Strenuous Endurance Exercise Research Articles

The Association Between Atrial Fibrillation and Endurance Physical Activity: How Much is too Much?

Atrial fibrillation (AF) is the most common arrhythmia in middle-aged athletes. Physical exercise performed in a regular basis has been shown to be beneficial for cardiovascular health. Moderate physical exercise, aside from producing a nice, peaceful and well-being sensation, has been associated with a reduced risk of AF. However, more strenuous endurance exercise, like the one experiencing marathon runners, seems to increase the risk of AF in healthy athletes without organic heart disease. On the other hand, low physical activity was found to be a risk factor for the appearance of AF. Nevertheless, the relationship of exercise to AF is complex, influenced by the intensity and the duration of the physical activity, and seems to have a U-shaped relationship with the greatest levels of physical activity possibly increasing AF incidence. There is cumulative data associating moderate physical activity to reduced AF incidence, hence physicians should recommend moderate exercise training to patients with AF. This may not only reduce AF risk, but would also contribute to an overall cardiovascular benefit. However, since there is also important data suggesting significant increased incidence of AF in elite athletes with long-term endurance physical activity, it may be a serious concern to go to the extreme. In most things in life it is much better and wiser to be well balanced, always in equilibrium.

Ischemic Preconditioning Improves Maximal Accumulated Oxygen Uptake and Time to Exhaustion in NCAA Division I Middle‐Distance Runners

PurposeIschemic preconditioning prevents reduction in blood flow after strenuous endurance exercise, and has been shown to improve swimming, cycling and running time trial performance, particularly at vigorous exercise intensities. However, not all studies have corroborated these findings. In addition, data supporting the role of ischemic preconditioning to improve supramaximal exercise is limited, particularly in competitive elite trained athletes seeking a performance advantage. The aim of the present study was to test the hypothesis that ischemic preconditioning improves supramaximal accumulated oxygen uptake and time to exhaustion in NCAA Division I middle‐distance runners.MethodsA randomized sham‐controlled crossover study was employed in which 10 NCAA Division I middle‐distance (800 to 1600 meter) track athletes (age: 21±1 yr; VO2 max: 65±7 mlO2·kg· −1·min−1) completed three supramaximal (110% VO2max) treadmill running protocols to volitional exhaustion coupled with indirect calorimetry to assess maximal accumulated oxygen uptake at baseline, after a sham control trial (mock preconditioning), and with limb‐based ischemic preconditioning (4×5 min cycles of brachial artery ischemia/reperfusion). Accumulated oxygen demand (mlO2·kg−1), the primary outcome variable, was calculated by multiplying VO2 (mlO2·kg· −1·min−1) by duration (min) of the respective supramaximal run. Total treadmill work (kg·m) was determined by multiplying body mass (kg) × velocity (m·min−1) × %grade × time (min). Experiments were conducted in accordance with the Declaration of Helsinki for protection of human subjects.Statistical AnalysisA three‐way repeated‐measures ANOVA with adjustment for multiple comparisons was used for within‐group differences (i.e., baseline vs sham vs ischemic preconditioning) in maximal accumulated oxygen uptake.ResultsIschemic preconditioning (122±38 sec) increased (P=0.0001) time to exhaustion by 22% compared with both baseline (99±23 sec, 95% CI: 4.8–40.6, P=0.014) and sham (101±30 sec, 95% CI: 6.7–34.2, P=0.001). Effect size for these trial differences as estimated by the Partial Eta2 (0.58) were large. As a result, the maximal accumulated oxygen demand was considerably greater (P=0.001) with ischemic preconditioning. During their supramaximal run in the presence of ischemic preconditioning, athletes accumulated 132±40 mlO2·kg−1, a substantial (Partial Eta2 = 0.64) increase compared with baseline (106±28 mlO2·kg−1, P=0.006, 95% CI:7.9–42.6) and sham (110±34 mlO2·kg−1, P=0.007. 95% CI: 6.6–36.5). Likewise, total treadmill work also significantly (P=0.002) increased (from baseline: 1908±204 kg·m to 2331±303 kg·m with ischemic preconditioning). There were no statistical differences in time to exhaustion, maximal accumulated oxygen demand, or treadmill work between baseline and sham.ConclusionsLimb‐based ischemic preconditioning considerably improves anaerobic treadmill time to exhaustion and accumulated oxygen uptake in NCAA Division I middle‐distance track athletes. Additional work is needed to confirm whether these laboratory‐based performance benefits can be translated to better outcomes in real competitive track meets.Support or Funding InformationWe thank the Department of Health and Nutritional Sciences for the equipment and supplies to conduct the study.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effects of Alpha-Lactalbumin or Whey Protein Isolate on Muscle Damage, Muscle Pain, and Mood States Following Prolonged Strenuous Endurance Exercise.

This study compared the effect of alpha-lactalbumin and whey protein on muscle damage, muscle pain, and mood states during short term recovery following strenuous prolonged exercise. In a two-stage crossover counterbalanced design, 12 endurance male runners were recruited (age: 30.4 ± 2.8 year, height: 172.7 ± 5.6 cm, body mass: 66.7 ± 6.5 kg, VO2max: 58.0 ± 6.9 ml/kg−/min), ran for 90 min at 70% VO2max, and followed by a 4-h recovery. Two treatments (carbohydrate+alpha-lactalbumin, CA; carbohydrate+whey protein isolate, CW) were applied during the main trials. During the first 2-h of recovery, CHO was served at the rate of 0.66 g/kg/h and PRO at 0.34 g/kg/h every 30 min. Creatine kinase (CK), interleukin-6 (IL-6), salivary cortisol, rating of muscle pain, pressure pain threshold (PPT), and mood states were evaluated before (Pre-ex), immediately (Post-ex0), 2 h (Post-ex2h) and 4 h (Post-ex4h) after exercise. 24 h after exercise (Post-ex24h), CK and IL-6, muscle pain, and PPT were evaluated. Compared with Pre-ex, Post-ex24h CK was higher in both trials of CA (398.16 ± 41.37 vs. 184.77 ± 22.68 IU/L, P = 0.039) and CW (418.17 ± 67.86 vs. 202.41 ± 22.26 IU/L, P = 0.037). IL-6 was also higher than Pre-ex at Post-ex0 and Post-ex2h in trials of CA (Post-ex0 vs. Pre-ex0: 7.87 ± 0.74 vs. 1.69 ± 0.23, P < 0.01; Post-ex2h vs. Pre-ex0: 5.39 ± 0.88 vs. 1.69 ± 0.23, P = 0.02) and CW (Post-ex0 vs. Pre-ex0: 8.63 ± 1.06 vs. 1.59 ± 0.19, P < 0.01; Post-ex2h vs. Pre-ex0: 5.75 ± 1.33 vs. 1.59 ± 0.19, P < 0.01). No difference was found in CK and IL-6 between two trials at all time points (all P > 0.05). Compared with Pre-ex0, salivary cortisol was elevated at Post-ex0 in both trials (CA: 0.96 ± 0.13 vs. 0.41 ± 0.05 ng/ml, P < 0.01; CW: 1.15 ± 0.18 vs. 0.43 ± 0.06 ng/ml, P < 0.01) and was lower at Post-ex24h than Pre-ex in CA trial (0.17 ± 0.02 vs. 0.41 ± 0.05 ng/ml, P < 0.01). Compared with CW, PPT was higher at Post-2h in CA trial (31.55 ± 3.09 vs. 26.99 ± 2.32 N/cm2, P < 0.01). Compared with Post-ex0, feeling of fatigue was lower at Post-ex2h (P = 0.014) and Post-ex4h (P < 0.01) in CA, while it was lower at Post-ex4h (P = 0.038) in CW. Compared with CW, feeling of fatigue was marginally lower in the CA trial at Post-ex2h (P = 0.056). In conclusion, compared with the co-ingestion of CHO and whey PRO isolate, co-ingestion of CHO and alpha-lactalbumin reduced sensitivity to the muscle pain, attenuated feeling of fatigue and was more beneficial to reduce the feeling of fatigue and cortisol responses during 4-h recovery following 90-min running at 70% VO2max.

The effect of carbohydrate and protein co-ingestion on energy substrate metabolism, sense of effort, and affective responses during prolonged strenuous endurance exercise

This study examined the effect of carbohydrate (CHO) and protein (PRO) co-ingestion on energy substrate metabolism, sense of effort, and affective responses during prolonged strenuous endurance exercise. In a four-stage randomized cross-over design, 10 male endurance runners (age: 27.3±1.4yrs; height: 172.9±1.1cm, weight: 63.5±1.6kg; body fat: 9.0±1.4%; V̇O2max: 62.9±1.8ml/kg/min) ran on a treadmill at 70% of their individual V̇O2max for 90min. There were two CHO and PRO treatments (CA: CHO+alpha-lactalbumin and CW: CHO+whey PRO isolate), one CHO treatment (CC: CHO+CHO), and a placebo control (CON). On each occasion, subjects consumed 5ml/kg according to their body weight (kg) immediately before and 2ml/kg every 15min during exercise. Blood samples were collected at 0min, 30min, 60min and 90min of exercise to measure glucose, lactate, insulin, and cortisol levels. The extent of physical sensation (abdominal discomfort, leg muscle pain), the sense of effort (rating of perceive exertion, RPE), and affective responses (pleasure-displeasure, arousal) were evaluated by numeric scales before, during, and immediately after exercise. Blood glucose and insulin concentrations in the CA, CW, and CC treatments were higher than in the CON at 90min (P<0.05). Muscle pain (evaluated by a single item, 0 to 10 pain intensity scale from “no pain at all” to “extremely unbearable”) was lower following CA ingestion than CON and CW ingestion, at 75min (vs. CON and CW, 1.95±0.61 vs. 3.70±1.00 and 3.60±1.02, P<0.05) and 90min (vs. CON & CW: 2.40±0.76 vs. 4.20±0.99 and 4.05±1.1, P<0.05). RPE (evaluated by a 15-point, 6 to 20 rating scale ranging from “very, very light” to “very, very hard”) following treatment with CA was lower than with CON and CW at 90min (vs. CON and CW: 11.30±1.14 vs. 14.20±1.30 and 13.30±1.24, P<0.05). Compared with CON and CW, CA enhanced the feeling of pleasure (evaluated by feeling scale from −5, “very bad” to +5, “very good”) at 90min (vs. CON and CW, 2.20±0.67 vs. −0.30±0.94 and 0.20±0.91, P<0.05). Co-ingestion of CHO and alpha-lactalbumin protein attenuates muscle pain, and therefore alleviates the sense of effort and enhances affective responses during 90min of strenuous running at 70% V̇O2max.

Pathophysiology of atrial fibrillation in endurance athletes: an overview of recent findings.

Exercise training in general has been associated with a reduced risk of atrial fibrillation and associated morbidity among patients with this condition.[1][1]–[3][2] However, more strenuous endurance exercise (e.g., marathon running) appears to increase the risk of paroxysmal atrial fibrillation

No evidence of adverse cardiac remodeling in former elite endurance athletes

BackgroundThe impact of high exercise loads on a previously healthy heart remains controversial. We examined the consequences of decades of strenuous endurance exercise at the highest competition level on heart dimensions and volumes as well as on serum biomarkers of cardiac fibrosis/remodeling. Methods and resultsWe compared echocardiographic measurements and serum biomarkers of cardiac fibrosis/remodeling [troponin I, galectin-3, matrix metallopeptidase-2 and -9, N-terminal pro-brain natriuretic peptide, carboxy-terminal propeptide of type I procollagen, and soluble suppressor of tumorigenicity-2 (sST-2)/interleukin(IL)-1R4] in 53 male athletes [11 former professional (‘elite’) and 42 amateur-level (‘sub-elite’) cyclists or runners, aged 40–70years] and 18 aged-matched controls. A subset of 15 subjects (5 controls, 3 sub-elite and 7 elite athletes) also underwent cardiac magnetic resonance imaging (cMRI).Elite and sub-elite athletes had greater echocardiography-determined left ventricular myocardial mass indexed to body surface area than controls (113±22, 115.2±23.1 and 94.8±21g/m2, respectively, p=0.008 for group effect), with similar results for left (50.5±4.4, 48.2±4.3 and 46.4±5.2mm, p=0.008) and right (38.6±3.8, 41.1±5.5 and 34.7±4.3mm, p<0.001) ventricular end-diastolic diameter, and cMRI-determined left atrial volume indexed to body surface area (62.7±8.1, 56.4±16.0 and 39.0±14.1ml/m2, p=0.026). Two athletes showed a non-coronary pattern of small, fibrotic left ventricular patches detected by late gadolinium enhancement. No group effect was noted for biomarkers. ConclusionsRegardless of their competition level at a younger age, veteran endurance athletes showed an overall healthy, non-pathological pattern of cardiac remodeling. Nonetheless, the physiopathology of the ventricular fibrotic patches detected warrants further investigation.

Impact of high-intensity endurance exercise on regional left and right ventricular myocardial mechanics.

Strenuous endurance exercise acutely increases myocardial wall stress and evokes transient functional cardiac perturbations. However, it is unclear whether exercise-induced functional cardiac disturbances are ubiquitous throughout the myocardium or are segment specific. The aim of this study was to examine the influence of high-intensity endurance exercise on global and segmental left (LV) and right (RV) ventricular tissue deformation (strain). Echocardiography was used to measure strain in 23 active men (age: 28 ± 2 years; VO2 peak: 4.5 ± 0.7 L min-1) at rest and during a standardized low-intensity exercise challenge, before and after a 90-min high-intensity endurance cycling intervention. Following the cycling intervention, LV and RV global strain decreased at rest (LV: -18.4 ± 0.4% vs. -17.7 ± 0.4%, P < 0.05; RV: -27.6 ± 0.7% vs. -26.4 ± 0.6%, P < 0.05) and by a greater extent during the low-intensity exercise challenge (LV: -21.3 ± 0.4% vs. -19.2 ± 0.5%, P < 0.01; RV: -28.4 ± 0.8% vs. -23.5 ± 0.9%, P < 0.01). Reductions in LV strain were unique to regions of RV attachment (e.g. LV septum: -24.4 ± 0.5% vs. -21.4 ± 0.6%, P < 0.01) with lateral (-18.9 ± 0.4% vs. -18.4 ± 0.5%) and posterior segments (-19.5 ± 0.4% vs. -18.8 ± 0.7%) unaffected. Similarly, augmentation of strain from rest to exercise was abolished in the RV free wall (-1.1 ± 1.0% vs. 2.9 ± 1.2%, P < 0.01), reduced in the septum (-4.6 ± 0.4% vs. -2.4 ± 0.5%, P < 0.01), and unchanged in the lateral (-1.2 ± 0.6% vs. -0.9 ± 0.6%) and posterior walls (-1.7 ± 0.6% vs. -1.3 ± 0.7%). Changes in ventricular strain following high-intensity exercise are more profound in the right ventricle than in the left ventricle. Reductions in LV strain were unique to the septal myocardium and may reflect ventricular interactions secondary to exercise-induced RV dysfunction.

Long-term leucine supplementation aggravates prolonged strenuous exercise-induced cardiovascular changes in trained rats.

What is the central question of this study? Can long-term leucine supplementation prevent prolonged strenuous endurance exercise induced cardiac injury? What is the main finding and its importance? Prolonged endurance exercise does not seem to exceed cardiac energetic capacity, hence it does not represent an energy threat to this organ, at least in trained subjects. However, it may induce, in susceptible individuals, a state of cardiac electrical instability, which has been associated with ventricular arrhythmias and sudden cardiac death. This situation might be worsened when combined with leucine supplementation, which leads to increased blood pressure and cardiac injury. Leucine supplementation failed to prevent cardiac fatigue symptoms and may aggravate prolonged strenuous exercise-induced cardiovascular disturbances in trained rats. Observational studies have raised concerns that prolonged strenuous exercise training may be associated with increased risk of cardiac arrhythmia and even primary cardiac arrest or sudden death. It has been demonstrated that leucine can reduce prolonged exercise-induced muscle damage and accelerate the recovery process. The aim of this study was to investigate the effects of prolonged strenuous endurance exercise on cardiovascular parameters and biomarkers of cardiac injury in trained adult male rats and assess the use of leucine as an auxiliary substance to prevent the likely cardiac adverse effects caused by strenuous exercise. Twenty-four male Wistar rats were randomly allocated to receive a balanced control diet (18% protein) or a leucine-rich diet (15% protein plus 3% leucine) for 6 weeks. The rats were submitted to 1h of exercise, 5days per week for 6weeks. Three days after the training period, the rats were submitted to swimming exercise until exhaustion, and cardiac parameters were assessed. Exercising until exhaustion significantly increased cardiac biomarker levels, cytokines and glycogen content inhibited protein synthesis signalling and led to cardiac electrical disturbances. When combined with exercise, leucine supplementation led to greater increases in the aforementioned parameters and also a significant increase in blood pressure and protein degradation signalling. We report, for the first time, that leucine supplementation not only fails to prevent cardiac fatigue symptoms, but may also aggravate prolonged strenuous exercise-induced cardiovascular disturbances in trained rats. Furthermore, we find that exercising until exhaustion can cause cardiac electrical disturbances and damage cardiac myocytes.

The Effects of Exercise on Natriuretic Peptides in Individuals without Heart Failure.

Cardiac natriuretic peptides (NPs) play an important role in the regulation of energy expenditure in skeletal muscle and adipose tissue. A systematic review on the effects of exercise on NPs in patients with heart failure reported that aerobic and resistance training reduced NPs; however, the effects of exercise on NPs and the underlying mechanism of exercise-induced NP secretion in subjects without heart failure remain unknown. In athletes and young, healthy subjects, the NP concentration at rest is not elevated, but strenuous endurance exercise significantly increases NPs. The exercise-induced increase in NPs may be caused by transient myocardial wall stress, cardiomyocyte metabolic changes, or neuroendocrinological response, which may have cytoprotective and growth-regulating effects on the heart. On the other hand, in elderly, overweight/obese subjects, and patients with hypertension, NP concentrations also increase during exercise; however, NP secretion may be more susceptible to cardiac stress compared to young, healthy individuals. Recent studies have shown that NPs are associated with thermogenesis in fat tissue and oxidative capacity in skeletal muscles. NPs may also have a protective role for skeletal muscle in humans, although further studies are warranted to elucidate the physiological mechanism of exercise-induced NP secretion.

Manipulating The Exercise Intensity-duration Matrix Has A Profound Impact On Exercise-induced Functional And Biochemical Perturbations In The Human Heart.

PURPOSE: Strenuous endurance exercise stimulates transient cardiac perturbations with ambiguous health outcomes. Therefore, this study aimed to alter the magnitude and time-course of exercise-induced functional and biochemical cardiac perturbations by manipulating the exercise intensity-duration matrix. METHODS: Echocardiograph-derived left (LV) and right (RV) ventricular global longitudinal strain (GLS), and serum high-sensitivity cardiac troponin (hs-cTnI) concentration, were examined in 10 males (Age: 27 ± 4 yr; VO2peak: 4.0 ± 0.8L•min-1) before, throughout (50-, 75- & 100-%), and during recovery (1-, 3-, 6- & 24-h) from two exercise trials. The two exercise trials consisted of cycling for either 90-min above, or 120-min within, the moderate-intensity exercise domain to complete an equivalent total mechanical work. RESULTS: LVGLS decreased (p&lt0.01) during the 90-min trial only, with reductions peaking at 1-h post (pre: -19.9 ± 0.6; 1-h post: -18.5 ± 0.7%) and persisting for >24-h into recovery. RVGLS decreased (p&lt0.05) during both exercise trials with reductions in the 90-min trial peaking at 1-h post (pre: -27.5 ± 0.7%; 1-h post: -25.1 ± 0.8%) and persisting for >24-h into recovery. Serum hs-cTnI increased (p&lt0.01) during both exercise trials with concentrations peaking at 3-h post, but only exceeding cardio-healthy reference limits (14ng/L) in the 90-min trial (pre: 4.2 ± 2.4ng/L; 3-h post: 25.1 ± 7.9ng/L). CONCLUSIONS: Exercise-induced reductions in ventricular strain and increases in cardiac injury markers persist for 24 hours following exercise that is typical of day-to-day endurance exercise training; however, the magnitude and time-course of this response can be altered by manipulating the intensity-duration matrix.

Influence of exercise intensity and duration on functional and biochemical perturbations in the human heart.

Strenuous endurance exercise induces transient functional and biochemical cardiac perturbations that persist for 24-48h. The magnitude and time-course of exercise-induced reductions in ventricular function and increases in cardiac injury markers are influenced by the intensity and duration of exercise. In a human experimental model, exercise-induced reductions in ventricular strain and increases in cardiac troponin are greater, and persist for longer, when exercise is performed within the heavy- compared to moderate-intensity exercise domain, despite matching for total mechanical work. The results of the present study help us better understand the dose-response relationship between endurance exercise and acute cardiac stress/injury, a finding that has implications for the prescription of day-to-day endurance exercise regimes. Strenuous endurance exercise induces transient cardiac perturbations with ambiguous health outcomes. The present study investigated the magnitude and time-course of exercise-induced functional and biochemical cardiac perturbations by manipulating the exercise intensity-duration matrix. Echocardiograph-derived left (LV) and right (RV) ventricular global longitudinal strain (GLS), and serum high-sensitivity cardiac troponin (hs-cTnI) concentration, were examined in 10 males (age: 27±4years; V̇O2, peak : 4.0±0.8lmin(-1) ) before, throughout (50%, 75% and 100%), and during recovery (1, 3, 6 and 24h) from two exercise trials. The two exercise trials consisted of 90 and 120min of heavy- and moderate-intensity cycling, respectively, with total mechanical work matched. LVGLS decreased (P<0.01) during the 90min trial only, with reductions peaking at 1h post (pre: -19.9±0.6%; 1h post: -18.5±0.7%) and persisting for >24h into recovery. RVGLS decreased (P<0.05) during both exercise trials with reductions in the 90min trial peaking at 1h post (pre: -27.5±0.7%; 1h post: -25.1±0.8%) and persisting for >24h into recovery. Serum hs-cTnI increased (P<0.01) during both exercise trials, with concentrations peaking at 3h post but only exceeding cardio-healthy reference limits (14ngl(-1) ) in the 90min trial (pre: 4.2±2.4ngl(-1) ; 3h post: 25.1±7.9ngl(-1) ). Exercise-induced reductions in ventricular strain and increases in cardiac injury markers persist for 24h following exercise that is typical of day-to-day endurance exercise training; however, the magnitude and time-course of this response can be altered by manipulating the intensity-duration matrix.

Impact of different running distances on muscle and lymphocyte DNA damage in amateur marathon runners.

[Purpose] The aim of this study was to investigate the impact of different marathon running distances (10 km, 21 km, and 42.195 km) on muscle and lymphocyte DNA damage in amateur marathon runners. [Subjects and Methods] Thirty male amateur runners were randomly assigned to 10 km, 21 km, and 42 km groups, with 10 subjects in each group. Blood samples were collected before and after the races and on the 3rd day of recovery to examine levels of muscle damage (creatine kinase and lactate dehydrogenase) and lymphocyte DNA damage (DNA in the tail, tail length, and tail moment). [Results] Serum creatine kinase, serum lactate dehydrogenase, and tail moment were significantly higher after the races compared with before the races in all groups. In addition, the 42 km group showed significantly higher levels of creatine kinase, lactate dehydrogenase, and tail moment than the 10 km and 21 km groups after the races. [Conclusion] Strenuous endurance exercise can cause muscle and lymphocyte DNA damage, and the extent of such damage can increase as running distance increases.

Endurance Exercise and the Heart: Friend or Foe?

Although low- to moderate-intensity exercise has well-known cardiovascular benefits, it has been increasingly suggested that prolonged strenuous endurance exercise (SEE) could have potential deleterious cardiac effects. In effect, the term 'cardiac overuse injury' (or 'over-exercise') has been recently reported to group all the possible deleterious cardiac consequences of repeated exposure to SEE or 'over-exercise'. In this article, we provide a balanced overview of the current state of knowledge regarding the 'pros' and 'cons' of SEE from a cardiological point of view.

Comparative changes in plasma, urine and sweat during endurance exercise using NMR-based metabolomics

Objective: The purpose of this study was to compare the relative metabolic profile of human biofluids before, during, and after strenuous endurance exercise. Method: Urine, blood, and sweat samples were collected from eleven healthy endurance trained cyclists at the beginning of, during, and immediately after a two hour cycle ergometer ride at 65% VO2peak. The exercised-induced metabolic changes in the sampled biofluids were followed using nuclear magnetic resonance (NMR) spectra recorded on a 700 MHz NMR spectrometer. Within the biofluids, group separation was accomplished based on relative changes in the distribution of metabolites based on their concentrations using a combination of principal component analysis (PCA), partial least squares discriminant analysis (PLS-DA) and orthogonal partial least squares discriminant analysis (OPLS-DA). Specific metabolites in the NMR spectra could be identified from their characteristic peak positions.Results: Urine profiles showed significant pre- vs post-exercise differences based on relative metabolite concentration changes. The significant contributors to this difference were creatinine and acetoacetate, which increased following exercise, and glycine, citrate and alanine which decreased. The differences seen in blood plasma were almost exclusively due to the substantial changes in glucose and lactate levels. The most novel of the biofluids, sweat, interestingly showed pre-, mid-, and post- exercise differences due to significant increases in lactate and to a lesser extent, changes in pyruvate and glycerol. In several instances plasma and sweat showed contrasting metabolite concentration changes across the exercise regimen.Conclusion: The metabolic profile (metabolome) of plasma, sweat, and urine all show significant, yet differing responses to strenuous endurance exercise.

Short-term powdered tart cherry supplementation encircling an acute endurance challenge potentially increases running performance and attenuates post-race markers of inflammation

Background Consumption of tart cherry juice has been reported to increase endurance aerobic performance and attenuate perceptions of muscle soreness by reducing inflammation and oxidative stress that cause secondary muscle damage following endurance exercise. The purpose of this study was to determine if consumption of a powdered form of tart cherries derived from tart cherry skins (CherryPURE Freeze Dried Tart Cherry Powder) prior to and following strenuous endurance exercise increases performance while attenuating markers of inflammation and oxidative stress.

Protein-leucine fed dose effects on muscle protein synthesis after endurance exercise.

Protein-leucine ingestion after strenuous endurance exercise accentuates muscle protein synthesis and improves recovery of muscle performance. The objective of this study is to determine whether a low-dose protein-leucine blend ingested after endurance exercise enhances skeletal muscle myofibrillar protein fractional synthetic rate (FSR). In a crossover design, 12 trained men completed 100 min of high-intensity cycling, then ingested either 70/15/180/30 g of protein/leucine/carbohydrate/fat (15LEU), 23/5/180/30 g of 5LEU, or 0/0/274/30 g of CON beverages in randomized order in four servings during the first 90 min of a 240-min recovery period. Muscle biopsies were collected at 30 and 240 min into recovery with FSR determined by L-[ring-13C6]phenylalanine incorporation and mTORC1 pathway phosphorylation by Western blot. The 33% (90% CL, ±12%) increase in FSR with 5LEU (mean, SD: 0.080, 0.014%·h(-1)) versus CON (0.060, 0.012%·h(-1)) represented near-maximal FSR stimulation. Tripling protein-leucine dose (15LEU: 0.090, 0.11%·h(-1)) negligibly increased FSR (13%, ±12% vs 5LEU). Despite similar FSR, mTORC1(Ser2448) phosphorylation only increased with 15LEU at 30 min, whereas p70S6K(Thr389), rpS6(Ser240/244), and 4E-BP1γ(Ser112) phosphorylation increased with protein-leucine quantity at one or both time points. Plasma leucine and essential amino acid concentrations decreased during recovery in CON but increased with protein-leucine dose. Serum insulin was increased in 15LEU versus CON (60%, ±20%) but was unaffected relative to 5LEU. Regression analysis revealed p70S6K-rpS6 phosphorylation moderately predicted FSR, but the associations with plasma leucine and essential amino acids were small. Ingesting 23 g of protein with 5 g of added leucine achieved near-maximal FSR after endurance exercise, an effect unlikely attributable to mTORC1-S6K-rpS6 signaling, insulin, or amino acids. Translating the effects of protein-leucine quantity on protein synthesis to optimizing adaptation and performance requires further research.

Atrial fibrillation and the athletic heart.

Endurance exercise, despite a plethora of proven health benefits, is increasingly recognized as a potential cause of lone atrial fibrillation. Moderate exercise reduces all-cause mortality and protects against developing atrial fibrillation. However, more intense exercise regimes confer modest incremental health benefits, induce cardiac remodelling and negate some of the cardiovascular benefits of exercise. The implications of endurance exercise and athletic heart are becoming increasingly relevant as the popularity of endurance exercise has increased 20-fold within a generation. An apparent dose-response relationship exists between endurance exercise and left atrial dilatation. Repeated strenuous endurance exercise overloads atria, resulting in stretch-induced 'microtears', inflammation and endocardial scarring. Although these findings are observational in humans, similar mechanisms have recently been confirmed in animal models suggesting causation. Currently, it is not known whether a ceiling for endurance exercise exists, and, if so, what factors determine the threshold of harm. Although preliminary research is promising, much work remains if we are to understand the mechanisms underpinning atrial fibrillation in athletes.

Strenuous endurance exercise and right ventricular systolic function: No evidence of long-term sequelae

a Faculty of Medicine, Department of Physiology, University of Valencia, Valencia, Spain b Fundacion de Investigacion del Hospital Clinico Universitario Valencia (FIHCUV-INCLIVA), Valencia, Spain c Faculty of Health and Sport Science, University of Zaragoza, Huesca, Spain d Hospital Universitario 12 de Octubre, Research Institute (i + 12), Madrid, Spain e HospitalUniversitario Miguel Servet, Zaragoza, Spain f Cardiology Service, Hospital Universitario Miguel Servet, Zaragoza, Spain g European University of Madrid, Madrid, Spain h Faculty of Medicine, Physical Education and Sports Section, University of Zaragoza, Zaragoza, Spain

Effects of mRNA, Protein Expression and Activity for Myocardial SOD2 by a Single Bout of or Long-Term Strenuous Endurance Exercise in Rats

Objective: To explore the effects of myocardial SOD2 by strenuous endurance exercise. Methods: 27 grown male SD rats were randomly divided into control group (C), a single bout of strenuous endurance exercise group (E1) and seventh-week strenuous endurance exercise group (E2). Real-time PCR was used to observe the changes of mRNA expression for myocardial SOD2. Western bolt was used to observe the changes of SOD2 protein expression. In addition, SOD2, T-SOD and SOD1 activity changes were observed. Results: Myocardial SOD2 expression level at mRNA and protein of Group E1, E2 was significantly higher than that in group C, and SOD2 and T-SOD activity in group E2 were significantly higher than those in group C. Those changes were more obvious in group E2. Conclusions: Strenuous endurance exercise can improve level of myocardial SOD2 expression at mRNA and protein, and enhance the activity for SOD2, thus increasing the activity for T-SOD. Effect of long-term strenuous endurance exercise was better than a single bout of one.

Endurance Exercise Diverts the Balance between Th17 Cells and Regulatory T Cells

Endurance, marathon-type exertion is known to induce adverse changes in the immune system. Increased airway hyper-responsiveness and airway inflammation are well documented in endurance athletes and endurance exercise is considered a major risk factor for asthma in elite athletes. Yet, the mechanisms underlying this phenomenon are still to be deduced. We studied the effect of strenuous endurance exercise (marathon and half-ironman triathlon) on CD4+ lymphocyte sub-populations and on the balance between effector and regulatory CD4+ lymphocytes in the peripheral blood of trained athletes, Endurance exercise induced a significant increase in Th17 cells and a sustained decrease in peripheral blood regulatory T cells (Tregs). While interleukin (IL)-2 levels remained undetectable, post-race serum IL-6 and transforming growth factor (TGF) β levels were significantly elevated. Treg levels in sedentary controls' decreased in vitro after incubation with athletes' post-exercise serum, an effect that was attenuated by supplements of IL-2 or anti IL-6 neutralizing antibodies. Our data suggest that exercise-induced changes in serum cytokine levels promote alterations in Tregs and Th17 cell populations, which may divert the subtle balance in the immune system towards inflammation. This may explain allergic and autoimmune phenomena previously reported in endurance athletes and contribute to our understanding of exercise-related asthma.