Hydrogen Ion Concentration Of Blood Research Articles

Repeated-sprint ability in professional and amateur soccer players

This study investigated the repeated-sprint ability (RSA) physiological responses to a standardized, high-intensity, intermittent running test (HIT), maximal oxygen uptake (VO(2) (max)) and oxygen uptake (VO(2)) kinetics in male soccer players (professional (N = 12) and amateur (N = 11)) of different playing standards. The relationships between each of these factors and RSA performance were determined. Mean RSA time (RSA(mean)) and RSA decrement were related to the physiological responses to HIT (blood lactate concentration ([La(-)]), r = 0.66 and 0.77; blood bicarbonate concentration ([HCO(3)-]), r = -0.71 and -0.75; and blood hydrogen ion concentration ([H(+)]), r = 0.61 and 0.73; all p < 0.05), VO(2) (max) (r = -0.45 and -0.65, p < 0.05), and time constant (tau) in VO(2) kinetics (r = 0.62 and 0.62, p < 0.05). VO(2) (max) was not different between playing standards (58.5 +/- 4.0 vs. 56.3 +/- 4.5 mL.kg(-1).min(-1); p = 0.227); however, the professional players demonstrated better RSA(mean) (7.17 +/- 0.09 vs. 7.41 +/- 0.19 s; p = 0.001), lower [La-] (5.7 +/- 1.5 vs. 8.2 +/- 2.2 mmol.L(-1); p = 0.004), lower [H+] (46.5 +/- 5.3 vs. 52.2 +/- 3.4 mmol.L(-1); p = 0.007), and higher [HCO3-] (20.1 +/- 2.1 vs. 17.7 +/- 1.7 mmol.L(-1); p = 0.006) after the HIT, and a shorter in VO2 kinetics (27.2 +/- 3.5 vs. 32.3 +/- 6.0 s; p = 0.019). These results show that RSA performance, the physiological response to the HIT, and differentiate between professional- and amateur-standard soccer players. Our results also show that RSA performance is related to VO(2) max, tau, and selected physiological responses to a standardized, high-intensity, intermittent exercise.

Net acid excretion capacity is related to blood hydrogen ion and serum carbon dioxide

Acid-base imbalance due to dietary food patterns has emerged as one of the hypotheses leading to modern-day diseases. This study examined if a new method to assess the renal ability to excrete an acid load, that is, the net acid excretion capacity (NAEC), constructed from net acid excretion (NAE) and urine pH, relates to blood hydrogen ion concentration ([H+]) and serum carbon dioxide concentration ([CO2]). In a second analysis, NAE to pH relationship was examined, and is de facto treated to be linear. This study used historical, cross-sectional data of 58 repeated measurements from 8 subjects for the primary measurements of NAEC, blood [H+], and serum [CO2]. Using fixed models, higher NAEC associated with lower [H+] and higher [CO2]. Using hierarchical models, the interindividual variations in [H+] and [CO2] explained the variations in NAEC. In the second analysis (n = 59), a quadratic NAE to pH relationship (NAE = −846.77 + 341.47 pH − 31.50 pH 2) can be reported. Net acid excretion capacity, a noninvasive tool to assess the renal ability to excrete an acid load, has a physiologic base to it, in that it captures the inherent nonlinear relations of NAE to pH explaining endogenous [H+] retention/excretion. A higher vegetable and fruit consumption might relieve NAEC and allow excess [H+] loss via both renal and respiratory routes.

The Importance of Calcium, Potassium, and Acid-Base Homeostasis in Bone Health and Osteoporosis Prevention

The Importance of Calcium, Potassium, and Acid-Base Homeostasis in Bone Health and Osteoporosis Prevention

Dietary sodium chloride intake independently predicts the degree of hyperchloremic metabolic acidosis in healthy humans consuming a net acid-producing diet

We previously demonstrated that typical American net acid-producing diets predict a low-grade metabolic acidosis of severity proportional to the diet net acid load as indexed by the steady-state renal net acid excretion rate (NAE). We now investigate whether a sodium (Na) chloride (Cl) containing diet likewise associates with a low-grade metabolic acidosis of severity proportional to the sodium chloride content of the diet as indexed by the steady-state Na and Cl excretion rates. In the steady-state preintervention periods of our previously reported studies comprising 77 healthy subjects, we averaged in each subject three to six values of blood hydrogen ion concentration ([H]b), plasma bicarbonate concentration ([HCO(3)(-)]p), the partial pressure of carbon dioxide (Pco(2)), the urinary excretion rates of Na, Cl, NAE, and renal function as measured by creatinine clearance (CrCl), and performed multivariate analyses. Dietary Cl strongly correlated positively with dietary Na (P < 0.001) and was an independent negative predictor of [HCO(3)(-)]p after adjustment for diet net acid load, Pco(2) and CrCl, and positive and negative predictors, respectively, of [H]b and [HCO(3)(-)]p after adjustment for diet acid load and Pco(2). These data provide the first evidence that, in healthy humans, the diet loads of NaCl and net acid independently predict systemic acid-base status, with increasing degrees of low-grade hyperchloremic metabolic acidosis as the loads increase. Assuming a causal relationship, over their respective ranges of variation, NaCl has approximately 50-100% of the acidosis-producing effect of the diet net acid load.

Plasma leptin concentration in patients with acute renal failure.

Acute renal failure (ARF) is characterized by impaired excretory, endocrine, homeostatic and metabolic function of the kidneys. It is well-known that leptin is an adipose-derived polypeptide hormone which is predominantly biodegraded by the kidneys. Therefore, plasma leptin concentration is increased in chronic renal failure (CRF). However, its' concentrations in patients with ARF were not investigated until now. The aim of the present study was to evaluate plasma leptin concentration in patients with ARF. 27 patients with ARF (age 44 +/- 4 years, BMI 26.0 +/- 0.9 kg/m2, means +/- SEM, 17 patients 15 M, 2 F recovered kidney function and 10 patients 7 M, 3 F died during the anuric phase), 27 hemodialysis patients (22 M, 5 F; age 45 +/- 2 years; BMI 26.2 +/- 0.8 kg/m2) with chronic renal failure (CRF) and 27 healthy subjects (HS) (22 M, 5 F; age 42 +/- 3 years; BMI 25.9 +/- 0.6 kg/m2) were examined. In patients with ARF, blood samples for plasma leptin and routinely assessed biochemical parameters were withdrawn before the first HD session (I), and in patients who survived a second time 5 days later during the anuric/oliguric phase (II), and a third one during the polyuric phase before discharge of the patient from hospital (III). In patients with CRF all examined parameters were estimated only once before a subsequent HD session. Patients with ARF (before the first HD session) and CRF did not differ significantly with respect to BMI, serum creatinine and blood hydrogen ion concentrations. Plasma leptin level in patients with ARF before the first HD session was similar to values obtained in HS, but significantly lower (p < 0.01) than in patients with CRF (2.5 (1.9 - 8.2) vs. 3.4 (2.5 - 8.3) vs. 8.4 (2.9 - 16.9) ng/ml in ARF, HS and CRF, respectively). There was no significant difference in leptinemia between patients with ARF who survived and who died. In patients with ARF who survived, improvement ofrenal function was accompanied by a slightly (not significant) declining tendency in plasma leptin concentration (5.6 +/- 2.2 vs. 4.8 +/- 1.7 vs. 4.5 +/- 1.3 ng/ml; I, II, III phases of ARF, respectively). In contrast to hemodialysis patients with chronic renal failure, patients with acute renal failure are characterized by normal plasma leptin concentration. Thus, difference in leptinemia between patients with chronic and acute renal failure seems to be due to preservation of large amounts of active renal parenchyma in ARF patients.

Acute metabolic acidosis: characterization and diagnosis of the disorder and the plasma potassium response.

ABSTRACT. Despite the high incidence of acute metabolic acidosis, there are no reliable human data to enable physicians to accurately diagnose this disorder. In addition, there is uncertainty about the direction and magnitude of plasma potassium changes in acute metabolic acidosis. The systemic and renal acid-base, electrolyte, and endocrine response to acute acid loads (imposed by three timed NH(4)Cl infusions into the duodenum, 0.9 mmol of NH(4)Cl per kg of body weight over 30 min each) was characterized in six healthy male subjects in whom a metabolic steady-state had been established. Arterialized blood CO(2) tension decreased by 0.85 mmHg per mmol/L decrease in plasma bicarbonate concentration and blood hydrogen ion concentration increased by 0.45 nmol/L per mmol/L decrease in plasma bicarbonate concentration. Plasma potassium did not change significantly (+0.02 +/- 0.02 mmol/L per mmol decrease in plasma bicarbonate concentration). Plasma insulin increased and plasma glucagon levels decreased in acute metabolic acidosis, while catecholamines and aldosterone were not affected significantly. These data provide the first diagnostic criteria for the diagnosis of acute metabolic acidosis in humans. The finding of a hyperinsulinemic response in acute metabolic acidosis suggests that an insulin response counterregulates any acidemia-induced cellular potassium efflux, resulting in stable plasma potassium concentrations.

The effect of exercise performed before and 24 hours after blood withdrawal on serum erythropoietin and growth hormone concentrations in humans.

In the present experiment we have studied the effect of exercise performed before and 24 h after withdrawal of 450 ml of blood on the serum erythropoietin and growth hormone (GH) levels, in humans. Twelve male subjects (x +/- SD) aged 23.2 +/- 2.6 y, with a body mass of 74.8 +/- 7.2 kg, height 178.0 +/- 7.6 cm, BMI 23.6 +/- 2.1 kg x m(-2), VO2 max 2937 +/- 324 ml x min(-1), participated in this study. The subjects performed twice an incremental exercise test until exhaustion, separated by a period of about 7 - 10 days. The second test was performed 24 h after withdrawal of 450 ml of blood (honorary blood donation). In the control study we found no effect of the incremental exercise on the serum erythropoietin concentration, which amounted to 14.24 +/- 7.66 mU x ml(-1) at rest and 14.97 +/- 6.07 mU x ml(-1) at the end of the incremental test. Serum GH level in the control study rose considerably from 0.158 +/- 0.024 nmol x l(-1) at rest to 1.523 +/- 0.336 nmol x l(-1) at the end of exercise and returned to initial value 2 h after the exercise. During the experiment performed 24 h after withdrawal of 450 ml of blood the serum erythropoietin concentration at rest was significantly elevated (p < 0.01) in relation to the control measurement (amounting to 24.85 +/- 13.60 mU x ml(-1)) and at the end of the incremental exercise a tendency towards further elevation (p = 0.09) in erythropoietin concentration up to 28.32 +/- 14.51 mU x m(-1) was observed. Serum GH level during the experiment after blood withdrawal was similar to that in control test and exercise caused a rise in the GH level to 1.056 +/- 0.52 nmol x l(-1), significantly less than in control test, but this increment fell to control value 2 h after exercise. The elevated level of erythropoietin 24 h after blood withdrawal was accompanied by a significant increase (p < 0.015) in blood hydrogen ion concentration [H +] b at rest from 48.2 +/- 2.8 nmol x l(-1) in the control study to 52.9 +/- 4.5 nmol x l(-1) after blood donation. No effect of blood withdrawal on pre-exercise level of plasma lactate concentration, end-tidal O2 and end-tidal CO2 was found. We concluded that withdrawal of 450 ml of blood, within 24 hours significantly increased serum erythropoietin concentration and caused non-lactic acidosis. A single bout of maximal incremental exercise, performed before and 24 hours after blood withdrawal, had no effect on serum erythropoietin concentration in humans but the exercise-induced increase in serum GH concentration performed after blood withdrawal tended to be lower than in the control study.

Influence of the Alpha-1-Adrenergic Receptor Blocker Doxazosin on Exercise-Induced Hyperkalemia in Hemodialysis Patients

Background/Aim: Hyperkalemic responses to both physical exercise and α-adrenergic stimulation are enhanced in patients with terminal renal failure. α-Adrenergic blockade was found to protect against hyperkalemia during vigorous exercise in healthy men. The aim of the study was to examine the effects of the α-adrenergic blocker doxazosin on exercise-induced hyperkalemia in hemodialysis patients. Methods: In a randomized, placebo-controlled, crossover design study, 15 anuric, chronic hemodialysis patients were included. Doxazosin or placebo was given in a random order for 4 days before exercise. At the end of each phase of the study, a 30-min treadmill exercise test with a constant workload of 2 metabolic equivalents was performed followed by a 30-min recovery period. Results: The patients achieved 64 ± 3 and 62 ± 3% of maximal heart rate during the exercise test on doxazosin and placebo, respectively. The baseline plasma concentration of potassium was similar both on active treatment and on placebo (5.1 ± 0.2 mmol/l on doxazosin and 4.9 ± 0.1 mmol/l on placebo). The serum potassium concentration increased significantly and to a similar extent during the tests. The mean rates of potassium increment during exercise were 8.4 ± 1.5 µmol/l/min on doxazosin and 6.9 ± 1.3 µmol/l/min on placebo. During the recovery period, the serum potassium concentration significantly decreased in both arms of the study. There were no significant changes in plasma sodium, calcium, and phosphate levels during the tests. Hydrogen ion concentration in blood, serum insulin and glucose, and plasma aldosterone and renin activity were similar before the exercise tests. Conclusion: α-Adrenergic blockade does not modulate the hyperkalemic response to moderate physical exercise in patients with terminal renal failure.

Interrelationship between plasma leptin concentration and severity of metabolic acidosis in haemodialysed patients with chronical renal failure.

Patients with chronic renal failure are frequently characterized by malnutrition, hyperleptinaemia and metabolic acidosis. Both hyperleptinaemia and chronic metabolic acidosis are presumed to contribute to the pathogenesis of malnutrition observed in this group of patients. It has been reported, that in vitro adipocytes exposed to acidotic medium decrease leptin secretion. The aim of present study was to analyze the possible impact of uraemic metabolic acidosis on leptinaemia in haemodialysis patients with chronic renal failure. - 94 haemodialysed patients (58 M, 36 F; mean age 45 +/- 1 years) were enrolled in this study. 56 patients were on haemodialysis treatment for one year using an acetate dialysis fluid, while 38 patients were haemodialysed at least for 3 months with a dialysate buffered with bicarbonate. Plasma leptin concentration, blood gases and body composition were assessed in all examined subjects. - Patients haemodialysed with an acetate and bicarbonate buffered dialysate did not differ with respect to body weight, body mass index (BMI), total fat mass (TFM) and plasma leptin concentration. Patients haemodialysed with an acetate buffered dialysate were characterized by a significantly more severe metabolic acidosis than patients on bicarbonate haemodialysis. Patients were divided according to the actual hydrogen ion concentration: over 60 nmol/l, 45-60 nmol/l and below 45 nmol/l. These subgroups did not differ significantly by body weight, BMI and TFM. Only a slightly (not significantly), lower median leptinaemia was found in patients with elevated hydrogen ion concentration. No significant correlation was noticed between blood hydrogen or hydrocarbonate ion concentration respectively and logarithmic values of plasma leptin concentration (tau = 0.025, p = 0.72; tau = - 0.021, p = 0.76 respectively). - From results obtained in this study we may conclude that, blood hydrogen ion concentration does not influence substantially or only moderately to plasma leptin concentration in haemodialysed patients.

Venous blood pressure in broilers during acute inhalation of five percent carbon dioxide or unilateral pulmonary artery occlusion

We evaluated the hypothesis that venous congestion (increased venous volume), as reflected by venous hypertension (increased venous pressure), can arise when the right ventricle is unable to elevate the pulmonary arterial pressure sufficiently to propel the cardiac output through an anatomically inadequate or inappropriately constricted pulmonary vasculature. Changes in venous pressure were evaluated in clinically healthy broilers during modest increases in pulmonary vascular resistance induced by inhalation of 5% CO2 and during large increases in pulmonary vascular resistance accomplished by acutely tightening a snare around one pulmonary artery. Inhalation of 5% CO2 induced a pronounced respiratory acidosis, as reflected by increases the partial pressure of CO2 and the hydrogen ion concentration in arterial blood. Inhalation of 5% CO2 also increased pulmonary arterial pressure by approximately 3 mm Hg and increased venous pressure by approximately 1 mm Hg when compared with the pre-inhalation venous pressure. Tightening the pulmonary artery snare increased the pulmonary arterial pressure by approximately 10 mm Hg, and this degree of pulmonary hypertension was sustained until the snare was released. When compared with the pre- and post-snare intervals, tightening of the pulmonary artery snare induced a sustained increase in venous pressure of > or = 1 mm Hg. Veins have highly compliant walls that permit an approximate doubling in volume with only small (4 to 6 mm Hg) increases in central venous pressure. Presumably the apparently modest 1 mm Hg increase in venous pressure measured after CO2 inhalation or unilateral pulmonary artery occlusion reflects a large increase in venous volume and, thus, substantial venous congestion. These observations support the hypothesis that increases in pulmonary vascular resistance can initiate increases in venous pressure by challenging the capacity of the right ventricle to propel all of the returning venous blood through the lungs. Central venous congestion predisposes broilers to the onset of cirrhosis and ascites by impeding the outflow of hepatic venous blood and increasing the hydrostatic pressure within hepatic sinusoids.

The infusion rate dependent influence of acute metabolic acidosis on pulmonary vascular resistance in broilers

Experiments were conducted to evaluate the pulmonary vascular responses of lightly anesthetized clinically healthy male broilers during acute metabolic acidosis induced by bolus i.v. injections or constant i.v. infusions of HCl. In Experiment 1, broilers received consecutive 1.5 mL i.v. bolus injections of 2.5% mannitol (volume control) and 0.4 N, 0.8 N, and 1.2 N HCl in 2.5% mannitol. Following each injection, equivalent concentrations of mannitol or HCl were infused i.v. at a rate of 0.05 mL/min.kg BW. In Experiment 2, repeated bolus injections of 2.5% mannitol and 1.2 N HCl were administered during ongoing constant infusion of 2.5% mannitol. The following variables were evaluated: pulmonary arterial pressure, pulmonary vascular resistance, mean arterial pressure, total peripheral resistance, cardiac output, stroke volume, heart rate, respiratory rate, hematocrit (HCT), and arterial blood gas (PaO2, PaCO2, pH, HCO3-). Mannitol alone did not alter any of the variables. The HCl loading protocols acidified the arterial blood to sustained (constant infusion) or transient (bolus injection) values averaging between pH 7.2 and 7.3. In both experiments, bolus injections of 1.2 N HCl caused transient increases in pulmonary vascular resistance and pulmonary arterial pressure, coincident with decreases in mean arterial pressure and cardiac output. When HCl was infused at a constant rate in Experiment 1, the arterial blood hydrogen ion concentration, [H+], was positively correlated with pulmonary arterial pressure and cardiac output, negatively correlated with mean arterial pressure and total peripheral resistance, and was not correlated with pulmonary vascular resistance. During constant i.v. infusion of mannitol or HCl in both experiments, pulmonary arterial pressure was positively correlated with pulmonary vascular resistance and cardiac output. Overall, bolus injections of 1.2 N HCl consistently triggered transient pulmonary vasoconstriction (increased pulmonary vascular resistance), leading to a transient increase in pulmonary arterial pressure in spite of opposing changes in cardiac output and mean arterial pressure. In contrast, equivalent or greater increases in [H+] during constant i.v. infusion of HCl caused a substantially lower increment in pulmonary arterial pressure, which, in, turn was primarily attributable to increases in cardiac output rather than pulmonary vascular resistance. Increments in either pulmonary vascular resistance or cardiac output induced by metabolic acidosis would be expected to contribute to the onset of pulmonary hypertension syndrome (PHS, ascites) in broilers.

Potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women.

Previously we demonstrated that low grade chronic metabolic acidosis exists normally in humans eating ordinary diets that yield normal net rates of endogenous acid production (EAP), and that the degree of acidosis increases with age. We hypothesize that such diet-dependent and age-amplifying low grade metabolic acidosis contributes to the decline in skeletal muscle mass that occurs normally with aging. This hypothesis is based on the reported finding that chronic metabolic acidosis induces muscle protein breakdown, and that correction of acidosis reverses the effect. Accordingly, in 14 healthy postmenopausal women residing in a General Clinical Research Center and eating a constant diet yielding a normal EAP rate, we tested whether correcting their "physiological" acidosis with orally administered potassium bicarbonate (KHCO3; 60-120 mmol/day for 18 days) reduces their urinary nitrogen loss. KHCO3 reduced EAP to nearly zero, significantly reduced the blood hydrogen ion concentration (P < 0.001), and increased the plasma bicarbonate concentration (P < 0.001), indicating that pre-KHCO3, diet-dependent EAP was significantly perturbing systemic acid-base equilibrium, causing a low grade metabolic acidosis. Urinary ammonia nitrogen, urea nitrogen, and total nitrogen levels significantly decreased. The cumulative reduction in nitrogen excretion was 14.1 +/- 12.3 g (P < 0.001). Renal creatinine clearance and urine volume remained unchanged. We conclude that in postmenopausal women, neutralization of diet-induced EAP with KHCO3 corrects their preexisting diet-dependent low grade metabolic acidosis and significantly reduces their urinary nitrogen wasting. The magnitude of the KHCO3-induced nitrogen-sparing effect is potentially sufficient to both prevent continuing age-related loss of muscle mass and restore previously accrued deficits.

Effect of age on blood acid-base composition in adult humans: role of age-related renal functional decline.

In 64 apparently healthy adult humans (ages 17-74 yr) ingesting controlled diets, we investigated the separate and combined effects of age, glomerular filtration rate (GFR, index of age-related renal functional decline), renal net acid excretion [NAE, index of endogenous acid production (EAP)], and blood PCO2 (PbCO2, index of respiratory set point) on steady-state blood hydrogen ion ([H+]b) and plasma bicarbonate concentration ([HCO3-]p). Independent predictors of [H+]b and [HCO3-]p were PbCO2, NAE, and either age or GFR, but not both, because the two were highly correlated (inversely). [H+]b increased with increasing PbCO2, NAE, and age and with decreasing GFR. [HCO3-]p decreased with increasing NAE and age but increased with increasing PbCO2 and GFR. Age (or GFR) at constant NAE had greater effect on both [H+]b and [HCO3-]p than did NAE at constant age (or GFR). Neither PbCO2 nor NAE correlated with age or GFR. Thus two metabolic factors, diet-dependent EAP and age (or GFR), operate independently to determine blood acid-base composition in adult humans. Otherwise healthy adults manifest a low-grade diet-dependent metabolic acidosis, the severity of which increases with age at constant EAP, apparently due in part to the normal age-related decline of renal function.

Age and systemic acid-base equilibrium: analysis of published data.

To investigate whether systemic acid-base equilibrium changes with aging in normal adult humans, we reviewed published articles reporting the acid-base composition of arterial, arterialized venous, or capillary blood in age-identified healthy subjects. We extracted or calculated blood hydrogen ion concentration ([H+]), plasma bicarbonate concentration ([HCO3(-)]), blood PCO2, and age, and computed a total of 61 age-group means, distributed among eight 10-year intervals from age 20 to 100 years. Using linear regression analysis, we found that with increasing age, there is a significant increase in the steady-state blood [H+] (p < .001), and reduction in steady-state plasma [HCO3(-)] (p < .001), indicative of a progressively worsening low-level metabolic acidosis. Blood PCO2 decreased with age (p < .05), in keeping with the expected respiratory adaptation to metabolic acidosis. Such age-related increasing metabolic acidosis may reflect in part the normal decline of renal function with increasing age. The role of age-related metabolic acidosis in the pathogenesis of the degenerative diseases of aging warrants consideration.

Blood hydrogen ion and lactate concentrations during strenuous exercise in the horse

SummaryExceptional findings in horses, such as metabolic alkalosis during exercise and an apparent absence of a distinct lactate threshold, led us to apply Stewart's acid‐base system and to develop a new statistical model for investigating lactate threshold. The lactate threshold was clearly demonstrated by an incremental exercise test using up to 14 steps. Lactate threshold was increased by training and by fat adaptation (prolonged interval training and a 10% corn oil diet). Fat adaptation appears to facilitate the metabolic regulation of glycolysis, sparing glucose and glycogen at work of low intensity, but promoting lactate production when power is needed for high intensity exercise. The blood lactate response to exercise was enhanced by fat adaptation and by oral supplementation of sodium bicarbonate. The synergistic effect of the combination suggested that inclusion of fat may enhance the advantage of a diet with a high cation‐anion balance. The lower CO2 production of fat‐adapted horses could be of benefit under hot and humid conditions, especially in horses with reduced pulmonary function.During repeated sprints, central venous [H+] increased (acidosis) but arterial [H+] decreased (alkalosis). These changes were consistent with concurrent changes in venous and arterial PCO2 but not [SID]. Arterial PO2 remained constant. These findings suggest that increasing ventilation to maintain arterial PO2 incidentally reduced PCO2, hence arterial [H+]. In terms of homeostatic priorities, regulation of respiration took precedence over regulation of acid‐base status.

Effect of acid-base balance on the growth hormone response to acute high-intensity cycle exercise

To investigate the effect of acid-base balance on serum human growth hormone (hGH) concentration after an acute high-intensity anaerobic exercise bout, 10 untrained but normally active men [age, 24.6 +/- 1.5 (SE) yr] participated in a randomized double-blind counterbalanced experiment. Each subject reported in a fasted state at the same time of day for two experimental sessions separated by 1 wk. For each session, subjects were administered a decaffeinated tea solution containing either 0.3 g NaHCO3/kg body wt [alkalosis (ALK)] or 0.04 g NaCl/kg body wt [control (CTRL)] over a 45-min ingestion period. Venous blood samples were obtained before [baseline (BL)] and 75 min after the ingestion period, as well as postexercise at 0, 5, 10, 15, 20, and 30 min. The exercise task immediately followed the preexercise blood draw and consisted of 90 s of maximal-effort cycle ergometry against an opposing force of 0.49 N (0.05 kg)/kg body wt. There were no differences between the ALK and CTRL conditions in mean or peak power output or total work during the exercise task. Whole blood pH was significantly (P < or = 0.05) elevated in ALK above CTRL at all time points except BL. Postexercise serum hGH concentration significantly increased above BL at 10, 15, 20, and 30 min in CTRL and at 20 and 30 min in ALK. The hGH concentration was significantly lower in ALK than in CTRL at 15, 20, and 30 min postexercise. These data indicate that an increase in blood hydrogen ion concentration may be partly responsible for the hGH response to acute high-intensity anaerobic exercise.

The Effect of Selected Minerals on the Acid-Base Balance of Growing Chicks

A study was conducted to determine the relative acidogenicities of dietary supplements of the anions, chloride, sulfate, and monohydrogen phosphate (HPO4−2) in diets of young Leghorn chicks. Chloride supplements ranged from 40 to 240 meq/kg, sulfate ranged from 100 to 240 meq/kg, and monohydrogen phosphate ranged from 120 to 240 meq/kg of diet. Anions were substituted on a charge-equivalent basis for dietary carbonate (CO3–2) at 7 to 10 days of age, and blood samples were taken for measurement of blood hydrogen ion concentration, carbon dioxide tension, and bicarbonate concentration (calculated) on the 1st day and after several (usually 8) days of experiment. The effects of anions on acid-base balance were evident on the 1st day and generally persisted for the duration of experiments. Chloride consistently depressed blood pH and blood bicarbonate concentration. Sulfate was acidogenic, but less so than chloride, whereas monohydrogen phosphate did not affect blood measures of acid-base balance.

Chronic Respiratory Alkalosis

In normal subjects, chronic hyperventilation lowers plasma bicarbonate concentration, primarily by inhibiting the urinary excretion of net acid. The quantitative relation between reduced arterial carbon dioxide tension (PaCO2) and the plasma bicarbonate concentration in the chronic steady state has not been studied in humans, however, and the laboratory criteria for the diagnosis of chronic respiratory alkalosis therefore remain undefined. We wished to provide such reference data for clinical use. Moreover, because chronic hyperventilation paradoxically lowers blood pH still further in dogs with metabolic acidosis, we desired to study the effect of chronic hypocapnia on the plasma bicarbonate concentration (and blood pH) in normal human subjects in whom acidosis had been induced with ammonium chloride. Under metabolic-balance conditions, we used altitude-induced hypobaric hypoxia to produce chronic hypocapnia in nine normal young men, five of whom received ammonium chloride daily to cause metabolic acidosis (the mean [+/- SE] steady-state plasma bicarbonate level in these five was 12.0 +/- 0.5 mmol per liter). For each decrease of 1 mm Hg (0.13 kPa) in the PaCO2, the plasma bicarbonate concentration decreased by 0.41 mmol per liter in the subjects who started with a normal plasma bicarbonate concentration and by 0.42 mmol per liter in the subjects with acidosis. In contrast to the findings in previous studies of dogs, hypocapnia increased blood pH similarly in both groups; the blood hydrogen ion concentration decreased by about 0.4 nmol per liter for every decrease of 1 mm Hg (0.13 kPa) in PaCO2. These results provide reference data for the diagnosis of chronic respiratory alkalosis in humans. Although chronic hypocapnia decreased plasma bicarbonate levels similarly in normal subjects with acidosis and without acidosis, the percent reduction in PaCO2 was always greater than the corresponding percent reduction in the plasma bicarbonate concentration. Therefore, as was not true of the response in dogs, the subjects' blood pH always increased with hyperventilation, regardless of the initial plasma bicarbonate concentration.

Effects of Warm-Up on Blood Gases, Lactate and Acid-Base Status During Sprint Swimming

A standardized 200-m front crawl sprint swim (SpS) was used to evaluate the effects of warm-up on pH, blood gases, and the concentrations of lactate ([La-]) and bicarbonate ([HCO3-]) in arterialized and venous blood. Eight trained male swimmers performed two randomly assigned 200-m front crawl swims at previously determined intensities corresponding to 120% VO2max. One swim was preceded by a warm-up (WU trial) which consisted of a 400-m front crawl swim (82% VO2max), 400-m flutter kicking (45% VO2max), and 4 x 50-m front crawl sprints (111% VO2max). The second was performed without warm-up (NWU trial). Blood was sampled from a hyperemized earlobe and an antecubital vein before the warm-up, 9 min after the warm-up (1 min before the swim), immediately following the SpS, and at 2, 5, 10, and 20 min after the SpS. The warm-up exercise resulted in a higher pre-SpS [La-] in arterialized blood (3.1 +/- 0.4 and 1.7 +/- 0.4 mmol x l-1, p less than 0.05), a higher hydrogen ion concentration ([H+]) in venous blood (45.9 +/- 0.9 and 42.2 +/- 0.8 nmol x l-1, p less than 0.001), and a lower arterialized blood [HCO3-] (25.1 +/- 0.9 and 22.2 +/- 0.8 mmol x l-1, p less than 0.05). The SpS was accompanied with higher heart rates during the WU trial (178 +/- 3 and 169 +/- 3 bpm; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

EFFECTS OF TRANSPORT AND ELECTROLYTE SUPPLEMENTATION ON ION CONCENTRATIONS, CARCASS YIELD AND QUALITY IN BULLS

Two experiments were completed to: (1) identify predictive acid-base and electrolyte parameters that might be correlated with meat quality in marketed bulls; and (2) to determine whether bulls could be treated with either glucose or electrolyte drinks while in lairage to improve electrolyte balance and meat quality. In the first experiment, 29 crossbred yearling bulls averaging 499 ± 13.4 kg were exposed to either a minimal stress of no mixing and 3 km transport (N = 13) or a moderate stress of mixing, 6 h transport 24 h off feed in lairage, plus an additional 3 km transport immediately prior to slaughter (N = 16). Animals exposed to moderate stress displayed higher serum chloride values (137 mmol L−1) compared to pre treatment control (121 mmol L−1) or minimal stress values (118 mmol L−1) (P ≤ 0.01). The moderate stress group also displayed lower blood hydrogen ion concentrations (P &lt; 0.05) and produced a high frequency of dark, firm and dry meat (9 out of 16 animals compared to 0 out of 13 in the control group). In the second experiment, 79 crossbred yearling bulls averaging 595 ± 6.5 kg were divided into treatment groups of either 19 or 20 animals each and subjected to mixing, handling and a 6-h transport period after which they were left in lairage for 18–20 h before slaughter. Treatment groups were: (1) no water during lairage; (2) water only; (3) electrolyte drink; or (4) a 5% glucose drink. Animals in exp. 2 given either water or no water displayed significantly higher serum sodium (P ≤ 0.01) and chloride ion (P ≤ 0.02) levels compared to animals offered an electrolyte or glucose drink. It was also found that the urine cation levels of animals offered no water or water only were significantly higher (P ≤ 0.05). In all animals, improved electrolyte balance coincided with improved meat quality traits and carcass yield. Key words: Electrolyte balance, transport stress, bulls, carcass quality