Ammonia and urea are left over when your body breaks down protein. The sweat leaves your skin through tiny holes called pores. When the sweat hits the air, the air makes it evaporate this means it turns from a liquid to a vapor.
As the sweat evaporates off your skin, you cool down. Sweat is a great cooling system, but if you're sweating a lot on a hot day or after playing hard you could be losing too much water through your skin. Then you need to put liquid back in your body by drinking plenty of water so you won't get dehydrated say: dee-HI-drayt-ed. Sweat isn't just wet — it can be kind of stinky, too.
But the next time you get a whiff of yourself after running around outside and want to blame your sweat glands, hold on! Sweat by itself doesn't smell at all. 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. Furthermore, BPA was detected in the sweat of 16 of the 20 subjects, but only two of the 20 subjects had BPA in their serum. In another study, PCB 52 concentration was higher in sweat than blood and urine [ ]. Given that interstitial fluid is the precursor to primary sweat secretion it is unlikely that the BPA or PCB 52 collected at the skin surface in these studies can be attributed to eccrine sweat if the chemical is absent in the blood.
Instead the chemicals could have originated from sebum secretions or epidermal cell contamination. One study lends support for this line of thinking: Porucznik et al. The primary avenue for heavy metals excretion, based on tracer studies, is fecal output [ ]. Meanwhile, there are no known mechanisms by which the sweat glands would preferentially secrete concentrate BPA, persistent organic pollutants, and trace metals to facilitate transport out of the body.
Thus direct evidence for sweating as an effective detoxification method is lacking. Still, future well-controlled studies designed to collect clean eccrine sweat are needed to clarify or refute any potential role of sweating as a therapeutic tool to eliminate toxins from the body. While therapeutic health benefits mostly subjective measures from detoxification protocols in some patient populations have been documented, it is important to note that sauna is only one component of a holistic intervention [ ].
Most protocols also include several weeks of strict changes in diet, exercise, and sleep and therefore it is not possible to attribute any benefit solely to sauna therapy [ , , — ]. The efficacy of lower rates of sweat loss, more realistic to the context of everyday life, is unknown [ ]. In fact, increased sweating is often considered a hangover symptom and is part of the Alcohol Hangover Severity Scale used as the standard in alcohol hangover research [ ].
Furthermore, it is commonly believed that an effective cure for hangovers after heavy drinking is to stimulate sweating via exercise or sauna bathing to accelerate recovery from alcohol intoxication.
However, the evidence to date does not support these ideas; not to mention there are significant health concerns with sauna bathing during alcohol hangover [ ]. Interestingly though, perceived sweating was not significantly different between the hangover and control groups in this naturalistic study, while all other individual symptoms successfully differentiated between the two conditions [ ].
Furthermore, alcohol intake has been found to have no or minimal impact on sweating rate in laboratory intervention studies [ , — ]. For instance, two separate studies found no differences in regional sweating rate chest or upper arm in response to hot water immersion [ ] or exercise-heat stress [ ] after alcohol ingestion that lead to 0.
However, the elevated sudomotor response was transient, as sweating rate decreased after 30 min and became even with the water trial by 40 min into heating [ ]. In addition, differences in sweating rates were very low up to 0. It does seem that sweat ethanol concentration increases with ethanol ingestion and rises linearly with increases in blood alcohol concentration.
For example, Buono et al. This nearly identical ethanol concentration between blood and sweat supports the idea that sweat ethanol originates from the interstitial fluid and its concentration is not significantly altered during transport through the duct onto the skin surface; which is counter to the suggestion that the sweat glands have homeostatic mechanisms to detoxify the blood via concentrating mechanisms.
Moreover, the main avenue of ethanol elimination from the body is known to be via oxidation by alcohol dehydrogenase and aldehyde dehydrogenase eventually breaking ethanol down to acetyl CoA, all of which occurs in the liver. Taken together the available evidence suggests that sweating likely plays a very small role in alcohol detoxification or hangover cures.
Another important function of the kidneys is excretion of metabolic and dietary waste products. Since some waste products appear in sweat the eccrine glands are also thought of as an excretory organ.
For example, sweat contains urea, the major nitrogen-containing metabolic product of protein catabolism. According to Sato [ 15 ], urea readily crosses the eccrine glandular wall and cell membrane and therefore concentrations of urea in sweat are expected to be about the same as that of the plasma. Some studies report very high urea concentrations in sweat [ — ], up to 50x that of serum [ ], and suggest that this is evidence for a selective transport mechanism across the sweat gland, especially in patients with kidney damage, to clear the blood of high urea concentrations [ ].
However, many of these studies used methods susceptible to sample evaporation collection of sweat drippage [ , ] or surface contamination sweat collected at onset of exercise [ ], which can lead to artificial increases in sweat urea concentrations see Table 2.
Other studies have shown that uric acid and creatinine excretion via sweat is insignificant compared with elimination rates through the kidneys [ , ]. Taken together, there is limited evidence that the sweat glands excretory function makes a substantial contribution to homeostasis [ , ].
As shown in Table 6 , certain medical conditions and medications can impact sweating rate and sweat composition. As discussed in the Thermoregulation section above, evaporation of sweat is crucial for temperature regulation in warm conditions and this is evident in patients suffering from anhidroses.
In particular, heat intolerance is well documented in patients with anhidrotic ectodermal dysplasia, a genetic condition resulting in a paucity of sweat glands over the entire body surface [ 3 , 15 ]. Other conditions associated with reduced sweating include burns and skin grafting [ — ], sunburn [ ], miliaria rubra [ , ], and atopic dermatitis [ , , ], as well as medications that interfere with neural sudomotor mechanisms e.
Hyperhidrosis, where sweating occurs in excess of thermoregulatory demands, can occur with primary etiology [ 3 , 29 ] or secondary to physiologic condition fever, pregnancy, menopause , pathology malignancy, endocrine, metabolic, or psychiatric disorder , or medication cholinesterase inhibitors, SSRIs, opioids [ 3 , — ].
The reader is referred to the supporting references in Table 6 for more details on each of the conditions and medications that alter sweat gland function. This paper discussed sweat gland physiology and the state of the evidence regarding various roles of sweating and sweat composition in human health.
Based on this review of the literature, the following conclusions were drawn:. It is well established that eccrine sweat glands have a tremendous capacity to secrete sweat for the liberation of heat during exercise and exposure to hot environments. They also have the capacity to enhance sweating rate with heat acclimation for improved heat tolerance. Eccrine sweat glands reabsorb NaCl and bicarbonate to minimize disruptions to whole-body electrolyte balance and acid—base balance, respectively.
NaCl reabsorption by the sweat glands improves with whole-body NaCl deficits heat acclimation, dietary restriction , but the response is somewhat delayed 1—3 days compared with that of the kidneys within 1—3 h. Individuals with salty sweat e. Eccrine gland mechanisms for secretion and reabsorption of other sweat solutes are poorly understood; nonetheless, sweating-induced deficiencies appear to be of minimal risk for trace minerals e. Ca and Fe , vitamins, and other constituents. Eccrine sweating may play a role in skin hydration and microbial defense, but additional research is required.
The role of the sweat glands in eliminating waste products and toxicants from the body seems to be minor compared with other avenues of breakdown liver and excretion kidneys and gastrointestinal tract. Evidence for a selective mechanism to excrete metabolic and dietary waste products and toxicants via the sweat glands is lacking. That is, sweat glands do not appear to adapt in any way to increase excretion rates of these substances either via concentrating sweat or increasing overall sweating rate as the kidneys do in contributing to the regulation of blood concentrations.
Unlike the renal system, sweat glands do not appear to conserve water loss or concentrate sweat fluid through AVP-mediated water reabsorption. Studies suggesting a larger role of sweat glands in clearing waste products or toxicants from the body e.
The utility of sweat composition as a biomarker for human physiology is currently limited; more research is needed to determine potential relations between sweat and blood solute concentrations.
Lindsay B. Lindsay has been conducting sports nutrition, hydration, and sweat studies for the GSSI research program since The views expressed in this article are those of the authors and do not necessarily reflect the position or policy of PepsiCo, Inc. National Center for Biotechnology Information , U.
Journal List Temperature Austin v. Temperature Austin. Published online Jul Author information Article notes Copyright and License information Disclaimer.
Baker moc. This article has been cited by other articles in PMC. Types of sweat glands The purpose of this section is to compare and contrast the three main types of sweat glands: eccrine, apocrine, and apoeccrine [ 5 , 6 ], which are illustrated in Figure 1. Open in a separate window. Figure 1. Comparison of the apocrine, eccrine, and apoeccrine glands in the axilla.
Eccrine sweat glands Eccrine glands were the first type of sweat gland discovered; as they were initially described in by Purkinje and Wendt and in by Breschet and Roussel de Vouzzeme, but were not named eccrine glands until almost years later by Schiefferdecker [ 11 ].
Apocrine sweat glands The apocrine gland is a second type of sweat gland, which was first recognized by Krause in and later named by Schiefferdecker in [ 20 , 21 ].
Apoeccrine sweat glands A third type of sweat gland, only recently described by Sato et al. Sebaceous glands Sebaceous glands are not a type of sweat gland but worth mentioning here since their secretions can impact the composition of sweat collected at the skin surface [ 25 ]. Structure and function of eccrine sweat glands Anatomy The anatomical structure of the eccrine sweat gland, illustrated in Figure 2 , consists of a secretory coil and duct made up of a simple tubular epithelium.
Figure 2. Mechanisms of secretion and reabsorption Secretion The basic mechanism by which secretion of primary sweat occurs in the clear cells, according to the Na-K-2Cl cotransport model, is illustrated in Figure 2 c. Ion reabsorption Figure 2 d shows the mechanism of ion reabsorption according to the modified Ussing leak-pump model.
Sweat gland metabolism Transport of Na across cellular membranes is an active process, thus sweat secretion in the clear cells and Na reabsorption in the duct require ATP. Control of eccrine sweating Eccrine sweat glands primarily respond to thermal stimuli; particularly increased body core temperature [ 40 ], but skin temperature and associated increases in skin blood flow also play a role [ 9 , 46 — 49 ].
Figure 3. Modifiers of eccrine sweating Several intra- and interindividual factors can modify the control of sweating [ 60 ], some of which are shown in Figure 3. Table 1. Host and environmental factors that modify sweat gland function. Limited data on sweat composition.
Sudomotor changes due to gland hypertrophy, increased cholinergic and aldosterone sensitivity, and decreased threshold for sweat onset see Figure 3. Aerobic training Chronic Increase in WBSR and RSR because of increased cholinergic sensitivity and decreased threshold for sweat onset [ 66 — 69 ] see Figure 3 ; limited data for sweat composition Sex Chronic Higher WBSR and RSR in men because of greater cholinergic responsiveness see Figure 3 and maximal sweating rate, but only at high evaporative requirements for heat balance [ 83 , 99 — ]; otherwise higher WBSR often observed in men are related to higher body mass and metabolic heat production, rather than sex per se [ — ].
Minimal differences in sweat [Na], [Cl], and [lactate] due to sex per se [ , , , — ]; limited data on other constituents Menstrual cycle Cyclical No effect on WBSR [ , — ], but lower RSR at a given body core temperature increased threshold and decreased slope during luteal phase [ — ]; no effect on sweat [Na], [Cl], or [K] [ ] Circadian Rhythm Cyclical Increased sweating threshold in the afternoon — h vs.
Limited data on sweat composition, but there seems to be no impact of age per se on sweat [Na] [ 67 ]. Table 2. Common methodological issues. Begin sweat collection after onset of sweating, i. When sealed during storage, no change in sweat [Na], [Cl], or [K] when refrigerated, frozen, or at room temperature for 7 days [ ]. Seal e. RSR: regional sweating rate. Table 3. Sweat micronutrients: Mechanisms and methodological considerations.
Primary sweat is nearly isotonic with blood plasma [ 6 , 8 , ]; Mixed results with respect to relation between flow rate and sweat [K] [ 6 , , , ]; thought to be secreted during sweat passage along the duct, but mechanism unknown [ — ] Often overestimated by up to x with arm bag technique due to surface contamination [ , ] Calcium b 0.
Table 4. Inverse relation between sweating rate and sweat lactate concentration dilution effect , but direct relation between sweating rate and lactate excretion rate [ — ]. Natural skin moisturizer [ 15 , ] Excretion of metabolic waste — not enough evidence [ ] Concentration varies with changes in sweating rate.
Readily crosses glandular wall and cell membrane and therefore concentrations expected to be same as or slightly higher than plasma [ 15 ]. However, measured concentrations are often significantly higher in sweat than plasma [ — ]; possibly because synthesis of urea by the gland [ 6 ] or surface contamination issues.
Natural skin moisturizer [ 15 ] Excretion of metabolic waste — not enough evidence [ ] Concentration changes with variation in sweating rate [ 6 ]. Primarily derived from plasma NH 3 by nonionic passive diffusion of NH 3 to acidic ductal sweat and ionic trapping of NH 4 [ 6 , 15 ]. HCO 3 reabsorption is inversely related to sweating rate i. Thus final sweat pH is lower more acidic at lower sweating rate [ 5 , 8 , 37 , ] Dictates pH of sweat [ 5 , 8 ] Concentration varies with changes in sweating rate [ 37 , ] Glucose 0.
Plasma glucose is the primary energy source for eccrine sweat gland secretory activity [ 6 , 41 ]. NA specific to its presence in sweat Possible skin surface contamination from residual glucose in sweat ducts Heavy Metals e. IgG, IgA and Antimicrobial peptides e. Potential for contamination by epidermal protein [ 6 ]. Cytokines e. Concentrations increase with increasing sweating rate [ ]. NA specific to its presence in sweat Skin surface contamination, both of epidermal origin and residual cytokines in the sweat gland lumen [ ] Amino acids e.
Skin maintenance and protection via desquamation of horny layer, hydrolysis of debris in the ductal lumen, allergen inhibition [ ] Skin surface contamination, both of epidermal origin [ ] and residual proteolytic enzymes in the sweat gland lumen [ ] Persistent Organic Pollutants e.
Persistent organic pollutants are lipophilic and thus may appear on skin surface through sebum secretions [ ]. BPA, phthalate, polybrominated diphenyl ethers a NA No [ , , ] Concentrations are often significantly higher in sweat than plasma [ , , ], but no known mechanisms for preferential secretion.
Table 5. Formula diet: Upper arm: 47 vs. Figure 4. Eccrine sweat composition Methodological considerations In science, the accuracy and reliability of study methodology are critical to interpret results and draw conclusions about the impact of an intervention or other factor on the outcome measure of interest. Overview of sweat composition Sweat is a very complex aqueous mixture of chemicals. Sodium chloride It is well established that sweat [Na] and [Cl] can vary considerably among individuals.
Figure 5. Effect of sweat flow rate Sodium chloride Sweat flow rate is another important factor determining final sweat [Na] and [Cl] and of other aspects of sweat composition. Figure 6. Figure 7. Figure 8. Figure 9. Bicarbonate, pH, and lactate 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 ]. Sweat composition as a biomarker 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.
Skin health 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. Role in micronutrient balance Sweat gland adjustments in response to deficiency or excess Heat acclimation Sodium chloride 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.
Trace minerals A common question on the topic of heat acclimation is whether or not electrolytes or minerals other than NaCl are conserved. Diet Sodium chloride It is a common perception that Na ingestion influences sweat [Na] or the rate of sweat Na excretion.
Trace minerals Several studies have investigated the hypothesis that dietary intake of trace minerals and vitamins influences sweat composition. Sweating-induced deficiencies Sodium chloride Of all the substances lost in sweat, Na and Cl are lost in the highest concentrations. Trace minerals and vitamins There have been some suggestions that athletes may require dietary supplementation of certain trace minerals due in part to excessive losses in sweat.
Comparison of sweat gland and kidney function Water conservation and excretion 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 [ ]. Excretion of toxicants 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 [ , ]. Excretion of metabolic waste Another important function of the kidneys is excretion of metabolic and dietary waste products.
Altered sweat gland function from conditions and medications As shown in Table 6 , certain medical conditions and medications can impact sweating rate and sweat composition. Table 6. Conditions and medications that alter sweat gland function. Etiology involves neurogenic overactivity of otherwise normal sweat glands [ 3 , 29 ]; associated with genetic predisposition [ , ].
Tattoos Chronic Reduced sweating rate and higher sweat [Na] in response to pharmacologically-induced local sweating than non-tattooed skin; unknown etiology [ — ].
More research involving exercise or heat-induced whole body sweating is needed. Conclusions This paper discussed sweat gland physiology and the state of the evidence regarding various roles of sweating and sweat composition in human health. Based on this review of the literature, the following conclusions were drawn: It is well established that eccrine sweat glands have a tremendous capacity to secrete sweat for the liberation of heat during exercise and exposure to hot environments.
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Pflugers Arch. Rapid regulation of electrolyte absorption in sweat duct. J Membr Biol. Hydrogen ion and electrolyte excretion of the single human sweat gland. The effect of intracutaneous d-aldosterone and hydrocortisone on human eccrine sweat gland function.
Sodium secretion and reabsorption in the human eccrine sweat gland. J Clin Invest. Glucose metabolism of the isolated eccrine sweat gland. The relation between glucose metabolism and sodium transport. The secretion of salt and water by the eccrine sweat gland. From a physiological perspective, sweating is absolutely a good thing. Our body would overheat if we did not sweat. But some of the activities that cause sweating excessive time in the heat, being nervous or sick is associated with other problems, such as heat exhaustion, anxiety and illness.
In contrast, activities such as exercise and controlled time in a sauna are healthy. This would suggest that it is not the sweating itself, but the activity behind it, which defines whether sweating is healthy or not. Sweating during exercise usually means you are reaching a level of exercise that promotes cardiovascular health. Some evidence suggests sweatier people are getting a more intense workout , and more fit individuals sweat sooner and more profusely , but tremendous variation in the timing and amount of sweat across individuals makes those claims unreliable.
Instead, focus on reaching a level of exercise or sauna time in which sweat actually shows up, rather than measuring the timing or amount.
Just because it is summer and hot outside, do not assume it means you should not work out. On those days, exercise in air-conditioned environments, choose the cooler times of the day, and keep hydrated. Stop exercising if you experience unusual symptoms, such as dizziness and nausea.
As for saunas, research is confirming some of the long-standing beliefs of Finnish people that sweating in saunas is beneficial to health. Heat-induced stress relief and possible positive effects on heart health may be the actual benefits. Similar to exercise, the activity behind the sweating not the sweating itself is what is actually making us healthy. To help people be healthy at every stage of life, Michigan State University Extension delivers affordable, relevant, evidence-based education to serve the needs of adults, youth and families in urban and rural communities.
Our programs cover all areas of health, from buying and preparing nutritious, budget-friendly food to managing stress, preventing or living well with diabetes and optimal aging — MSU Extension has the information you need in a format you can use, in-person and online.
Contact your local MSU Extension county office to find a class near you. This article was published by Michigan State University Extension. Is sweating good for you?
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