## 1 Introduction  
Exercise performance in hot environmental conditions is compromised due to increased physiological strain, compared to when undertaken in temperate or cool conditions [1, 2, 3]. While exercising in the heat, central and peripheral thermosensitivity mechanisms control body temperature regulation [4]. Sensory thermoreceptors transmit signals to the preoptic anterior hypothalamus (POAH) in response to increased core temperature, thereby initiating independent thermoreceptor loops to elicit thermoregulatory sweating in an effort to cool the body through heat dissipation [4, 5]. However, this sudomotor response is accompanied by a loss of electrolytes (i.e., sodium [Na\({}^{+}\)], chloride [Cl\({}^{-}\)], and potassium [K\({}^{+}\)]) in the sweat [6]. Electrolytes are critical substances that aid with maintaining water balance by shifting fluid between intracellular and extracellular compartments, maintaining membrane electrochemical potentials, and transporting nutrients into and waste out of the cell [7]. The loss of electrolytes in sweat and subsequent fluid imbalances often lead to hypophoration, which negatively influences exercise performance, health, and thermoregulatory mechanisms [8, 9, 10] (Figure 1). The physiological actions of electrolytes operate in both the extracellular compartments of the blood and intracellular compartments within the cell. During exercise in the heat, several physiological impairments occur as a result of reduced plasma electrolyte concentrations from the increased electrolyte concentrations lost in sweat [11]. For example, increases in plasma osmolality occur because plasma Na\({}^{+}\) (Na\({}^{+}\)p) and Cl\({}^{-}\) (Cl\({}^{-}\)p) are directly associated with plasma osmolality, as they are the primary regulators of extracellular volume and function to maintain water absorption [11, 12, 13]. In addition, plasma volume is partially regulated by Na+p and Cl-p, as these electrolytes exert osmotic pressure and redistribute fluid between the blood and cells [11]. Consequently, plasma volume reductions may be observed due to the increased electrolyte concentration lost in sweat as opposed to circulating in plasma. Furthermore, it has been suggested that there may be a relationship between electrolytes and the neuromuscular properties associated with exercise performance (i.e., skeletal muscle membrane potential, exercise-induced muscle cramps [EIMC]) [14; 15]. Indeed, muscle tissue is composed of approximately 76% water, with electrolytes being a primary modulator of water flux [16]; however, it is difficult to surmise the impact of this as it remains under contention amongst the scientific community and requires more research [15; 17]. Collectively, electrolyte imbalances due to exercise in the heat can lead to various physiological impairments. Blood flow patterns experience significant alterations during exercise compared to resting conditions [18]. When an individual performs exercise, particularly under thermal stress, blood circulation to the skin can increase by as much as 30-40% in healthy young men as part of the body's efforts at temperature regulation [18]. This increased skin blood flow leads to a higher concentration of plasma electrolytes and blood in the dermis, which is the skin layer composed of collagen, elastic tissue, and extracellular components, including blood vessels, nerve endings, and excrine glands [19]. The secretion of sweat occurs within the dermis in the secretory coils and proximal ducts, more precisely following the Na-K-2 Cl cotransport model within the clear cells of the secretory coil [20]. When the POAH signals for sweating to occur, acetylcholine is released from sympathetic post-ganglionic neurons and binds to muscarinic receptors on the basolateral membrane of the clear cells [20]. This initiates the release of intracellular calcium (Ca2+) stores and an influx of extracellular Ca2+ into the cell's cytoplasm [20].