Long-term Intensive Exercise Research Articles

Do athletic ECG changes predict athletic performance in Gurkha recruits?

IntroductionECG changes are associated with regular long-term intensive exercise due to electrical manifestations of increased vagal tone, increased ventricular wall thickness and enlarged chamber size. The aim of this study...

Wnt1 gene expression in the heart left ventricle as a response to the various durations of the intensive exercise: An experimental study.

Objective. Myocardial fibrosis is a devastating condition causing millions of deaths yearly. Several factors, such as aging, cause myocardial fibrosis. The Wnt/β-catenin pathway is one of the critical intracellular signaling for the development of cardiac fibrosis. Molecular and cellular mechanism of myocardial fibrosis induced by intensive exercise is not well-understood. The current study evaluates the effects of short- and long-term intensive exercise on the Wnt1 gene expression in a heart left ventricle in an animal model. Methods. Twenty-one male Wistar rats (mean weight 250±50 g) were divided into three groups (n=7): 1) control group (C); 2) short-term regular intensive exercise group (S-RIE, high-intensity exercise for one month six days weekly for 60 min with speed of 35 m/min), and 3) long-term regular intensive exercise group (L-RIE, high-intensity exercise for six months six days daily for 60 min with speed of 35 m/min). The heart left ventricle was isolated at the end of the experiment, and the relative gene expression of the Wnt1 gene was measured by the Real-Time PCR. Results. The L-RIE group showed a significant increase in the Wnt1 expression compared to the S-RIE and the control group. Although no difference was observed in the Wnt1 mRNA level in the S-RIE group compared to the control group, Wnt1 mRNA level increased in the L-RIE group compared to the S-RIE group. Conclusion. The exercise duration was of a great importance in the Wnt1 gene expression. Regular intensive exercise may be involved in the formation of the myocardial fibrosis by increasing the expression of the Wnt1 gene.

Relationship between Nutritional Status, Anthropometric Measurements and Dietary Inflammatory Index in Professional Football Players

Objective: This study was carried out to evaluate the relationship between the nutritional status, anthropometric measurements and dietary inflammatory index (DII) of professional football players exposed to long-term intense exercise.
 Method: Twenty-one professional male football players with a mean age of 26.00±5.69 years playing in the same club participated in the study. The nutritional status of the football players was evaluated with 3-day food consumption record (2 days of training and 1 match day). DII scores were calculated using data on 34 nutrient/nutritional ingredients obtained from the food consumption records. Body fat percentage in the anthropometric evaluations were determined by caliper and skinfold thicknesses.
 Results: The median DII scores of the football players were found as – 3.42 (-9.95 – 0.95), and their nutritional intake were found to be antiinflammatory. When the relationship between the DII scores of the football players and their anthropometric measurements was examined, a positive and significant correlation (R: .476; p: .029) was found between their DII score and their abdominal adiposity. However, there was no significant correlation (p> .05) between the DII scores and the other anthropometric measurements. In addition, there was a significant negative correlation (R: – .468; p: .032) between fiber consumption and abdominal adiposity, and a significant positive correlation between carbohydrate and fat consumption and body weight (respectively R= .730 p= .000; R= .526 p= .014).
 Conclusion: It has been revealed that the football players participating in our study generally have an anti-inflammatory diet. It was also found that abdominal adiposity was higher in the football players with high DII scores.

Long-term intensive endurance exercise training is associated to reduced markers of cellular senescence in the colon mucosa of older adults

Regular endurance exercise training is an effective intervention for the maintenance of metabolic health and the prevention of many age-associated chronic diseases. Several metabolic and inflammatory factors are involved in the health-promoting effects of exercise training, but regulatory mechanisms remain poorly understood. Cellular senescence—a state of irreversible growth arrest—is considered a basic mechanism of aging. Senescent cells accumulate over time and promote a variety of age-related pathologies from neurodegenerative disorders to cancer. Whether long-term intensive exercise training affect the accumulation of age-associated cellular senescence is still unclear. Here, we show that the classical senescence markers p16 and IL-6 were markedly higher in the colon mucosa of middle-aged and older overweight adults than in young sedentary individuals, but this upregulation was significantly blunted in age-matched endurance runners. Interestingly, we observe a linear correlation between the level of p16 and the triglycerides to HDL ratio, a marker of colon adenoma risk and cardiometabolic dysfunction. Our data suggest that chronic high-volume high-intensity endurance exercise can play a role in preventing the accumulation of senescent cells in cancer-prone tissues like colon mucosa with age. Future studies are warranted to elucidate if other tissues are also affected, and what are the molecular and cellular mechanisms that mediate the senopreventative effects of different forms of exercise training.

Absence of cardiac damage induced by long-term intensive endurance exercise training: A cardiac magnetic resonance and exercise echocardiography analysis in masters athletes

ObjectivesIt is under debate whether the long-term practice of intensive endurance exercise induces chronic cardiac damage such as myocardial fibrosis and ventricle contractile dysfunction. Multimodality analysis was performed to evaluate myocardial damage induced by long term intensive endurance training in master athletes. MethodsThirty-three asymptomatic endurance master athletes (47 ± 6 year-old, 9,6 ± 1,7 h training/week for 26 ± 6 years), were compared to 18 sedentary controls (49 ± 7 year-old). They underwent a CMR protocol including 4 chambers morphological and late gadolinium-enhancement (LGE) analysis, left (LV) and right ventricular (RV) T1 mapping and calculation of cardiac extracellular volume (ECV). A maximal exercise echocardiography with left and right ventricular longitudinal global strain (LGS) analysis was performed. Cardiac biomarkers of fibrosis (high sensitive cardiac Troponin T, N-Terminal pro brain natriuretic peptide, N-terminal propeptide of procollagen type I and N-terminal propeptide of procollagen type III) were analysed. ResultsAthletes had larger left and right atrial volume, LV and RV end diastolic volume and increased LV and RV mass compared to controls. LGE was not found in athletes. Native T1 values of LV and RV were not significantly different in athletes compared with controls. ECV was normal in both groups (21,5%± 1,6% [18.3 – 23%] in athletes, 22%± 2,2% [18.5 – 27%] in controls). LV and RV peak exercise LGS values were higher in athletes. Cardiac biomarkers levels were normal. ConclusionDespite significant physiological cardiac remodelling, consistent with previous descriptions of athlete's heart, there was no evidence of myocardial fibrosis or exercise left or right ventricular dysfunction or cardiac fibrosis in endurance athletes. Our results are not supporting the hypothesis of deleterious cardiac effects induced by long term and intensive endurance exercise training.

Assessment of left ventricular systolic function by non-invasive pressure-strain loop area in young male strength athletes

BackgroundThe health of athletes has been recognized as a worldwide public concern with more reported sudden cardiac deaths (SCD). Therefore, early detection of abnormal heart function in athletes can help reduce the risk of exercise. A novel valid non-invasive method to evaluate left ventricular (LV) myocardial work (MW) using LV pressure-strain loop (PSL), was used in this paper to explore LV systolic function in young male strength athletes.MethodsThirty-six professional young male strength athletes (the athlete group) and 32 healthy, age-matched young men (the control group) were involved in the study. The LVMW parameters were calculated as the area of PSL by two-dimensional speckle tracking echocardiography (2D-STE) and peak systolic LV pressure. The differences between two groups of data and the predictive efficacy of MW parameters for LV systolic function were analyzed.ResultsThe athlete group had significantly higher values of global wasted myocardial work (GWW) and peak strain dispersion (PSD) than did the control group (P<0.05). Global myocardial work index (GWI), global constructive myocardial work (GCW) and global longitudinal strain (GLS) were lower in the athlete group than that in the control group, although statistical significance was not reached (P>0.05). Due to the proportion of GWW and GCW, statistically significant reduction was found in global myocardial work efficiency (GWE) in the athlete group. Conventional echocardiography parameters were well correlated with GWW and GWE (P<0.05). The best predictor of LV myocardial contractile performance in the athletes using receiver operating characteristic curve (ROC) was GWE, with the area under ROC (AUC) of 0.733, sensitivity of 83.3% and specificity of 59.4%.ConclusionsSubclinical changes have appeared in the hearts of young male strength athletes after long-term intensive exercise and LVMW parameters by PSL play an important role in the evaluation of athlete’s LV contractile performance.

Moxibustion at CV 8 alleviates the myocardial inflammatory response in rats with long-term exercise-induced fatigue through inhibition of the p38 MAPK/NF-κβ signaling pathway

Pathological cardiac remodeling is an important cause of sudden cardiac death and other cardiovascular diseases in athletes. Unfortunately, people involved in long-term intense endurance exercise (especially professional athletes) do not fully understand the cause and health risks of pathological cardiac remodeling, resulting in pathological cardiac remodeling developing into irreversible damage, which seriously affects sports careers and the postretirement life of athletes. Studies have shown that myocardial inflammation caused by long-term and repeated high-intensity exercise is a prerequisite for inducing pathological remodeling and that effective inhibition of inflammation can block or reverse the pathological process of pathological remodeling. This preliminary study showed that moxibustion at CV 8 inhibited the p38 mitogen-activated protein kinases/nuclear factor-κβ (p38 MAPK/NF-κβ) signaling pathway in myocardium, reduced the expression of cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), and tumor necrosis factor(TNF-α), significantly improved myocardial morphology and function in rats under going long-term and repeated high-intensity exercise, and effectively prevented pathological cardiac remodeling. Moxibustion at CV 8 provides a new physical therapy and experimental basis for the treatment of pathological cardiac remodeling in clinical practice.

Long-Term Intense Exercise Training in Becker Muscular Dystrophy

Long-Term Intense Exercise Training in Becker Muscular Dystrophy

Long-term Intense Exercise Training in Becker Muscular Dystrophy: Three-year follow-up

Long-term Intense Exercise Training in Becker Muscular Dystrophy: Three-year follow-up

Long-term intense exercise training in becker muscular dystrophy: 3-year follow-up

Long-term intense exercise training in becker muscular dystrophy: 3-year follow-up

732-P: Insulin Sensitivity Nonresponders after Long-Term Intensive Exercise Training Are Characterized by Perturbed Amino Acid Metabolism and Mitochondrial Dysfunction

Exercise may effectively improve insulin sensitivity, although some individuals do not reap this benefit. Yet, mechanisms underlying variations in training-improved insulin sensitivity remain unknown. We investigated men with or without dysglycemia subjected to 12 w of high-intensity endurance and strength exercise, and classified them as nonresponders (n=5) or responders (n=21) based on glucose infusion rate (GIR) from euglycemic hyperinsulinemic clamping. We explored variables related to variation in training-improved GIR. VO2max, muscle strength, fat depots, adipose tissue (AT) and skeletal muscle (SkM) lipidomics, mRNA sequencing, and blood amino acid profiles were evaluated pre- and post-training. By design, nonresponders did not improve their GIR, whereas responders exhibited a pronounced increase (42%). There was no difference in attendance to training sessions between the groups, or any correlation between attendance rate and training-improved GIR. Both groups improved VO2max, leg press, pull down and chest press strength, but responders increased significantly more in VO2max and chest press strength. Nonresponders exhibited higher baseline plasma concentrations of leucine, isoleucine, valine, homocysteine and cysteine, more intraperitoneal AT and impaired insulin signaling, branched-chain amino acids and methionine and cysteine metabolism in AT, and higher SkM triacylglycerol, free fatty acids and cholesterol levels and impaired SkM oxidative phosphorylation, branched-chain amino acids degradation and tricarboxylic acid cycle. Failing to improve insulin sensitivity after long-term intensive training may relate to perturbed amino acids metabolism and mitochondrial dysfunction. Initial plasma levels of branched-chain and sulphur amino acids may determine individuals not obtaining glucometabolic improvements after training. Disclosure S. Lee: None. H.L. Gulseth: Consultant; Self; Novo Nordisk A/S. Speaker’s Bureau; Self; Merck Sharp &amp; Dohme Corp., Sanofi-Aventis. C.A. Drevon: Board Member; Self; Vitas AS. Consultant; Self; Vitas AS. K.I. Birkeland: Research Support; Self; AstraZeneca, Boehringer Ingelheim International GmbH, Lifecare, Inc., Merck Sharp &amp; Dohme Corp., Roche Diabetes Care. Other Relationship; Self; Norwegian Diabetes Association.

Exercise-induced shift in right ventricular contraction pattern: novel marker of athlete's heart?

Data about the functional adaptation of the right ventricle (RV) to intense exercise are limited. Our aim was to characterize the RV mechanical pattern in top-level athletes using three-dimensional echocardiography. A total of 60 elite water polo athletes (19 ± 4 yr, 17 ± 6 h of training/wk, 50% women and 50% men) and 40 healthy sedentary control subjects were enrolled. We measured the RV end-diastolic volume index (RVEDVi) and ejection fraction (RVEF) using dedicated software. Furthermore, we determined RV global longitudinal (RV GLS) and circumferential strain (RV GCS) and the relative contribution of longitudinal ejection fraction (LEF) and radial ejection fraction (REF) to RVEF using the ReVISION method. Athletes also underwent cardiopulmonary exercise testing [O2 consumption (V̇o2)/kg]. Athletes had significantly higher RVEDVi compared with control subjects (athletes vs. control subjects, 88 ± 11 vs. 65 ± 10 ml/m2, P < 0.001); however, they also demonstrated lower RVEF (56 ± 4% vs. 61 ± 5%, P < 0.001). RV GLS was comparable between the two groups (-22 ± 5% vs. -23 ± 5%, P = 0.24), whereas RV GCS was significantly lower in athletes (-21 ± 4% vs. -26 ± 7%, P < 0.001). Athletes had higher LEF and lower REF contribution to RVEF (LEF/RVEF: 0.50 ± 0.07 vs. 0.42 ± 0.07, P < 0.001; REF/RVEF: 0.33 ± 0.08 vs. 0.45 ± 0.08, P < 0.001). Moreover, the pattern of RV functional shift correlated with V̇o2/kg (LEF/RVEF: r = 0.30, P < 0.05; REF/RVEF: r = -0.27, P < 0.05). RV mechanical adaptation to long-term intense exercise implies a functional shift; the relative contribution of longitudinal motion to global function was increased, whereas the radial shortening was significantly decreased, in athletes. Moreover, this functional pattern correlates with aerobic exercise performance, representing a potential new resting marker of an athlete's heart. NEW & NOTEWORTHY Intensive regular physical exercise results in significant changes of right ventricular morphology and function. By separate quantification of the right ventricular longitudinal and radial function, a relative dominance of longitudinal motion and a decrease in radial motion can be observed compared with sedentary controls. Moreover, this contraction pattern correlates with cardiopulmonary fitness. According to these results, this functional shift of the right ventricle may represent a novel marker of an athlete's heart.

Exercise induced Right Ventricular Fibrosis is Associated with Myocardial Damage and Inflammation.

Background and ObjectivesIntense exercise (IE) induced myocardial fibrosis (MF) showed contradictory findings in human studies, making the relationship between IE and the development of MF unclear. This study aims to demonstrate exercise induced MF is associated with cardiac damage, and inflammation is essential to the development of exercise induced MF.MethodsSprague-Dawley rats were submitted to daily 60-minutes treadmill exercise sessions at vigorous or moderate intensity, with 8-, 12-, and 16-week durations; time-matched sedentary rats served as controls. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum cardiac troponin I (cTnI) concentration. After completion of the exercise protocol rats were euthanized. Biventricular morphology, ultrastructure, and collagen deposition were then examined. Protein expression of interleukin (IL)-1β and monocyte chemotactic protein (MCP)-1 was evaluated in both ventricles.ResultsAfter IE, right but not left ventricle (LV) MF occurred. Serum cTnI levels increased and right ventricular damage was observed at the ultrastructure level in rats that were subjected to long-term IE. Leukocyte infiltration into the right ventricle (RV) rather than LV was observed after long-term IE. Long-term IE also increased protein expression of pro-inflammation factors including IL-1β and MCP-1 in the RV.ConclusionsRight ventricular damage induced by long-term IE is pathological and the following inflammatory response is essential to the development of exercise induced MF.

Proteomics analysis of intensive exercise-induced disorders of gametogenesis in the testis using isobaric tags for relative and absolute quantification (iTRAQ) analysis.

In the present study we screened a panel of regulatory proteins associated with gametogenesis disorders in the testis that are induced by intensive exercise. Four-week-old Sprague-Dawley male rats were randomly divided into three groups: a control group, a no-load exercise group and an intensive exercise group. Rats in the control group were free to move in their cage. Rats in the no-load exercise and intensive exercise groups swam for 60minday-1, six times each week, for a total 9-week exercise regimen; rats in the intensive exercise group swam with a load of 6% body mass. After the last exercise session (or at the end of the 9-week period), a sperm count, reproductive hormone assays, histological analysis of the testis and proteomics analysis were performed for each rat. Mean (±s.d.) sperm concentration was significantly lower in the intensive exercise group than in the control and no-load exercise groups (1.36±0.63 vs 2.12±0.53 and 2.57±0.48×106 spermatozoa mL-1 respectively; P<0.05). Serum testosterone concentrations were also significantly lower in the intensive exercise group (P<0.01), whereas gonadotrophin-releasing hormone, LH and FSH concentrations were slightly decreased in the intensive exercise group, but not significantly (P>0.05). Histological analysis showed that the number of spermatogenic cells in the seminiferous tubules was lower in the intensive exercise group than in the control and no-load exercise groups. Proteomics analysis identified 54 proteins that were differentially expressed between the control and intensive exercise groups (31 downregulated, 23 upregulated). Pathway enrichment analysis showed that ribosome and extracellular matrix-receptor interaction pathways play an important role in the signal transduction of testicular gametogenic disorders. Four differentially expressed proteins that were involved in the regulation of reproduction were identified by bioinformatics analysis and validated by targeted mass spectrometry analysis, namely vimentin, collagen α-1(I) chain, fatty acid-binding protein 9 and 40S ribosomal protein S3a. The data suggest that changes in the abundance of differentially expressed proteins after long-term intensive exercise affect the cycle and progression of spermatogenesis, resulting in spermatogenic disorders.

Long-term Intensive Exercise Induced Atrial Fibrosis Is Associated With Tgf-β1-Mir-21 Signaling Pathway

Long-term Intensive Exercise Induced Atrial Fibrosis Is Associated With Tgf-β1-Mir-21 Signaling Pathway

Does long-term intensive diet and exercise reduce the biomechanical burden in overweight and obese adults with knee osteoarthritis? the intensive diet and exercise for arthritis (idea) trial

Does long-term intensive diet and exercise reduce the biomechanical burden in overweight and obese adults with knee osteoarthritis? the intensive diet and exercise for arthritis (idea) trial

The Impaired Function of Macrophages Induced by Strenuous Exercise Could Not Be Ameliorated by BCAA Supplementation.

The aim of this study was to evaluate the effect of strenuous exercise on the functions of peritoneal macrophages in rats and to test the hypothesis that branched-chain amino acid (BCAA) supplementation will be beneficial to the macrophages of rats from strenuous exercise. Forty male Wistar rats were randomly divided into five groups: (C) Control, E) Exercise, (E1) Exercise with one week to recover, (ES) Exercise + Supplementation and (ES1) Exercise + Supplementation with 1 week to recover. All rats except those of the sedentary control were subjected to four weeks of strenuous exercise. Blood hemoglobin, serum testosterone and BCAA levels were tested. Peritoneal macrophages functions were also determined at the same time. The data showed that hemoglobin, testosterone, BCAA levels, and body weight in group E decreased significantly as compared with that of group C. Meanwhile, phagocytosis capacity (decreased by 17.07%, p = 0.031), reactive oxygen species (ROS) production (decreased by 26%, p = 0.003) and MHC II mRNA (decreased by 22%, p = 0.041) of macrophages decreased in the strenuous exercise group as compared with group C. However, the chemotaxis of macrophages did not change significantly. In addition, BCAA supplementation could slightly increase the serum BCAA levels of rats from strenuous exercise (increased by 6.70%, p > 0.05). Moreover, the body weight, the blood hemoglobin, the serum testosterone and the function of peritoneal macrophages in group ES did not change significantly as compared with group E. These results suggest that long-term intensive exercise impairs the function of macrophages, which is essential for microbicidal capability. This may represent a novel mechanism of immunosuppression induced by strenuous exercise. Moreover, the impaired function of macrophage induced by strenuous exercise could not be ameliorated by BCAA supplementation in the dosing and timing used for this study.

Right heart structural and functional remodeling in athletes.

Long-term intensive exercise training programs lead to numerous progressive cardiac adaptations, which are collectively termed "athlete's heart." Noninvasive diagnostic techniques, such as color Doppler echocardiography, have been widely used in the analysis of the athlete's heart. Initial experiences focused mainly on left heart adaptations to training. However, in recent years, substantial structural and functional adaptations of the right heart have been documented. The present review article focuses on recent data defining right heart adaptation to short- and long-term periods of exercise training. Right ventricular (RV) morphology and function may be more profoundly affected by intense exercise and, in some cases, functional recovery may be incomplete. Moreover, there is speculation that such changes may represent a substrate for proarrhythmic RV remodeling in some highly trained athletes, even in the absence of a known familial redisposition.

Changes in joint loads, leptin, and MMP-3 subsequent to long-term intensive weight loss and exercise: secondary outcomes from the intensive diet and exercise for arthritis randomized clinical trial

Changes in joint loads, leptin, and MMP-3 subsequent to long-term intensive weight loss and exercise: secondary outcomes from the intensive diet and exercise for arthritis randomized clinical trial

Losartan Prevents Heart Fibrosis Induced by Long-Term Intensive Exercise in an Animal Model

RationaleRecently it has been shown that long-term intensive exercise practice is able to induce myocardial fibrosis in an animal model. Angiotensin II is a profibrotic hormone that could be involved in the cardiac remodeling resulting from endurance exercise.ObjectiveThis study examined the antifibrotic effect of losartan, an angiotensin II type 1 receptor antagonist, in an animal model of heart fibrosis induced by long-term intense exercise.Methods and ResultsMale Wistar rats were randomly distributed into 4 experimental groups: Exercise, Exercise plus losartan, Sedentary and Sedentary plus losartan. Exercise groups were conditioned to run vigorously for 16 weeks. Losartan was orally administered daily before each training session (50 mg/kg/day). Time-matched sedentary rats served as controls. After euthanasia, heart hypertrophy was evaluated by histological studies; ventricular collagen deposition was quantified by histological and biochemical studies; and messenger RNA and protein expression of transforming growth factor-β1, fibronectin-1, matrix metalloproteinase-2, tissue inhibitor of metalloproteinase-1, procollagen-I and procollagen-III was evaluated in all 4 cardiac chambers. Daily intensive exercise caused hypertrophy in the left ventricular heart wall and originated collagen deposition in the right ventricle. Additionally long-term intensive exercise induced a significant increase in messenger RNA expression and protein synthesis of the major fibrotic markers in both atria and in the right ventricle. Losartan treatment was able to reduce all increases in messenger RNA expression and protein levels caused by exercise, although it could not completely reverse the heart hypertrophy.ConclusionsLosartan treatment prevents the heart fibrosis induced by endurance exercise in training animals.