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The concentrations of extracellular and intracellular potassium (K+) in skeletal muscle influence muscle cell function and are also important determinants of cardiovascular and respiratory function. Several studies over the years have shown that exercise results in a release of K+ ions from contracting muscles which produces a decrease in intracellular K+ concentrations and an increase in plasma K+ concentrations. Following exercise there is a recovery of intracellular K+ concentrations in previously contracting muscle and plasma K+ concentrations rapidly return to resting values. The cardiovascular and respiratory responses to K+ released by contracting muscle produce some changes which aid exercise performance. Increases in the interstitial K+ concentrations of contracting muscles stimulate CIII and CIV afferents to directly stimulate heart rate and the rate of ventilation. Localised K+ release causes a vasodilatation of the vascular bed within contracting muscle. This, together with the increase in cardiac output (through increased heart rate), results in an increase in blood flow to isometrically contracted muscle upon cessation of contraction and to dynamically contracting muscle. This exercise hyperaemia aids in the delivery of metabolic substrates to, and in the removal of metabolic endproducts from, contracting and recovering muscle tissues. In contrast to the beneficial respiratory and cardiovascular effects of elevations in interstitial and plasma K+ concentrations, the responses of contracting muscle to decreases in intracellular K+ concentrations and increases in intracellular Na+ concentrations and extracellular K+ concentrations contribute to a reduction in the strength of muscular contraction. Muscle K+ loss has thus been cited as a major factor associated with or contributing to muscle fatigue. The sarcolemma, because of changes in intracellular and extracellular K+ concentrations and Na+ concentrations on the membrane potential and cell excitability, contributes to a fatigue ‘safety mechanism’. The purpose of this safety mechanism would be to prevent the muscle cell from the self-destruction which is evident upon overload (metabolic insufficiency) of the tissues. The net loss of K+ and associated net gain of Na+ by contracting muscles may contribute to the pain and degenerative changes seen with prolonged exercise. During exercise, mechanisms are brought into play which serve to regulate cellular and whole body K+ homeostasis. Increased rates of uptake of K+ by contracting muscles and inactive tissues through activation of the Na+-K+ pump serve to restore active muscle intracellular K+ concentrations towards precontraction levels and to prevent plasma K+ concentrations from rising to toxic levels. These effects are at least partially mediated by exercise-induced increases in plasma catecholamines, particularly adrenaline. Upon cessation of exercise intracellular K+ concentrations rapidly recover towards resting values, and this is associated with improvements in muscle contraction. Training may result in an increase in intracellular K+ concentrations of resting muscle and relatively lower plasma K+ concentrations compared to values reported in untrained individuals. Also, a blunting of the exercise-induced hyperkalaemia in trained individuals is associated with a decrease in the net loss of K+ from contracting muscle; these observations have been attributed to an upregulation of Na+-K+ pump activity in both inactive tissues and active muscle.
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... Reduced intracellular potassium during exercise can impact muscle performance and physiological responses. A decrease in intracellular potassium may impair muscle contraction, leading to increased fatigue and reduced strength, which can hinder performance and increase injury risk due to muscle weakness [41]. Low intracellular potassium can also disrupt neuronal function, potentially causing muscle cramps. ...
... Additionally, caffeine may stimulate the beta-adrenergic system, increasing renin secretion and activating the renin-angiotensin-aldosterone system, leading to increased potassium loss [41]. The T allele may affect potassium transport and regulation, such as those encoding the Na + -K + ATPase pump. ...
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... The beneficial impact of this part of MO on athletic performance can be attributed to its high content of (a) calcium, which plays a crucial role in neuromuscular excitability, (b) potassium, essential for muscle contraction control and regulation of water balance between intracellular and extracellular environments, and (c) protein intake, which aids in the maintenance and growth of muscle mass [5][6][7]. The presence of flavonoids in the plant's leaf could also contribute to improved athletic performance. ...
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... Among the wide variety of molecules and ions, potassium (K + ) was selected as an optimal candidate for the first validation the ion biosensing. Sweat potassium ion monitoring represents an interesting biomarker to be correlated with several pathological conditions, such as cardiovascular issues, muscular fatigue, or dehydration [10]. Potentiometric sensors selective for K + were designed relying on a standard layout with 2 electrodes, a reference (RE) and a working electrode (WE). ...
... Maintaining blood sodium concentrations is critical for an athlete's health, with the effects of exercise-associated hyponatraemia being a major source of concern. Potassium ions, on the other hand, are released from contracting muscles during exercise, leading to an increase in plasma potassium concentrations and a decrease in intracellular potassium concentrations [108]. Within the urinary system, aldosterone, a mineralocorticoid hormone, plays an important role in the regulation of electrolytes by acting on the distal renal tubes [109]. ...
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Physiological and biological markers in different body fluids are used to measure the body’s physiological or pathological status. In the field of sports and exercise medicine, the use of these markers has recently become more popular for monitoring an athlete’s training response and assessing the immediate or long-term effects of exercise. Although the effect of exercise on different physiological markers using various body fluids is well substantiated, no article has undertaken a review across multiple body fluids such as blood, saliva, urine and sweat. This narrative review aims to assess various physiological markers in blood, urine and saliva, at rest and after exercise and examines physiological marker levels obtained across similar studies, with a focus on the population and study methodology used. Literature searches were conducted using PRISMA guidelines for keywords such as exercise, physical activity, serum, sweat, urine, and biomarkers, resulting in an analysis of 15 studies for this review paper. When comparing the effects of exercise on physiological markers across different body fluids (blood, urine, and saliva), the changes detected were generally in the same direction. However, the extent of the change varied, potentially as a result of the type and duration of exercise, the sample population and subject numbers, fitness levels, and/or dietary intake. In addition, none of the studies used solely female participants; instead, including males only or both male and female subjects together. The results of some physiological markers are sex-dependent. Therefore, to better understand how the levels of these biomarkers change in relation to exercise and performance, the sex of the participants should also be taken into consideration.
... During the 4-month research period, the strength endurance training was replaced with more tactical training and games, in line with this, after the end of the regular season, we detected an elevated level of triglyceride, uric acid, and potassium, and a decreased level of urea, creatinine kinase, and Vitamin D. A higher triglyceride level might be caused by the relatively higher fat intake (5.44 g/kg/day), while signi cantly higher uric acid level by the higher training volume and exercise intensity [21]. The high potassium concentration in the blood is a response for muscle contraction, therefore also associated with higher training volume [22]. The insu cient protein intake can also be determined with the low urea level, while the decreased level of vitamin D may be associated with the overload of players. ...
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... In this study, although not different between groups, potassium ratios changed significantly within each group but remained within the normal range and appeared to consistent with the physiological response of potassium during acute exercise. Potassium loss is a major factor contributing to muscle fatigue (Lindinger & Sjogaard, 1991); but in the study, the participants in both groups had higher potassium levels before the intervention. This may be related to a potassium shift following strenuous exercise, change in blood flow to skeletal muscles, intracellular acidosis or possible insufficient fluid intake (Warburton et al., 2002). ...
... A higher triglyceride level might be caused by the relatively higher fat intake (5.44 g/kg/day), while significantly higher uric acid level by the higher training volume and exercise intensity [23]. The high potassium concentration in the blood is a response to muscle contraction and therefore also associated with higher training volume [24]. The insufficient protein intake can also be determined with the low urea level, while the decreased level of vitamin D may be associated with the overload of players. ...
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