Alterations of irisin concentrations in saliva and serum of obese and normal-weight subjects,before and after 45 min of a Turkish bath or running

The purpose of this study was to ascertain (1) whether human saliva contains irisin and whether its level correlates with serum irisin concentration, (2) whether salivary glands, eccrine glands and sebaceous glands in human skin produce irisin, (3) how the changes in saliva and serum irisin concentrations after the Turkish bath at 47 ± 3 °C compare with the changes caused by moderate exercise in obese and normal weight subjects. Seven obese male subjects and seven normal weight subjects were enrolled for Turkish bath. Seven obese male subjects and seven normal weight subjects were also enrolled for moderate outdoor exercise, and thirteen male normal weight subjects neither exercised nor showered at the Turkish bath. From each participant, 1.5 ml of saliva and 5 ml blood were collected simultaneously before and after the moderate exercise and Turkish bath. Salivary glands and eccrine and sebaceous glands in the skin were screened immunohistochemically for irisin while serum and saliva irisin were measured with an ELISA. Submandibular glands, eccrine glands and sebaceous glands in the human skin showed strong irisin immunoreactivity. Human saliva contained irisin and its level was significantly higher than the serum levels in both obese and normal weight subjects. However, irisin concentrations were more markedly increased in both saliva and serum samples from subjects who had showered at a Turkish bath than in obese subjects who had exercised or in normal weight subjects. Human submandibular glands, eccrine sweat glands and sebaceous glands synthesize irisin.     

Primate models to study eccrine sweating

The histochemistry and histology of the eccrine sweat gland in the rhesus monkey (Macaca mulatta) are described. The histochemical distribution and localization of enzymes and substrates are very similar to those found in the human; innervation is cholinergic. Active eccrine glands on the general body surface average 136 glands/cm². Above the thermal neutral zone (TNZ), sweating is the major avenue for heat loss and the role of panting in dissipating heat is relatively insignificant. The intrahypothalamic administration of prostaglandin E₁ (PGE₁) suppresses sweating and leads to an increase in core temperature. A linear relation is found between local sweat rates on the general body surface and clamped hypothalamic temperature. Studies also provide direct support for the concept that brain temperature and skin temperature interact additively in the control of sweating in higher primates. The functional characteristics of eccrine sweating in the patas monkey (Erythocebus) are qualitatively similar to those in the rhesus monkey. The patas monkey maintains a relatively constant rectal temperature (37.6–38.4°C) when equilibrated to a wide range of ambient temperaures of 15–40°C. Eccrine sweating is the main effector system for heat dissipation above the TNZ. We emphasize here that evaporative heat loss that is due to sweating is related to both mean skin and mean body temperature and at 40°C is 40% higher than that recorded from the rhesus monkey. These results indicate that the patas monkey, because of its high sweating capacity and other similarities with the human eccrine system, is a most appropriate animal model for comparative studies of eccrine sweat gland function in primates in general.     

Transition duration of ingested deuterium oxide to eccrine sweat during exercise in the heat

The time necessary for the initial appearance of ingested water as sweat during exercise in the heat remains unknown. Based on the current literature, we estimated fluid transition through the body, from ingestion to appearance as sweat, to have a minimum time duration of approximately three minutes. The purpose of this study was to test this prediction and identify the time necessary for the initial enrichment of deuterium oxide (D₂O) in sweat following ingestion during exercise in the heat. Eight participants performed moderate intensity (40% of maximal oxygen uptake) treadmill exercise in an environmental chamber (40 °C, 40% rH) to induce active sweating. After fifteen minutes, while continuing to walk, participants consumed D₂O (0.15 ml kg⁻¹) in a final volume of 50 ml water. Scapular sweat samples were collected one minute prior to and ten minutes post-ingestion. Samples were analyzed for sweat D₂O concentration using isotope ratio mass spectrometry and compared to baseline. Mean±SD ∆ sweat D₂O concentration at minutes one and two post-ingestion were not significantly higher than baseline (0 min). Minutes three (9±3 ppm) through ten (23±11 ppm) post-ingestion had ∆ sweat D₂O concentrations significantly (P<0.05) higher than baseline. Such results suggest that ingested water rapidly transports across the mucosal membrane of the alimentary canal into the vasculature space, enters the extravascular fluid, and is actively secreted by the eccrine sweat glands onto the surface of the skin for potential evaporation in as little as three minutes during exercise in the heat.     

Gross Cystic Disease Fluid Protein 15 in Stratum Corneum Is a Potential Marker of Decreased Eccrine Sweating for Atopic Dermatitis

It is well known that eccrine sweating is attenuated in patients with atopic dermatitis (AD). We have reported by using proteome analysis that gross cystic disease fluid protein 15 (GCDFP15), a substance secreted from eccrine sweat glands, is decreased in tape-stripped stratum corneum (SC) samples from AD patients. The aim of this study was to evaluate GCDFP15 production by eccrine glands with SC samples and to assess sweating in AD. SC samples were obtained from 51 healthy control (HC) and 51 AD individuals. Sweat samples were from 18 HC and 12 AD subjects. GCDFP15 was quantified by ELISA. By immunohistochemistry, the expression of GCDFP15 in eccrine glands was examined in normal and AD skin specimens. To identify GCDFP15-producing cells, double immunofluorescence staining for GCDFP15 and S100 protein was performed in frozen sections. To address the mechanism underlying the decreased eccrine sweating in AD patients, we examined the expression of cholinergic receptor M3 (CHRM3), a receptor for acetylcholine-induced sweating, in eccrine sweat glands. The amounts of GCDFP15 in the SC extracts were significantly lower in AD than HC (P < 0.0001). The sweat samples from AD patients also had lower levels of GCDFP15 concentration (P < 0.05). Immunohistochemistry showed positive GCDFP15 staining in the eccrine gland secretory cells and the ductal and acrosyringial lumen in normal skin, but AD lacked clear staining. Immunofluorescence staining revealed that GCDFP15 was co-expressed with S100 protein, suggesting that the clear cell of eccrine glands produces GCDFP15. Finally, we found that the expression of CHRM3 was depressed in AD, suggesting contribution to the low sweating. The SC of AD patients contains a low amount of GCDFP15 due to both low sweating and low GCDFP15 concentration in the sweat. GCDFP15 in SC is a potential marker for dysregulated sweating in AD.     

Effect of stride frequency on thermoregulatory responses during endurance running in distance runners

Changing stride frequency may influence oxygen uptake and heart rate during running as a function of running economy and central command. This study investigated the influence of stride frequency manipulation on thermoregulatory responses during endurance running. Seven healthy endurance runners ran on a treadmill at a velocity of 15 km/h for 60 min in a controlled environmental chamber (ambient temperature 27 °C and relative humidity 50%), and stride frequency was manipulated. Stride frequency was intermittently manipulated by increasing and decreasing frequency by 10% from the pre-determined preferred frequency. These periods of increase or decrease were separated by free frequency running in the order of free stride frequency, stride frequency manipulation (increase or decrease), free stride frequency, and stride frequency manipulation (increase or decrease) for 15 min each. The increased and decreased stride frequencies were 110% and 91% of the free running frequency, respectively (196±6, 162±5, and 178±5 steps/min, respectively, P<0.01). Compared to the control, stride frequency manipulation did not affect rectal temperature, heart rate, or the rate of perceived exhaustion during running. Whole-body sweat loss increased significantly when stride frequency was manipulated (1.48±0.11 and 1.57±0.11 kg for control and manipulated stride frequencies, respectively, P<0.05), but stride frequency had a small effect on sweat loss overall (Cohen's d=0.31). A higher mean skin temperature was also observed under mixed frequency conditions compared to that in the control (P<0.05). While the precise mechanisms underlying these changes remain unknown (e.g. running economy or central command), our results suggest that manipulation of stride frequency does not have a large effect on sweat loss or other physiological variables, but does increase mean skin temperature during endurance running.     

An analysis on the rates and regulation of insensible water loss through the eccrine sweat glands

An analysis is presented on insensible water loss from the human body at rest through exposed skin surfaces into still air. Possible sites of moisture release are identified as the stratum corneum of the skin, free surfaces of dilute sweat liquids perpetually present in the microscopic ducts of a large population of eccrine sweat glands, and moist microvillous processes which line part of the periductal surfaces in the glands, particularly in the helical coils within the stratum spinosum of the epidermis. Water supply to the sites involves transepidermal migration across skin tissue layers, secretion and partial reabsorption of solutes and water within eccrine glands, and transport across periductal lining of eccrine glands from the surrounding connective tissues respectively. Evaporation and gas phase diffusion within eccrine ducts were modelled. Basal loss rates of water (as regulated by the ambient temperature and relative humidity and by aspects of the anatomy of and physiological factors for eccrine glands, the epidermis and the dermis) were calculated at between 1 and 20 g hr-1 at an ambient temperature of 25 degrees C and a relative humidity of 60% as an example. Such rates are significant fractions of experimental values for insensible water loss rates reported at between 4 and 35 g hr-1 in air at 22-30 degrees C and a relative humidity of 30-60%.     

Cholinergic- rather than adrenergic-induced sweating play a role in developing and developed rat eccrine sweat glands

Both cholinergic and adrenergic stimulation can induce sweat secretion in human eccrine sweat glands, but whether cholinergic and adrenergic stimulation play same roles in rat eccrine sweat glands is still controversial. To explore the innervations, and adrenergic- and cholinergic-induced secretory response in developing and developed rat eccrine sweat glands, rat hind footpads from embryonic day (E) 15.5–20.5, postanal day (P) 1–14, P21 and adult were fixed, embedded, sectioned and subjected to immunofluorescence staining for general fiber marker protein gene product 9.5 (PGP 9.5), adrenergic fiber marker tyrosine hydroxylase (TH) and cholinergic fiber marker vasoactive intestinal peptide (VIP), and cholinergic- and adrenergic-induced sweat secretion was detected at P1–P21 and adult rats by starch-iodine test. The results showed that eccrine sweat gland placodes of SD rats were first appeared at E19.5, and the expression of PGP 9.5 was detected surrounding the sweat gland placodes at E19.5, TH at P7, and VIP at P11. Pilocarpine-induced sweat secretion was first detected at P16 in hind footpads by starch-iodine test. There was no measurable sweating when stimulated by alpha- or beta-adrenergic agonists at all the examined time points. We conclude that rat eccrine sweat glands, just as human eccrine sweat glands, co-express adrenergic and cholinergic fibers, but different from human eccrine sweat glands, cholinergic- rather than adrenergic-induced sweating plays a role in the developing and developed rat eccrine sweat glands.     

The skin of primates. XXX. The skin of the woolly monkey. (Lagothrix lagotricha)

The anatomical and histochemical features of the skin of the woolly monkey are intermediate between those of the Cercopithecoidea and the Pithecoidea. The animal has a prehensile tail, the glabrous, friction surface of which is similar to that of the fingers. The epidermis is heavily pigmented. The dermal vascularization is relatively well-developed and similar to that of the skin of the Cercopithecoidea. Hair follicles grow in groups of 4 to 15, as in the skin of the Pithecoidea. In the hairy skin, eccrine sweat glands occur only in the tail and genitalia. The woolly monkey, like the green monkey, possesses only acetylcholinesterase-containing nerve fibers around its eccrine sweat glands.     

Immunohistochemical localization of activated EGF receptor in human eccrine and apocrine sweat glands.

Epidermal growth factor (EGF) is secreted into sweat from secretory cells of human sweat glands. The function of EGF in sweat is poorly understood. The biological function of EGF is exerted by the binding of EGF to the receptor (EGFR) and its activation. Therefore, we immunohistochemically localized the activated form of EGFR in human eccrine and apocrine sweat glands to assess the functional importance of the EGF-EGFR system in human sweat glands. Frozen sections of human skin were stained with a monoclonal antibody (MAb) specific for tyrosine-phosphorylated (activated) EGFR and with an MAb that stains both activated and non-activated EGFR. In the secretory portion of eccrine sweat glands, nuclei of the secretory cells were stained with the anti-activated EGFR MAb. In coiled and straight portions of eccrine sweat ducts, nuclei of luminal and peripheral cells were stained with the antibody specific for activated EGFR. Luminal cell membranes and luminal cytoplasm of inner ductal cells possessed non-activated EGFR. In the secretory portion of apocrine sweat glands, activated EGFRs were present in cytoplasm and nuclei of secretory cells. These data suggest that EGF, already known to be present in the cytoplasm of secretory cells in eccrine and apocrine sweat glands, activates EGFR in the nuclei of secretory cells themselves in an intracrine manner. Because ductal cells do not express EGF, EGF in the sweat secreted from the secretory cells should activate EGFR in the ductal cells in a paracrine manner. (J Histochem Cytochem 49:597-601, 2001)     

Neural control and mechanisms of eccrine sweating during heat stress and exercise.

In humans, evaporative heat loss from eccrine sweat glands is critical for thermoregulation during exercise and/or exposure to hot environmental conditions, particularly when environmental temperature is greater than skin temperature. Since the time of the ancient Greeks, the significance of sweating has been recognized, whereas our understanding of the mechanisms and controllers of sweating has largely developed during the past century. This review initially focuses on the basic mechanisms of eccrine sweat secretion during heat stress and/or exercise along with a review of the primary controllers of thermoregulatory sweating (i.e., internal and skin temperatures). This is followed by a review of key nonthermal factors associated with prolonged heat stress and exercise that have been proposed to modulate the sweating response. Finally, mechanisms pertaining to the effects of heat acclimation and microgravity exposure are presented.     

Effect of age on heat-activated sweat gland density and flow during exercise in dry heat

Physiological responses of eight postmenopausal older women (age 52-62 yr) and eight younger women (age 20-30 yr) were compared during moderate intensity exercise in a hot dry environment (48 degrees C dry bulb, 25 degrees C wet bulb). The age groups were matched on the basis of maximal O2 consumption (VO2max), body surface area, and body fatness. After heat acclimation the women walked at 40% VO2max for up to 2 h in the hot dry environment while heart rate (HR), rectal temperature (Tre), mean skin temperature (Tsk), whole-body sweating rate (Msw), and local sweating rates (msw; forearm, chest, and scapula) were measured. Additionally, the density of heat-activated sweat glands (HASG) was determined and average sweat gland flow (SGF) was calculated for the scapular area. Although no differences between age groups were found in HR response (when analyzed as percent of maximal HR) or Tsk, the older women had a significantly higher Tre throughout the heat-exercise session. The greater heat storage of the older women may be explained by their significantly lower Msw and msw. There were no differences between the younger and older women in the density of HASG after 30 min; therefore, the lower msw reflects a diminished output per HASG rather than a decrease in the number of sweat glands recruited. The diminished thermoregulatory ability of the older women, unrelated to differences in VO2max, appears to reflect either 1) a diminished response of the sweat glands to central and/or peripheral stimuli, or 2) an age-related structural alteration in the eccrine glands or surrounding skin cells.     

The metabolism and hormonal responses of human eccrine sweat glands isolated by collagenase digestion.

1. Collagenase digestion of biopsies of human skin yields eccrine sweat glands that can be picked out under binocular light microscopy. The glands are viable as determined by the exclusion of Trypan Blue, the uptake of Methylene Blue, electron microscopy, the rate of lactate dehydrogenase release, ATP content and the rates of glucose oxidation and lactate release. 2. It is proposed that eccrine sweat glands engage in aerobic glycolysis, which accounts for the high content of lactate in sweat (15--60 mM) and the high lactate/pyruvate ratio (100: 1) [Emrich & Zwiebel (1966) Pfluegers Arch. 290, 315--319]. 3. Acetylcholine causes a 4-fold increase in cyclic GMP content, dilatation of the intercellular canaliculi and a reversible, atropine-sensitive, 2-fold increase in the rates of glucose oxidation and lactate release. 4. Isoprenaline causes a 2.5-fold increase in cyclic AMP content. Phenylephrine does not significantly alter cyclic nucleotide metabolism.     

Effects of heat acclimation on sweating during graded exercise until exhaustion

The aim of the present study was to test the hypothesis that the sweating during graded exercise until exhaustion in a temperate environment would be greater after heat acclimation. Six healthy young males performed an exercise–heat stress acclimation protocol during 9 days. Before (PRE) and after (POS) the acclimation protocol they performed a graded exercise until exhaustion and the sweat loss during exercise increased after acclimation (3.94±1.10, PRE, and 4.86±1.70 g m⁻² min⁻¹, POS; p<0.05). The results showed that daily prolonged exposures to exercise-heat stress increased sweating during a graded and short duration exercise in a temperate environment.     

The effect of perspiration on the sEMG amplitude and power spectrum

Sweat accumulation underneath surface EMG (sEMG) electrodes is a common problem in workplace studies which compromises electrode adherence to the skin as well as signal fidelity. In this study, the effect of sweat accumulation on signal amplitude and mean frequency (MF) was examined to determine if the sEMG signal becomes altered through the sweat layer and whether this effect can be avoided by interrupting the pool of sweat using a thin strip of medical adhesive between the electrode snaps. Nine males performed a maximum, isometric contraction of their right quadriceps as sEMG was collected. Skin conditions under the electrode were dry and wet in incremental layers of 0.02 mm of artificial sweat. The results demonstrated that sweat accumulation under sEMG electrodes dampens the amplitude of the EMG signal in a predictable way (r = .88 and .97 for double and single snap electrodes, respectively) with almost 2% and 3% deterioration for every 0.02 mm of sweat depending on the type of electrode used. The medical adhesive proved to be highly effective at preventing amplitude deterioration indicating that signal shunting can be prevented. MF was not influenced by sweat accumulation even under the extreme wet condition.     

The skin of primates. XXXVII. The skin of the pig-tail macaque (Macaca nemestrina)

The skin of the pig-tail macaque is basically similar to that of the rhesus monkey and the stump-tail macaque. The epidermis is thin and contains occasional basal melanocytes. The dermis, rich in elastic fibers, is practically free of pigment-containing cells. The upper dermis is highly vascular in the perianal region and sex skin. Cholinesterase-reactive nerve endings are plentiful beneath the friction surfaces of the pes and manus, mucous membranes, and junction of the hairy gluteus and glabrous ischial callosity. Hederiform-like endings are present in the eyelid, pinna, and frontal scalp. Apocrine and eccrine sweat glands occur throughout the hairy skin in a 2–3: 1 ratio. Both types are invested by nerves reactive for acetyl- and butyrylcholinesterase.     

Tropical Malaysians and temperate Koreans exhibit significant differences in sweating sensitivity in response to iontophoretically administered acetylcholine

Natives of the tropics are able to tolerate high ambient temperatures. This results from their long-term residence in hot and often humid tropical climates. This study was designed to compare the peripheral mechanisms of thermal sweating in tropical natives with that of their temperate counterparts. Fifty-five healthy male subjects including 20 native Koreans who live in the temperate Korean climate (Temperate-N) and 35 native tropical Malaysian men that have lived all of their lives in Malaysia (Tropical-N) were enrolled in this study after providing written informed consent to participate. Quantitative sudomotor axon reflex testing after iontophoresis (2 mA for 5 min) with 10% acetylcholine (ACh) was used to determine directly activated (DIR) and axon reflex-mediated (AXR) sweating during ACh iontophoresis. The sweat rate, activated sweat gland density, sweat gland output per single gland activated, and oral and skin temperature changes were measured. The sweat onset time of AXR (nicotinic-receptor-mediated) was 56 s shorter in the Temperate-N than in the Tropical-N subjects (P < 0.0001). The nicotinic-receptor-mediated sweating activity AXR (1), and the muscarinic-receptor-mediated sweating activity DIR, in terms of sweat volume, were 103% and 59% higher in the Temperate-N compared to the Tropical-N subjects (P < 0.0001). The Temperate-N group also had a 17.8% (P < 0.0001) higher active sweat gland density, 35.4% higher sweat output per gland, 0.24°C higher resting oral temperature, and 0.62°C higher resting forearm skin temperature compared to the Tropical-N subjects (P < 0.01). ACh iontophoresis did not influence oral temperature, but increased skin temperature near where the ACh was administered, in both groups. These results suggest that suppressed thermal sweating in the Tropical-N subjects was, at least in part, due to suppressed sweat gland sensitivity to ACh through both recruitment of active sweat glands and the sweat gland output per each gland. This physiological trait guarantees a more economical use of body fluids, thus ensuring more efficient protection against heat stress.     

Evaporative heat loss in Bos taurus: Do different cattle breeds cope with heat stress in the same way?

The aim of this study was to compare two Portuguese (Alentejana and Mertolenga) and two exotic (Frisian and Limousine) cattle breeds in terms of the relationship between the increase in ambient temperature and the responses of the evaporative heat loss pathways and the effects on homeothermy. In the experiment, six heifers of the Alentejana, Frisian, and Mertolenga breeds and four heifers of the Limousine breed were used. The animals were placed in four temperature levels, the first one under thermoneutral conditions and the other ones with increase levels of thermal stress. When submitted to severe heat stress, the Frisian developed high thermal tachypnea (125 mov/min) and moderate sweating rates (117 g m⁻² h⁻¹), which did not prevent an increase in the rectal temperature (from 38.4 °C to 40.0 °C). Moderate increases in rectal temperature were observed in the Alentejana (from 38.8 °C to 39.4 °C) and Limousine (from 38.6 °C to 39.4 °C), especially in the period of highest heat stress. The Limousine showed moderate levels of tachypnea (101 mov/min) while showing the lowest sweating rates. The Alentejana showed significant increases in sweating rate (156 g m⁻² h⁻¹) that played a major role in homeothermy. The Mertolenga showed a superior stability of body temperature, even in the period of highest heat stress (from 38.5 °C to 39.1 °C). Uncommonly, the maintenance of homeothermy during moderate heat stress was achieved primarily by intense tachypnea (122 mov/min). The sweating rate remained abnormally low under conditions of moderate heat stress, rising significantly (110 g m⁻² h⁻¹) without evidence of stabilization, only when tendency for heat storage occurred. This unusual response of the evaporative heat loss pathways infers a different thermoregulatory strategy, suggesting a different adaptation to semi-arid environment and strong association with water metabolism.     

Three-dimensional reconstructed eccrine sweat glands with vascularization and cholinergic and adrenergic innervation

Functional integrity of the regenerated tissues requires not only structural integrity but also vascularization and innervation. We previously demonstrated that the three-dimensional (3D) reconstructed eccrine sweat glands had similar structures as those of the native ones did, but whether the 3D reconstructed glands possessing vascularization and innervation was still unknown. In the study, Matrigel-embedded eccrine sweat gland cells were implanted under the inguinal skin. Ten weeks post-implantation, the vascularization, and innervation in the 10-week reconstructed eccrine sweat glands and native human eccrine sweat glands were detected by immunofluorescence staining. The results showed that the fluorescent signals of general neuronal marker protein gene product 9.5, adrenergic nerve fiber marker tyrosine hydroxylase, and cholinergic nerve fiber markers acetylcholinesterase and vasoactive intestinal peptide embraced the 3D reconstructed glands in circular patterns, as the signals appeared in native eccrine sweat glands. There were many CD31- and von Willebrand factor-positive vessels growing into the plugs. We demonstrated that the 3D reconstructed eccrine sweat glands were nourished by blood vessels, and we for the first time demonstrated that the engineering sweat glands were innervated by both cholinergic and adrenergic fibers. In conclusion, the 3D reconstructed eccrine sweat glands may have functions as the native ones do.     

Rhinarium temperature dynamics in domestic dogs

Many mammals have specialized nose-tips with glabrous and often wet skin, called rhinaria. The function of the rhinarium is unknown in most species. Rhinaria differ not only in shape and skin structure, but also in skin temperature. They are considerably colder in carnivorans than in herbivorous artio- and perissodactyls. Domestic dogs are carnivorans and their noses often feel cold, such that they can be used as an abundant and easily accessible model species. We performed a study on rhinarium temperature in dogs under various ambient temperatures as well as in different behavioral and physiological contexts, breeds, and age groups. The rhinaria of adult, alert, and comfortable dogs are colder than ambient temperature from 30 °C (approximately 5 °C colder) down to a break point at about 15 °C. At an ambient temperature of 0 °C, rhinarium temperature is approximately 8 °C and the decrease in skin surface temperature with decreasing ambient temperature has not yet leveled off. The dog rhinarium warms up under a number of circumstances. In contrast to the continuously warm rhinaria of herbivores, our results suggest strongly that the cold state is the operating state of the dog rhinarium.     

Preslaughter spray-washing effects on physiological stress responses and skin and carcass microbial counts in goats

Preslaughter management procedures that decrease fecal contamination of skins/hides are likely to reduce biological hazards on carcass surfaces during slaughter and processing. This trial was conducted to determine the effects of preslaughter spray-washing on stress responses and skin and carcass bacterial counts in goats. Twenty meat goats were slaughtered in two groups (replicate) on 2 different days (10 goats/replicate). Animals were randomly allotted to treatment (1 min spray-wash) or control (no wash) groups (n = 5/(treatment replicate)). Blood and skin swab samples were collected from control and treated animals before and after the washing treatment. Bacterial counts on the carcasses immediately after dressing were also recorded. Treatment, sampling time or treatment × sampling time did not affect the plasma cortisol, glucose and non-esterified fatty acid (NEFA) concentrations. Skin aerobic plate counts were the same in both treated and control groups prior to washing treatment, but were significantly less in the treated group when sampled after washing (treatment × sampling time, P < 0.05). Aerobic plate counts were 3.6 and 4.4 log₁₀ CFU/cm² in the treated and control groups, respectively. However, skin Escherichia coli counts did not significantly decrease due to spray-washing treatment. Spray-washing treatment also did not influence carcass E. coli or aerobic plate counts. Results indicate that skin bacterial counts can be significantly reduced by preslaughter spray-washing, without increasing stress in goats. Preslaughter spray-washing may be a cost-effective skin decontamination method that can be easily adopted in goat slaughter plants.