Perspiration is what type of secretion

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This content does not have an English version. This content does not have an Arabic version. See more conditions. Sweat glands. Previous papers have comprehensively reviewed the effect of methodology on intra- and inter-individual variability in sweating rate and sweat composition as well as made suggestions for best practices [ 16 , 83 , ].

Therefore, this topic will not be reviewed extensively here. Instead, these methodological considerations and supporting references have been summarized in Table 2. Specific examples illustrating the importance of valid methodology in interpreting study results are discussed throughout the remaining sections of this paper. However, it is worth noting a couple of overarching themes.

First, it is important to realize that depending upon the methodology used, sweat collected from the surface of the skin may contain, not only thermal sweat secreted by the eccrine sweat gland but also, residual contents of the sweat duct, sebum secretions, epidermal cells, and other skin surface contaminants. This can lead to artificial elevations in sweat constituent concentrations and, in some cases, the overestimation is not small.

For example, as shown in Table 2 , two- to five-fold increases in constituent concentrations have been reported for trace minerals such as Fe and Ca.

Unless care is taken to avoid contaminants it is difficult to draw conclusions about sweat composition and its utility as a biomarker, its impact on micronutrient balance, and assess the effectiveness of the sweat gland in excretion of waste products or toxicants.

By contrast, dermal contamination from extra-sweat NaCl seems to be negligible compared with NaCl contained in the sweat itself, as studies have reported only 0. Another important methodological consideration is to ensure that the conditions of the protocol, including the method of sweat stimulation and anatomical location of sweat collection, are specific to the research question of interest.

As described in Table 2 sudomotor responses vary among pharmacological-, passive heat-, and exercise-induced sweating and so these methods should not be used interchangeably. Similarly, because of regional variability in sweating rate and sweat constituent concentrations, data from one region cannot be generalized to other regions or the whole body. Sweat is a very complex aqueous mixture of chemicals.

Although sweat is mostly water and NaCl, it also contains a multitude of other solutes in varying concentrations [ 6 , — ]. Tables 3 and 4 list some of the micronutrients and non-micronutrients, respectively, present in sweat. This is obviously not an exhaustive list but includes some of the more commonly researched constituents.

Tables 3 and 4 include the range in sweat constituent concentrations, mechanisms of secretion and reabsorption, and functional role in health, where known or applicable.

Micronutrients include the electrolytes Na and Cl, which are the constituents found in the highest concentrations in sweat, as well as K, vitamins, and trace minerals. Non-micronutrient ingredients listed in Table 4 include products of metabolism, proteins, amino acids, and toxicants.

It is important to note that concentrations listed in these tables are approximate ranges and are not intended to reflect normal reference ranges. There are insufficient data, perhaps with the exception of Na, Cl, and K, to inform normative ranges for sweat constituents at this time. Instead the ranges listed are meant to provide some context in terms of relative order of magnitude of concentrations across all of the constituents, in order of higher e.

NaCl to lower e. For some constituents, higher values outside the range listed have been reported, but are relatively rare, involve individuals with medical conditions, or may be inflated because of methodological issues; all of these points are discussed in more detail in later sections of this paper. Because interstitial fluid is the precursor fluid for primary sweat, it follows that many components of final sweat originate from this fluid space.

However, the exact mechanisms of secretion are largely unknown for most constituents other than Na and Cl. Potential mechanisms and supporting references are listed in Tables 3 and 4 and may include active or passive diffusion across membranes or paracellular transport mechanisms of transport. Some sweat constituents do not originate from the interstitial fluid, but instead, appear in sweat as a result of sweat gland metabolism e.

Yet others e. It should be noted that many other chemicals not in Tables 3 and 4 , such as cortisol [ , ] neuropeptides, bradykinin, cyclic AMP, angiotensins, and histamines [ 9 , 15 ] are also present in sweat. For a more comprehensive list of sweat constituents, the reader is referred to other published reviews [ 6 , ] and studies [ , ], including metabolomic analysis of sweat [ — ].

It is well established that sweat [Na] and [Cl] can vary considerably among individuals. Table 1 shows the host and environmental factors that account for some of the variability in sweat [Na] and [Cl]. The [Na] and [Cl] of final sweat are determined predominately by the rate of Na reabsorption in the duct relative to the rate of Na secretion in the clear cells. The vertical line represents the mean value.

Reprinted from Baker et al. Circulating aldosterone also changes acutely in response to non-genomic factors such as exercise and dehydration. Yoshida et al. Therefore the genomic action of aldosterone may have a stronger impact on inter-individual variations in sweat [Na] than the rapid non-genomic action of aldosterone during exercise in humans [ ].

Sweat flow rate is another important factor determining final sweat [Na] and [Cl] and of other aspects of sweat composition. This concept has been known since as early as [ ] and several studies since then have confirmed a direct relation between sweating rate and final sweat [Na] and [Cl] [ 5 , 6 , 11 , 15 , 40 , , ]. In , Buono et al. An important point is that the absolute rate of Na reabsorption actually increased continuously with increases in sweating rate.

However, the percentage of secreted Na that was reabsorbed in the duct decreased with a rise in sweating rate. Therefore, the faster the primary sweat travels along the duct the smaller the percentage of Na that can be reabsorbed [ 39 ]. Underlying mechanisms are unclear, but Buono et al. Relation between regional sweating rate and regional sweat [Na]. The mean r for the group was 0. Reprinted from Buono et al. Given the well-established relation between sweat flow rate and sweat electrolyte concentrations, it follows that any factors stimulating acute increases in sweating rate e.

This has been found at the whole-body level [ ] Figure 7 as well as within isolated sweat glands [ 6 ] and given skin regions [ 39 ]. The effect of sweat flow rate on relative Na reabsorption may also partially explain regional differences in sweat [Na] and [Cl] within subjects.

Solid circles show individual data. Redrawn from Baker et al. Regional sweating rate vs. To date, the relation between sweat flow rate and sweat [Na] has been well-established in studies in which subjects served as their own control e. Figure 6 — 8.

However, the regional sweating rate vs. When plotting regional sweating rate vs. On the other hand, acute changes in sweating rate play a significant role in intra-individual differences in sweat [Na] and [Cl] [ 39 , ]. Regression of regional sweating rate vs. In addition to Na and Cl conservation, another important function of the sweat gland is reabsorption of bicarbonate for the maintenance of acid-base balance of the blood [ 8 ].

In the process, sweat fluid in the ductal lumen is acidified before excretion onto the skin surface [ 36 ]. Bicarbonate reabsorption in the duct is inversely related to sweating rate [ 5 , 8 , 37 , ].

As discussed previously, lactate is produced by eccrine sweat gland metabolism [ 13 , 15 , 45 , , ]. However, because of the diluting effect of higher sweat fluid volume, there is an inverse relation between sweating rate and sweat lactate concentration [ — ]. Accordingly, sweat lactate concentration decreases with increasing exercise intensity [ , ].

More details regarding the effect of sweat flow rate on sweat composition are provided in Tables 3 and 4. There has been considerable interest recently in the use of sweat as a non-invasive alternative to blood analysis to provide insights to human physiology, health, and performance.

The development of wearable devices and sensing techniques for sweat diagnostics is an expanding field. Perhaps the best example of a sweat biomarker is the use of sweat [Cl] for the diagnosis of cystic fibrosis, although this practice is not new [ ]. Individuals with cystic fibrosis have higher than normal sweat [Cl] because of a genetic absence of a functioning CFTR two defective genes, homozygote [ — ]. However, sweat [Cl] in cystic fibrosis patients can be much higher, with values in the 80— range commonly reported [ , , — ].

Because the epithelial Na channels depend upon a functioning CFTR, Na is also poorly reabsorbed in individuals with cystic fibrosis [ ]. For more details, the reader is referred to the following reviews on cystic fibrosis [ , — ]. Apart from the use of sweat [Cl] for the diagnosis of cystic fibrosis, the application of sweat diagnostics has been limited to date [ , ]. There are perhaps a few constituents in sweat whose concentrations may change in accordance with large disturbances in homeostasis.

In addition, iron-deficient anemic patients have lower than normal [Fe] in sweat especially in cell-rich sweat [ ] and sweat [Fe] has been shown to increase with iron therapy [ ]. However, the utility of glucose, micronutrients, and other constituents as sweat biomarkers is questionable, especially as a real-time monitoring tool, because correlations between sweat and blood have not been established.

As shown in Tables 3 and 4 , the literature has reported mixed results regarding the correlation between sweat and blood for glucose, cytokines, urea, ammonia, and bicarbonate and no significant correlation for micronutrients, lactate, heavy metals, or environmental toxicants. However, a fundamental issue with this assertion is that sweat [Na] and [Cl] are known to vary considerably within and among individuals; and a change in hydration status is only one of many factors that could play a role in this variability [ ].

This is further complicated by the fact that dehydration could have differential effects on sweat [Na] and [Cl]. Dehydration-induced hemoconcentration would increase extracellular [Na] and in turn increase Na of the primary sweat, in theory leading to a small increase in final sweat [Na].

On the other hand, dehydration would also be expected to reduce sweating rate Figure 3 , which would, in turn, lead to lower sweat [Na]. These confounding factors likely explain the discrepancy in results across studies measuring sweat composition and changes in hydration status. Dehydration has been associated with increased [ , , ], decreased [ , ], or no change [ — ] in sweat [Na] and [Cl].

Sweat [K] and pH are also poor indicators of hydration status [ ]. In summary, while the notion of a non-invasive tool for real-time hydration, nutrition, and health monitoring is attractive, more research is needed to determine the utility of sweat composition as a biomarker for human physiological status.

To date, few well-designed, adequately powered studies have investigated the correlation between sweat and blood solute concentrations. Moreover, as discussed throughout this paper, final sweat composition is not only influenced by blood solute concentrations, but also the method of sweat stimulation active vs. These challenges need to be considered in future research and applications of sweat diagnostics. It is well-established that the primary physiological function of sweating is heat dissipation for body temperature regulation.

In addition, heat is transferred from the air to the body when ambient temperature is greater than skin temperature. With sweating, heat is transferred from the body to water on the surface of the skin. The latent heat of vaporization of sweat is kcal of heat per 1 kg of evaporated sweat J per gram of sweat [ ].

According to heat-balance theory, the amount of sweat production is determined by the relation between the evaporative requirement for heat balance E req and maximum evaporative capacity of the environment [ , ]. E req is represented by the following equation [ ]:. The primary means by which the body gains heat is from metabolism which is directly proportional to exercise intensity and the environment; therefore, these factors are also the primary determinants of sudomotor activity [ , ].

It is important to note that some sweat can drip from the body and not be evaporated. Therefore during conditions of low sweat efficiency e. For a more comprehensive discussion on the role of sweat evaporation in human thermoregulation, the reader is referred to other reviews [ 83 , , ]. Eccrine sweat is thought to play a role in epidermal barrier homeostasis through its delivery of water, natural moisturizing factors, and antimicrobial peptides to the skin surface.

Natural moisturizing factors include amino acids or their derivatives , lactate, urea, Na, and K; which can act as humectants allowing the outermost layers of the stratum corneum to remain hydrated [ ]. Some of these natural moisturizing factors, such as lactate, urea, Na, and K originate from eccrine sweat [ ], while amino acids on the skin surface may be produced in the stratum corneum [ ]. Nevertheless studies have shown that perspiration increases stratum corneum hydration [ , ] and this may occur via moisture transfer from the eccrine gland coil directly into the skin before commencement of surface sweating [ 13 , ].

Therefore, it has been proposed that preservation of sweating may be an important therapeutic strategy for improving atopic dermatitis or other conditions of dry skin [ , ], albeit direct evidence is still needed.

On a related topic, wetting of the skin with eccrine sweat on the palmar surfaces can improve tactile sense and enhance grip as an aspect of the fight or flight response in humans [ ]. Finally, recent immunohistochemistry studies suggest that sweat glands produce and excrete antimicrobial peptides such as dermcidin [ ], cathelicidin [ ], and lactoferrin [ ], pointing to a potential role of sweating in host defense against skin infection [ ].

The reader is referred to recent reviews for more details on the role of sweat in skin hydration [ , , ] and microbial defense [ ]. The changes in sweat [Na] and [Cl] during heat acclimation have been well established and reviewed in previous papers [ , ] and therefore will not be comprehensively discussed here. In brief, adaptation to the heat leads to improved salt conservation through a decrease in sweat [Na] and [Cl] [ 62 , 63 , , , — ].

Most studies have involved a 7—day heat acclimation protocol, but Buono et al. Somewhat paradoxically, the decrease in sweat [Na] and [Cl] occurs despite increases in sweating rate that accompany heat acclimation.

This can be explained by the disparate effects of acute changes in sweat flow rate discussed above versus the longer-term adaptations in the sweat gland that occur with heat acclimation. Buono et al. The slope of the relation did not change after heat acclimation. Thus, at any given sweating rate on the forearm, heat acclimation resulted in significantly lower forearm sweat [Na] [ ]. However, changes in the slope and y-intercept in response to heat acclimation have not been established for the relation between whole-body sweating rate and whole-body sweat [Na] or [Cl].

Most heat acclimation studies have measured regional sweat electrolyte concentrations. Because of the variable effects of heat acclimation on regional sweating rate, such that regional sweating rate on the limbs forearm tend to increase proportionally more than at central sites chest, back [ , ], future research is needed to confirm the effects of heat acclimation on whole-body sweat [Na] and [Cl] and its relation with whole-body sweating rate. The underlying mechanism for NaCl conservation is thought to be related to increased sensitivity of the sweat gland to circulating aldosterone [ 62 ].

However, it is important to clarify that the presence of a salt deficit is required for NaCl conservation to occur with heat acclimation. In studies where subjects consumed enough NaCl to replace losses incurred during the repeated exercise-heat stress, sweat [Na] and [Cl] did not change or increased slightly [ 45 , , , ].

This topic will be discussed further in the Diet — Sodium Chloride section below. A common question on the topic of heat acclimation is whether or not electrolytes or minerals other than NaCl are conserved. Only a few studies have investigated this and mixed results have been reported.

In , Chinevere et al. However, in a subsequent heat acclimation study from the same laboratory, Ely et al. However, there were no changes in sweat mineral concentrations with heat acclimation at the scapular site that had been thoroughly washed [ ]. That is, progressive flushing of mineral residue lying on the skin surface with daily-repeated profuse sweating may have contributed to the decrease in sweat mineral concentrations over the 10 days of testing [ ].

There have been some suggestions that conservation of sweat trace mineral loss occurs on an acute basis during a single bout of exercise. For example, several studies have shown decreases in sweat mineral Fe, Zn, Mg, Ca concentrations during 1—7 h of exercise [ — ]. Because sweat mineral concentrations decreased despite stable or increasing sweating rates over time, it was hypothesized that mineral conservation may have been taking place.

However, again, this is likely an artifact of skin surface contamination, as studies using methodology to collect clean or cell-free sweat have shown no evidence of trace mineral conservation in response to acute exercise-induced sweating [ , , ]. Moreover, there are no known physiological mechanisms by which Ca, Mg, Fe, Cu, and other trace minerals would be reabsorbed by the eccrine sweat gland duct in order to facilitate conservation of loss via sweating.

It is a common perception that Na ingestion influences sweat [Na] or the rate of sweat Na excretion. However, study results to date have been mixed.

For example, in a systematic review of six endurance exercise studies, McCubbin and Costa found no relation between the change in Na intake and the change in sweat [Na] across studies. For example, in one study Costa et al. On the other hand, Hargreaves et al. Thus, McCubbin and Costa concluded that the impact of dietary Na intake on sweat [Na] during exercise is uncertain and future studies are needed [ ].

As noted by Robinson in the early s, while the renal system responds to a salt deficiency or excess within 1—3 h, the sweat glands typically require 1—4 days [ , ]. The literature summary in Table 5 is in general agreement with this notion. Indeed, most studies have shown that several days to weeks of dietary Na manipulation are associated with changes in sweat [Na] [ 45 , , , , , — ].

Other studies, usually of shorter duration up to 3 days [ , ] or with relatively small changes in daily Na ingestion [ , ] have reported no or minimal effect of dietary Na on sweat [Na] or the rate of Na excretion. The relation between acute i.

However, in one investigation, Hamouti et al. This result is perhaps not surprising based on the time course of sweat gland responsiveness, which is also in agreement with the notion that genomic effects of aldosterone on sweat [Na] are stronger than non-genomic actions as discussed above in the Overview of Sweat Composition section [ ].

Regardless of duration, all studies have been consistent in finding no effect of salt deficiency or excess on sweating rate Table 5. Therefore, any change in the rate of sweat NaCl excretion associated with dietary NaCl is likely due to changes in sweat concentrations. Finally, it is important to discuss the dietary Na vs. Several studies have employed study designs with large, perhaps unrealistic changes in dietary Na intake. The low Na diet in these same studies was 0.

The variation in sweat [Na] as a result of smaller deviations in Na intake, more realistic to a free-living individual, is yet to be fully elucidated. In addition, some studies measured sweat [Na] via regional techniques [ , ], which may not be indicative of changes at the whole-body level. Others have used a parallel study design where sweat [Na] was not matched between groups at baseline [ ]. Thus, it is important that future studies address these and other methodological limitations as also pointed out by McCubbin and Costa [ ].

Several studies have investigated the hypothesis that dietary intake of trace minerals and vitamins influences sweat composition. However, most [ , , — ] but not all [ , , ] studies reported no association between dietary intake of trace minerals Zn, Fe, Ca, Cu and their concentrations or excretion rates in sweat.

Regardless of study duration, the impact of diet on sweat mineral and vitamin loss seems to be minimal, at least in healthy individuals with no known deficiencies. For example, Vellar et al. There was no change in sweat [Fe] or sweating rate during 60 min of passive heat stress as a result of the acute iron load [ ]. Similarly, Lug and Ellis [ ] found no significant changes in sweat vitamin concentrations in healthy heat-acclimatized men after administration of a dietary supplement of mg L-ascorbic acid during the 24 h before sweat collection.

Furthermore, in a day controlled diet study in healthy men, Jacob et al. A few studies have found a significant change in sweat mineral concentrations associated with dietary intake [ , , ] and the commonality of these studies is that they included patient populations with known mineral deficiencies or involved controlled interventions designed to deplete and subsequently replete mineral stores of healthy subjects.

For example, Milne et al. For the first 5 weeks, Zn intake was 8. Corresponding sweat Zn loss was 0. It is also important to interpret these results within the context of the source of mineral concentrations found in sweat. As pointed out by Milne et al. Therefore, in this study [ ] it is difficult to discern how much of the sweat Zn originated from the body surface epidermal cells versus the interstitial fluid secreted by the eccrine sweat gland , as changes in body mineral homeostasis can impact the mineral stores of the skin as well as that of the interstitial fluid [ , , ].

Some studies have compared mineral concentrations of cell-free and cell-rich sweat in Fe and Zn-deficient patient populations versus healthy normal controls [ , ]. Prasad et al. However, in cell-free sweat, only [Zn] was lower in patients, while there were no differences in [Fe] between Fe and Zn-deficient patients and healthy controls.

This study suggests that most of the Fe collected at the skin surface originates from desquamated epithelial cells, while most of the Zn is present in the cell-free portion of sweat.

This may also partly explain why an acute increase in blood [Fe] in the study by Vellar et al. There are no known reabsorption or secretion mechanisms by which the eccrine sweat gland could actively conserve or preferentially excrete minerals. Therefore, sweat mineral concentrations may be altered in situations of depletion in intervention studies or chronic deficiencies in patient populations. Note that this is not necessarily evidence of a homeostatic mechanism; rather a result of passive transport of minerals in accordance with concentration gradients during secretion of primary sweat in the secretory coil cell-free sweat and an artifact of surface contamination cell-rich sweat.

Furthermore, the impact of diet on cell-rich and cell-free sweat mineral concentrations will differ depending upon the mineral of interest. As discussed above, Fe and Ca are found in much higher concentrations, and Zn in lower concentrations in cell-rich versus cell-free sweat [ , , , , ]; further complicating the interpretation of study results. Future studies on diet, mineral balance, and sweat mineral losses should carefully choose the methodology employed and consider the source of the minerals measured in the sweat.

Regardless, based on the available evidence to date, the take-home message for healthy individuals is that small fluctuations in dietary mineral intake that do not significantly alter mineral status or whole-body stores seem to have minimal impact on sweat mineral loss.

Of all the substances lost in sweat, Na and Cl are lost in the highest concentrations. Therefore, it has been suggested that Na and Cl are the principal electrolytes whose loss may affect homeostasis [ 7 , , ]. Hyponatremia has been reported in healthy athletes [ ], laborers [ , , ], and soldiers [ , ], as well as clinical populations e.

Based on mathematical models using the prediction equation developed by Ngyuen and Kurtz [ ], plasma [Na] is most sensitive to changes in total body water and thus the primary cause of hyponatremia is an increase in body mass due to overdrinking of water or other hypotonic fluid relative to body water losses [ ].

However, the model also predicts that plasma [Na] is moderately sensitive to changes in the mass balance of Na and K [ ], such as through loss of electrolytes in sweat.

Excessive sweat Na losses can exacerbate decreases in plasma [Na] caused primarily by overdrinking for a long period of time [ ] e. Hyponatremia has also been documented concomitant with dehydration, suggesting that in these cases excessive sweat Na loss was the primary etiology underlying a fall in plasma [Na] [ , , — ].

Regardless of the underlying cause of the high sweat [Na] and [Cl], case reports and theoretical models alike demonstrate that excessive electrolyte losses through sweating can contribute to the development of Na and Cl imbalances.

There have been some suggestions that athletes may require dietary supplementation of certain trace minerals due in part to excessive losses in sweat. The two trace minerals that have received the most attention in terms of sweat-induced deficiencies are Ca and Fe. For example, the most recent consensus statement from the International Olympic Committee mentions that excess losses in sweat, in combination with other factors, may lead to suboptimal Fe status in athletes and therefore may require dietary supplementation [ ].

Other papers have suggested that sweat or dermal Ca losses in athletes may contribute to reduced bone mineral density through stimulation of parathyroid hormone during training [ , , ]. However, the balance of the evidence suggests that sweat losses probably contribute minimally to whole-body trace mineral and vitamin deficiencies [ , , , , — ]. First, it is important to reiterate that many of the studies reporting substantial trace mineral and vitamin losses in sweat have used methods e.

For example, 65 years ago Robinson and Robinson [ ] recognized that a primary source of Ca and Fe found in sweat is associated with desquamated cell debris, which is characteristic of the arm bag technique. Regional measures of sweat trace minerals are also higher and more variable e.

Studies have shown that during an acute bout of 1—2 h exercise serum ionized [Ca] decreases, resulting in subsequent elevation of parathyroid hormone and activation of bone reabsorption.

While the underlying mechanisms are yet to be elucidated, one hypothesis is that the exercise-induced increase in PTH is triggered by sweat Ca loss.

However, only one study has reported an association between sweat Ca loss and any measure of Ca homeostasis or bone mineral density.

Several other studies have reported no association between sweat Ca loss and measures of Ca homeostasis bone mineral density, parathyroid hormone, C-terminal telopeptide of Type I collagen, or bone-specific alkaline phosphatase in female cyclists [ ], male cyclists [ , ], basketball players [ ], or firefighters [ ].

It is important to note that Ca supplementation or infusion can attenuate increases in PTH and activation of bone resorption during exercise [ , , ]; however, the underlying mechanism is apparently unrelated to replacement of sweat Ca loss. In addition to the lack of evidence discussed above, the timing of changes in Ca homeostasis during exercise does not agree with the sweat Ca loss hypothesis.

As pointed out by Kohrt et al. Furthermore, while in extreme circumstances excess mineral loss cannot be ruled out as a contributing factor to suboptimal trace mineral status [ ], for most athletes the main routes of loss are likely through other avenues such as urine or the gastrointestinal tract [ , , ]. Taken together, micronutrient supplementation does not seem to be necessary on the basis of sweat excretion during physical activity, provided that dietary intakes are normal [ ]. The sweat glands are often compared to the nephrons of the kidneys, whose main function, among others, is to conserve the vital constituents of the body [ ].

Indeed, sweat glands share some similarities with the renal system; as eccrine glands have mechanisms to conserve Na, Cl, and bicarbonate losses in sweat as discussed in detail in the Mechanisms of secretion and reabsorption section above.

For example, in response to aldosterone, sweat glands increase Na reabsorption in the duct leading to a decrease in sweat [Na], albeit with a greater time lag than that of the kidneys. These adjustments are mediated through changes in renal water reabsorption in response to arginine vasopressin AVP concentrations in the plasma [ ]. With hyperosmotic hypovolemia, AVP binds to vasopressin type 2 receptors of the distal tubule and collecting duct of the kidneys, stimulating aquaporin transport of water.

It has been suggested that AVP might facilitate eccrine gland water reabsorption in a similar manner, resulting in attenuated sweating rates and more concentrated sweat as a consequence of water removal from the primary fluid along the duct [ — ].

However, the majority of studies have concluded that neither administration of AVP e. These studies also reported no correlation between plasma AVP concentrations and sweating rate or sweat [Na] [ , , ].

Moreover, one study showed that pharmacological manipulation of vasopressin type 2 receptors with an agonist desmopressin or antagonist tolvaptan prior to exercise had no effect on sweat [Na] [ ]. These results may be explained in part by the relatively sparse ductal membrane expression of aquaporin-5 compared with the secretory coil [ ].

Taken together it appears that AVP does not regulate water loss via the sweat glands as it does in the kidneys; and the sweat duct does not play an important role in water conservation during exercise-heat stress [ , , , ]. Additionally, a recent study suggests that intradermal administration of atrial natriuretic peptide, a cardiac hormone that promotes urinary excretion of sodium and water, has no effect on sweating rate in young adults nor does it affect sweating in response to muscarinic receptor activation [ ].

The notion that sweating is a means to accelerate the elimination of persistent environmental contaminants from the human body has been around for many years [ , ]. Detoxification methods include several hours per day of sauna bathing to stimulate excessive sweating, resulting supposedly in purification of the body and release of toxins from the blood.

Some proponents of this method claim that increasing sweating via exercise or heat stress sauna is an effective clinical tool to protect against or overcome illness and disease [ — ]. Others suggest that physical activity leads to better health outcomes as a result of accelerated toxin elimination via thermal sweating [ , ].

As attractive as this idea sounds, there is little if any evidence to date that supports these claims [ , ]. In a series of studies, Genuis et al. The overall finding of these studies was that many chemicals, including persistent organic pollutants, heavy metals, bisphenol A BPA , and phthalate are excreted in sweat. Such reports [ , , ] have led some to hypothesize that these chemicals are perhaps preferentially excreted in sweat to reduce the body burden.

However there are several important methodological limitations to consider when measuring environmental toxicants in sweat. First, many of these studies used sweat collection methods that are susceptible to surface contamination and sweat evaporation, which would artificially increase the concentration of toxicants measured in sweat samples. For instance, in most of these studies [ — , — ], sweat was collected by the subjects on their own uncontrolled, unsupervised , from any site on their body, by scraping sweat from the skin surface with a stainless steel spatula into a glass jar.

With these methods, it is probable that sweat samples were tainted with sebum secretions. Scraping methods increase the likelihood of skin surface epidermal cells contamination because scraped sweat contains x more lipid than clean sweat [ ]; potentially explaining the high concentrations of some the of lipophilic toxicants in sweat.

Furthermore, the method of sweat stimulation exercise, sauna and timing with respect to how long sweating had commenced before collection were not controlled [ — , — ]. Other studies [ , ] used the arm bag method which is also susceptible to skin surface contamination.

As previously discussed the epidermis contains many contaminants, including heavy metals measured in these studies arsenic and lead [ , ]. When using these methods Genuis et al. Take a look at this sebaceous gland. Can you identify the sebaceous gland and duct, the hair, arrector pili muscle, and the IRS and ERS internal and external root sheaths of the hair? Notice the changes in the ERS and IRS near the duct, the cells of the sebaceous gland disintegrate near the duct, and the duct opens out upwards onto the hair.

These are only found in the axillae, breast, and pubic and perineal regions. They are similar to apocrine sweat glands, but open out onto the upper regions of hair follicles, like sebacous glands. They only secrete after puberty. They produce a cloudy secretion, which starts to smell if bacteria react with it.