Diagnostic Values of Venous Peak Lactate, Lactate-to-pyruvate Ratio, and fold Increase in Lactate from Baseline in Aerobic Exercise Tests in Patients with Mitochondrial Diseases

Background: Female who are in fertile period of their life and prefer a sedentary life style rather than performing regular physical exercise, whether light or heavy exercise show different hormonal pattern which effect their physical health. Such hormonal changes are directly related to the level of ovarian reserve of hormones which are negatively affected by lack of exercise. The ovarian pool of hormones decline with age and also lack of physical exercise. Among the large pool of biochemical markers AMH (anti-mullerian hormone) appears to be the most important and helpful indicator of ovarian reserve. Inclusion criteria: Healthy females between 25 to 35 years of age were included in the study. Exclusion criteria: Females below 25 years and above 35 years of age were excluded from the study, in addition those females having some medical problem or using some medication were also excluded from the study. Material and Methods: 20 females consented to participate in the study who were divided in two groups. These females were living a sedentary life before they joined the gymnasium. One group was subjected to light aerobic exercise and other group to heavy physical exercise. Tests before the start of study were conducted and were repeated after 08 weeks of study to observe the effect of both exercises on the ovarian reserves of different hormones. Results: The comparison between both groups were observed, the values before and after exercise has a remarkable difference, a decrease in values were observed in body weight, BMI, waist and hip ratio after exercise. Slight reduction in E2 and FSH level after aerobic exercises was observed. Whereas in heavy exercise group significant difference i.e. increase in level of FSH was observed at the same time, significant decrease in AMH level was also observed. The difference between E2 and LH had no significance in heavy exercise group. Conclusion: Those females who were living sedentary life and performed light aerobic exercise, even for a longer time period did not showed significant change in the E2, LH, FSH and AMH level of hormones. However, heavy exercise reduces the level of AMH and increases the level of FSH. These finding suggest heavy exercise may affect fertility in a negative way especially in females with low ovarian reserves. Keywords: Exercise, spinning, ovarian reserve, AMHh anti-mullerian hormone

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Effects of Antioxidant Supplementation on Exercise Performance in Acute Normobaric Hypoxia

International Journal of Sport Nutrition and Exercise Metabolism ◽

10.1123/ijsnem.2013-0118 ◽

2014 ◽

Vol 24 (2) ◽

pp. 227-235 ◽

Cited By ~ 3

Author(s):

Christian Mariacher ◽

Hannes Gatterer ◽

Joachim Greilberger ◽

Radoslav Djukic ◽

Michaela Greilberger ◽

...

Keyword(s):

Aerobic Exercise ◽

Exercise Performance ◽

Beta Carotene ◽

Cycling Performance ◽

Normobaric Hypoxia ◽

Alpha Tocopherol ◽

Maximal Heart Rate ◽

Exercise Tests ◽

Double Blind ◽

Concentrate Supplementation

Background/Objectives:To compare the effects of a 3-week supplementation between two different mixtures of antioxidants and placebo on aerobic exercise performance in acute normobaric hypoxia.Subjects/Methods:Seventeen subjects were randomly assigned in a double-blind fashion to receive a broad-based antioxidants supplement containing beta-carotene, ascorbic acid, d-alpha-tocopherol-succinate, N-acetylcysteine, riboflavin, zinc, and selenium (antioxidant capsule group [AO group]), or a combination of alpha-ketoglutaric acid (α-KG) and 5-hydroxymethylfurfural (5-HMF; CYL concentrate supplementation group [CS group]), or placebo (PL group). Before and after supplementation, subjects performed two incremental cycle-exercise tests until exhaustion. The first test was conducted under normoxic conditions (LA, FiO2 of 20.9%, ~547 m) and the second after the 3-week supplementation period under normobaric hypoxic conditions (AHA, FiO2 of 12.9%, ~4300m).Results:In CS peak cycling performance (peak power) declined from LA to AHA 7.3% (90% CI: 2.2–12.4) less compared with PL (p = .04) and 6.7% (90%CI: 3.2–10.2) less compared with AO (p = .03). Better maintenance of aerobic exercise capacity in CS was associated with an attenuated reduction in maximal heart rate in hypoxia.Conclusions:Aerobic exercise performance was less impaired in acute normobaric hypoxia after 3 weeks with supplementation of α-KG and 5-HMF compared with a broad-based antioxidants supplement or PL.

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Metabolic effects of d-glyceraldehyde in isolated hepatocytes

Biochemical Journal ◽

10.1042/bj2400771 ◽

1986 ◽

Vol 240 (3) ◽

pp. 771-776 ◽

Cited By ~ 11

Author(s):

S M Maswoswe ◽

F Daneshmand ◽

D R Davies

Keyword(s):

Fold Increase ◽

Isolated Hepatocytes ◽

High Rate ◽

Metabolic Effects ◽

Temporary Increase ◽

Dihydroxyacetone Phosphate ◽

Phosphate Content ◽

Intracellular Content ◽

Fructose 1,6 Bisphosphate ◽

Pyruvate Ratio

The effects of D-glyceraldehyde on the hepatocyte contents of various metabolites were examined and compared with the effects of fructose, glycerol and dihydroxyacetone, which all enter the glycolytic/gluconeogenic pathways at the triose phosphate level. D-Glyceraldehyde (10 MM) caused a substantial depletion of hepatocyte ATP, as did equimolar concentrations of fructose and glycerol. D-Glyceraldehyde and fructose each caused a 2-fold increase in fructose 1,6-bisphosphate and the accumulation of millimolar quantities of fructose 1-phosphate in the cells. D-Glyceraldehyde caused an increase in the glycerol 3-phosphate content and a decrease in the dihydroxyacetone phosphate content, whereas dihydroxyacetone increased the content of both metabolites. The increase in the [glycerol 3-phosphate]/[dihydroxyacetone phosphate] ratio caused by D-glyceraldehyde was not accompanied by a change in the cytoplasmic [NAD+]/[NADH] ratio, as indicated by the unchanged [lactate]/[pyruvate] ratio. The accumulation of fructose 1-phosphate from D-glyceraldehyde and dihydroxyacetone phosphate in the hepatocyte can account for the depletion of the intracellular content of the latter. Presumably ATP is depleted as the result of the accumulation of millimolar amounts of a phosphorylated intermediate, as is the case with fructose and glycerol. It is suggested that the accumulation of fructose 1-phosphate during hepatic fructose metabolism is the result of a temporary increase in the D-glyceraldehyde concentration because of the high rate of fructose phosphorylation compared with triokinase activity. The equilibrium constant of aldolase favours the formation and thus the accumulation of fructose 1-phosphate.

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A microfluidic antibody bioarray for fast detection of human interleukins in low sample volumes

Canadian Journal of Chemistry ◽

10.1139/cjc-2018-0506 ◽

2019 ◽

Vol 97 (10) ◽

pp. 737-744

Author(s):

Mahsa Gharibi ◽

Samar Haroun ◽

Jonathan C. Choy ◽

Paul C.H. Li

Keyword(s):

Method Development ◽

Physical Adsorption ◽

Fold Increase ◽

Covalent Immobilization ◽

Detection Methods ◽

Fluorescence Signal ◽

Fast Detection ◽

Promising Tool ◽

Diagnostic Values ◽

Capture Antibody

The antibody bioarray is a promising tool for the detection of proteins, which can be used as disease biomarkers. Therefore, we have developed a sandwich immunoassay-type bioarray using a microfluidic method to detect human interleukins that have diagnostic values. In the method development, we studied the effect of different factors that affect capture antibody immobilization, antibody–antigen interactions, and detection methods on the bioarray surface. The fluorescence signal obtained from different detection strategies was compared based on the signal fold-increase. This comparison showed that the use of covalent immobilization of capture antibodies, as opposed to their physical adsorption on the bioarray surface, increases the signal by 1.5 fold. Moreover, the use of protein G to achieve a better oriented immobilized capture antibody has resulted in a more than 3-fold signal enhancement.

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POS5 Gene of Saccharomyces cerevisiae Encodes a Mitochondrial NADH Kinase Required for Stability of Mitochondrial DNA

Eukaryotic Cell ◽

10.1128/ec.2.4.809-820.2003 ◽

2003 ◽

Vol 2 (4) ◽

pp. 809-820 ◽

Cited By ~ 81

Author(s):

Micheline K. Strand ◽

Gregory R. Stuart ◽

Matthew J. Longley ◽

Maria A. Graziewicz ◽

Olivia C. Dominick ◽

...

Keyword(s):

Saccharomyces Cerevisiae ◽

Mitochondrial Dna ◽

Gene Product ◽

Critical Role ◽

Mitochondrial Diseases ◽

Fold Increase ◽

Mitochondrial Targeting ◽

Nuclear Mutations ◽

Mitochondrial Dna Stability ◽

Nadh Kinase

ABSTRACT In a search for nuclear genes that affect mutagenesis of mitochondrial DNA in Saccharomyces cerevisiae, an ATP-NAD (NADH) kinase, encoded by POS5, that functions exclusively in mitochondria was identified. The POS5 gene product was overproduced in Escherichia coli and purified without a mitochondrial targeting sequence. A direct biochemical assay demonstrated that the POS5 gene product utilizes ATP to phosphorylate both NADH and NAD+, with a twofold preference for NADH. Disruption of POS5 increased minus-one frameshift mutations in mitochondrial DNA 50-fold, as measured by the arg8m reversion assay, with no increase in nuclear mutations. Also, a dramatic increase in petite colony formation and slow growth on glycerol or limited glucose were observed. POS5 was previously described as a gene required for resistance to hydrogen peroxide. Consistent with a role in the mitochondrial response to oxidative stress, a pos5 deletion exhibited a 28-fold increase in oxidative damage to mitochondrial proteins and hypersensitivity to exogenous copper. Furthermore, disruption of POS5 induced mitochondrial biogenesis as a response to mitochondrial dysfunction. Thus, the POS5 NADH kinase is required for mitochondrial DNA stability with a critical role in detoxification of reactive oxygen species. These results predict a role for NADH kinase in human mitochondrial diseases.

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Chronic Oral Lactate Supplementation Does Not Affect Lactate Disappearance from Blood after Exercise

International Journal of Sport Nutrition ◽

10.1123/ijsn.5.2.117 ◽

1995 ◽

Vol 5 (2) ◽

pp. 117-124 ◽

Cited By ~ 6

Author(s):

Fred Brouns ◽

Mikael Fogelholm ◽

Gerrit van Hall ◽

Anton Wagenmakers ◽

Wim H.M. Saris

Keyword(s):

Treatment Period ◽

Blood Lactate ◽

Potassium Salts ◽

Exercise Tests ◽

Treatment Groups ◽

Supplementation Period ◽

Peak Lactate ◽

The Given ◽

Male Subjects ◽

Sodium And Potassium

This study tested the hypothesis that a 3-week oral lactate supplementation affects postexercise blood lactate disappearance in untrained male subjects. Fifteen men were randomly assigned to either a lactate supplementation (n = 8) or a placebo (n = 7) treatment. During the treatment period they drank an oral lactate or a maltodextrin (placebo) supplement twice a day. The lactate drink contained 10 g of lactate as calcium, sodium, and potassium salts. Blood lactate concentrations were studied before, during, and immediately after three exercise tests, both pre-and posttreatment. Peak lactate values for placebo (PL) or lactate (L) treatment groups during different tests were as follows: Test 1 PL, 13.49 ± 3.71; L, 13.70 ± 1.90; Test 2 PL, 12.64 ± 2.32; L, 12.00 ± 2.23; Test 3 PL, 12.29 ± 2.92; L, 11.35 ± 1.38 and were reached 3 min postexercise. The decrease in blood lactate during the long (30- to 45-min) recovery periods amounted to @ 10 mmol/L. Blood lactate changes were highly reproducible. However, a 3-week oral lactate supplementation did not result in differences in lactate disappearance. This study does not support the hypothesis that regular oral lactate intake at rest enhances the removal of lactate during and following exercise, that is, not with the given lactate load and supplementation period.

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Association of Hemodynamic and Cerebrovascular Responses to Exercise With Symptom Severity in Adolescents and Young Adults With Concussion

Neurology ◽

10.1212/wnl.0000000000012929 ◽

2021 ◽

pp. 10.1212/WNL.0000000000012929

Author(s):

David R Howell ◽

Danielle L Hunt ◽

Stacey E Aaron ◽

Jason W Hamner ◽

William P Meehan ◽

...

Keyword(s):

Heart Rate ◽

Young Adults ◽

Aerobic Exercise ◽

Symptom Severity ◽

Adolescents And Young Adults ◽

Exercise Protocol ◽

Exercise Tests ◽

Cerebrovascular Function ◽

Symptom Exacerbation ◽

Exercise Induced

Background and Objectives:Aerobic exercise has become a useful method to assist with post-concussion management. Exercise can exacerbate concussion symptoms even when symptoms are not apparent at rest. Few studies have examined the reasons for symptom exacerbation during exercise following a concussion. We had two primary objectives. 1) To delineate cardiopulmonary and cerebrovascular responses to exercise in adolescents and young adults with a concussion and healthy controls. 2) To determine the association between cerebrovascular responses and symptom burden.Methods:We recruited participants with a recent concussion from a sport concussion clinic between 9/1/2018-2/22/2020. They were included if their concussion occurred <3 weeks before initial testing and if they were symptomatic at rest. Participants were excluded if they sustained a concussion in the past year (excluding index injury), reported history of neurological disorders, or were using medications/devices that may alter neurological function. Participants completed a progressive, symptom-limited, sub-maximal exercise protocol on a stationary bike. We assessed heart rate, blood pressure, fraction of end tidal CO2 (FETCO2) and middle cerebral artery blood flow velocity (CBF) and cerebrovascular function (vasoreactivity and autoregulation) at seated rest and during exercise.Results:We conducted 107 exercise tests (40 concussed, 37 healthy participants initially; 30 concussed at follow-up). Concussed participants were tested initially (mean=17.6±2.2 [SD] years old; 55% female; mean=12.5±4.7 days post-concussion) and again 8 weeks later (mean=73.3±9.5 days post-concussion). Control participants (mean=18.3±2.4 years; 62% female) were tested once. FETCO2 increased throughout the exercise protocol as heart rate increased, reached a plateau, and declined at higher exercise intensities. CO2 explained >25% of the variation in resting CBF (R2>0.25; p<0.01) in most (73% individuals). Within the concussion group, resting symptom severity and the heart rate at which FETCO2 reached a plateau explained ∼two-thirds of variation in exercise-induced symptom exacerbation (R2=0.65; FETCO2 β=-1.210±0.517[S.E.], p<0.05). There was a moderate, statistically significant relationship between cerebrovascular responses to CO2 at rest (cerebral vasoreactivity) and cerebrovascular responses to exercise-induced changes in FETCO2 (R2=0.13, p=0.01).Discussion:The arterial CO2 response and symptom exacerbation relationship during post-concussion aerobic exercise may be mediated by increased sensitivity of cerebral vasculature to exercise-related increase in CO2.

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Abstract 428: Shear Stress-Induced Mitochondrial Biogenesis: Implications for Salutary Effects of Aerobic Exercise on Endothelial Homeostasis

Hypertension ◽

10.1161/hyp.64.suppl_1.428 ◽

2014 ◽

Vol 64 (suppl_1) ◽

Author(s):

Ji-Seok Kim ◽

Boa Kim ◽

Hojun Lee ◽

Sunny Thakkar ◽

Dianne M Babbitt ◽

...

Keyword(s):

Endothelial Cells ◽

Shear Stress ◽

Exercise Training ◽

Aerobic Exercise ◽

Mitochondrial Biogenesis ◽

Vascular Endothelium ◽

Fold Increase ◽

Endothelial Activation ◽

Aerobic Exercise Training ◽

Antimycin A

Enhancing structural/functional integrity of mitochondria in the vascular endothelium has emerged as a novel therapeutic approach for vascular disease. Aerobic exercise stimulates mitochondrial biogenesis via a shear stress (SS)-dependent mechanism in the vasculature. However, functional consequences of SS-induced mitochondrial remodeling in the vascular endothelium remain largely unknown. The purpose of this study was to examine effects of aerobic exercise on endothelial activation/apoptosis and to elucidate the underlying mechanism. In in vivo study, twenty-one prehypertensive individuals underwent a 6-month supervised aerobic exercise training (65% HRmax, 40 min/day, 3 days/week). In in vitro study, cultured Human Umbilical Vein Endothelial Cells (HUVECs) were exposed to SS using a cone-and-plate shear apparatus. Endothelial cells (ECs) were harvested for protein analysis and cell-culture media were collected to assess endothelial microparticle (EMP) production. Antimycin A, SIRT1 siRNA and PGC-1α siRNA were used for the disruption of mitochondrial functional/structural integrity. Protein expressions were analyzed by western-blotting. EMP productions were measured by flow cytometry. Circulating levels of activated (CD62E+) and apoptotic (CD31+/CD42a-) EMPs were significantly decreased (49±6 to 20±2 and 4.0 to 2.4 events/μL, respectively p<0.01) after 6-month aerobic exercise training in prehypertensives. In ECs, laminar SS attenuated productions of activated EMPs (3.18 to 1.43 events/μL) and apoptotic EMPs (0.24 to 0.07 events/μL), which were accompanied by an increase in mitochondrial content (7.8-fold increase). SIRT1 knockdown using siRNA completely abolished the protective effect of laminar SS. Disruption of mitochondrial integrity by either antimycin A or PGC-1α siRNA provoked the activated- (1.7-fold and 2.4-fold increase, respectively) and apoptotic- statuses (2.1-fold and 1.7-fold increase, respectively) and shear stress normalized these impairments. In conclusion, aerobic exercise attenuates endothelial activation and apoptosis by SS-induced mitochondrial biogenesis. This study expands the understanding of implications of mitochondrial biogenesis in endothelial cell homeostasis.

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Distinguishing Gouty Arthritis from Calcium Pyrophosphate Disease and Other Arthritides

The Journal of Rheumatology ◽

10.3899/jrheum.140634 ◽

2014 ◽

Vol 42 (3) ◽

pp. 513-520 ◽

Cited By ~ 36

Author(s):

Christian Löffler ◽

Horst Sattler ◽

Lena Peters ◽

Uta Löffler ◽

Michael Uppenkamp ◽

...

Keyword(s):

Gouty Arthritis ◽

Diagnostic Algorithm ◽

Fold Increase ◽

Diagnostic Value ◽

Calcium Pyrophosphate ◽

Predictive Values ◽

Calcium Pyrophosphate Deposition Disease ◽

Doppler Signals ◽

Diagnostic Values ◽

Sensitivity Specificity

Objective.Differentiating gout, calcium pyrophosphate deposition disease (CPPD), and non–crystal-related inflammatory arthropathies (non-CRA) is essential but often clinically impossible. The sonographic double contour (DC) sign may have good specificity for gout in highly specialized centers, but it can be challenging to use it to distinguish gout from cartilage hyperenhancements in CPPD. We evaluated the diagnostic value of the DC sign alone and in combination with Doppler signals and uric acid (UA) levels in patients with acute arthritis.Methods.We retrospectively investigated 225 acutely inflamed joints and documented the presence of DC, Doppler hypervascularization, and serum UA (SUA) levels. All patients underwent synovial fluid (SF) analysis. Sensitivity, specificity, and positive predictive values were calculated, and correlation analyses and a binary regression model were used to investigate their diagnostic values.Results.The sensitivity of DC sign for crystalline arthritides was 85% and specificity 80%. Its specificity for gout was 64%, for CPPD 52%. In contrast to non-CRA hypervascularization, degree 2 and 3 Doppler signals were highly associated with gout and less with CPPD (p < 0.01). The combination of DC sign with hypervascularization and elevated UA levels increased specificity for gout to more than 90% and resulted in a 7-fold increase of the likelihood of diagnosis of gout (p < 0.01), but with a loss of sensitivity (42%).Conclusion.The DC sign alone is suitable for predicting crystal-related arthropathies, but it cannot reliably distinguish gout from CPPD in everyday clinical routine. Combining hypervascularization and SUA levels increases the diagnostic value, leading us to propose a diagnostic algorithm.

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