Plasma Lactic Acid Concentrations Research Articles

Effects of dietary rumen-protected choline supplementation to periparturient dairy cattle on inflammation, metabolism, and performance during an intramammary lipopolysaccharide challenge

Recent studies have suggested that dietary rumen-protected choline (RPC) supplementation can modulate immune function, attenuate inflammation, and improve performance in periparturient dairy cattle; however, this has yet to be evaluated during a mastitis challenge. Therefore, the objective of this study was to examine the effects of supplementation and dose of RPC on metabolism, inflammation, and performance during an intramammary lipopolysaccharide (LPS) challenge. Parous Holstein cows (parity, mean ± SD, 1.9 ± 1.1 at enrollment) were blocked by calving month and randomly assigned within block to receive either 45 g/d of RPC (20.4 g/d of choline ions; CHOL45, n = 18), 30 g/d of RPC (13.6 g/d of choline ions; CHOL30, n = 21), or no RPC (CON, n = 19) as a top-dress starting 24 d before expected calving until 21 d postpartum. Cows were alternately assigned within treatment group to either receive an intramammary LPS challenge (200 μg in each rear quarter; Escherichia coli O111:B4) or not at 17 DIM. Before the challenge, CHOL45 and CHOL30 cows produced 3.4 and 3.8 (±1.2 SED) kg/d more milk than CON, respectively. Dietary RPC supplementation did not mitigate the milk loss associated with the intramammary LPS challenge; however, CHOL45 and CHOL30 cows produced 3.1 and 3.5 (±1.4 SED) kg/d more milk than CON, respectively in the carryover period (22 to 84 DIM). Dietary RPC supplementation enhanced plasma β-hydroxybutyrate (BHB) concentrations before the LPS challenge, and increased plasma nonesterified fatty acids (NEFA) and acetylcarnitine concentrations during the LPS challenge, potentially reflecting greater adipose tissue mobilization, fatty acid transport and oxidation. Aside from trimethylamine N-oxide and sarcosine, which were increased in CHOL45-LPS as compared with CON-LPS, most other choline metabolite concentrations in plasma were unaffected by treatment, likely because more choline was being secreted in milk. Plasma lactic acid concentrations were decreased in CHOL45-LPS and CHOL30-LPS as compared with CON-LPS, suggesting a reduction in glycolysis or an enhancement in the flux through the lactic acid cycle to support gluconeogenesis. Plasma concentrations of fumaric acid, a byproduct of AA catabolism and the urea cycle, were increased in both choline groups as compared with CON-LPS during the LPS challenge. Cows in the CHOL45 group had greater plasma antioxidant potential before the LPS challenge and reduced plasma methionine sulfoxide concentrations during the LPS challenge compared with CON-LPS, suggesting an improvement in oxidant status. Nevertheless, concentrations of inflammatory markers such as haptoglobin and tumor necrosis factor α (TNFα) were not affected by treatment. Taken together, our data suggest that the effects of dietary RPC supplementation on milk yield could be mediated through metabolic pathways and are unlikely to be related to the resolution of inflammation in periparturient dairy cattle. Lastly, dose responses to dietary RPC supplementation were not found for various economically important outcomes including milk yield, limiting the justification for feeding a greater dietary RPC dose in industry.

The Influence of Exercise Intensity on Tryptophan Metabolites in Thoroughbred Horses.

Catabolism of tryptophan (Trp) is modulated by physical activity and provides a pool of active compounds: Trp is considered a calmative agent, kynurenine (Kyn) and 3-hydroxykynurenine (3-HKyn) show neurotoxic effects, kynurenic acid (Kyna) and xanthurenic acid (XA) have neuroprotective properties like nicotinamide (NAm), while serotonin is the neurotransmitter. The study was conducted to investigate the dependence of exercise intensity, measured by plasma lactic acid (LA) concentration, on the level of Trp, its catabolites (serotonin, Kyn, 3-HKyn, Kyna and XA), and NAm in Thoroughbred horses. A total of 18 young race Thoroughbred horses were investigated during exercise tests. Blood samples for analysis were collected: at rest, 10 min after the end of the exercise, and 60 min after the end of the exercise. Plasma LA was determined by the enzymatic method, Trp, and other metabolites using liquid chromatography coupled with mass spectrometry. In horses performing intense exercise, the concentration of LA, Kyn, XA and NAm was increased, while Trp was decreased. Significant correlations were detected for exercise-induced increase in LA and 3-HKyn, XA, and NAm. Considering the scope of changes in analyzed data, there is an expected neutral effect on the health status of exercised horses.

Trimetazidine restores the positive adaptation to exercise training by mitigating statin-induced skeletal muscle injury.

BackgroundExercise rehabilitation is demonstrated to improve the prognosis of patients with coronary heart disease (CHD). Statins, as the key medicine to lower cholesterol in CHD, result in skeletal muscle injury and impair exercise training adaptation. Energy metabolism dysfunction is identified as the potential mechanism underlying statin‐induced skeletal muscle injury. In this study, we investigated the effects of the metabolic modulator trimetazidine on skeletal muscle energy metabolism and statin‐associated exercise intolerance.MethodsHigh‐fat fed apolipoprotein E knockout (ApoE−/−) mice were given aerobic exercise and administrated simvastatin, trimetazidine, or simvastatin plus trimetazidine by gavage. Exercise capacity was evaluated at the end of the treatment by hanging grid test, forelimb grip strength, and running tolerance test. Plasma glucose, lipid, and creatine kinase concentrations were measured at the end of the treatment. After sacrifice, gastrocnemii were stored for assessment of muscle morphology and fibre type. Energy metabolism was estimated by plasma lactic acid concentration, ragged red fibres, and glycogen stores. Activities of mitochondrial complex III, citrate synthase activity, and membrane potential were measured to assess mitochondrial function. Oxidative stress was also evaluated by superoxide in mitochondria, superoxide dismutase activity, and glutathione redox state.ResultsIn high‐fat fed ApoE−/− mice, exercise training had no effect on lipid concentrations. Lower lipid concentrations with increased creatine kinase were observed with additional simvastatin treatment. Exercise capacity increased significantly in response to exercise training alone but was blunted by the addition of simvastatin. Similarly, cross‐sectional area of muscle fibres and the proportion of slow‐twitch fibres increased in the exercise group but decreased in the simvastatin plus exercise group. Additionally, simvastatin increased centronucleated fibres and induced energy metabolism dysfunction by inhibiting complex III activity and thus promoted oxidative stress in gastrocnemius. We demonstrated that trimetazidine could reverse simvastatin‐induced exercise intolerance and muscle damages. We also found the ability of trimetazidine in restoration of muscle fibre hypertrophy and facilitating fast‐to‐slow type shift. The energy metabolism dysfunction and oxidative stress in gastrocnemii were rescued by trimetazidine.ConclusionsTrimetazidine alleviated statin‐related skeletal muscle injury by restoration of oxidative phenotype and increasing fibre cross‐sectional areas in response to exercise training. Correspondingly, the exercise training adaptation were improved in high‐fat fed ApoE−/− mice. Moreover, trimetazidine is able to exert its positive effects without affecting the beneficial lipid‐lowering properties of the statins. Thus, trimetazidine could be prescribed to remedy the undesirable statins‐induced exercise intolerance during cardiac rehabilitation in patients with CHD.

Qualitative analysis of platelet rich plasma prepared by acute plateletpheresis in patients undergoing heart surgery

This study was aimed to evaluate the efficiency and effectiveness of platelet-rich plasma(PRP) prepared by acute plateletpheresis in patients undergoing open heart surgery, and to analyze the quality of prepared platelet-rich plasma. Whole blood from 20 patients with ASAII-III was collected and PRP was harvested by machine after induction of anesthesia. Platelet count (Plt), mean platelet volume (MPV), platelet distribution width (PDW), plasma pH, plasma lactic acid (LA) concentration, and lactic dehydrogenase (LDH) concentration, germiculture result, CD62p and PAC-1 positive rate of inactivated and activated platelets by ADP in the whole blood before plateletpheresis (T1) , in the PRP after plateletpheresis (T2) and PRP before back-transfusion (T3) were determinated. The results showed that as compared with whole blood the platelet count in the PRP at T2 was (783 ± 184) ×10(9)/L, MPV, PDW and pH significantly decreased (P < 0.01) , while the plasma LDH, LA concentration, CD62p and PAC-1 positive rate of inactivated platelets were not significantly different from the whole blood at T1. In the PRP at T3, the platelet count, MPV, PDW and pH significantly decreased (P < 0.01) , while plasma LDH concentration, CD62p and PAC-1 positive rate of inactivated platelet significantly increased (P < 0.05 or P < 0.01) compared with the whole blood at T1. There were no significant difference among the CD62p and PAC-1 positive rate of activated platelets in the whole blood and PRP. It is concluded that PRP can be efficiently obtained from the patients undergoing open heart surgery by acute plateletpheresis, and the platelets in PRP are not activated during the preparing process. Some platelets in PRP are activated during the preserving process, but the whole activating function of platelets keeps normal.

The Effect of Furosemide on Intravascular Volume Status and Electrolytes in Patients Receiving Mannitol

Mannitol is often used during intracranial surgery to improve surgical exposure. Furosemide is often added to mannitol to augment this effect. The concern exists, however, that the augmented diuresis caused by the addition of furosemide to mannitol may cause hypovolemia and hypoperfusion, hypokalemia, and hyponatremia. We examined the intraoperative safety of low-dose furosemide (0.3 mg/kg) combined with mannitol (1 g/kg). We observed 23 patients in a double-blind, block randomized, placebo-controlled study to examine the effects of furosemide (0.3 mg/kg) when combined with mannitol (1 g/kg) on surgical brain relaxation for tumor surgery. Mannitol and the study drug (furosemide or placebo) were administered, and arterial blood gases with electrolytes (sodium, potassium, and lactic acid) and urine output volume were recorded every 30 minutes for 3 hours. Plasma sodium, potassium, and lactic acid concentrations, and interval urine outputs, were compared across time and between furosemide-placebo assignment groupings, with a P<0.01 considered significant. Although mannitol produced a large volume of diuresis (1533±335 mL), the addition of a low dose of furosemide substantially increased both the rate of production of urine for the first 90 minutes after administration and the total volume of urine produced (2561±611 mL, P<0.001, compared with placebo group). The addition of furosemide did not produce a serum potassium level below 3.8±0.7 mEq/L, a serum sodium level below 128.3±3.4 mEq/L, or a serum lactic acid level above 2.4±0.9 mmol/L. There were no differences in the plasma potassium concentration, sodium concentration, or lactic acid concentration between the drug groups at any time point. Despite an increase in urine output by as much as 67%, adding low-dose furosemide to mannitol does not seem to produce significant electrolyte derangements or hypovolemia compared with the administration of mannitol alone.

Increased plasma d-lactic acid associated with impaired memory in rats

d-Lactic acidosis is associated with memory impairment in humans. Recent research indicates that d-lactic acid may inhibit the supply of energy from astrocytes to neurons involved with memory formation. However, little is known about the effects of increased hind-gut fermentation due to changes in diet on circulating lactic acid concentrations and memory. Thirty-six male Wistar rats were fed three dietary treatments: a commercial rat and mouse chow, a soluble carbohydrate based diet or a fermentable carbohydrate based diet. The parameters estimating memory were examined by employing the object recognition test. Physical parameters of fermentation including hind-gut and plasma lactic acid concentrations were examined after sacrifice, either 3 or 21h after feeding. Increased fermentation in the hind-gut of rats, indicated by lower caecum pH, was associated with increased plasma l-lactic acid (r=-0.41, p=0.020) and d-lactic acid (r=-0.33, p=0.087). Memory, being able to discriminate between a familiar and a novel object during the object recognition test, was reduced with increasing plasma d-lactic acid (r=-0.51, p=0.021). Memory impairment was associated with alterations in plasma d-lactic acid following the fermentation of carbohydrate in the hind-gut. Further work is still required to determine whether these effects are mediated centrally or via direct connections through the enteric nervous system.

Mechanism of dichloroacetate-induced hypolactatemia in humans with or without cirrhosis

Dichloroacetate (DCA) has been used as an experimental treatment for lactic acidosis because it lowers plasma lactic acid concentration. Three potential mechanisms could underlie the hypolactatemic action of DCA, but the dominant mechanism in vivo remains unclear. This study tested whether DCA-induced hypolactatemia occurs via decreased lactate production, increased lactate clearance, or decreased rate of glycolysis in healthy humans and in patients with end-stage cirrhosis. Cirrhosis is associated with decreased hepatic pyruvate dehydrogenase (PDH) content. Six healthy volunteers and 7 cirrhotic patients received a primed, constant infusion of 1- 13C-pyruvate and 15N-alanine for 5 hours. DCA (35 mg/kg intravenously) was administered at 2 hours. Plasma isotopic enrichment was measured by gas chromatography/mass spectrometry (GC/MS), and exhaled CO 2 enrichment by isotope ratio mass spectrometry. Pyruvate and alanine production rates (Ra) were determined by isotope dilution, and pyruvate oxidation calculated as 13CO 2 production from 13C-pyruvate. Ra lactate was calculated as the difference between Ra pyruvate and its disposal by oxidation to CO 2 and conversion to alanine. Baseline plasma lactate kinetics in cirrhotic patients did not differ from controls. DCA decreased lactate concentration in both groups by approximately 53%. DCA decreased glycolysis (Ra pyruvate) by 24%, increased the fraction of pyruvate oxidized to CO 2 by 26%, and decreased pyruvate transamination to alanine by 25%. DCA also inhibited lactate production by 85%, but decreased plasma lactate clearance by 60% in both groups. DCA reduces plasma lactic acid concentration by inhibiting production, via stimulating pyruvate oxidation and inhibiting glycolysis, rather than increasing clearance. In addition, end-stage cirrhosis does not alter either the mechanism or the magnitude of the metabolic response to DCA.

Metformin-Induced Lacticacidemia in Patients with Type 2 Diabetes Mellitus

To determine whether metformin therapy can predispose patients with type 2 diabetes and normal renal function to lactic acidosis when certain conditions are present. We undertook this prospective cohort study in 110 consecutive patients (age range, 27 to 85 years) with normal serum creatinine levels (<1.5 mg/dL in men; <1.4 mg/dL in women), receiving metformin as monotherapy or in combination with sulfonylurea or insulin, who were undergoing assessment on a regular basis for diabetes care. Clinical evaluations were performed at 4- to 12-week intervals for up to 2 years. Serum electrolytes and creatinine as well as plasma lactic acid determinations were done in all patients, regardless of symptoms. The anion gap was calculated. Plasma lactic acid concentrations were normal in 47 patients (mean, 9.4 +/- 18.0 mg/dL or 1.053 +/- 0.194 mmol/L) and high in 63 patients (19.63 +/- 5.11 mg/dL or 2.208 +/- 0.569 mmol/L; P<0.001). The anion gap was increased in the high lactic acid group in comparison with the normal group (P<0.001). Comorbid conditions (for example, cardiovascular or respiratory disease) that may predispose to hypoxemia or compromise tissue perfusion were significantly more prevalent in patients in the high lactic acid group than in those with normal lactic acid values. Lacticacidemia may occur in metformin-treated patients with type 2 diabetes mellitus who have normal renal function. An increased anion gap and certain clinical symptoms may serve as clues for the presence of lacticacidemia. Progression from lacticacidemia to clinical lactic acidosis, under certain hemodynamic or respiratory adverse conditions, remains conjectural and needs further evaluation.

Attenuated cardiovascular adjustment to sustained static exercise after carbohydrate loading

We examined whether a higher plasma lactic acid (LA) concentration resulting from carbohydrate (CHO)-loading affects the cardiovascular responses to exercise through a greater activation of LA-induced metaboreflex. Before and after CHO-loading, LA concentration, mean arterial blood pressure (MAP), heart rate (HR), cardiac output (CO), rating perceived exertion (RPE), and integrated electromyogram (iEMG) of the vastus lateralis were studied during a sustained static knee extension of single legs in 16 volunteers. The CHO-loading comprised an exhaustive bout of one-legged cycling (73±3% of maximal oxygen uptake for 130–160 min) and consuming a low-CHO diet for 2–3 days and a high-CHO diet for the next 3 days. In the leg that performed the exercise (the experimental leg), the LA concentration after CHO-loading was significantly increased, but the magnitude of MAP, HR, and CO responses during static exercise was significantly decreased in parallel with a significant reduction of RPE and iEMG. In the control leg, there were no changes in the variables before and after CHO-loading. These results suggest that the increased LA concentration resulting from CHO-loading did not affect the cardiovascular adjustment to the sustained exercise. Other mechanisms related to the reduction of RPE and iEMG seem to be responsible for the attenuated cardiovascular responses observed in the experimental leg after CHO-loading.

Effects of Calcitonin Gene-Related Peptide on Hemodynamic Responses, Catecholamine Release, and Carbohydrate Metabolism during Sevoflurane Anesthesia

Calcitonin gene-related peptide (CGRP) induces vasodilation, hypotension, and tachycardia. Tachycardia induced by CGRP may be due to sympathetic activation. The volatile anesthetic sevoflurane attenuates arterial baroreflexes. We examined the hemodynamic, endocrine, and metabolic effects of CGRP infusion (4μg·kg-1) in dogs anesthetized with sevoflurane. Hemodynamic variables, plasma catecholamine, glucose and lactic acid were measured before, during, and after CGRP infusion. Anesthesia consisted of induction with pentobarbital, followed by 2.4% sevoflurane in oxygen. The decrease in mean arterial pressure induced by CGRP was due to a reduction in systemic vascular resistance associated with an increase in cardiac index, but was not accompanied by any change in heart rate. Mean pulmonary artery and pulmonary capillary wedge pressures remained unchanged during infusion but mean pulmonary artery pressure increased after infusion. Plasma norepinephrine concentrations increased, but epinephrine levels did not increase during infusion. Plasma glucose concentrations increased only during infusion, but plasma lactic acid concentrations increased throughout the observation perod. In conclusion, the current study demonstrated that the suppression in CGRP-induced tachycardia might be due to catecholamines resulting from sevoflurane-induced sympathetic suppression. These findings suggested that CGRP may be a useful vasodilator agent during sevoflurane anesthesia.

Influence of malic acid supplementation on ruminal pH, lactic acid utilization, and digestive function in steers fed high-concentrate finishing diets.

Two trials were conducted to evaluate the influence of malic acid supplementation on ruminal fermentation. In Trial 1, six Holstein steers (300 kg) with ruminal cannulas were used in a crossover design experiment to study the influence of malic acid (MA) on ruminal metabolism during glucose-induced lactic acidosis. Treatments consisted of a 77% steam-flaked barley-based finishing diet supplemented to provide 0 or 80 g/d of MA. After a 13-d dietary adjustment period, 1 kg of glucose was infused into the rumen 1 h after the morning feeding. Ruminal pH was closely associated (R2 = .70) with ruminal DL-lactate concentration. Malic acid supplementation increased (P < .01) ruminal pH 3 h after the glucose infusion. However, there were no treatment effects (P > .10) on ruminal VFA molar proportions or ruminal and plasma DL-lactate concentrations. In Trial 2, four Holstein steers (150 kg) with cannulas in the rumen and proximal duodenum were used in a crossover design experiment to evaluate the influence of MA supplementation on characteristics of digestion. Treatments consisted of an 81% steam-flaked barley-based finishing diet supplemented to provide 0 or 80 g/d of MA. There were no treatment effects (P > .10) on ruminal and total tract digestion of OM, ADF, starch, and feed N or on ruminal microbial efficiency. Malic acid supplementation increased (P < .05) ruminal pH 2 h after feeding. As with Trial 1, there were no treatment effects (P > .10) on ruminal VFA and DL-lactate concentrations. We conclude that supplementation of high-grain finishing diets with MA may be beneficial in promoting a higher ruminal pH during periods of peak acid production without detrimental effects on ruminal microbial efficiency or starch, fiber, and protein digestion. There were no detectable beneficial effects of MA supplementation on ruminal and plasma lactic acid concentrations in cattle fed high-grain diets.

Mechanisms of fatigue-induced activation of group IV muscle afferents: the roles played by lactic acid and inflammatory mediators

We already showed that group IV muscle afferents are activated during electrically-induced fatigue. The purpose of this study is to identify the mechanisms of stimulation of these muscle afferents by electrically-induced fatigue at a high (100 Hz; high frequency fatigue, HFF) or a low rate (10 Hz; low frequency fatigue, LFF) of stimulation. In 23 paralyzed and anaesthetized rabbits, group IV afferent activity from the tibialis anterior muscle was recorded before and after 3-min HFF or 5-min LFF runs eliciting the same force failure. Plasma lactic acid concentration (LA) was also measured in leg venous blood. We tested the effects of dichloroacetate (DCA), which reduces lactic acid production, and of acetylsalicylic acid (ASA), a blocker of cyclooxygenase, on fatigue-induced activation of group IV muscle afferents after HFF and LFF trials. Pretreatment by ASA or DCA did not modify HFF-induced activation of muscle afferents. On the other hand, LFF-induced response was markedly depressed by each pharmacological agent (−44% after ASA and −75% after DCA). We verified that DCA markedly lowered LA production after LFF. The present results show that the activation of group IV muscle afferents by LFF or HFF results from different mechanisms and also demonstrate the major role played by lactic acid production and, to a lesser extent, the release of inflammatory mediators in LFF-induced activation of group IV muscle afferents.

MECHANISM OF DICHLOROACETATE-INDUCED HYPOLACTATEMIA IN HUMANS WITH OR WITHOUT CIRRHOSIS

Dichloroacetate (DCA) has been used as an experimental treatment for lactic acidosis because it lowers plasma lactic acid concentration. Three potential mechanisms could underlie the hypolactatemic action of DCA, but the dominant mechanism in vivo remains unclear. This study tested whether DCA-induced hypolactatemia occurs via decreased lactate production, increased lactate clearance, or decreased rate of glycolysis in healthy humans and in patients with end-stage cirrhosis. Cirrhosis is associated with decreased hepatic pyruvate dehydrogenase (PDH) content. Six healthy volunteers and 7 cirrhotic patients received a primed, constant infusion of 1-13C-pyruvate and 15N-alanine for 5 hours. DCA (35 mg/kg intravenously) was administered at 2 hours. Plasma isotopic enrichment was measured by gas chromatography/mass spectrometry (GC/MS), and exhaled CO2 enrichment by isotope ratio mass spectrometry. Pyruvate and alanine production rates (Ra) were determined by isotope dilution, and pyruvate oxidation calculated as 13CO2 production from 13C-pyruvate. Ra lactate was calculated as the difference between Ra pyruvate and its disposal by oxidation to CO2 and conversion to alanine. Baseline plasma lactate kinetics in cirrhotic patients did not differ from controls. DCA decreased lactate concentration in both groups by approximately 53%. DCA decreased glycolysis (Ra pyruvate) by 24%, increased the fraction of pyruvate oxidized to CO2 by 26%, and decreased pyruvate transamination to alanine by 25%. DCA also inhibited lactate production by 85%, but decreased plasma lactate clearance by 60% in both groups. DCA reduces plasma lactic acid concentration by inhibiting production, via stimulating pyruvate oxidation and inhibiting glycolysis, rather than increasing clearance. In addition, end-stage cirrhosis does not alter either the mechanism or the magnitude of the metabolic response to DCA.

Effects of KRN2391-induced hypotension on the endocrine system and carbohydrate metabolism in halothane-anesthetized dogs.

The hemodynamic profiles of KRN2391-induced hypotension have been reported to be a hyperdynamic state. However, the endocrine effects of KRN2391-induced hypotension remain to be elucidated. We investigated the endocrine and metabolic effects of KRN2391-induced hypotension on the plasma concentrations of catecholamines, aldosterone, cortisol, glucose, and lactic acid and on plasma renin activity. Eight dogs were anesthetized with 087% halothane in oxygen. After a baseline period, mean arterial pressure (MAP) was lowered to 60 mmHg for 60min by the infusion of KRN2391. KRN2391-induced hypotension resulted in a 50% decrease (P<0.01) in MAP due to a 80% reduction (P<0.01) in systemic vascular resistance associated with a 224% increase (P<0.01) in cardiac index. Plasma norepinephrine concentrations increased (P<0.01) after 60 min of hypotension. Plasma epinephrine concentrations and plasma renin activity both increased (P<0.05) during the hypotensive period. Plasma aldosterone concentrations remained unchanged during the hypotensive period, but then increased (P<0.05) after termination of KRN2391. Plasma cortisol concentrations remained unchanged throughout the observation period. Plasma glucose concentrations increased (P<0.01) during the hypotensive period. Plasma lactic acid concentrations increased (P<0.01) throughout the observation period. KRN2391-induced hypotension activates the sympathetic nervous system and consequently may modulate the renin-angiotensin-aldosterone axis and carbohydrate metabolism.

Actual management: partial separation of excess lipid from plasma

We formulated a hypothesis to explain our patient's progressively worsening metabolic acidosis despite treatment for shock and hyperglycaemia. We proposed that the oxygen carrying capacity of her blood was impaired...

Adaptation to a Fat-Supplemented Diet by Cutting Horses

Summary In a crossover experiment, eight mature Quarter Horses were exercised by simulated cutting-horse training and fed either a control concentrate (C) or a 10% fat-supplemented concentrate (F) with Bermuda grass hay in a 60:40 ratio. The experiment consisted of two 28-day experimental periods with a 28-day standardization period between treatments. Digestion trials and standardized exercise tests (SET) were conducted every 7 days during experimental periods. Dietary fat had no detrimental effect on digestion of diet constituents, and all digestion coefficients were within expected ranges. Likewise, there was no significant difference in heart rates between treatments or SET days. Plasma lactic acid concentrations did not differ (P > .05) between treatments, however, there was a decline (P .05) in muscle glycogen over time when horses were fed C. On days 7, 14, and 28, muscle glycogen utilization increased (P

Lack of Heart Rate Variation Between Morning and Afternoon Exercise Testing in Coronary Artery Disease Patients

The purpose of this study was to investigate cardiovascular [heart rate (HR), blood pressures, rate-pressure product (RPP)], physiological (oxygen uptake), and metabolic (blood plasma lactic acid concentration) responses during symptom-limited graded exercise testing (SL-GXT) during early morning and late afternoon hours in an unmedicated, regularly exercising, coronary artery disease population. Subjects, males ages 41-71 yr (n = 11), underwent SL-GXT via cycle ergometry at 8:30 A.M. and 4:30 P.M. HR, systolic blood pressure, diastolic blood pressure, and RPP were evaluated at rest and at submaximal and peak work. Oxygen uptake and rate of perceived exertion were also determined at submaximal and peak power output, with blood plasma lactic acid concentration measured at peak work. Data, analyzed by the paired t test, failed to demonstrate any significant variation in HR, systolic blood pressure, diastolic blood pressure, RPP, or blood plasma lactic acid responses during exercise at the two points used. Oxygen uptake did not significantly change at any submaximal intensity. Thus SL-GXT results obtained at early morning (8:30 A.M.) and late afternoon (4:30 P.M.) are a reproducible, reliable means of prescribing exercise HR and work intensities.

Lack of heart rate variation between morning and afternoon exercise testing in coronary artery disease patients.

The purpose of this study was to investigate cardiovascular [heart rate (HR), blood pressures, rate-pressure product (RPP)], physiological (oxygen uptake), and metabolic (blood plasma lactic acid concentration) responses during symptom-limited graded exercise testing (SL-GXT) during early morning and late afternoon hours in an unmedicated, regularly exercising, coronary artery disease population. Subjects, males ages 41-71 yr (n = 11), underwent SL-GXT via cycle ergometry at 8:30 A.M. and 4:30 P.M. HR, systolic blood pressure, diastolic blood pressure, and RPP were evaluated at rest and at submaximal and peak work. Oxygen uptake and rate of perceived exertion were also determined at submaximal and peak power output, with blood plasma lactic acid concentration measured at peak work. Data, analyzed by the paired t test, failed to demonstrate any significant variation in HR, systolic blood pressure, diastolic blood pressure, RPP, or blood plasma lactic acid responses during exercise at the two points used. Oxygen uptake did not significantly change at any submaximal intensity. Thus SL-GXT results obtained at early morning (8:30 A.M.) and late afternoon (4:30 P.M.) are a reproducible, reliable means of prescribing exercise HR and work intensities.

Mechanisms of impaired exercise capacity in short duration experimental hyperthyroidism.

To investigate the mechanism of reduced exercise tolerance in hyperthyroidism, we characterized cardiovascular function and determinants of skeletal muscle metabolism in 18 healthy subjects aged 26 +/- 1 yr (mean +/- SE) before and after 2 wk of daily ingestion of 100 micrograms of triiodothyronine (T3). Resting oxygen uptake, heart rate, and cardiac output increased and heart rate and cardiac output at the same submaximal exercise intensity were higher in the hyperthyroid state (P less than 0.05). However, maximal oxygen uptake decreased after T3 administration (3.08 +/- 0.17 vs. 2.94 +/- 0.19 l/min; P less than 0.001) despite increased heart rate and cardiac output at maximal exercise (P less than 0.05). Plasma lactic acid concentration at an equivalent submaximal exercise intensity was elevated 25% (P less than 0.01) and the arteriovenous oxygen difference at maximal effort was reduced (P less than 0.05) in the hyperthyroid state. These effects were associated with a 21-37% decline in activities of oxidative (P less than 0.001) and glycolytic (P less than 0.05) enzymes in skeletal muscle and a 15% decrease in type IIA muscle fiber cross-sectional area (P less than 0.05). Lean body mass was reduced (P less than 0.001) and the rates of whole body leucine oxidation and protein breakdown were enhanced (P less than 0.05). Thus, exercise tolerance is impaired in short duration hyperthyroidism because of decreased skeletal muscle mass and oxidative capacity related to accelerated protein catabolism but cardiac pump function is not reduced.

Heat stress and thermal dehydration: lactacidemia and plasma volume regulation

This investigation was undertaken to study heat stress and dehydration effects on 1) plasma lactic acid (LA) concentration and 2) plasma LA effect on plasma volume conservation during thermal dehydration. Experiments were performed on conscious nonacclimated and heat-acclimated laboratory rats subjected to various levels of heat stress and/or dehydration (37-42 degrees C with and without drinking water). During the exposures, rectal temperature (Tre), plasma LA pyruvic acids, and hematocrit were measured. From these data, excess LA, indicative of anaerobic metabolism, was calculated. In separate experiments, transvascular protein efflux (half time of Evans blue-labeled albumin) was measured before and after plasma LA elevation, either by LA infusion or thermal dehydration. The results show that elevation of plasma LA was associated with a rise in Tre, with accelerated elevation within a Tre range of 41-42 degrees C. LA concentrations were similar for the same Tre in all experimental groups. In nonacclimated rats, this rise was accompanied by a significant rise in excess LA. In acclimated rats, only a minor rise in excess LA was observed. A positive correlation was found between plasma LA elevation and the increase in plasma protein efflux. It is concluded that there is a temperature threshold for the rise in plasma LA. In nonacclimated rats, local hypoxia may contribute to this rise. The data also suggest that, in nonacclimated rats, lactacidemia accelerates plasma protein and fluid loss, leading to circulatory failure during acute thermal dehydration.