Content uploaded by Michael I Lindinger
Author content
All content in this area was uploaded by Michael I Lindinger on Nov 10, 2015
Content may be subject to copyright.
A preview of the PDF is not available
Potassium Regulation during Exercise and Recovery
Abstract and Figures
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.
Figures - uploaded by Michael I Lindinger
Author content
All figure content in this area was uploaded by Michael I Lindinger
Content may be subject to copyright.
... 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. ...
Background: The monocarboxylate transporter 1 (MCT1) plays a crucial role in regulating lactate and pyruvate transport across cell membranes, which is essential for energy metabolism during exercise. The MCT1 A1470T (rs1049434) polymorphism has been suggested to influence lactate transport, with the T (major) allele associated with greater transport efficiency. This study aimed to investigate the effect of the MCT1 polymorphism on lactate and potassium (K⁺) concentrations in response to resistance exercise (RE) following caffeine (CAF) ingestion. Methods: Thirty resistance-trained athletes were randomly selected to participate in a randomized, double-blind, placebo-controlled crossover study. Participants consumed either CAF (6 mg/kg of body weight) or a placebo (PL; 6 mg of maltodextrin per kg of body weight) one hour before performing RE. Serum lactate and potassium concentrations were measured before exercise (Pre), immediately after (Post), and 15 min post-exercise (15 min Post). The RE protocol consisted of three sets to failure at 85% of 1RM for each exercise, with 2 min rest intervals between sets. Results: The findings indicate that under caffeine consumption, individuals carrying the A (minor) allele had significantly higher blood lactate levels before (p = 0.037) and immediately after (p = 0.0001) resistance exercise compared to those with the TT genotype. Additionally, caffeine consumption moderated the increase in plasma potassium levels in TT genotype carriers, while A allele carriers exhibited elevated potassium levels 15 min post-exercise, regardless of caffeine or placebo intake (p < 0.05). Conclusions: Our findings suggest that the MCT1 A1470T polymorphism may influence lactate metabolism and clearance under caffeine consumption, potentially impacting exercise performance and recovery.
... Physical activity with repetitive action potentials that occur across myocyte membranes is associated with the release of large amounts of K+ from contracting skeletal muscle. Moreover, blood potassium is also elevated due to the exercise-evoked haemoconcentration, which is caused by the shift of fluid from plasma into the interstitial and intracellular compartments (Lindinger and Sjøgaard 1991). During repeated bouts of exercise and generation of action potentials, the efficiency of muscular sodium-potassium pumps to pump back the same amount of K+ that was lost with repolarizing K+ currents appears to be insufficient. ...
... Sejersted 1990). Such high plasma potassium is closely related to muscle fatigue and exercise cessation, preventing further K+ rise to toxic levels (Lindinger and Sjøgaard 1991). In addition, it seems that right after exercise cessation, the sympathetic drive with high catecholamines may contribute to increased sodium-potassium pump efficiency, possibly by raising the pump's sensitivity to elevated intracellular sodium concentration, which initiates rapid K+ fall (Medbø and Sejersted 1990). ...
Life-threatening electrolyte abnormalities, such as sudden changes in serum potassium, cause or contribute to fatal cardiac consequences, including cardiac arrest. Here we present a case of a 57-year-old man with unrecognized hypokalaemia who experienced exercise-related out-of-hospital cardiac arrest (OHCA). Successful CPR was initiated immediately; however, he remained in a coma for four days. The patient had no other comor-bidities except a history of mild hypertension treated with low doses of angiotensin receptor blocker (ARB) combined with thiazide. On admission: sinus heart rhythm 80 bpm, potassium level 2.8 mmol/l, Glasgow Coma Scale 3, blood pressure normal. Coronary angiography did not show any coronary occlusion. Other additional tests were nonspecific. Upon awakening, he had major confusion with severe memory deficits. A week later, he was able to walk and was discharged from the hospital. Seventeen months later, the patient still struggles with severe cognitive impairment, lack of motivation, muscle weakness, and fatigue. He requires special care, including supervision and help with activities of daily living. Although the exact cause of hypokalaemia remained unrecognized, several probable mechanisms were taken into consideration.
... 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]. ...
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. ...
Background: Water polo is unique among aquatic - and generally other - sports and in general compared to other sports as it includes cyclic elements typical in swimming and acyclic elements occurring mainly in ball games. Moreover, Wwater polo includes high- and low-intensity activities and demands high level of technical and tactical skills. Players need an optimal nutritional and physical condition to achieve a high athletic performance, which is to a great extend also influenced by nutritional habits. We aim to highlight possible shortfalls in players’ nutritional intake in relation to positions played within the team.
Methods: In the present study, we determined the anthropometric and body composition characteristics, dietary habits, and laboratory parameters of elite adult male water polo players (n=19) before the start of the championship and at the end of the regular season, which meant a 4-month intervention period. Analyses of body composition characteristics and nutritional habits were performed using bioimpedance analyzer InBody 770 and3-day nutrition diary. Variance analysis and paired-sample t-test were used to determine the differences between the variables measured before and after the championship. Correlations Association between the anthropometric and body composition characteristics and different serum parameters were analyzed using linear correlation calculation and deep learning multivariable regression method. K-mean cluster analysis was performed using the anthropometric and body composition characteristics of the athletes.
Results: Based on anthropometric and body composition characteristics, players can be divided into two significantly different clusters that shows an association with specific playing positions. Cluster I included goalkeepers and wing players, while cluster II contained defenders, centers centers, and shooters belonged to Cluster II. We observed differences between in the physical composition and nutritional habits of the clusters. Cluster I players were 5 cm shorter on average, while their mean body weight, skeletal muscle mass and body fat mass data were lower by 19 kg, 7kg and 7 kg, respectively. Various body composition characteristics can predict the InBody Score with 92% efficacy using the deep learning method, while laboratory parameters can predict it with 95% efficacy. Body composition characteristics and laboratory parameters can predict the InBody Score with 92% and 95% efficacy using multivariable regression method. These results may be applicable in sport sciences for elite athletes and sports coaches.
Conclusions: Cluster differences between anthropometric and body compositional characteristics can help to develop position-specific training and nutritional recommendations in the future, thereby the results may be applicable in sport sciences for elite athletes and sports coaches.
... 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. ...
Background
Water polo is unique among aquatic—and generally other—sports as it includes cyclic elements typical in swimming and acyclic elements occurring mainly in ball games. Moreover, water polo demands high level of technical and tactical skills. Players need an optimal nutritional and physical condition to achieve high athletic performance, which is to a great extend influenced by nutritional habits. We aim to highlight possible shortfalls in players’ nutritional intake in relation to positions played within the team.
Methods
In the present study, we determined the anthropometric and body composition characteristics, dietary habits and laboratory parameters of elite adult male water polo players (n = 19) before the start of the championship and at the end of the regular season, which meant a 4-month intervention period. Analyses of body composition characteristics and nutritional habits were performed using bioimpedance analyzer InBody 770 and a 3-day nutrition diary, respectively. Paired-sample t-test were used to determine the differences between the variables measured before and after the championship. Correlations between the anthropometric and body composition characteristics and different serum parameters were analyzed using linear correlation calculation. K-mean cluster analysis was performed using the anthropometric and body composition characteristics of the athletes.
Results
Based on anthropometric and body composition characteristics, players can be divided into two significantly different clusters that shows an association with specific playing positions. Cluster I included goalkeepers and wing players, while defenders, centers, and shooters belonged to Cluster II. We observed significant differences in the physical composition and slight but not significant differences in nutritional habits of the clusters. Cluster I players were 5 cm shorter on average, while their mean body weight, skeletal muscle mass and body fat mass data were lower by 19 kg, 7 kg, and 7 kg, respectively. We studied the correlation between initial anthropometric and body composition parameters and the changes in laboratory parameters before and after the regular season. As a result, we detected numerous significant differences between the two clusters, such as the changes in glucose and magnesium levels, which showed a strong correlation with several body composition parameters in cluster II, but did not in cluster I.
Conclusions
Cluster differences between anthropometric and body compositional characteristics, and the changes in laboratory parameters can help to develop position-specific training and nutritional recommendations in the future. Therefore, the results may be applicable in sport sciences for elite athletes and sports coaches.
Skeletal muscle fatigue is defined as the fall of force or power in response to contractile activity. Both the mechanisms of fatigue and the modes used to elicit it vary tremendously. Conceptual and technological advances allow the examination of fatigue from the level of the single molecule to the intact organism. Evaluation of muscle fatigue in a wide range of disease states builds on our understanding of basic function by revealing the sources of dysfunction in response to disease. © 2012 American Physiological Society. Compr Physiol 2:997‐1044, 2012.
Spontaneous pneumomediastinum is an infrequent condition typically secondary to smoking, illicit drug use, or asthma. The condition often follows barotrauma or bronchial hyperactivity, causing alveolar destruction and air trapping within the mediastinum. Rarely, it may present following strenuous exercise, particularly in tall, thin males, resembling the presentation of pneumothorax. In this case, a 23‐year‐old male with no prior medical history presented to the emergency department with chest pain and dyspnea following intense training for a triathlon. Following a normal chest x‐ray, a high‐resolution computed tomography imaging revealed the presence of spontaneous pneumomediastinum. The patient was admitted for observation and managed conservatively with close monitoring for potential complications such as pneumothorax or pneumopericardium. Emergency physicians should maintain a high index of suspicion for spontaneous pneumomediastinum in patients presenting with acute chest pain and dyspnea, especially in the absence of significant comorbidities. This condition can mimic other cardiopulmonary emergencies, necessitating its inclusion in the differential diagnosis to ensure accurate and timely management.
Adding potassium nitrate (KNO3) to the diet improves the physiological properties of mammalian muscles (rebuilds weakened muscle, improves structure and functionality). The aim of this study was to investigate the effect of KNO3 supplementation in a mouse model. BALB/c mice were fed a KNO3 diet for three weeks, followed by a normal diet without nitrates. After the feeding period, the Extensor digitorum longus (EDL) muscle was evaluated ex vivo for contraction force and fatigue. To evaluate the possible pathological changes, the histology of EDL tissues was performed in control and KNO3-fed groups after 21 days. The histological analysis showed an absence of negative effects in EDL muscles. We also analyzed 15 biochemical blood parameters. After 21 days of KNO3 supplementation, the EDL mass was, on average, 13% larger in the experimental group compared to the controls (p < 0.05). The muscle-specific force increased by 38% in comparison with the control group (p < 0.05). The results indicate that KNO3 has effects in an experimental mouse model, showing nitrate-diet-induced muscle strength. This study contributes to a better understanding of the molecular changes in muscles following nutritional intervention and may help develop strategies and products designated to treat muscle-related issues.
It is well established that a decrease in body weight of more than 2% by heat and/or exercise induced sweating causes an impairment in physical work capacity [1, 7, 17]. Studies have indicated that after a given sweat loss due to prolonged exercise the physical work capacity is more reduced than when sweating is stimulated by environmental heat stress. KozLowsxl and SALTIN [14] have demonstrated a marked difference in the distribution of body water when men reduced body weight (4%) by either exercise or thermally induced sweating. During exercise dehydration the major part of the sweating was achieved at the expense of intracellular water losses (−8,4%), whereas a similar degree of weight loss brought aboilt by inactive exposure to a hot, dry environment resulted in a significantly smaller loss of water from the intracellular compartment (−4,7%). Calculations of total body and plasma sodium, potassium and chloride changes suggested that during thermal dehydration there was a larger loss of sodium and chloride and a smaller loss of potassium from the extracellular space than during exercise dehydration. It seems possible that these variations in muscle water and electrolytes may alter the muscular excitability, thereby affecting the functional capacity of muscle.
A new method based on vanadate facilitated binding of 3H-ouabain has been applied for the quantitative determination of the number of 3H-ouabain binding sites (Na-K-pumps) in needle biopsies of human skeletal muscle.
Samples of the vastus lateralis muscle weighing 2-8 mg showed specific and saturable binding of 3H-ouabain with an apparent KD of 1.9 × 10−8 mol/l. In 20 healthy human subjects in the age range 25-80 years, the number of 3H-ouabain binding sites was 278 ± 15 pmol/g wet weight with no relation to age or sex. In samples of the intercostal and rectus abdominis muscles, the number of 3H-ouabain binding sites varied from 225 to 280 pmol/g wet weight. These values are at least 2 times higher than those previously reported for human skeletal muscle. The number of 3 H-ouabain and 3H-digoxin binding sites were identical, and ouabain (103 mol/l) completely displaced specifically bound 3H-digoxin. When biopsies were frozen in liquid N2 immediately after withdrawal, storage at 20 °C for up to II weeks caused no significant change in the number of 3H-ouabain binding sites.
The method allows quantitative determination of the number of 3H-ouabain binding sites in standard biopsies of human skeletal muscle to be performed by simple procedures within a few hours. This can be used for the study of conditions where the number of Na-K-pumps is known to undergo fluctuations.
Since beta-adrenergic stimulation enhances extrarenal potassium uptake, we postulated an opposite effect of the alpha-adrenergic nervous system. Seven healthy subjects were given intravenous potassium chloride (0.5 mmol per kilogram of body weight), in the presence and absence of the alpha-agonist phenylephrine. After potassium chloride alone, the potassium level rose to 0.64 +/- 0.03 mmol (mean +/- S.E.M.); phenylephrine augmented the rise (0.93 +/- 0.09 mmol, P less than 0.025) and prolonged it, without changing urinary potassium excretion. Subsequent administration of potassium and phenylephrine together with the alpha-antagonist phentolamine blocked the rise in the potassium level due to phenylephrine and shortened the duration of elevation, again without affecting urinary potassium excretion. No changes in plasma renin and aldosterone levels or in serum insulin concentrations occurred, to account for these findings. Stimulation of alpha-adrenergic receptors impairs extrarenal disposal of an acute potassium load--the opposite effect of beta-adrenergic stimulation. The alpha-adrenergic effect may act to preserve a normal serum potassium level or may contribute to hyperkalemia under certain circumstances, such as vigorous exercise.
One aim of the present study was to examine the compensatory mechanisms of lactacidosis in subjects habituated to metabolic acidosis (i.e. sprint trained subjects) and in marathon runners with little or no exposure to lactacidosis. The second aim of the investigation was to examine the water and electrolyte shifts during repeated bouts of maximal exercise and during the recovery period. Experiments were performed on four sprint trained and four endurance trained (marathon) subjects.
1.1. Intact rat extensor digitorum longus muscles soaked in l-isoproterenol plus 10−5 M ouabain gained less sarcoplasmic Na+ than did muscle soaked in ouabain alone. Half maximal effect was produced by 10−8 M l-isoproterenol.2.2. d-Isoproterenol and oxidized l-isoproterenol were only 3 and 1%, respectively, as potent as l-isoproterenol. Other catechols tested had no effect.3.3. The effect of l-isoproterenol on sarcoplasmic Na+ content appears to be a β-adrenergic function in that it was blocked by propranolol, but not by phentolamine, and could be mimicked by dibutyryl cyclic AMP or by caffeine.4.4. Reduced gain in sarcoplasmic Na+ was accompanied by reduced loss of sarcoplasmic K+.5.5. l-Isoproterenol increased loss of sarcoplasmic Na+ in the absence of ouabain, in muscles recovering from cold treatment.6.6. Results suggest that the β-adrenergic system stimulates a coupled Na+-K+ pump.7.7. A model is proposed in which stimulation of the Na+-K+ pump in response to β-adrenergic agents involves a number of intermediate steps, identified tentatively.
Nine volunteers have been examined during prolonged physical exercise to exhaustion at a load of about 60 per cent of W 170 . Ordinary circulatory parameters were measured as well as the quantities of glycogen, water and electrolytes in muscle tissue obtained by needle biopsy. In a separate study 6 subjects were examined for respiratory quotient under similar exercising conditions. The muscle glycogen fell considerably from a mean of 6.9 per 100g glycogen and fat‐free solids to a mean of 1.7 g at the end of exercise. The quantity of muscle glycogen used was correlated both to total energy developed during exercise and also to duration of exercise.
The electrolyte and water content in muscle tissue showed only small changes. Some increase was found in muscle sodium and chloride, and also in the chloride space. The potassium content fell significantly by about 4 per cent of the basal value. None of the circulatory parameters measured showed changes of such magnitude as to have a limiting effect on performance. Two subjects were examined also with glucose infusion during the exercise. The reduction of glycogen, as also the performance of these two subjects, was of the same order of magnitude with and without infusion of glucose. The results suggest that the capacity for prolonged work is directly correlated to the glycogen store in the working muscles.