min) intensifi es germ cell apoptosis [ 21 ].
D. Durairajanayagam et al.
Similarly, higher heat exposure (45 °C for
15 min) causes generalized, nonspecifi c damage
to many different germ cell types in adult rats.
Besides apoptosis, heat stress also causes
defects in DNA synapsis and DNA strand breaks
in pachytene spermatocytes and induces DNA
damage in mature spermatozoa [ 20 ]. Sperm DNA
damage that occurs in the heat-stressed testis is
likely due to excessive generation of reactive
oxygen species (which causes the sperm cell to
be in a state of oxidative stress) as well impaired
DNA repair in the germ cells [
20 , 22 ]. In experi-
mentally cryptorchid rats, heat stress (due to
increased scrotal temperatures) increases genera-
tion of reactive oxygen species leading to oxida-
tive stress [
23 , 24 ]. Moreover, in adult rats, the
effects of scrotal hyperthermia (43 °C for 30 min
once daily for 6 consecutive days) include
decreased levels of glutathione, superoxide dis-
mutase, and glutathione peroxidase and increased
lipid peroxidation in the testes [
18 ]. Further, gene
expression for DNA repair and cellular antioxi-
dants are suppressed during testicular heat stress
[ 25 ] (Fig. 8.1 ).
Fig. 8.1 Schematic highlighting various mechanisms by which testicular heat stress causes germ cell apoptosis, DNA
damage in mature and immature sperm and male infertility
8 Testicular Heat Stress and Sperm Quality
In summary, heat-induced changes due to
increased scrotal temperatures in the testes lead
to apoptosis of germ cells and sperm DNA dam-
age, which subsequently suppresses spermato-
genesis [ 18 , 20 ].
Impact of Failed Thermoregulation
on Semen Parameters
Semen analysis is carried out as a routine labora-
tory assessment of the infertile male. Fundamental
sperm parameters evaluated during a standard
semen analysis include sperm concentration,
motility, and morphology [ 26 ]. The total count
and concentration of sperm refl ect semen quality
and the male reproductive potential whereas
sperm concentration and motility are best able to
predict fertility [ 27 ]. Repeated testicular expo-
sure to elevated levels of heat could lead to
chronic thermo-dysregulation, which in time
could lead to signifi cant changes in sperm char-
acteristics [ 1 , 28 ].
Mean scrotal temperature is higher in infertile
men than in fertile ones [ 29 ], and the higher the
scrotal temperature, the more sperm quality is
altered [ 29 ]. Men (mean age 31.8 years) who
were infertile for at least 2 years (without female
factor infertility) were found to have lower sperm
count, percentage of motile sperm and testicular
volume in both testes and higher mean scrotal
temperatures compared to fertile men [ 29 ].
However, testicular hyperthermia causes modifi -
cation of sperm characteristics in both the fertile
and infertile male [ 29 ]. Physiological increases in
scrotal temperature are associated with substan-
tially reduced sperm concentration that results in
poor semen quality [ 30 ]. An increase of 1 °C
above baseline values suppresses spermatogene-
sis by 14 %, decreasing sperm production [ 31 ].
Elevated testicular and epididymal tempera-
tures decrease the synthesis of sperm membrane
coating protein, resulting in higher amounts of
morphologically abnormal sperm [ 31 ]. Within
6–8 months of exposure to elevated temperatures,
the mean value of sperm with abnormal morphol-
ogy was found to double [ 31 ]. Sperm motility is
also suppressed in the hyperthermic testis [ 32 ].
Exposure to high temperature causes deteriora-
tion in sperm morphology and impairs motility as
well as sperm production, all of which have a del-
eterious effect on male fertility [ 33 , 34 ].
Pathological Failure
of Thermoregulation
Increased testicular temperatures due to either
endogenous or exogenous stimuli decrease sperm
concentration, motility, and the number of mor-
phologically normal sperm [ 11 , 35 ]. Pathophys-
iological abnormalities such as varicocele and
cryptorchidism cause testicular hyperthermia,
which could lead to male infertility [ 36 ]. Thus,
any disruption (either acute or chronic) to the
thermoregulation of the testis would have severe
adverse effects on the spermatogenic process.
Febrile Episodes
When the hypothalamic thermoregulation of the
core body temperature is compromised with
the onset of fever, thermoregulation at the level of
the testes is also impacted. In a case study of a
fertile patient with infl uenza who was febrile
(39.9 °C) for 1 day, semen samples analyzed
18–66 days post fever showed underlying effects
on sperm chromatin structure and a temporary
release of abnormal sperm [ 37 ]. In another study,
the incidence of fever was reported to have a sig-
nifi cant effect on spermatogenesis, and the more
days of fever (between 1 and 11 days); the more
increasingly adverse were its effects on sperm
concentration, percentage of normal and immo-
tile sperm [ 11 ]. Certain stages of spermatogenesis
were found to be more predisposed to the effects
of higher temperatures caused by a fever than oth-
ers: sperm concentration was affected when fever
occurred during meiosis (33–56 days before
ejaculation) and spermiogenesis (post-meiotic
phase, 9–32 days before ejaculation) while sperm
morphology and motility were affected when
fever occurred during spermiogenesis [ 11 ].
D. Durairajanayagam et al.
Varicocele is the most common and treatable
cause of male infertility and it affects 15 % of the
male population. It is implicated in 40 % of men
with primary infertility and in 80 % of men with
secondary infertility [ 38 , 39 ]. A varicocele is the
abnormal tortuosity and dilatation of the testicular
veins in the pampiniform plexus causing retro-
grade blood fl ow in the internal spermatic veins
and venous stasis. Consequently, the cooling of
the testicular arterial blood via the counter current
heat exchange becomes ineffective and testicular
temperature increases towards that of the core
body [ 40 ]. Increased scrotal temperature found in
infertile men is most commonly caused by varico-
cele [ 29 , 41 ]. Both Mieusset et al. [ 29 ] and
Goldstein and Eid [ 42 ] reported that infertile men
with varicocele have higher mean scrotal tempera-
tures on (1) the affected testis compared to the
unaffected side and (2) both testes compared to
that in fertile men. Intra-testicular temperatures in
the affected testis were 2.43–2.72 °C higher than
that of a normal testis [ 42 ]. The underlying mech-
anism of varicocele-related infertility is not clear
but is attributable to factors such as increased
scrotal temperature, oxidative stress, and hor-
monal imbalance [ 43 ]. Varicocele patients have
increased apoptosis (programmed cell death) [ 44 ],
and the increase in scrotal temperature (but not
varicocele grade) is associated with oxidative
stress-induced apoptosis [ 43 ]. Chan et al. [ 45 ]
found that heat shock proteins 70 and 90 were sig-
nifi cantly upregulated in varicocele patients. Heat
shock proteins are produced in response to various
stress inducers including heat, and their increased
expression suggest that they play a role in the
mechanism of varicocele- related infertility [ 45 ].
Cryptorchidism is among the most common con-
genital defects in newborns and occurs in 2–4 %
of full-term male births [ 46 ]. About 50 % of these
cases resolve spontaneously within the fi rst year
of birth and those that do not resolve naturally
require surgical intervention. Failure of the testis
to descend leads to infertility and increased risk
of testicular cancer. The severity of infertility in
human cryptorchidism depends on the position of
the testis, whether one or both of the testis is mal-
descended, how soon it is surgically corrected
and perhaps the underlying pathology [ 47 ]. In its
supra-scrotal position, the testis is hyperthermic.
This causes heat-induced loss of spermatogonial
differentiation and apoptosis of all germ cells
(including germ stem cells) as well as an indirect
effect of increased oxidative stress and abnormal
energy metabolism [ 23 , 48 , 49 ]. In addition, the
changes in Sertoli cell junctions and abnormal
levels of Leydig cell hormones noted in the crypt-
orchid testis are linked to hyperthermia [ 50 , 51 ].
Furthermore, despite sperm appearing to be mor-
phologically normal [ 52 ], heat stress produced in
conditions of cryptorchidism and varicocele
induces sperm DNA fragmentation [ 52 , 53 ].
Assessing Testicular Temperature
Testicular and intra-scrotal temperatures can be
measured either directly or indirectly and in the
form of either a single or continuous measurement
(Table 8.1 ). Intra-scrotal skin surface temperatures
refl ect the temperature of the underlying testis as
the testis and epididymis constitute the largest ther-
mal mass in the hemiscrotum [ 36 , 54 ]. Testicular
temperature may range between 31 and 36 °C
depending on the method used for the measure-
ment of temperature and the presence of any under-
lying pathology [ 55 ]. Accuracy and reproducibility
of the temperature are important as temperature dif-
ferences in a normal (euthermic) and pathologic
(hyperthermic) testis may be as small as 0.6–1.4 °C
[ 36 ]. Even these small increases can hamper sper-
matogenesis and epididymal maturation [ 36 ].
Single or Discontinuous
In this method evolved by Zorgniotti and MacLeod
[ 36 ], the subject disrobes from the waist below and
lays supine for about 6 min (to equilibrate to
an ambient room temperature of about 21–23 °C)
[ 32 , 36 ]. A mercury thermometer is pre-warmed by
placing the bulb of the thermometer in contact with
8 Testicular Heat Stress and Sperm Quality
Table 8.1 Methods of measuring scrotal (testicular) temperature in humans
Method Description Advantage Disadvantage Reference(s)
Single measurement or discontinuous method
Mercury thermometer 1. Pre-warmed bulb positioned directly
over the most prominent part of the
anterior testis
1. Simple and inexpensive 1. Clinical thermometer unsuitable as its
mercury column is constricted
[ 32 , 36 , 54 , 55 ]
2. Thermometer bulb held longitudinally
against the scrotum
2. Provides accurate measurements 2. Applicable only when subject is
3. Loose scrotal skin drawn around the
thermometer bulb using the thumb and
index fi nger
3. Gives repeatable and standardized
3. Reproducible only under static
conditions (e.g., lying down for several
Skin surface
1. Attached to the scrotal skin overlying
the anterior testis using an adhesive
1. Small dimensions 1. May be displaced from the site of
contact with the testis beneath
[ 55 , 65 ]
2. Electrode cables secured at trouser
2. Light weigh 2. Minor movements of the scrotum could
alter the readings
3. Assessment done in a clothed state
Thermal resistor
(thermistor) needles
1. Placed within the scrotum or testis 1. Direct measurement 1. Invasive procedure [
4 , 54 , 55 , 108 ]
2. Depth of thermistor placement could
contribute to differences in reading
(temperature in the peripheral testis is
lower than the mediastinum testis)
3. Use of anesthesia and evaporation of
the antiseptic solution applied during
scrotal skin preparation would alter the
4. Extremes of ambient temperature,
scrotal skin infl ammation, and
intrascrotal disease would affect the
D. Durairajanayagam et al.
Infrared thermometry 1. Measures heat emitted from the
scrotal skin
1. Easy way to measure temperature
in different body positions
1. For better accuracy, these thermometers
needs to be calibrated using a black
body prior to use
[ 55 , 109 , 110 ]
2. A pistol-type, non-contact, digital
infrared thermometer with an accuracy
of ±0.1 °C was preferred
2. Permits repeated measurement
on the same area
2. Variations in skin’s thermal radiation or
emissivity could affect readings
3. Replicate readings taken at the skin
over the most prominent part of the
3. Only the surface temperature is
measured and not deep scrotal
4. Lacks sensitivity to record small
differences in temperature
Thermography 1. Measured heat emitted from the
scrotal skin
1. Does not provide the required accuracy
for research as the comparison with the
grey scale can introduce inaccuracies
[ 55 ]
2. Provides relative differences but not
absolute numbers
3. Unable to obtain a preferred sensitivity
of ±0.1 °C
Liquid crystal
1. Measured using temperature- sensitive
1. Unable to obtain a preferred sensitivity
of ±0.1 °C
[ 55 , 109 ]
Continuous measurement method
thermocouples or
1. Attached to skin on the anterior face of
the each scrotum using transparent tape
1. Allows for a dynamic recording
of temperature
[ 5658 ]
2. Connected to a portable data recorder
attached to a belt
2. Representative of testicular
temperature during normal daily
Thermistor 1. Thermistor attached to underwear [ 54 , 55 ]
2. Connected to a light-weight data logger
8 Testicular Heat Stress and Sperm Quality
a light source or immersing it in warm water, allow-
ing the mercury column in the thermometer to
expand to a temperature that is slightly higher than
the estimated temperature of the testis (i.e., around
37 °C). The thermometer is then quickly positioned
directly over the most prominent part of the ante-
rior testis and the bulb is held longitudinally against
the scrotum. The loose scrotal skin is drawn around
the thermometer bulb using the thumb and index
nger (to include the immersion mark, if present).
The mercury column will begin to drop until it
reaches equilibrium (usually about 8 s). The read-
ing at that point plus 0.1 °C represents the intra-
scrotal temperature [ 36 ]. The process is then
repeated in the contralateral testis. This method
was modifi ed from the “invagination method” by
Brindley [ 32 ] and allows for repeatable and consis-
tent values to be obtained for use in a clinical evalu-
ation of, for example, a varicocele [ 56 ].
Continuous Measurements
During continuous measurement, two cutaneous
thermocouples (thermoprobes) are attached to
the skin on the anterior face of the each scrotum
using transparent tape, and these are connected to
a small portable data recorder attached to a belt.
Temperatures are recorded at 2-min intervals.
Measurements recorded in the data recorder are
downloaded to a computer through a specifi c pro-
gram [ 57 ]. The use of a portable data recorder for
continuous determination of scrotal temperature
allows for a dynamic recording of temperature
[ 58 ]. However, scrotal skin temperatures have also
been measured noninvasively for an entire day
using a thermistor attached to underwear that is
connected to a light-weight data logger [ 56 ].
Risk Factors for Scrotal
The temperature difference between the body and
scrotum can be affected by a variety of external
thermogenic factors including body posture or
position, clothing, obesity, lifestyle and occupa-
tional exposure, and ambient seasonal tempera-
ture changes (Fig. 8.2 ).
Changes in posture affect testicular tempera-
ture. Scrotal temperature is lowest when stand-
ing disrobed [ 36 , 59 ]. Heat dissipation can
occur unhindered from the unsupported testis
when the body is unclothed and in an upright
position. When comparing body positions,
scrotal temperature in the supine or seated posi-
tion is higher than that in the standing position
[ 32 , 36 , 58 , 59 ]. When walking (upright and
moving), scrotal temperatures are 0.3–1 °C
lower than those generated when sitting regard-
less of clothing type [ 32 , 59 ]. Scrotal tempera-
tures are highest during sleep when the body is
supine and movement is minimized [ 32 , 58 , 60 ]
compared to other body positions. When com-
paring sleepwear, scrotal temperatures were the
lowest when sleeping in the nude compared to
sleeping in pyjamas or underwear [ 32 ]. When
in a supine position, the testes are resting on the
thighs and are in direct contact (conduction)
with the relatively higher body temperature.
Additional layers of clothing trap air and con-
serve heat. Using an electric blanket or quilt on
top of typical nightclothes while lying down in
bed after a hot bath will give a cumulative effect
that is likely to lead to genital heat stress. When
assessing diurnal variation, Hjollund et al. [ 56 ]
found that scrotal temperatures, when measured
at a 5-min interval for a continuous 24 h, were
higher at night by 1.2 °C compared to those
during the day.
The length of time spent in a seated position,
either due to occupational nature, long commutes
and sedentary leisure activities, also contributes
to testicular heat stress. A predominantly seden-
tary (sitting) position at work has been shown to
increase scrotal temperatures [ 30 , 56 , 57 ]. When
sitting, the testes are trapped between the thighs.
Moreover, the normal seated position leads to
poor ventilation in the groin area, which contrib-
utes to an increase in scrotal temperature. The
positioning of the legs while sitting (i.e., legs
together, apart or crossed) impacts the scrotal
temperature in both the disrobed [ 59 ] and clothed
state [ 32 , 57 ].
D. Durairajanayagam et al.
Paraplegic men in wheelchairs who remain
seated for extended periods with closed and unmov-
ing legs were found to have higher deep scrotal
temperature and poor sperm motility than normal
men who were seated freely for 20 min or more
(without the position of their thighs being specifi ed,
i.e., kept close together or apart) [ 32 ]. However,
when compared in a supine position, there was
no signifi cant difference in scrotal temperatures
between the paraplegic and normal men [ 32 ].
The insulating effect of the seated posture is
compounded by being sedentary but counter-
acted by physical activity. The average scrotal
temperature in healthy volunteers while sitting
on a conventional chair for a period longer than
35 min is 36.4 °C compared to 34.5 °C during
walking [ 61 ]. Increased limb movement during
physical activity increases perigenital air circula-
tion, and this allows for better dissipation of heat,
which then results in lower scrotal temperatures,
compared to when being seated in a sedentary
In a study comparing the increase in scrotal
temperatures while seated on different types of
chairs, Koskelo et al. [ 62 ] reported a 3 °C increase
in scrotal temperature upon 20 min of sitting on a
conventional cushioned offi ce chair. However,
they found no difference in temperature when
subjects sat in a saddle chair. This is probably due
to the open hip and knee angles, which allow for
adequate scrotal ventilation [
62 ]. Similarly, sit-
ting with crossed legs causes a bigger increase in
scrotal temperature than sitting with the legs
apart (at an angle of about 70°) [ 63 ]. After
remaining in a seated position with crossed legs
for 15 min, the thermogenic effect caused by this
position further persisted for a minimum of
5 min, even after standing up [
63 ].
Fig. 8.2 Various lifestyle, occupational, postural, and environmental factors contributing to testicular heat stress
8 Testicular Heat Stress and Sperm Quality
When sitting on surfaces with a higher tem-
perature, the increase in scrotal temperature attrib-
uted to the seated posture is further compounded
by the warmth exuding from the seated surface. In
a Korean study, Song and Seo [ 64 ] investigated
the effects of sitting directly on a heated fl oor on
scrotal temperature among 6 healthy male volun-
teers in a controlled environmental chamber. They
concluded that the fl oor surface temperature and
the rate of metabolism while in a sedentary pos-
ture affect scrotal temperature and recommended
that surface temperature of a heated fl oor be main-
tained within 23–33 °C to avoid impairment of
spermatogenesis [ 64 ].
Irrespective of the body position, wearing cloth-
ing has an insulating effect that increases scrotal
temperature. In the standing and supine posi-
tions, clothing increases scrotal temperatures by
1.5–2 °C compared to the naked state [ 63 , 65 ]. In
men at rest who are lightly clothed, the layer of
air trapped in the space between the skin and
clothes is on average 3.5 °C higher than that of
ambient air (at a temperature of between 21 and
32 °C) [ 66 ]. The reduction in air exchange when
in a clothed state contributes to the increase in
scrotal skin temperature [ 63 ]. Clothing that per-
mits better air fl ow would mean that scrotal heat
could be more easily dissipated, keeping temper-
atures closer to physiological levels. Kompanje
[ 27 ] suggested that Scottish kilt-wearing possibly
produced a more ideal physiological scrotal envi-
ronment, especially since nearly 70 % of men
chose to not wear anything underneath their kilt.
In the Asian region, men often wear only a sarong
when at leisure, which similarly helps in dispers-
ing body and environmental heat to keep lower
testicular temperatures.
Tight Underwear, Boxers, Jockey Shorts
It is still debated whether the type of underwear
has a signifi cant impact on testicular temperature
and hence, male fertility. Studies have reported
that the regular use of tight underwear over a
period of time leads to a reduction in sperm
motility [ 67 , 68 ]. Another study found that men
who wear tight underwear have decreased sperm
count and sperm motility compared to those who
wear loose underwear [ 69 ]. Conversely, in a
study involving 97 men presenting for primary
infertility (aged between 25 and 52 years), scrotal
temperatures did not differ between men who
wore boxer shorts and those who wore brief style
underwear [ 12 ]. The authors further reasoned
that brief style underwear gives a supportive
effect that pushes the testes closer to the body
while the boxer shorts lacks this effect. However,
any additional layer of clothing that is worn over
the underwear (e.g., trousers) would result in the
same supportive effect on the testes [ 12 ].
The use of disposable plastic-lined diapers is
more common these days than cotton, reusable
diapers. Even cotton diapers are usually used in
combination with a plastic lining as a protective
covering to prevent leakages. The use of plastic
material reduces the skin’s breathability, which
would lead to a warm and moist perigenital area,
thereby contributing to higher scrotal tempera-
ture. Partsch et al. [ 70 ] studied 14 neonates (term
aged 0–4 weeks) and pre-term with a gestational
age of 28–36 weeks (postnatal age 14–85 days),
22 infants (aged 1–12 months), and 12 toddlers
(age 13–55 months) and reported that young
boys wearing disposable plastic-lined nappies
have increased scrotal temperatures compared to
those wearing reusable cotton diapers (without
protective pants). However, in another study,
Grove et al. [ 71 ] found no differences in the scro-
tal temperature profi les of approximately 70
young boys (aged 3–25 months) wearing dispos-
able diapers with a plastic lining compared to
those wearing reusable cotton diapers covered
with plastic pants. Only when the cotton diapers
were used without any plastic covering were
scrotal temperatures lower than those in the boys
using disposable diapers [ 70 , 71 ]. That being
said, as cotton diapers are almost always used
along with the plastic pants, it would seem that
practically speaking, both the classic and modern
diaper choices did not differ signifi cantly on their
effect on scrotal temperature. As to whether
D. Durairajanayagam et al.
diapering preferences (and the higher scrotal
temperatures is generates) at a young age could
contribute towards a compromised male fertility
potential as an adult, Jung and Schuppe [ 72 ] rea-
soned that pachytene spermatocytes and round
spermatids (the most temperature-sensitive tes-
ticular cells) [ 10 ] are not yet present in the age
group when most children use diapers. The
authors concluded that there was no convincing
evidence linking genital heat stress with poor
semen quality in their adulthood [ 72 ].
Obesity is a common lifestyle-related societal
problem of the modern era. Many adults who are
in the reproductive age group have a higher than
normal body mass index (BMI, normal range:
18.0–24.9). In fact, the rate of obesity is higher in
infertile men than in men with normal semen
parameters [ 73 ]. A BMI 25 is associated with
an average 25 % reduction in sperm count and
motility [ 74 ]. Obesity is often associated with
decreased physical activity and prolonged peri-
ods of sitting or being sedentary, which have been
found to increase testicular temperatures and con-
sequently suppress sperm production [ 75 ]. Obese
males are more likely to have increased fat depo-
sition in the abdomen and upper thighs and larger
waist and hip circumferences. Additionally, scro-
tal lipomatosis (deposition of fat around the sper-
matic cord) in obese men could inhibit
spermatogenesis by several means, i.e., (1) pro-
vide insulation that could disrupt the radiation of
testicular heat, (2) compress blood vessels, lead-
ing to testicular congestion (venous stasis) and
impaired heat exchange, (3) compress the testicu-
lar artery leading to ischemia of the testis, (4)
hamper the cord’s ability to reposition the testes
in response to temperature changes, and (5) dis-
rupt local thermoregulation due to excess fat in
the suprapubic region [ 76 , 77 ]. The compromised
effi ciency of testicular thermoregulation may
well lead to elevated testicular temperatures.
However, scrotal lipomatosis could also occur in
those who are not obese [ 76 ]. In one study,
removal of excess fat in the scrotal and suprapu-
bic region helped improve sperm count, motility,
and morphology in nearly 65 % of infertile
patients, and nearly 20 % of these patients went
on to initiate a pregnancy [ 77 ].
Saunas are a popular method of relaxation and
detoxifi cation or cleansing in many parts of the
world. Temperatures in saunas typically range
between 80 and 100 °C at the level of the bather’s
head, with humidity ranging from 40 to 60 g of
water/kg dry air [ 78 ]. Conventional saunas pro-
vide wet heat through warmed, humid air (radia-
tion and convection) as well as warmed surfaces
(radiation and conduction), while modern saunas
such as infrared saunas provide dry, radiant heat.
Brown-Woodman et al. [ 79 ] examined the
effect of a single sauna exposure (85 °C for
20 min) on sperm parameters at 10 weeks post-
exposure compared to 3 weeks preexposure.
They found that this one acute testicular heat
stress episode was suffi cient to cause the sperm
count to reduce within a week post-exposure,
only to normalize in the fi fth-week post-exposure
[ 79 ]. In a study that continuously (i.e., every 5 s)
monitored scrotal temperature during a sauna
exposure (87.6 ± 1.3 °C and <15 % humidity),
scrotal temperatures were found to reach core
body temperature within about 10 min of expo-
sure to the exogenous heat [ 58 ]. Saikhun’s group
assessed the effects of sauna exposure on sperm
parameters after a 2-week sauna exposure
(at 80–90 °C for 30 min) [ 35 ]. They found that
sperm movement characteristics had declined but
were restored within a week after concluding the
sauna exposure. They reported that sperm param-
eters such as semen volume, sperm count, num-
ber of motile and morphologically normal sperm
as well as sperm penetration levels had remained
unchanged [ 35 ]. More recently, Garolla et al.
[ 80 ] investigated the effects of biweekly Finnish
(dry) sauna sessions (89–90 °C for 15 min) for
3 months on ten normozoospermic men. They
found that these frequent sauna exposures (that
lasted long enough to cover an entire spermato-
genic cycle) caused a signifi cant reduction in
sperm count and progressive motility (although
8 Testicular Heat Stress and Sperm Quality
they were still within normal range) and altered
mitochondrial function, DNA protamination, and
chromatin condensation in the sperm [ 80 ].
However, sperm morphology and viability
remained unaffected while heat shock proteins
(and their regulating heat shock factors) that con-
fer a protective effect were found to be upregu-
lated after testicular heating [ 80 ]. These studies
collectively showed that following sauna expo-
sure, the negative impact on spermatogenesis was
signifi cant but reversible.
Hot Baths
Other lifestyle habits such as indulging in a relax-
ing soak in a hot tub, heated whirlpool, or a warm
bath could negatively impact male fertility. Shefi
et al. [ 81 ] studied the effects of wet heat exposure
in a group of 11 infertile men (mean age
36.5 years) who practiced whole body immersion
in either a hot tub, heated jacuzzi, or warm bath
(at temperatures that were higher than that of
body temperature) for more than 30 min weekly
(mean weekly exposure was 149 min) for longer
than 3 months. Comparison of semen parameters
in samples analyzed before vs. 3 months after the
discontinuation of the wet hyperthermia, showed
improvements, mainly in sperm motility [ 81 ].
They concluded that in certain infertile men,
refraining from these types of heat exposure
could perhaps reverse the detrimental effects of
hyperthermia on their semen quality.
A regular, moderate exercise regimen bestows
numerous health benefi ts. However, certain forms
of exercise done in the pursuit of fi tness, cycling,
for example, may negatively affect male fertility.
Scrotal temperatures during cycling may be
infl uenced by the duration and intensity of the
exercise as well as posture [ 82 ] and clothing. As
a physical activity, cycling improves perigenital
air circulation, which aids in the dissipation of
testicular heat [ 82 ]. At the same time, cycling
involves extended periods of being in a seated
posture on a saddle seat for the majority of the
exercise and wearing a body-fi tting spandex out-
t, which would contribute an insulating effect
on scrotal temperatures, especially in profes-
sional cyclists [ 83 ]. However, in their study, Jung
et al. [ 82 ] found that 25 healthy volunteers
(median BMI of 23.2) who wore cotton wool
clothing while performing moderate cycling
(median speed of 25.5 km/h, power around 25 W)
sitting on the saddle of a stationary cycle for
60 min had mean scrotal temperatures below
35.6 °C. Increases in scrotal temperatures did not
differ signifi cantly between the left and right
scrotum and with time [ 82 ].
Laptop Usage
Sheynkin et al. [ 84 ] demonstrated among 29
healthy volunteers that using a laptop in a lap
position close to the genital area (i.e., a seated
position with approximated thighs) for an hour
contributes to a 0.6–0.8 °C increase in scrotal
temperatures compared to a 2.1 °C increase in
scrotal temperatures in the same sitting position
without using a working laptop. This increase in
genital heat could be attributed to heat exposure
from laptops that have internal operating temper-
atures of more than 70 °C and to the seated pos-
ture for those 60 min. Although this study did not
examine changes in semen parameters, the
authors suggested that since scrotal heat impairs
spermatogenesis, then laptop usage also likely
affects these parameters [ 84 ].
Welders: Radiant Heat
Welders are occupationally exposed to intense
radiant heat, toxic metals and their oxides, and
toxic welding fumes during welding. Bonde [ 85 ]
reported that 17 manual metal arc alloyed steel
welders (mean age 35.9 years) with moderate
exposure to radiant heat (31.1–44.8 °C) and with
minimal exposure to welding fume toxicants
experienced a reversible decrease in semen qual-
ity. The percentage of sperm with normal mor-
phology decreased within 6 weeks of exposure to
radiant heat but increased 4 weeks after cessation
of exposure [ 85 ]. In another study, 17 welders
(mean age 43.8 years) with 1–10 years or
more of welding exposure possibly had some
adverse effects on sperm motility, morphology
and physiologic function, although they main-
tained a normal range of sperm concentration [ 86 ].
D. Durairajanayagam et al.
Bakers: Radiant Heat
Bakers are reported to take longer to initiate a
pregnancy than controls, as only 14 % of bakers’
partners were pregnant within 3 months
(compared to 55 % of controls) and 29 % of
bakers’ partners were pregnant within 6 months
(compared to 74 % of controls) [ 87 ]. This sug-
gests that the bakers’ occupational exposure to
heat may be a contributory factor to subfertility.
Ceramic Oven Operators: Radiant Heat
Figà-Talamanca et al. [ 88 ] reported that healthy
ceramics oven operators with chronic occupa-
tional exposure to high temperatures (37 °C, 8 h/
day) had a higher incidence of abnormal sperm
parameters compared to controls. These individ-
uals faced diffi culty in establishing a pregnancy
and had a higher occurrence of not being able to
father a child compared to controls [ 88 ].
Professional Drivers
Long hours of driving and remaining in a seated
position have shown to have detrimental effects
on male reproductive function. The negative
effect of extended periods of driving on sperm
parameters is attributed to an increase in scrotal
temperature [ 57 ].
Sas and Szollosi [ 89 ] investigated the effects
of prolonged driving on spermiogenesis in 2,984
patients, of whom 281 were occupational drivers.
They found that the incidence of abnormal sperm
was higher among the patients who drove profes-
sionally and more severe in those with longer
occupational driving experience. Similarly,
workers involved in the transport occupational
group had lower sperm concentrations [ 90 ] and
a higher risk of abnormal sperm motility [ 91 ]
compared to other occupational groups. Figà-
Talamanca et al. [ 92 ] reported that compared to
control subjects, taxi drivers in the city of Rome
had a higher amount of sperm with abnormal
morphology and that this was more apparent in
the longer-serving drivers. However, sperm con-
centration and motility in these drivers ( n = 72)
were comparable to that of the 50 healthy control
subjects, who were of similar age and had similar
smoking habits. This study also suggested that
prolonged driving time could compromise sperm
morphology and thereby sperm quality [ 92 ].
In a study of 402 fertile couples in France,
Thonneau et al. [ 93 ] found that compared to other
couples, the time to pregnancy was signifi cantly
prolonged for those couples in which the male
partner remained seated driving in a vehicle for
longer than 3 h daily.
In addition to the effect of prolonged sitting on
a car seat (which in itself causes about a 2 °C
increase in scrotal temperature) [ 57 ], the use of a
heated car seat for longer than 60 min was shown
to cause an increase in scrotal temperature of
0.5–0.6 °C, nearing core body temperature [ 94 ].
This additional factor would likely add towards
the decline in sperm quality.
Velez de la Calle [ 95 ] and co-workers looked into
the infertility risk factors in a military population
from a large military naval base in Brest, France.
They found that male mechanics, cooks, and sub-
mariners who were occupationally exposed to
very hot working conditions while in the subma-
rine (temperatures in the rear end of the subma-
rine close to the motor range between 40 and
60 °C) had sought help for infertility issues.
Ambient Temperature
and Seasonality
A 1 °C increase in ambient temperature induces
a 0.1 °C increase in scrotal temperature [ 32 ].
In a study of semen samples taken from more
than 1,000 fertile men from four European cit-
ies (Copenhagen, Denmark; Paris, France;
Edinburgh, Scotland; and Turku; Finland),
Jorgenson’s group found a general seasonal vari-
ation in sperm concentration (summer values
were 70 % of winter values) and total sperm
count (summer values were 72 % of winter val-
ues), but not for sperm motility or morphology
[ 96 ]. The difference of approximately 30 % in
sperm count from winter (highest) to summer
(lowest) could be attributed to differences in life-
style or environmental exposures among the men
[ 96 ]. Similarly, in a preliminary study of 4,435
pre-vasectomy patients, Tjoa et al. [ 97 ] reported
8 Testicular Heat Stress and Sperm Quality
a circannual rhythm (biological rhythmicity
approximating 1 year) in human sperm concen-
tration and total sperm count, with a higher sperm
count in winter compared to summer. Gyllenborg
et al. [ 98 ] found that sperm counts among a group
of unselected Danish semen donor candidates
were lowest in the summer although semen vol-
ume and sperm motility remained unchanged.
However, Mallidis et al. [ 99 ] did not fi nd any
effect of season in semen samples provided by
normal healthy Australian men.
Mild Scrotal Heating as a Method
of Contraception
Scrotal temperatures that are maintained lower
than that of the core body temperature would
help improve spermatogenesis and the fertility
potential of men facing infertility issues.
However, fertile men may fi nd that higher scrotal
temperatures could work in their favor.
Commonly used methods of male contraception
include hormonal approach, the use of condoms
and vasectomy [ 100 ]. However, local application
of heat could provide the means for a non-
hormonal, noninvasive, reversible method of
contraception targeting the testicular level [ 100 ].
In a preliminary study, Mieusset and Bujan [ 101 ]
induced mild testicular heating (assumed as
1–2 °C) by immobilizing the testis close to the
inguinal canal daily during waking hours in 9
men aged between 23 and 34 years. These meth-
ods did not affect the men’s libido or sexual
rhythm, and no pregnancies were reported during
the study period [ 101 ]. Sperm count and motility
normalized within 1–1.5 years in all the subjects
involved in this study [ 101 ]. In another clinical
study, Wang et al. [ 102 ] reported that hot water
baths taken in combination with testosterone sup-
pressed sperm count and motility. Thus, it would
seem that mild scrotal heating could potentially
serve as an alternate contraceptive method.
However, the endocrine parameters involved in
regulating spermatogenesis such as the hypotha-
lamic and pituitary hormones may well be
affected by the intentional increase in scrotal
Scrotal Cooling
Several studies have showed that scrotal cooling
can improve sperm count, motility, and morphol-
ogy [ 103 ]. Devices that have been used for tes-
ticular cooling include a curved rubber collar
lled with ice cubes that was taped to both the
thighs for 30 min daily for 14 consecutive days
[ 104 ] and a gel ice pack that solidifi ed upon freez-
ing, which was wrapped in a cloth or towel and
inserted in the underwear on the anterior aspect of
the scrotum nightly for 2 months—the cooling
effect occurred upon the thawing of the ice pack
within 3–4 h [ 105 ]. Other techniques included a
cotton suspensory bandage placed in close con-
tact with the scrotum (worn for 16–22 h from 8 to
20 weeks) that released fl uid (water or alcohol) to
maintain a damp scrotum [ 106 ] and a device
attached with a belt to the abdomen and scrotum
that released a continuous air stream to achieve
scrotal cooling nightly for 12 weeks [ 107 ]. In a
study to assess the feasibility of a clinical trial,
Osman and his group evaluated the use of a non-
greasy hydrogel pad, the Babystart
® FertilMate™
Scrotum Cooling Patch, in patients with mild,
moderate, and severe oligoasthenospermia [ 103 ].
The pad contained 0.5 % w/w natural I-menthol
and was reported to be more practical and com-
fortable to use than other cooling devices [ 103 ].
When the testes were cooled, spermatogenesis
improved and pregnancy occurred leading to the
suggestion that hyperthermia played a role in
causing or aggravating male infertility [ 29 ]. The
factors affecting scrotal (testicular) temperatures
and their effect on sperm parameters and male
infertility are summarized in Table 8.2 .
Scrotal hyperthermia is a substantial risk factor
for male infertility. Repetitive transient scrotal
hyperthermia in the current modern lifestyle is
likely to have a negative impact upon spermato-
genesis, specifi cally in men who are of repro-
ductive age and desire to have children. The
normal healthy male is equipped with local
D. Durairajanayagam et al.
Table 8.2 Factors affecting scrotal (testicular) temperatures and their effect on sperm parameters and male fertility
Exogenous factors
contributing to heat stress
Effects on scrotal/
testicular temperature Reference(s) Impact on sperm parameters and male fertility Reference(s)
Posture (physical inactivity)
1. Standing Lower (vs. sitting or supine) [
32 , 36 , 58 , 59 ] No data
2. Sitting (regardless of position
of legs, i.e., crossed, close
together or apart)
Increased (vs. standing or supine) [
32 , 36 , 5759 ] Reduced motility (legs close together) [ 32 ]
3. Sitting (legs apart) Lower (when legs apart vs. when
legs close together or crossed)
[ 57 , 63 ] No data
4. Sitting (on different chair
types—cushioned and non-
cushioned, plywood and wooden,
knee-support, saddle chair)
Increased (in conventional offi ce
chair—legs narrowly apart) vs.
saddle chair—legs wide apart
[ 62 ] No data
5. Sitting (on heated fl oor, car seat) Increased (vs. conventional fl oor
or car seat)
[ 64 , 94 ] No data
6. Supine (and during night sleep) Increased close to core body
temperature (vs. standing or sitting)
[ 16 , 30 , 32 , 56 ,
58 , 60 , 61 , 107 ]
No effect on semen parameter [
16 ]
Lower (when naked vs. clothed or
wearing underwear)
7. Sitting (sedentary position
at work)
Increased (vs. standing or supine) [
30 , 56 , 57 ] Not a risk factor for abnormal semen quality [ 30 ]
Strong correlation between scrotal
temperatures and duration of
sedentary work
Posture (physical activity)
8. Moderate walking Lower (vs. sitting) [
16 , 30 , 32 ,
5661 , 107 ]
No data
1. Clothed state Increased (vs. naked or unclothed
[ 32 , 57 , 6366 ] No data
2. Underwear (form-fi tting) Increased (vs. loose-fi tting) [
32 , 59 , 68 , 111 ] No data
No difference (vs. loose-fi tting) [
12 , 65 ] No data
8 Testicular Heat Stress and Sperm Quality
Table 8.2 (continued)
Exogenous factors
contributing to heat stress
Effects on scrotal/
testicular temperature Reference(s) Impact on sperm parameters and male fertility Reference(s)
3. Diapers (disposable) No difference (vs. reusable cloth
diapers with plastic covering)
[ 71 ] No data
Higher (vs. reusable cloth diapers
without plastic covering)
[ 70 , 71 ] No data
1. Obesity Increased [ 76 , 77 ] Suppressed sperm production [ 75 ]
2. Sauna Increased to core body temperature [
58 ] Reduced sperm count within a week [ 79 ]
Increased to core body temperature [
35 ] No change in semen volume, sperm count, morphology [ 35 ]
Reduced motility, reversible once exposure is discontinued
Increased to core body temperature [
80 ] Reduced sperm count (less effi cient spermatogenesis but
reversible) and lower (but reversible) progressive motility
[ 80 ]
No change in sperm morphology and viability
Altered DNA protamination and nuclear condensation
Increased expression of genes associated with hypoxia
and heat stress (up-regulation of heat shock proteins
and their regulating heat shock factors)
3. Hot baths Increased [ 68 , 81 ] Reduced sperm motility [ 81 ]
4. Exercise—moderate cycling Lowered during cycling
(maximum value reached is above
physiological range)
[ 72 ] Sperm density and morphology unaffected
(in professional cyclists during competition year)
[ 83 ]
5. Laptop usage in lap position Increased [
84 ] No data
Occupational exposure
1. Welders—radiant heat No data Adverse effects on sperm count, motility, concentration,
and proportion of sperm with normal morphology reduced
[ 85 , 86 ]
2. Bakers—radiant heat No data Longer time to pregnancy [
87 ]
3. Ceramic oven operators—
radiant heat
No data Longer time to pregnancy [
88 ]
D. Durairajanayagam et al.
Exogenous factors
contributing to heat stress
Effects on scrotal/
testicular temperature Reference(s) Impact on sperm parameters and male fertility Reference(s)
4. Professional drivers No data Lower percentage of sperm with normal morphology,
higher risk of lowered sperm motility
[ 89 , 92 , 93 ]
5. Submariners in a
nuclear-powered submarine
No data Increased infertility issues [ 95 ]
Temperature variations
1. Ambient temperature Increased [ 32 ] No data
No effect [ 63 ] No data
2. Seasonal changes No data Circannual rhythm in sperm count [
97 , 98 ]
Higher sperm count in winter
No data No effect [ 99 ]
Exogenous factors contributing to heat stress
Pathological conditions
1. Febrile episode Reduced sperm concentration, sperm morphology
and motility affected if fever occurs during spermiogenesis
[ 11 , 37 ]
2. Varicocele Increased [ 29 , 36 , 58 , 63 ] Induces sperm DNA fragmentation [ 52 , 53 ]
3. Cryptorchidism Increased [ 3 , 36 , 112 ] Lower sperm output [ 52 , 53 ]
Induces sperm DNA fragmentation
Exogenous application or removal of heat
1. Mild scrotal heating Increased [ 29 , 59 , 101 ,
113 , 114 ]
Reduced sperm count and percentage of motile sperm
and sperm with normal morphology
[ 29 , 101 ,
113 , 114 ]
No pregnancy established during exposure period
2. Scrotal cooling Decreased [ 29 , 104107 ,
111 ]
Improved spermatogenesis [ 29 ,
104107 ,
111 , 115 ]
Improved semen quality
Improved sperm density and motility
8 Testicular Heat Stress and Sperm Quality
thermoregulatory mechanisms to maintain a
hypothermic testis. However, posture, clothing,
lifestyle factors, occupation, and environmental
exposure can cause testicular heat stress.
Extended hours of exposure to genital heat stress
factors exacerbate their effect on semen quality
and sperm parameters. Each of these factors does
not occur solitarily, but many of them occur
simultaneously at any given time, compounding
their effect on testicular temperatures. This is
especially pertinent in infertile men who already
have a compromised reproductive potential.
Nevertheless, simple but signifi cant measures
can be taken by individuals to help alleviate the
deleterious impact of heat stress on male fertility.
These include interspersing periods of activity or
movement (walking, running) between extended
time spent sitting or lying down, wearing clothing
that does not restrict genital airfl ow, maintaining a
healthy weight, and making lifestyle modifi ca-
tions that will promote scrotal hypothermia (e.g.,
avoiding sauna or hot baths or using a laptop on
the lap). Understandably, the occupational require-
ments of certain lines of work and seasonal varia-
tions, although less easily tackled, should not be a
deterrent for achieving scrotal hypothermia.
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8 Testicular Heat Stress and Sperm Quality
... In addition, genital insulation while sleeping, excessive hot occupational environment (e.g., bakers and welders), placing laptop or electrical gadgets on the lap for long hours, heated car seats or floor and frequent sauna sessions are possible mediators of male infertility through GHS. The clinical disorders owing to high scrotal temperature and GHS include cryptorchidism, varicocele and acute/chronic febrile illnesses (Durairajanayagam, Sharma, Plessis, & Agarwal, 2014). ...
... The mechanism of GHS-induced spermatogenic impairments includes induction of oxidative stress with high reactive oxygen species (ROS) concentration and reduced antioxidants in the genital tract and ejaculate, sperm chromatin disintegration, DNA fragmentation, sperm mitochondrial dysfunction and increased rate of germ cell apoptosis (Durairajanayagam et al., 2015(Durairajanayagam et al., , 2014. Spermatozoa may be most susceptible to damage in the pre-meiotic stage at which chromatin remains mostly unstable due to the ongoing processes of histone modifications and hyperacetylation. ...
Alongside an increasing prevalence of couple and male infertility, evidence suggests there is a global declining trend in male fertility parameters over the past few decades. This may, at least in part, be explained through detrimental lifestyle practices and exposures. These include alcohol and tobacco consumption, use of recreational drugs (e.g., cannabis, opioids and anabolic steroids), poor nutritional habits, obesity and metabolic syndrome, genital heat stress (e.g., radiation exposure through cell phones and laptops, prolonged periods of sitting, tight‐fitting underwear and recurrent hot baths or saunas), exposure to endocrine‐disrupting chemicals (e.g., pesticide residue, bisphenol A, phthalates and dioxins) and psychological stress. This review discusses these lifestyle practices and the current evidence associated with male infertility. Furthermore, known mechanisms of action are also discussed for each of these. Common mechanisms associated with a reduction in spermatogenesis and/or steroidogenesis due to unfavourable lifestyle practices include inflammation and oxidative stress locally or systemically. It is recommended that relevant lifestyle practices are investigated in clinical history of male infertility cases, particularly in unexplained or idiopathic male infertility. Appropriate modification of detrimental lifestyle practices is further suggested and recommended in the management of male infertility.
... These finding correlated with studies done internationally. [33][34][35] The textile industry workers showed slightly similar results to oven workers, who were exposed to chemicals, had increased frequency of abnormal sperm morphology predominantly coiled tail, midpiece and tapering head defects, decreased total count and motility. Out of 120 samples 19 were (Azoospermia). ...
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Aim: To determine whether there is a relation between abnormal semen parameters and occupational exposure to excess heat, chemical solvents and pesticides. Study design: Cross sectional study. Place and duration of study: Life Medicare and Areeba Clinic of Fertility Centres, District Faisalabad, Punjab from 1 st January 2019 to 30 th June 2019. Methodology: Three hundred and sixty semen samples were collected from married men between 25 to 55 years of age, with different occupations. Semen analysis was done using computer assisted semen analysis (CASA) technique. Results: There was a strong association between industrial hazards and their effects on male reproductive health. Exposure to high heat in bakers and oven workers (Tandoor) showed remarkable decrease in sperm count, motility and morphology. Workers who were exposed to textile chemicals had disturbed sperm morphology and moderately decreased sperm count along with motility. Conclusions: High heat has strong association with spermatogenesis and influences normal sperm motility. Working environment for bakers and oven workers (Tandoor) seems to be very hostile for their reproductive health, while textile chemical industry worker had better working environment and their results were slightly better than oven workers. Farmers and gardeners seem to be on safer side due to their working environment in open fields and garden. Their sperm count, motility and morphology were much better than other two groups.
... [25] Tight underwear, jeans Decrease the temperature of the scrotum that hampers spermatogenesis. [26] Drug history Antidepressants (SSRI) Spermatogenesis, sperm motility and sperm density. [27] Calcium channel blocker (nifedipine) CCB inhibits sperm capacitation and prevents fertilization. ...
Full-text available
According to the latest data, globally 15% of couples have infertility and male infertility contributes to 10% of all cases. Infertility can be caused by certain biological changes in the gonads and the reproductive system like azoospermia, oligospermia, asthenospermia, teratozoospermia and hypospermatogenesis. Genetic causes of azoospermia include chromosomal abnormalities, Y chromosome microdeletions and deletion or other mutations of Y-linked genes. The maximum number of the genes are located in the azoospermia factor region of the long arm (Yq) of the Y chromosome. Y chromosome microdeletion is known as the second major genetic cause of spermatogenetic failure. This article aims to review the latest updates on the involvement of Yq microdeletions in male infertility. The diagnostics, prevalence and phenotypic spectrum related to Yq gene microdeletions are discussed.
... Adipokines (the cytokines produced by adipose tissue) may stimulate the production of reactive oxygen species (ROS) [22]; Further, obesity has also been associated with increased intestinal permeability and metabolic endotoxemia on male reproductive function, which then increase sperm DNA fragmentation and chromatin alterations [23]. Reportedly, increased scrotal adiposity is associated with testicular heat and oxidative stress, which negatively affect semen quality, sperm concentration, motility, and morphology [24,25]. In this study, we observed that the prevalence of patients with MetS among infertile cases was higher than the general prevalence of MetS in Vietnamese [17] and Chinese [26] men. ...
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Background A direct association between metabolic syndrome (MetS) and sperm production/function has been proposed. In this cross-sectional study, we aimed to determine the impact of MetS on sperm survival. Men from infertile couples treated at Hue University Hospital, Vietnam, were enrolled in this study, which spanned the October 2018 to October 2020 period. The general characteristics of the patients, including body mass index (BMI), waist-to-hip ratio (WHR), the levels of different biochemicals, and semen parameters were determined, and sperm survival tests (SSTs) were performed. The modified National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III for the Asian population was used for MetS diagnosis. Results Men with an abnormal waist circumference (≥ 90 cm) showed a higher rate of abnormal SST results (30.1% vs. 16.7%, p = 0.012). The frequency of abnormal SST results in patients with MetS (72.3%) was significantly higher than that in individuals without MetS (53.4%) ( p = 0.02). Furthermore, the percentage of abnormal SST results in patients with MetS and with BMI ≥ 23 was significantly higher than those in individuals without MetS (77.1% vs. 55.2%, p = 0.03). Weak negative correlations were also observed between the patients’ age and the SST results. Conclusion Sperm viability was lower in men with MetS. We also observed that age and BMI were independent factors associated with abnormal SST.
Background: Temperature changes cause testicular dysfunction. It has been observed that testicular hyperthermia leads to oxidative stress and as a result a severe reduction in testicular parameters. Causes a severe reduction in Sperm parameters to become oxidative due to stress. Recently, natural plant materials and magnetic nanoparticles have been considered. In the internal mitochondrial apoptosis pathway, gen bcl2 is a target of miR455. Objectives: The present study aimed to investigate the effects of titanium dioxide nanoparticles and improve their impacts by using the antioxidant curcumin on sperm parameters by investigating changes in expression miR455 in response to temperature-induced stress in scrotal hyperthermia rats. Methods: After preparation, the rats were placed in a hot water bath at 43°C. for 30 minutes for six consecutive days. The rats were then divided into eight groups. We used TiO2 nanoparticles at a concentration of 0.03 mg/kg of body weight and curcumin at a concentration of 0.02 mg/kg of body weight. After killing the animals, such parameters of sperm as viability, concentration, motility, and morphology of spermatozoa were studied. RNA extraction and cDNA synthesis were performed using appropriate kits. A gene primer was designed and RT-PCR was used to assess gene expression. The t-test and ANOVA were used to examine differences between different groups. Data analysis was performed using Prism8 software and SPSS version 26. Results: The results showed that miR455 expression was lower in the treatment groups and was associated with curcumin (P < 0.05). A positive effect of curcumin on improving sperm parameters in rats with scrotum hyperthermia and a negative and toxic effect of TiO2 nanoparticles were shown. However, a significant improvement in sperm parameters was observed when rats were given TiO2 nanoparticles along with curcumin. Conclusions: The changes in the expression miR455, shown in curcumin have controlled the damage to TiO2 nanoparticles. It seems that miRNA455 can be used as a marker to predict sperm health status. So Curcumin can play a protective role in reducing the toxic effects of testicular hyperthermia as well as titanium dioxide nanoparticles.
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Both the animals and humans with generalized lipodystrophy develop signs of infertility syndrome in the absence of semen health. Infertility is defined as not being able to get pregnant (conceive) after one year (or longer) of unprotected sex. The treatment of disease is usually expensive. Their expertise and experience provide the most current knowledge to promote future research. Dietary habits need to be altered, for most of world people. Therefore, the conclusions and recommendations from the part of this chapters will provide a basis for change. We welcome your offers and criticisms for book improvement in next editions. Bisphenol has been used since the 1950s, in food packaging, industrial materials, dental sealants, and personal hygiene products. Everyone is exposed to Bisphenol through the skin, inhalation, and digestive system. Bisphenol disrupts endocrine pathways because it has weak estrogenic, antiandrogenic, and antithyroid activities. Known endocrine disruptor bisphenol A (BPA) has been shown to be a reproductive toxicant in animal models. This book chapter the current epidemiological literature on fertility outcomes associated with Bisphenol exposure. It also provides relevant resources for health care providers who are in a unique position to provide guidance in reducing exposure to this endocrine-disrupting chemical.
Exposure to heat in the male reproductive system can lead to transient periods of partial or complete infertility. The current study aimed to examine the beneficial effects of Fisetin against spermatogenic disorders in mice affected by long-term scrotal hyperthermia. For this purpose, hyperthermia was induced daily by exposure to the temperature of 43 °C for 20 min for 5 weeks. Except for the Healthy group, six other groups were exposed to heat stress: two treated groups including Preventive and Curative which received oral administration of fisetin (10 mg/kg/day) starting immediately before heat exposure and 15 consecutive days after the end of the heat exposure, respectively. And for each treated group, two groups including Positive Control (Pre/Cur+PC group) and vehicle (Pre/Cur+DMSO group) were considered. Our results showed that the testicular volume; the density of spermatogonia, primary spermatocyte, round spermatid, and Sertoli and Leydig cells; and sperm parameters, as well biochemical properties of the testis tissue, were remarkably higher in both Preventive and Curative groups compared to the other hyperthermia-induced groups and were highest in Preventive ones. Unlike the c-kit gene transcript which was significantly increased in the Fisetin treatment groups (specially the Preventive group), the expression of HSP72 and NF-kβ genes, Caspase3 protein, and DFI in sperm cells were significantly more decreased in Preventive and Curative groups compared to other hyperthermia-induced groups and were lowest in Preventive ones. Overall, Fisetin exerts preventive and curative effects against spermatogenic disorders induced by long-term scrotal hyperthermia.
Hyperthermia (HT) is a significant risk factor for male infertility. Most researchers investigated the effect of localized and short‐term HT on male fertility. This study aimed to assess the harmful impacts of prolonged and generalized HT on testicular histology and ultrastructure in rats. The possible protective effects of vitamin E (Vit E), Vit C, and their combination were also investigated. Thirty male adult Wister rats were used (5 groups). 1‐ control, 2‐ HT, 3‐ Vit C, 4‐ Vit E, and 5‐ Vit C + Vit E. Rats in groups 2–5 were subjected to HT (41°C), 1 hr daily for 2 weeks. HT‐induced a significant decrease in body weight gain, food and water intake, and serum testosterone. HT showed a damaging effect on the testicular and coda epididymis tissue. HT significantly (p ≤ .05) produced oxidative stress (decreased serum catalase (145.49 ± 8.98), glutathione peroxidase (20.27 ± 4.46), superoxide dismutase (2.68 ± 0.54), and reduced glutathione (5.18 ± 0.33), and increased malondialdehyde (9.46 ± 1.55). Vit E alone and combined with Vit C, significantly protected the gonads against the deleterious effects of HT. The results recommended that prolonged HT of the whole body is harmful to male fertility. Prophylactic therapy with Vit E could help decrease the HT‐induced male gonadal harm.
The testis is a temperature-sensitive organ that needs to be maintained 2–7°C below core body temperature to ensure the production of normal sperm. Failure to maintain testicular temperature in mammals impairs spermatogenesis and leads to low sperm counts, poor sperm motility and abnormal sperm morphology in the ejaculate. This review discusses the recent knowledge on the response of testicular somatic cells to heat stress and, specifically, regarding the relevant contributions of heat, germ cell depletion and inflammatory reactions on the functions of Sertoli and Leydig cells. It also outlines mechanisms of testicular thermoregulation, as well as the thermogenic factors that impact testicular function.
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Objective: To evaluate the recovery of semen quality in a cohort of infertile men after known hyperthermic exposure to hot tubs, hot baths or whirlpool baths. Materials and methods: A consecutive cohort of infertile men had a history remarkable for wet heat exposure in the forms of hot tubs, Jacuzzi or hot baths. Clinical characteristics and exposure parameters were assessed before exposure was discontinued, and semen parameters analyzed before and after discontinuation of hyperthermic exposure. A significant seminal response to withdrawal of hyperthermia was defined as >or= 200% increase in the total motile sperm count (TMC = volume x concentration x motile fraction) during follow-up after cessation of wet heat exposure. Results: Eleven infertile men (mean age 36.5 years, range 31-44) exposed to hyperthermia were evaluated pre and post-exposure. Five patients (45%) responded favorably to cessation of heat exposure and had a mean increase in total motile sperm counts of 491%. This increase was largely the result of a statistically significant increase in sperm motility from a mean of 12% at baseline to 34% post-intervention (p = 0.02). Among non-responders, a smoking history revealed a mean of 5.6 pack-years, compared to 0.11 pack-years among responders. The prevalence of varicoceles was similar in both cohorts. Conclusions: The toxic effect of hyperthermia on semen quality may be reversible in some infertile men. We observed that the seminal response to exposure elimination varies biologically among individuals and can be profound in magnitude. Among non-responders, other risk factors that could explain a lack of response to elimination of hyperthermia should be considered.
We studied the use of a testicular hypothermia device worn daily for at least 16 weeks in 64 men with subfertile semen and elevated testicular temperature, who had had an infertile marriage for 2 or more years in which the wife was judged fertile. Improvement in 1 or more semen parameters was seen in 42 patients (65.6 per cent). Semen analysis was converted into the motile oval index, a numerical value representing the count, motility and normal morphology. The motile oval index helps to predict pregnancy outcome. Of 21 patients with pre-treatment motile oval indexes greater than 4.8 million per ml. 11 (52.4 per cent) produced pregnancy. Patients with lower starting indexes did not fare as well. Of 20 patients who met the criteria, and who wore the device for less than 2 weeks or not at all and had no other treatment 1 (5.0 per cent) produced pregnancy. Mean hypothermia time to date of missed menses was 4.2 months. Six patients with nonobstructive azoospermia showed no semen change with the testicular hypothermia device.
Short term exposure of the testis to heat causes degeneration of germ cells. However, the mechanisms underlying this process are poorly understood. The major objectives of this study were to determine whether the heat-induced loss of germ cells in the adult rat occurs via apoptosis, to document its stage-specific and cell-specific distribution, and to examine whether intratesticular testosterone (T) plays any role in the stage specificity of heat-induced germ cell death. Testes of adult male Sprague-Dawley rats were exposed to 22 C (control) or 43 C for 15 min. Animals were killed on days 1, 2, 9, and 56 after heat exposure. Germ cell apoptosis was characterized by DNA gel electrophoresis and in situ terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick end labeling assay. The incidence of germ cell apoptosis [apoptotic index (AI)] was quite low in control rats (AI = 0.04–0.1). Mild hyperthermia within 1 or 2 days resulted in a marked activation (AI = 4.7–5.6) of germ cell apoptosis predominantly ...
Objective To test the hypothesis that men with varicocele who have already fathered children are immune to the detrimental effect of varicocele on their fertility and will continue to be fertile. If this were the case, one would expect a very low incidence of varicocele in currently infertile men who were able to father a child in the past (secondary infertility) compared with men who have never been fertile (primary infertility). Design Survey of men with male factor infertility. Setting Tertiary care university medical center. Patients One thousand ninety-nine infertile men of whom 98 (9%) met our criteria for secondary infertility. Men with prior vasectomy and men whose partners were over age 40 were excluded. Main Outcome Measure Difference in the incidence of varicocele in men with secondary infertility versus primary infertility. Results A varicocele was palpable in 35% (352/1,001) of men with primary infertility and 81% (79/98) of men with secondary infertility. This difference in the incidence of varicocele was highly significant. Men with secondary infertility and varicocele were slightly older (37.9 versus 33.5 years), had a lower mean sperm concentration (30.2 versus 46.1×10 6 /mL), more abnormally shaped sperm (72% versus 40%,), and higher mean serum follicle-stimulating hormone levels (17.6 versus 7.9mIU/mL,) compared with men with primary infertility and varicocele. Conclusions The incidence of varicocele is much higher in male factor secondary infertility compared with primary infertility. These findings suggest that varicocele causes a progressive decline in fertility and that prior fertility in men with varicocele does not predict resistance to varicocele induced impairment of spermatogenesis. Men with a varicocele may benefit from early evaluation and prophylactic varicocelectomy to prevent future infertility.
Experimental cryptorchidism in the adult rat induces lipid peroxidation as a sign of oxidative stress. To further elucidate the role of free radicals and antioxidant enzymes in the degeneration of testis in cryptorchidism, we first studied testes of untreated rats before and after the normal testicular descent. In the second experiment, primary unilateral cryptorchidism was induced by surgically attaching one testis of each rat to the abdomen before testicular descent. The level of lipid peroxidation was detected by formation of fluorescent chromolipids and diene conjugates. At the age of testicular descent (18-21 days), the level of fluorescent chromolipids dropped to one third (p < 0.05). Correspondingly, the level of diene conjugates was 69% (p < 0.05) higher at 18 than at 30 days of age. The antioxidant enzyme activities did not change at the time of testicular descent. Primary unilateral cryptorchidism was induced at the age of 13 days. At 25 or 35 days of age, the level of diene conjugates was higher in the cryptorchid testes than in the contralateral scrotal testes (+39%, p < 0.01, and +51%, p < 0.001, respectively). In the abdominal testes, the mRNA of CuZn superoxide dismutase (SOD) was increased by 69% (p < 0.05) at 25 days, whereas by 35 days of age enzymatic CuZn SOD activity was slightly decreased and catalase activity increased. The present results show that the abdominal position of the testis, either before normal testicular descent or in experimental cryptorchidism, is associated with a high level of lipid peroxidation. The data provide evidence that increased production of reactive oxygen species could contribute to degeneration of the cryptorchid testis. The oxidative testis. The oxidative stress in the cryptorchid testis is not explained by inactivation of antioxidant enzymes.
Alterations of intrascrotal temperature markedly affect spermatogenesis and sperm counts. In euspermic subjects, scrotal exposure for 30 minutes to a 150-watt electric light bulb resulted in reversal of the scrotal-rectal temperature ratio by a mean of 2.9 C. Such treatment on 14 consecutive days caused depression of spermatogenesis followed by rebounds to temporarily high sperm counts. Application of an ice bag to the scrotum for a mean of about 30 minutes cooled the testicular environment by a mean of 6.9 C. Such cold treatment on 14 consecutive days, beginning not less than 12 days following cessation of exposure to heat, stimulated spermatogenesis without initial inhibition, nearly trebling the mean pretreatment count. Oligospermic subjects responded to both heating and cooling faster and to a relatively greater degree, but less predictably, than did euspermics. The greatest increase in spermatogenesis followed sequential application of heat and cold, which suggested possible therapeusis in oligospermia.