scholarly journals Exercise-Induced Cardiac Troponin Elevations: From Underlying Mechanisms to Clinical Relevance

Circulation ◽  
2021 ◽  
Vol 144 (24) ◽  
pp. 1955-1972
Author(s):  
Vincent L. Aengevaeren ◽  
Aaron L. Baggish ◽  
Eugene H. Chung ◽  
Keith George ◽  
Øyunn Kleiven ◽  
...  
Keyword(s):  
Clinical Relevance ◽  
Release Kinetics ◽  
Future Research ◽  
Key Factors ◽  
Free Survival ◽  
Reference Limit ◽  
Underlying Mechanisms ◽  
Exercise Induced ◽  
Upper Reference Limit ◽  
Number Of Individuals

Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field.

scholarly journals The emerging role of lactate as a mediator of exercise-induced appetite suppression

2020 ◽  
Vol 319 (4) ◽  
pp. E814-E819
Author(s):  
Seth F. McCarthy ◽  
Hashim Islam ◽  
Tom J. Hazell
Keyword(s):  
Overweight And Obesity ◽  
Future Research ◽  
Ghrelin Receptor ◽  
Cellular Models ◽  
Regulatory Molecule ◽  
Blood Lactate Accumulation ◽  
Underlying Mechanisms ◽  
Exercise Induced

Lactate, a molecule originally considered metabolic waste, is now associated with a number of important physiological functions. Although the roles of lactate as a signaling molecule, fuel source, and gluconeogenic substrate have garnered significant attention in recent reviews, a relatively underexplored and emerging role of lactate is its control of energy intake (EI). To expand our understanding of the physiological roles of lactate, we present evidence from early infusion studies demonstrating the ability of lactate to suppress EI in both rodents and humans. We then discuss findings from recent human studies that have utilized exercise intensity and/or sodium bicarbonate supplementation to modulate endogenous lactate and examine its impact on appetite regulation. These studies consistently demonstrate that greater blood lactate accumulation is associated with greater suppression of the hunger hormone ghrelin and subjective appetite, thereby supporting a role of lactate in the control of EI. To stimulate future research investigating the role of lactate as an appetite-regulatory molecule, we also highlight potential underlying mechanisms explaining the appetite-suppressive effects of lactate using evidence from rodent and in vitro cellular models. Specifically, we discuss the ability of lactate to 1) inhibit the secretory function of ghrelin producing gastric cells, 2) modulate the signaling cascades that control hypothalamic neuropeptide expression/release, and 3) inhibit signaling through the ghrelin receptor in the hypothalamus. Unravelling the role of lactate as an appetite-regulatory molecule can shed important insight into the regulation of EI, thereby contributing to the development of interventions aimed at combatting overweight and obesity.

scholarly journals Cardiac Troponin T Release after Football 7 in Healthy Children and Adults

2020 ◽  
Vol 17 (3) ◽  
pp. 956 ◽  
Author(s):  
Rafel Cirer-Sastre ◽  
Alejandro Legaz-Arrese ◽  
Francisco Corbi ◽  
Isaac López-Laval ◽  
Juan José Puente-Lanzarote ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Troponin T ◽  
Football Players ◽  
Cardiac Troponin T ◽  
Healthy Children ◽  
Training Experience ◽  
Exercise Load ◽  
Reference Limit ◽  
Exercise Induced ◽  
Upper Reference Limit

The objective of this study was to compare the release of cardiac troponin T (cTnT) after a football 7 match between two cohorts of children and adult players. Thirty-six male football players (children = 24, adult = 12) played a football 7 match, and cTnT was measured before, and 3 h after exercise. Concentrations of cTnT were compared between groups and time, and correlated with participants’ characteristics, as well as internal and external exercise load. Cardiac troponin T was elevated in all participants (p < 0.001), and exceeded the upper reference limit for myocardial infarction in 25 (~70%) of them. Baseline concentrations were higher in adults (p < 0.001), but the elevation of cTnT was comparable between the groups (p = 0.37). Age (p < 0.001), body mass (p = 0.001) and height (p < 0.001), and training experience (p = 0.001) were associated to baseline cTnT values, while distance (p < 0.001), mean speed (p < 0.001), and peak (p = 0.013) and mean (p = 0.016) heart rate were associated to the elevation of cTnT. The present study suggests that a football 7 match evoked elevations of cTnT during the subsequent hours in healthy players regardless of their age. However, adults might present higher resting values of cTnT than children. In addition, results suggest that the exercise-induced elevations of cTnT might be mediated by exercise load but not participant characteristics.

Does Vitamin K Intake Influence High Phosphate Induced Vascular Pseudo-ossification: An Underappreciated Therapeutic Prospect in General Population?

2019 ◽  
Vol 20 (4) ◽  
pp. 421-430
Author(s):  
Zar Chi Thent ◽  
Gabriele R.A. Froemming ◽  
Suhaila Abd Muid
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Prolonged Exposure ◽  
Vascular Complication ◽  
Key Factors ◽  
The Matrix ◽  
Underlying Mechanisms ◽  
High Phosphate

Increasing interest in vascular pseudo-ossification has alarmed the modern atherosclerotic society. High phosphate is one of the key factors in vascular pseudo ossification, also known as vascular calcification. The active process of deposition of the phosphate crystals in vascular tissues results in arterial stiffness. High phosphate condition is mainly observed in chronic kidney disease patients. However, prolonged exposure with high phosphate enriched foods such as canned drinks, dietary foods, etc. can be considered as modifiable risk factors for vascular complication in a population regardless of chronic kidney disease. High intake of vitamin K regulates the vascular calcification by exerting its anti-calcification effect. The changes in serum phosphate and vitamin K levels in a normal individual with high phosphate intake are not well investigated. This review summarised the underlying mechanisms of high phosphate induced vascular pseudo ossification such as vascular transdifferentiation, vascular apoptosis and phosphate uptake by sodium-dependent co-transporters. Pubmed, Science Direct, Scopus, ISI Web of Knowledge and Google Scholar were searched using the terms ‘vitamin K’, ‘vascular calcification, ‘phosphate’, ‘transdifferentiation’ and ‘vascular pseudoossification’. Vitamin K certainly activates the matrix GIA protein and inhibits vascular transition and apoptosis in vascular pseudo-ossification. The present view highlighted the possible therapeutic linkage between vitamin K and the disease. Understanding the role of vitamin K will be considered as potent prophylaxis agent against the vascular disease in near future.

scholarly journals Structural and Functional Remodeling of Mitochondria in Cardiac Diseases

2021 ◽  
Vol 22 (8) ◽  
pp. 4167
Author(s):  
Xiaonan Sun ◽  
Jalen Alford ◽  
Hongyu Qiu
Keyword(s):  
Regulatory Network ◽  
Molecular Basis ◽  
Therapeutic Potential ◽  
Research Direction ◽  
Future Research ◽  
Cardiac Diseases ◽  
Functional Remodeling ◽  
Underlying Mechanisms ◽  
Mitochondrial Remodeling ◽  
Normal Cellular Function

Mitochondria undergo structural and functional remodeling to meet the cell demand in response to the intracellular and extracellular stimulations, playing an essential role in maintaining normal cellular function. Merging evidence demonstrated that dysregulation of mitochondrial remodeling is a fundamental driving force of complex human diseases, highlighting its crucial pathophysiological roles and therapeutic potential. In this review, we outlined the progress of the molecular basis of mitochondrial structural and functional remodeling and their regulatory network. In particular, we summarized the latest evidence of the fundamental association of impaired mitochondrial remodeling in developing diverse cardiac diseases and the underlying mechanisms. We also explored the therapeutic potential related to mitochondrial remodeling and future research direction. This updated information would improve our knowledge of mitochondrial biology and cardiac diseases’ pathogenesis, which would inspire new potential strategies for treating these diseases by targeting mitochondria remodeling.

scholarly journals Increased canine pancreatic lipase immunoreactivity (cPLI) and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) lipase in dogs with evidence of portal hypertension and normal pancreatic histology: a pilot study

2021 ◽  
pp. 104063872110039
Author(s):  
Gonçalo Serrano ◽  
Dominique Paepe ◽  
Tim Williams ◽  
Penny Watson
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Pilot Study ◽  
Pancreatic Lipase ◽  
Glutaric Acid ◽  
Inclusion Criteria ◽  
Reference Limit ◽  
Clinical Presentations ◽  
Upper Reference Limit

The clinical presentations of both liver disease and pancreatitis are nonspecific and overlapping, which may cause difficulty in diagnosis. In our retrospective pilot study, we assessed whether dogs with evidence of portal hypertension and absence of pancreatitis on pancreatic histology have increases in canine pancreatic lipase immunoreactivity (cPLI) and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) lipase. We included dogs that had been presented between 2008 and 2019 if they had normal pancreatic histology, histologically confirmed hepatopathy, and if canine pancreas-specific lipase (Spec cPL; Idexx) or DGGR lipase had been measured. Only dogs with portal hypertension were included. Six dogs fulfilled the inclusion criteria. Four of 6 and 2 of 6 dogs had Spec cPL and DGGR lipase exceeding the upper reference limit, respectively. From the 4 dogs with increased Spec cPL, 2 had concentrations of 200–400 µg/L and 2 had concentrations ≥ 400 µg/L. Our results suggest that canine portal hypertension might lead to increased Spec cPL and DGGR lipase values in the absence of pancreatitis on histology. Until more evidence in a larger number of dogs with portal hypertension is available, both tests should be interpreted cautiously in the presence of portal hypertension.

Clinical and analytical evaluation of kits for measurement of creatine kinase isoenzyme MB.

1986 ◽  
Vol 32 (1) ◽  
pp. 186-191 ◽  
Author(s):  
T R Koch ◽  
U J Mehta ◽  
H C Nipper
Keyword(s):  
Creatine Kinase ◽  
Clinical Performance ◽  
Reference Population ◽  
Reference Ranges ◽  
Diagnostic Specificity ◽  
Electrophoretic Method ◽  
Reference Limit ◽  
Coronary Care ◽  
Upper Reference Limit ◽  
Creatine Kinase Isoenzyme Mb

Abstract We studied the analytical and clinical performance of six methods for creatine kinase (EC 2.7.3.2) isoenzyme MB (CK-MB): three immunoassays (Behring, Hybritech, and International Immunoassay Labs); one immunoinhibition assay (Roche); one immunoinhibition/column method (Du Pont); and one electrophoretic method (Beckman). Between-day precision for all kits was poor at the upper reference limit. All methods gave results linearly related to CK-MB concentration and all were free from CK-MM, CK-BB, and adenylate kinase interference. Only the Du Pont method was adversely affected by atypical isoenzymes. For diagnosis of acute myocardial infarction in a coronary care population (n = 40; prevalence = 45%), all methods were approximately 95% efficient, when appropriate reference criteria were used. Some manufacturers fail to provide data for an appropriate (acutely ill, non-infarct) reference population; decreased diagnostic specificity may result from use of reference ranges based on results for healthy subjects. Expression of CK-MB as a percent of total CK degrades efficiency unless total CK is markedly increased.

scholarly journals PHYSIOLOGY OF SUCCESSFUL AGING: IMPLICATIONS FOR HEALTH AND WELL-BEING

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S434-S434
Author(s):  
Konstantinos Mantantzis ◽  
Denis Gerstorf ◽  
Thomas M Hess
Keyword(s):  
Older Adults ◽  
Successful Aging ◽  
Well Being ◽  
Empathic Accuracy ◽  
Future Research ◽  
Subjective Well Being ◽  
Use Of Data ◽  
Aging Study ◽  
Underlying Mechanisms ◽  
Relationship Factors

Abstract Research into peripheral physiology and its association with cognition, emotionality, and social/physical functioning has received considerable attention over the years. However, many of the underlying mechanisms are not well understood. In this symposium, we have compiled a set of four empirical projects that showcase current and future endeavors to address some of the long-standing questions about when, how, and why physiology shapes and is shaped by key psychosocial resources. Hawkley et al. make use of data from the NSHAP and HRS longitudinal studies to investigate whether social relationships such as number of friends predicts risk of diabetes among older adults. Wilson et al. use dyadic data from young and middle-aged couples to examine cardiometabolic similarity among spouses, and how such concordance is shaped by key relationship factors such as emotional closeness. Pauly et al. use data from two daily-life studies of older couples to investigate how physiological synchrony in cortisol is modulated by partner interactions, empathy, and empathic accuracy. Finally, Mantantzis et al. make use of multi-year longitudinal data from the Berlin Aging Study II to examine the role of glucose regulation capacity for trajectories of subjective well-being among older adults. Thomas Hess will discuss the importance of these papers, discuss strengths and weaknesses of the approaches chosen, and consider implications for future research.

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