## 1 Introduction
Following this, an efflux of K+ via K+ channels on the basolateral membrane and Cl- through Cl- channels on the apical membrane occurs, thus causing cell shrinkage [20]. This cell shrinkage leads to an inflow of Na+, K+, and Cl- through Na-K-2 Cl cotransporters on the basolateral membrane and, subsequently, an efflux of Na+ and K+ through Na-K-ATPase and K+ channels into the extracellular space, along with an efflux of Cl- through Cl- channels into the lumen [20]. The increased Cl- concentration in the lumen creates an electrochemical gradient that promotes the movement of Na+ across the cell junction [20; 21; 22]. In turn, this leads to a net efflux of K+ and Cl- from the cell, creating an osmotic gradient for the movement of water into the lumen via aquaporin-5 channels [20; 23; 24; 25]. Lastly, the water and electrolytes transported into the lumen combine to form primary sweat. This entire process elucidates how electrolytes from the blood are utilized in the formation of sweat. The homeostasis of body fluid regulation and electrolyte excretion via sweat glands during and after exercise in the heat is also impacted by aldosterone and antidiuretic hormone, as well as sympathetic nervous system activity. Aldosterone is a mineralocorticoid hormone whose primary function is water and Na+ regulation via reabsorption in the kidney, specifically the late distal tubules and collecting ducts of nephrons [26]. The  
Figure 1: Impact of sweat electrolyte loss in sports performance across physiological and physical performance metrics. antidiuretic hormone is typically co-released with aldosteroneone, whereby it supports the extracellular fluid reabsorption of water through the mobilization of aquaporin channels to the apical membrane of the collecting tubule [26]. During exercise in the heat, aldosteroneone and antidiuretic hormone secretions are increased, which promotes water and Na+ reabsorption in the kidneys and counteracts the loss of fluids and electrolyte caused by sweating [27]. In contrast, sympathetic nervous system activity modulates fluid regulation during exercise in the heat by activating sweat glands to excrete fluid via sweating [28]. This function is imperative to allow for adequate heat dissipation, but it subsequently results in fluid and electrolyte losses. Therefore, the body is in a constant flux of fluid and electrolyte reabsorption (i.e., aldosteroneone and the antidiuretic hormone) and excretion (i.e., sympathetic nervous system activity). The loss of electrolytes via sweating, along with several other decremental physiological responses from exercising in the heat, has been investigated in the hope of reducing these effects. A popular strategy that has been explored is the implementation of heat training, either via heat acclimation (HA; training in a hot artificial environment) or heat acclimatization (HAz; training in a naturally hot environment). One of the positive adaptations that occurs with heat training is reduced electrolyte concentrations in the sweat, inferring that more electrolytes are kept in the blood, possibly due to improved reabsorption within the proximal duct during sweat secretion. As primary sweat propagates in the lumen towards the skin surface, Na+ and Cl- are reabsorbed via the luminal and basal cells of the duct [20]. This results in the final form of sweat being hypotonic; however, there still remain electrolytes in the sweat that is then lost on the skin's surface. Investigation into the heat training adaptation of reduced electrolytes in the sweat has been carried out using various methodologies. patches) [6; 29; 30; 33; 38; 39; 40; 41]. However, there are no current reviews available, to the authors' knowledge, on electrolyte concentration adaptations from heat training and differences in assessment results dependent on the method employed. Therefore, the objective of this review was to explore the differences between sweat electrolyte measurement techniques from the adaptations incurred following heat training.