Arterial Potassium Concentration Research Articles

A single oral glucose load decreases arterial plasma [K+ ] during exercise and recovery.

AimWe investigated whether acute carbohydrate ingestion reduced arterial potassium concentration ([K+]) during and after intense exercise and delayed fatigue.MethodsIn a randomized, double‐blind crossover design, eight males ingested 300 ml water containing 75 g glucose (CHO) or placebo (CON); rested for 60 min, then performed high‐intensity intermittent cycling (HIIC) at 130% V˙O2peak, comprising three 45‐s exercise bouts (EB), then a fourth EB until fatigue. Radial arterial (a) and antecubital venous (v) blood was sampled at rest, before, during and after HIIC and analyzed for plasma ions and metabolites, with forearm arteriovenous differences (a‐v diff) calculated to assess inactive forearm muscle effects.ResultsGlucose ingestion elevated [glucose]a and [insulin]a above CON (p = .001), being, respectively, ~2‐ and ~5‐fold higher during CHO at 60 min after ingestion (p = .001). Plasma [K+]a rose during and declined following each exercise bout in HIIC (p = .001), falling below baseline at 5 min post‐exercise (p = .007). Both [K+]a and [K+]v were lower during CHO (p = .036, p = .001, respectively, treatment main effect). The [K+]a‐v diff across the forearm widened during exercise (p = .001), returned to baseline during recovery, and was greater in CHO than CON during EB1, EB2 (p = .001) and EB3 (p = .005). Time to fatigue did not differ between trials.ConclusionAcute oral glucose ingestion, as used in a glucose tolerance test, induced a small, systemic K+‐lowering effect before, during, and after HIIC, that was detectable in both arterial and venous plasma. This likely reflects insulin‐mediated, increased Na+,K+‐ATPase induced K+ uptake into non‐contracting muscles. However, glucose ingestion did not delay fatigue.

Effect of Aerosolised Salbutamol Administration on Arterial Potassium Concentration in Anaesthetised Horses

Aerosolized salbutamol has been associated with hypokalemia in horses undergoing colic surgery. The objective of this study was to evaluate the effect of aerosolized salbutamol on arterial potassium concentration ([K +]) in healthy anaesthetized horses undergoing elective surgery.Anesthetic records were reviewed from healthy adult horses undergoing elective surgery over a 3-year period with two complete sets of arterial electrolyte (sodium [Na +], potassium [K +], chloride [Cl -], calcium [Ca 2+]) concentration measurements. Records were excluded if intra-operative electrolyte supplementation, antimicrobial administration or noncrystalloid fluid administration were documented or if salbutamol was administered prior to electrolyte measurement. Sixty records which fulfilled inclusion criteria were divided into two groups depending on whether or not aerosolized salbutamol (2μg kg -1) (to treat hypoxemia) was administered after baseline electrolyte measurement and before the second electrolyte measurement. Aerosolized salbutamol was administered (Group S) in 22 horses and not administered (group NS) in 38 horses. There was a significant reduction in [K +] and [Ca 2+] between baseline and the second electrolyte measurement in both groups (P< .001). The reduction in [K +] between baseline and the second electrolyte measurement was significantly greater in group S (12.3%) compared to group NS (6.9%) (P= .017) and was significantly associated with salbutamol administration (P= .04). The results of this study indicate that monitoring [K +] is important in anaesthetized horses, particularly after aerosolized salbutamol administration.

Salbutamol effects on systemic potassium dynamics during and following intense continuous and intermittent exercise.

Salbutamol inhalation is permissible by WADA in athletic competition for asthma management and affects potassium regulation, which is vital for muscle function. Salbutamol effects on arterial potassium concentration ([K+]a) during and after high-intensity continuous exercise (HIcont) and intermittent exercise comprising repeated, brief sprints (HIint), and on performance during HIint are unknown and were investigated. Seven recreationally active men participated in a double-blind, randomised, cross-over design, inhaling 1000µg salbutamol or placebo. Participants cycled continuously for 5min at 40% [Formula: see text]O2peak and 60% [Formula: see text]O2peak, then HIcont (90s at 130% [Formula: see text]O2peak), 20min recovery, and then HIint (3 sets, 5×4s sprints), with 30min recovery. Plasma [K+]a increased throughout exercise and subsequently declined below baseline (P<0.001). Plasma [K+]a was greater during HIcont than HIint (P<0.001, HIcont 5.94±0.65 vs HIint set 1, 4.71±0.40mM); the change in [K+]a from baseline (Δ[K+]a) was 2.6-fold greater during HIcont than HIint (P<0.001). The Δ[K+] throughout the trial was less with salbutamol than placebo (P<0.001, treatment main effect, 0.03±0.67 vs 0.22±0.69mM, respectively); and remained less after correction for fluid shifts (P<0.001). The Δ[K+] during HIcont was less after salbutamol (P<0.05), but not during HIint. Blood lactate, plasma pH, and the work output during HIint did not differ between trials. Inhaled salbutamol modulated the [K+]a rise across the trial, comprising intense continuous and intermittent exercise and recovery, lowering Δ[K+] during HIcont. The limited [K+]a changes during HIint suggest that salbutamol is unlikely to influence systemic [K+] during periods of intense effort in intermittent sports.

Mesangial proliferative glomerulonephritis with aldosterone-producing adenoma

We describe a case of mesangial proliferative glomerulonephritis (MesPGN), the clinical symptoms of which were exacerbated by aldosterone-producing adenoma (APA). A 45-year-old man, who had had a history of hypertension for several years, presented with renal derangement, with serum creatinine at its upper normal limit and with microhematuria and proteinuria. He also presented with hypokalemia, with a plasma aldosterone concentration at its upper normal limit and plasma renin activity at its lower normal limit. After the administration of spironolactone, we resected his left adrenal gland, which had a nodular lesion as well as aldosterone hypersecretion. The treatment normalized his arterial blood pressure and serum potassium concentration. Although his proteinuria disappeared with the reduction in arterial blood pressure, the microhematuria continued. The administration of losartan because of the histological finding of MesPGN reduced the amount of hematuria. A dissociated response of hematuria and proteinuria to antihypertensive treatment indicated that MesPGN was coincidental with APA.

Potassium kinetics and its relationship with ventilation during repeated bouts of exercise in women

The purpose of this study was to determine the electrolyte concentration changes in arterial plasma from high-intensity repeated bouts of cycling exercise in well-trained females and to determine the relationships between arterial plasma lactate, potassium (K+), bicarbonate (HCO3(-)), and pH with minute ventilation. Fourteen female subjects (mean age = 27 +/- 4 years; mean height = 170 +/- 7 cm; mean weight = 62 +/- 7 kg; maximal oxygen uptake = 50 +/- 6 ml/kg/min) were recruited to perform 3 x 5 min bouts of exercise at 236 +/- 27 W with 10 min recovery between each set. Minute ventilation, arterial plasma lactate, potassium, calcium, chloride, and sodium ion concentrations were measured a minute 0, 1, 2, 3, 4, 5 of each set and midway through recovery (21 sampling points total per subject). The results showed that the strongest relationship was between arterial plasma K+ concentration and minute ventilation (r2 = 0.91), and, that arterial plasma lactate mirrored both arterial plasma HCO3(-) and pH. In conclusion, this study demonstrates that women exhibit similar electrolyte responses as reported elsewhere in men, and support the idea that K+ may partly contribute to controlling ventilation during high-intensity exercise and recovery.

Exercise-induced Rise in Arterial Potassium is Enhanced in Patients with Impaired Exercise Tolerance.

We assessed the changes in arterial potassium concentration during exercise and recovery in relation to exercise tolerance in patients with impaired exercise tolerance. Sixteen patients with cardiac disease were subjected to a cardiopulmonary exercise test on a cycle ergometer. Arterial potassium and lactate concentrations were measured every minute during and after exercise, and ventilatory threshold (VT) and lactate threshold (LT) were identified. Before exercise, arterial potassium concentration was 3.8 +/- 0.3 mEq/l. It increased to 4.1 +/- 0.3 mEq/l at LT (p < 0.002 versus at rest), to 4.2 +/- 0.3 mEq/l at VT, and to 4.8 +/- 0.5 mEq/l at peak exercise (p < 0.001 versus at LT, p < 0.001 versus at VT). At an exercise intensity equivalent to 30, 40, 50 or 60% of predicted maximum oxygen uptake, the increase in arterial potassium showed a negative and significant correlation with %LT (r = -0.62 approximately -0.72, p < 0.01 approximately 0.05) and %VT (r = -0.62 approximately -0.75, p < 0.001 approximately 0.05), where %LT and %VT represent the ratios of LT and VT to the predicted maximum oxygen uptake, respectively. There was a good correlation between the rate of fall in potassium concentration during recovery and its increase during exercise. It was concluded that in patients with impaired exercise tolerance, the greater the degree of exercise intolerance, the greater the increase in arterial potassium concentration during exercise, and the steeper the fall in potassium concentration during recovery. Because the rise in potassium concentration during exercise and its fall during recovery were greater when the exercise level exceeded the anaerobic threshold, exercise levels below the anaerobic threshold are recommended for patients with cardiac diseases.

Effect of hypoxia on arterial potassium concentration at rest and during exercise in man

Hypoxia has been reported to increase arterial potassium concentration ([K+]a) in anaesthetized cats (Paterson, Estavillo & Nye, 1988). The purpose of this study was to determine whether this phenomenon occurs in humans. The effect of hypoxia on [K+]a was measured in ten male subjects, at rest and during light exercise, before and after 8 weeks of physical training. The [K+]a increased by 0.15 +/- 0.04 mM (mean +/- S.E.M.) at rest, when end-tidal PO2 (PET,O2) was lowered from 100 to 51 +/- 1.6 Torr, and by 0.10 +/- 0.02 mM during exercise, when PET,O2 was lowered from 100 to 66 +/- 6.2 Torr. Physical training did not alter the rise in [K+]a significantly. The magnitude of this effect is small in comparison with that of exercise-induced hyperkalaemia, and is unlikely to be of great physiological significance at moderate levels of hypoxia.

Effect of physical training on exercise-induced hyperkalemia in chronic heart failure. Relation with ventilation and catecholamines.

The exercise-induced rise in arterial potassium concentration ([K+]a) may contribute to exercise hyperpnea and could play a role in exertional fatigue. This study was designed to determine whether the exercise-induced rise in [K+]a is altered in patients with chronic heart failure (CHF) and whether physical training affects K+ homeostasis. We evaluated 10 subjects with CHF (ejection fraction, 23 +/- 3.9%) and 10 subjects with normal left ventricular function (NLVF) who had undergone previous coronary artery graft surgery (ejection fraction, 63 +/- 8.6%). Subjects performed an incremental cycle ergometer exercise test before and after a physical training or detraining program. Changes in [K+]a and ventilation (VE) during exercise were closely related in both groups. Subjects with CHF did less absolute work and had reduced maximal oxygen consumption (VO2max) compared with subjects with NLVF (P < .01). Exercise-induced rises in [K+]a, VE, norepinephrine, lactate, and heart rate were greater at matched absolute work rates in subjects with CHF than in subjects with NLVF (P < .01). However, when the rise in [K+]a was plotted against percentage of VO2max to match for relative submaximal effort, there were no differences between the two groups. Physical training resulted in reduced exercise-induced hyperkalemia at matched submaximal work rates in both groups (P < .01) despite no associated change in the concentration of arterial catecholamines. At maximal exercise when trained, peak increases in [K+]a were unaltered, but peak concentrations of catecholamines were raised (P < .05). The decrease in VE at submaximal work rates after training was not significant with this incremental exercise protocol, but both groups had an increased peak VE when trained (P < .01). Exercise-induced rises in [K+]a, catecholamines, and VE are greater at submaximal work rates in subjects with CHF than in subjects with NLVF. Physical training reduces the exercise-induced rise in [K+]a but does not significantly decrease VE during submaximal exercise with this incremental cycle ergometry protocol. The reduction in exercise-induced hyperkalemia after training is not the result of altered concentrations of arterial catecholamines. The pathophysiological significance of the increased exercise-induced hyperkalemia in CHF and the mechanisms of improved K+ homeostasis with training have yet to be established.

IMPROVEMENT OF BRAIN ELECTRICAL ACTIVITY DURING TREATMENT OF PORCINE MALIGNANT HYPERTHERMIA WITH DANTROLENE

Three months before this study, susceptibility for malignant hyperthermia (MH) had been tested in 15 pigs. In all pigs, MH was triggered by administration of 1% halothane. Brain electrical activity was examined during therapy of MH with and without administration of dantrolene. From the EEG, power densities in selected frequencies and the median frequency of the power spectrum were calculated. Therapy was started when severe respiratory changes were observed (PaCO2 > 10 kPa, mixed venous oxygen tension (PvO2) < 4 kPa). At this time, heart rate exceeded 150 beat min-1, mean arterial pressure (MAP) was less than 60 mm Hg and median frequency was less than 2 Hz. EEG was isoelectric (n = 6) or showed slow polymorphic delta-activity. For therapy, administration of all anaesthetics was terminated, 100% oxygen was delivered and ventilation was increased four-fold. Acidosis was treated by administration of sodium bicarbonate 2-4 mmol litre-1 kg-1. Animals were allocated randomly to one of two groups: group I (control, n = 7) received no dantrolene; group II (n = 8) received dantrolene 2.5 mg kg-1 i.v. All variables were measured over a period of 60 min after therapy: EEG, HR and MAP were recorded continuously and blood-gas tensions, arterial potassium and glucose concentrations and pH were measured every 150 s. In group I (no dantrolene) minor, transient improvements in EEG activity were noted, but all animals died within 15-25 min after the start of therapy. In dantrolene-treated animals, EEG total power and median frequency increased within 5 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of the correction of renal anaemia by erythropoietin on physiological changes during exercise

The effects of treating the anaemia of end-stage renal failure with erythropoietin were studied in nine dialysis patients. The increase in haemoglobin concentration (by 59% from 7.0 +/- 1.2 to 11.1 +/- 1.1 g dl-1) was associated with increases in exercise duration (by 41%) and maximum oxygen consumption (by 34%). Treatment reduced resting heart rate but did not significantly alter heart rate at maximum exercise, nor resting or exercise blood pressure. Resting arterial potassium concentrations were slightly increased after treatment, but they increased similarly in relation to minute ventilation during exercise. Lactic acidaemia developed during exercise at both levels of haemoglobin, and was accompanied by similar reductions in arterial pH and bicarbonate levels but constant PaO2 and PaCO2. Ventilation was coupled to the metabolic rate of carbon dioxide production, ventilatory dead-space and arterial PCO2 before and after treatment of anaemia, the ventilatory requirement for carbon dioxide elimination being unchanged. Treatment of anaemia did not alter resting arterial lactate concentration; the concentration of lactate at maximum exercise was increased slightly following treatment but this increase did not reach statistical significance. The rate of increase in arterial lactate concentration as a function of oxygen consumption, assessed both with respect to the 'lactate threshold' and 'lactate slope index', was significantly delayed by treatment. Treatment of anaemia also delayed the 'anaerobic threshold', and there was good correlation between lactate and anaerobic thresholds. Treatment of renal anaemia by erythropoietin thus results in improved tissue oxygen supply during exercise, reflected by delay in the onset of lactic acidaemia.

Control of breathing during exercise

Although the control of breathing during exercise has been studied extensively that both neural and humoral factors may play a role in mediating the exercise hyperpnea, it remains unresolved whether the response is due solely to neural or humoral mechanisms and how the pulmonary gas exchange matches to the tissue exchange rates. At just onset of exercise ventilation can increase abruptly within 1 to 2 breathes (Phase I). Such a rapid increment of ventilation is not attributed to the humoral factor(s) due to the circulation delay from muscle metabolites. More rapid mechanism(s) such as irradiation from brain stream, afferent neurogenic control, blood flow increment as cardiodynamic theory might be considered. During moderate exercise intensity with a step function, ventilation increased exponentially to the steady state (phase II) after an abrupt increase at just onset of exercise. In this phase II, the breathing is controlled as to exchange the oxygen and carbon dioxide at rates appropriate for the acid-base homeostasis regulation. As a result, arterial blood gases and acid-base status must maintain within a narrow range despite of extremely enlarged metabolic rates by exercise. Some humoral factor(s) might be mediated for the control of breathing such as mean steady state error theory, arterial blood gases oscillation theory, feedback system by CO2, or optimization theory. At the heavy exercise intensity, anaerobic metabolism was supplemented to product for the enhanced energy requirement, so that ventilation increased non-linearly with oxygen uptake due to the lactoacidosis and its buffering activity. There has been a debate concerning cause and effect relationship between blood lactate increment and hyperpnea during exercise. Recently, arterial potassium concentration resulted from depolarization due to muscle contraction during exercise might stimulate to carotid bodies for increasing ventilation.

Ventilatory response and arterial potassium concentration during incremental exercise in patients with chronic airways obstruction

The relationship of ventilation response (VE) to arterial potassium concentration (K+) during ramp incremental exercise was assessed in nine patients with chronic obstructive pulmonary disease (COPD), and in 10 healthy subjects. For COPD patients the maximum oxygen uptake (VOmax) was 19.6 +/- 3.8 ml kg-1 min-1 (+/- SD), and percentage of forced expired volume at 1 s (% FEV1) was 47.8 +/- 10.4%. In healthy subjects, VO2max was 44.4 +/- 7.0 ml kg-1 min-1 and FEV1 was 89.7 +/- 7.4%. Breath-by-breath determinations for VE, oxygen uptake (VO2) and carbon dioxide output (VCO2), as well as determinations for K+, partial pressure of oxygen (PO2), partial pressure of carbon dioxide (PCO2), pH and lactate in arterial blood were performed during a workout on an exercise bicycle at a ramp function work rate of 20 W min-1, preceded by a 40 min warm-up period. The major findings in the present study are: (1) that there is a linear relation between ventilation and arterial K+ concentration during ramp exercise in both healthy subjects and COPD patients; (2) that the slope of the VE-K+ relationship is significantly lower in COPD patients (16.2 +/- 7.3 l min-1 mM-1) than in normal subjects (37.4 +/- 6.9 l min-1 mM-1, P less than 0.01); and, (3) that the slope of the VE-K+ relationship is significantly related to the ability to ventilate during maximal exercise in both healthy subjects and COPD patients (P less than 0.05). It is thought that the significantly reduced slope of the VE-K+ relationship in the COPD patients could be interpreted as a reduced sensitivity to the stimulus and/or as a mechanical impairment of the ventilation.

Potassium as a respiratory signal in humans

Six renal transplant recipients underwent a series of incremental exercise experiments. Minute ventilation (VE), carbon dioxide production rate (VCO2), and arterial blood chemistry were measured at rest and while subjects exercised on a stationary bicycle. Four of the subjects performed a similar experiment while exercising on a static rowing machine. Within each subject, arterial potassium concentration ([K+]a) was linearly related to VCO2 and VE during exercise. The slope of the relationship between [K+]a and VCO2 was similar in the cycling and rowing experiments. This implies that the absorption of potassium by resting muscle does not significantly limit the arterial hyperkalemia seen during exercise. When VE, VCO2, and [K+]a were measured 1 and 5 min after the end of cycling there was no correlation, whereas VE continued to be closely correlated with VCO2. The relationship demonstrated between change in [K+]a and VCO2 in these experiments is compatible with change of [K+]a acting as a respiratory signal during exercise but not during recovery from exercise in humans.

Effects of central bolus injections of potassium chloride on arterial potassium concentration in patients undergoing cardiopulmona0ry bypass

The effects of central venous bolus injections of potassium chloride (KCI) on arterial potassium concentration were studied in patients undergoing cardiopulmonary bypass. Ten subjects were studied, and each received a rapid bolus injection of KCI, 33 μEq/kg, both before and after cardiopulmonary bypass. Injections were delivered through the proximal infusion port of a 7.5F pulmonary artery catheter, which was situated in either the superior vena cava or the right atrium. Monitored variables included the electrocardiogram, mean arterial, central venous, and pulmonary artery pressures, end-tidal carbon dioxide and inspired oxygen concentrations, and temperature. Blood was sampled continuously at either the radial artery alone or both the radial artery and aortic root at 2 mL/4.3 s. The difference in magnitude between the maximal potassium concentration achieved and the prebolus baseline potassium concentration (delta K) was correlated with cardiac output, stroke volume, and prebolus baseline potassium concentration (baseline [K +]), using simple linear regression analysis. Although significant hyperkalemia leg, 7 to 9 mEq/L) developed in both the aortic root and radial artery, this was of no electrocardiographic or hemodynamic consequence, presumably because of the transient nature of the hyperkalemic response, following bolus injection of KCl. There was no significant correlation between delta K and cardiac output or stroke volume; however, delta K did correlate significantly with the Baseline [K +] in a direct linear relationship. It is concluded that central bolus injections of KCI through the proximal infusion port of the pulmonary artery catheter at 33 μEq/kg are safe. This technique should be used cautiously in patients with extremely low cardiac outputs or where intracardiac shunting of blood may exist, as these situations could potentially result in greater hyperkalemic responses than those observed in the current study.

Relationship between ventilation and arterial potassium concentration during incremental exercise and recovery

The purpose of this study was to compare the relationship of ventilation (VE) with pH, arterial concentrations of potassium [( K+]a), bicarbonate [( HCO3-]a), lactate [( la]a), and acid-base parameters which would affect hyperpnoea during exercise and recovery. To assess this relationship, ten healthy male subjects exercised with intensity increasing as a ramp function of 20 W.min-1 until voluntary exhaustion and they were then allowed a 5-min recovery period. Breath-by-breath gas exchange data, [HCO3-]a, pH, [la]a, [K+]a and blood gases were determined during both exercise and recovery. Using a linear regression method, the VE/[K+]a relationship was analysed during both exercise and recovery. Several interesting results were obtained: a significant relationship between [K+]a and VE was observed during recovery as well as during exercise; the VE at any given values of [K+]a was significantly higher during recovery than during exercise and out of those factors affecting exercise hyperpnoea, only [K+]a had a similar time-course to VE during recovery. Changes in [K+]a during recovery were shown to occur significantly faster than VE with an [K+]a time constant of 70.0 s, SD 16.2 as opposed to 105.5 s, SD 10.0 for VE (P less than 0.01). These results provided further evidence that [K+]a might play an important role as a substance which can stimulate exercise hyperpnoea as has been suggested by other workers. The present study also showed that during recovery [K+]a contributed significantly to the control of VE.

Effects of Selective and Nonselective β-Adrenoceptor Antagonism on Isoproterenol-Stimulated Myocardial Potassium Uptake in the Intact Dog

In intact anesthetized dogs, we measured myocardial potassium uptake, as calculated from the aortocoronary sinus difference in potassium concentration and myocardial blood flow, before and during beta-adrenergic stimulation with isoproterenol. Isoproterenol (10 and 30 ng/kg/min, n = 16) lowered arterial potassium concentration from 3.48 +/- 0.08 mmol/L by 0.20 +/- 0.07 and 0.32 +/- 0.06 mmol/L, coronary sinus potassium from 3.45 +/- 0.08 mmol/L by 0.20 +/- 0.06 and 0.35 +/- 0.06 mmol/L, increasing/myocardial potassium uptake from 1.94 +/- 0.99 mumol/min to 2.33 +/- 0.97 and 5.36 +/- 1.29 mumol/min. Unselective beta blockade (propranolol 0.1 mg/kg) significantly attenuated the fall in arterial and coronary sinus serum potassium and the increase in myocardial potassium uptake. Selective beta 1 blockade (metoprolol 0.1 mg/kg) did not significantly influence these effects. We conclude that beta-adrenergic stimulation increases myocardial potassium uptake, lowering serum potassium in the coronary bed, in addition to causing a systemic hypokalemia. This effect is mediated predominantly by beta 2 adrenoceptors.

Decrease in serum potassium concentration during epidural anaesthesia.

A mean decrease in the arterial serum potassium concentration (S-K) of 0.40 mmol/l (range 0-1.0) was found in 45 elderly men who were studied before and after induction of epidural anaesthesia (using mepivacaine 2% with adrenaline). The decrease was similar in patients who received acetated Ringer solution or dextran 40 in normal saline as intravenous fluid supplementation. No difference in S-K change was found between patients with a normal (less than 115 mumol/l) or elevated serum creatinine concentration. The decrease in S-K prevailed at the end of surgery except in patients with an elevated serum creatinine. Corrections of S-K for changes in arterial blood pH and rectal temperature during induction of anaesthesia did not explain the decrease in S-K. Correlations of clinical parameters such as the extension of anaesthesia, amount of intravenous fluid given and blood pressure changes gave conflicting results. A smaller decrease or no change in S-K was usually seen in arterial (n = 7) and venous (n = 7) samples when no intravenous fluid was given, as well as in venous samples when acetated Ringer solution was given (n = 6).

Blood biochemical status of miniature swine during submaximal and exhaustive exercise

Simultaneous arterial (left atrial) and mixed venous (right atrial) blood samples were anaerobically drawn from 14 miniature swine (mean weight = 25.0 +/- 1.7 [SE] kg) in order to examine the adequacy of these animals as a model for the exercising human. Samples were drawn: 1) at rest; 2) during exercise that elicited 80.4 +/- 1.2% of the animals' measured maximal heart rates; 3) at exhaustion; and 4) during the 4th min of a standing, resting recovery period. At rest, the animals were mildly alkalotic (pHa = 7.497 +/- 0.016) and hypocapnic (pCO2a = 29.6 +/- 1.2 torr), with low hematological values (arterial hemoglobin = 6.66 +/- 0.18 mmol X 1-1; arterial hematocrit = 32.0 +/- 0.9%) and slightly elevated catecholamine concentrations. During the submaximal exercise, there were no statistically significant changes in the arterial blood pH or in plasma sodium (Na+) and chloride (Cl-) concentrations, with significant decreases observed in Hcta, pCO2a, and increases in arterial plasma norepinephrine, total protein, and potassium (K+) concentrations. At exhaustion, pHa and pCO2a decreased further, with increases noted in the arterial plasma concentrations of K+, epinephrine, total protein, and the Hct but not in Na+ or Cl-. During recovery, arterial lactate averaged 20.54 +/- 0.71 mmol X 1-1. Venous changes were similar to those observed in arterial blood, with a mean pHv of 7.168 +/- 0.043 and arterial lactate = 21.08 +/- 0.90 mmol X 1-1 during recovery. Exercise-induced hemoconcentration was similar for both arterial and venous sample sites during both the submaximal and exhaustive exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of potassium carotid chemoreceptor activity and ventilation in the cat

Intravenous injections of potassium chloride were given to anaesthetised cats to produce rises in arterial plasma potassium within the range of those occuring in man during exercise. Carotid chemo-receptor activity was recorded as action potentials from a single or few fibre preparation of the right sinus nerve. Arterial potassium was recorded continuosly using a potassium electrode placed in the abdomial aorta. In response to the potassium injections there was an increase in carotid chemoreceptor activity, which closely followed the arterial potassium concentration, and an increase in ventilation. It is suggested that potassium released from muscle may be an important drive to ventilation in exercise.

Intracellular pH and electrolytes in human skeletal muscle during adrenaline and insulin infusions.

There is evidence that both beta-adrenergic stimulation and insulin are of importance in controlling intracellular pH. Therefore we have investigated the influence of intravenous infusion of adrenaline or insulin glucose (euglycaemic clamp) on pH and electrolyte composition in resting skeletal muscle (m. quadriceps femoris) and arterial blood in six healthy subjects. A decrease in the arterial potassium concentration was observed during infusion of adrenaline and is in conformity with previous studies. Both adrenaline and insulin infusions resulted in an increased lactate content of muscle and blood, indicating an enhanced glycolysis. The intracellular concentrations of K+, Na+, Mg2+ and H+, however, remained unchanged during the adrenaline infusions as well as during infusions of insulin. It is concluded that increasing the plasma adrenaline and insulin concentrations to levels well above the physiological range (adrenaline) or in the upper physiological range (insulin) does not affect the concentrations of electrolytes and hydrogen ions in resting human muscle to any appreciable extent.