Running Capacity Research Articles

Atrial Myocyte Function and Ca2+ Handling Is Associated with Inborn Aerobic Capacity

BackgroundAlthough high aerobic capacity is associated with effective cardiac function, the effect of aerobic capacity on atrial function, especially in terms of cellular mechanisms, is not known. We aimed to investigate whether rats with low inborn maximal oxygen uptake (VO2 max) had impaired atrial myocyte contractile function when compared to rats with high inborn VO2 max.Methods and ResultsAtrial myocyte function was depressed in Low Capacity Runners (LCR) relative to High Capacity Runners (HCR) which was associated with impaired Ca2+ handling. Fractional shortening was 52% lower at 2 Hz and 60% lower at 5 Hz stimulation while time to 50% relengthening was 43% prolonged and 55% prolonged, respectively. Differences in Ca2+ amplitude and diastolic Ca2+ level were observed at 5 Hz stimulation where Ca2+ amplitude was 70% lower and diastolic Ca2+ level was 11% higher in LCR rats. Prolonged time to 50% Ca2+ decay was associated with reduced sarcoplasmic reticulum (SR) Ca2+ ATPase function in LCR (39%). Na+/Ca2+ exchanger activity was comparable between the groups. Diastolic SR Ca2+ leak was increased by 109%. This could be partly explained by increased ryanodine receptors phosphorylation at the Ca2+-calmodulin-dependent protein kinase-II specific Ser-2814 site in LCR rats. T-tubules were present in 68% of HCR cells whereas only 33% LCR cells had these structures. In HCR, the significantly higher numbers of cells with T-tubules were combined with greater numbers of myocytes where Ca2+ release in the cell occurred simultaneously in central and peripheral regions, giving rise to faster and more spatial homogenous Ca2+-signal onset.ConclusionThis data demonstrates that contrasting for low or high aerobic capacity leads to diverse functional and structural remodelling of atrial myocytes, with impaired contractile function in LCR compared to HCR rats.

Genetic Analysis of a Rat Model of Aerobic Capacity and Metabolic Fitness

Aerobic capacity is a strong predictor of all-cause mortality and can influence many complex traits. To explore the biological basis underlying this connection, we developed via artificial selection two rat lines that diverge for intrinsic (i.e. inborn) aerobic capacity and differ in risk for complex disease traits. Here we conduct the first in-depth pedigree and molecular genetic analysis of these lines, the high capacity runners (HCR) and low capacity runners (LCR). Our results show that both HCR and LCR lines maintain considerable narrow-sense heritability (h2) for the running capacity phenotype over 28 generations (h2 = 0.47 ± 0.02 and 0.43 ± 0.02, respectively). To minimize inbreeding, the lines were maintained by rotational mating. Pedigree records predict that the inbreeding coefficient increases at a rate of <1% per generation, ~37-38% slower than expected for random mating. Genome-wide 10K SNP genotype data for generations 5, 14, and 26 demonstrate substantial genomic evolution: between-line differentiation increased progressively, while within-line diversity deceased. Genome-wide average heterozygosity decreased at a rate of <1% per generation, consistent with pedigree-based predictions and confirming the effectiveness of rotational breeding. Linkage disequilibrium index r2 decreases to 0.3 at ~3 Mb, suggesting that the resolution for mapping quantitative trait loci (QTL) can be as high as 2-3 cM. To establish a test population for QTL mapping, we conducted an HCR-LCR intercross. Running capacity of the F1 population (n=176) was intermediate of the HCR and LCR parentals (28 pairs); and the F2 population (n=645) showed a wider range of phenotypic distribution. Importantly, heritability in the F0-F2 pedigree remained high (h2~0.6). These results suggest that the HCR-LCR lines can serve as a valuable system for studying genomic evolution, and a powerful resource for mapping QTL for a host of characters relevant to human health.

Reliability and Validity of a New Maximal Anaerobic Shuttle Running Test

The purpose of this study was twofold: first to assess the relative and absolute reliability of a new Maximal Anaerobic Shuttle Running Test (MASRT), and second to evaluate the criterion validity of the MASRT. 16 team sport players participated in this study. The velocity (VMASRT) and the number of shuttles achieved at volitional exhaustion were measured. To assess the reliability of the MASRT, each player performed the MASRT twice, on separate days. The criterion validity of the MASRT was determined by examining the relationship between MASRT indices and the Wingate test (WingT) performances. Results showed no difference between test-retest MASRT scores for VMASRT and the number of shuttles (P>0.05). The intraclass correlation coefficients (ICC) values for VMASRT and Shuttle number were 0.84 and 0.80, respectively. The coefficients of variation (CV) and the mean difference (bias)±the 95% limits of agreement for the same variables were 3.6 and 12.9%, and 0.02±0.37m·s-1 and 0.3±6.7, respectively. The strongest correlation was found between mean power output relative to body mass (MPO) measured during the WingT and VMASRT (r=0.77, P<0.001). The MASRT constitutes a reliable and valid field tool for assessing short term repeated running capacity of team sport players.

Physiological assessment of isolated running does not directly replicate running capacity after triathlon-specific cycling

Triathlon running is affected by prior cycling and power output during triathlon cycling is variable in nature. We compared constant and triathlon-specific variable power cycling and their effect on subsequent submaximal running physiology. Nine well-trained male triathletes (age 24.6 ± 4.6 years, 4.5 ± 0.4 L · min−1; mean ± SD) performed a submaximal incremental run test, under three conditions: no prior exercise and after a 1 h cycling trial at 65% of maximal aerobic power with either a constant or a variable power profile. The variable power protocol involved multiple 10–90 s intermittent efforts at 40–140% maximal aerobic power. During cycling, pulmonary ventilation (22%, ±14%; mean; ±90% confidence limits), blood lactate (179%, ±48%) and rating of perceived exertion (7.3%, ±10.2%) were all substantially higher during variable than during constant power cycling. At the start of the run, blood lactate was 64%, ±61% higher after variable compared to constant power cycling, which decreased running velocity at 4 mM lactate threshold by 0.6, ±0.9 km · h−1. Physiological responses to incremental running are negatively affected by prior cycling and, to a greater extent, by variable compared to even-paced cycling. Testing and training of triathletes should account foe higher physiological cost of triathlon-specific cycling and its effect on subsequent running.

Abstract 507: Combined Exercise Training Induces Additional Cardiovascular Autonomic Benefits in Comparison to Dynamic Resistance Training in Ovariectomized Diabetic Rats

The purpose of this study was to compare the cardiovascular autonomic effects between dynamic aerobic, resistance and combined exercise training in ovariectomized diabetic female rats. Female Wistar rats (200-220g) were divided into 4 ovariectomized (bilateral ovaries removal) diabetic (streptozotocin, 50mg/kg, iv) groups: sedentary (DOS) and trained by an aerobic protocol on a treadmill (DOTA), by a resistance protocol in ladder (DOTR), or by a combined protocol in ladder+treadmill on alternate days (DOTC). After 8 weeks of training, the animals were cannulated to arterial pressure (AP) recording and baroreflex sensitivity (BS) evaluation. Heart rate (HR) and systolic AP variabilities were analyzed in the time and frequency domains. Exercise training induced an increase of 77% in the run capacity in the DOTA group (DOS: 8.6±0.6; DOTA: 15.3±0.4; DOTR: 11.5±1.6; DOTC: 15.0±0.2 min), 60% in the maximum load in DOTR group (DOS: 179.7±11.0; DOTA: 167.3±1.5; DOTR: 288.4±7.5; DOTC: 284.6±10.2 % of body weight), and increases in both exercise tests in DOTC (75% and 58%, respectively). All trained animals showed normalization of diabetic induced-resting hypotension and bradycardia, associated with increased HR variance (DOS: 39.6±2.6; DOTA: 71.2±7.2; DOTR: 70.9±12.1; DOTC: 65.7±6.1 ms2) and normalization of the LF band of pulse interval (DOS: 2.7±0.3; DOTA: 5.3±0.4; DOTR: 7.2±1.5; DOTC: 6.8±0.8 ms2) (vs. DOS). The DOTA and DOTC groups (but not DOTR) had higher BS (tachycardic and bradycardic responses), and attenuation in SAP variability (DOS: 7.4±0.8; DOTA: 12.7±1.1; DOTR: 8.9±1.0; DOTC: 13.3±1.0 mmHg2) in relation to DOS. Mortality was higher in DOS group when compared to trained group. In conclusion, the results showed that dynamic aerobic, resistance or combined exercise training induced benefits in physical capacity, hemodynamic and autonomic parameters after ovarian hormone deprivation in diabetic rats. However, the combined exercise training promoted additional effects than aerobic or resistance training in this condition.

Catechins Suppress Muscle Inflammation and Hasten Performance Recovery after Exercise

Catechins, abundant in green tea, exhibit many biological actions for potential clinical applications. Our purpose was to explore the potential benefits of catechin ingestion on recovery of physical performance after downhill running. Institute of Cancer Research mice were used to examine the effects of prior catechin ingestion (0.5% w/w in diet for 3 wk) on 1) wheel-running activity, 2) running endurance, 3) muscle force, and 4) muscle oxidative stress and inflammation after downhill running (16 m·min for 5 min, 18 m·min for 5 min, 20 m·min for 10 min, and 22 m·min for 130 min). Voluntary wheel-running activity and the contractile force of the isolated soleus muscle decreased (P < 0.05) after downhill running. Notably, catechin ingestion significantly alleviated the running-induced decrease in voluntary wheel-running activity by 35%; the catechin-treated mice maintained endurance running capacity (214 ± 9 vs 189 ± 10 min, P < 0.05). Furthermore, catechins alleviated (P < 0.05) the decrease in tetanic force evident in the soleus muscle after downhill running. Catechins suppressed the running-induced increases in plasma creatine phosphokinase levels by 52%; this was also true of the carbonylated protein content of the soleus muscle by 17% (P < 0.05), malondialdehyde levels by 32% in the gastrocnemius muscle, and myeloperoxidase activity of the gastrocnemius by 22% (P < 0.05). The levels of tumor necrosis factor-α, interleukin-1β, and monocyte chemoattractant protein-1 in the gastrocnemius muscle were significantly lower (P < 0.05) by 33%, 29%, and 35%, respectively, in treated mice; the expression levels of mRNAs encoding these fell in parallel. Our results suggest that long-term intake of catechins, perhaps through their antioxidant properties, attenuates downhill running-induced muscle damage by suppressing muscle oxidative stress and inflammation, hastening recovery of physical performance in mice.

Analysis of Mechanical Characteristic of Three-Phase Asynchronous Motor

The functional relationship is analyzed between three-phase asynchronous motor electromagnetic torque and some factors; Mechanical characteristic curve of motor performance is drawn; The inherent mechanical properties and human mechanical properties are explored in a specific application. Facts prove that mechanical characteristic analysis of three-phase asynchronous motors, to reduce the failure rate of the three-phase induction motor, to improve the running capacity and production efficiency are important.

Mitochondrial and performance adaptations to exercise training in mice lacking skeletal muscle LKB1

LKB1 and its downstream targets of the AMP-activated protein kinase family are important regulators of many aspects of skeletal muscle cell function, including control of mitochondrial content and capillarity. LKB1 deficiency in skeletal and cardiac muscle (mLKB1-KO) greatly impairs exercise capacity. However, cardiac dysfunction in that genetic model prevents a clear assessment of the role of skeletal muscle LKB1 in the observed effects. Our purposes here were to determine whether skeletal muscle-specific knockout of LKB1 (skmLKB1-KO) decreases exercise capacity and mitochondrial protein content, impairs accretion of mitochondrial proteins after exercise training, and attenuates improvement in running performance after exercise training. We found that treadmill and voluntary wheel running capacity was reduced in skmLKB1-KO vs. control (CON) mice. Citrate synthase activity, succinate dehydrogenase activity, and pyruvate dehydrogenase kinase content were lower in KO vs. CON muscles. Three weeks of treadmill training resulted in significantly increased treadmill running performance in both CON and skmLKB1-KO mice. Citrate synthase activity increased significantly with training in both genotypes, but protein content and activity for components of the mitochondrial electron transport chain increased only in CON mice. Capillarity and VEGF protein was lower in skmLKB1-KO vs. CON muscles, but VEGF increased with training only in skmLKB1-KO. Three hours after an acute bout of muscle contractions, PGC-1α, cytochrome c, and VEGF gene expression all increased in CON but not skmLKB1-KO muscles. Our findings indicate that skeletal muscle LKB1 is required for accretion of some mitochondrial proteins but not for early exercise capacity improvements with exercise training.

Influence of individual energy cost on running capacity in warm, humid environments

Challenging environmental conditions including heat and humidity are associated with particular risks to the health of runners and triathletes during prolonged events. The heat production of a runner is the product of its energy cost of running (C r) by its velocity. Since C r varies greatly among humans, those individuals with high C r are more exposed to heat stress in warm and humid conditions. Although risk factor awareness is crucial to the prevention of heat stroke and potential fatalities associated therewith, how C r affects the highest sustainable velocity (V) at which maximal heat loss matches heat production has not been quantified to date. Here, we computed in virtual runners weighting 45-75kg, the influence of C r variability from 3.8 to 4.4J·m(-1)·kg(-1) on V. Heat loss by radiation, convection, and conduction was assessed from known equations including body dimensions, running velocity (3.4-6.2m·s(-1)), air temperature (T a, 10-35°C) and relative humidity (r h, 50, 70 and 90%). We demonstrated a marked and almost linear influence of C r on V in hot and humid conditions: +0.1J·kg(-1)·m(-1) in C r corresponded to -4% in V. For instance, in conditions25°C r h 70%, 65-kg runners with low C r could sustain a running speed of 5.7m·s(-1) as compared to only 4.3m·s(-1) in runners with high C r, which is huge. We conclude that prior knowledge of individual C r in athletes exposed to somewhat warm and humid environments during prolonged running is one obvious recommendation for minimizing heat illness risk.

Exercise training enhances white adipose tissue metabolism in rats selectively bred for low- or high-endurance running capacity

Impaired visceral white adipose tissue (WAT) metabolism has been implicated in the pathogenesis of several lifestyle-related disease states, with diminished expression of several WAT mitochondrial genes reported in both insulin-resistant humans and rodents. We have used rat models selectively bred for low- (LCR) or high-intrinsic running capacity (HCR) that present simultaneously with divergent metabolic phenotypes to test the hypothesis that oxidative enzyme expression is reduced in epididymal WAT from LCR animals. Based on this assumption, we further hypothesized that short-term exercise training (6 wk of treadmill running) would ameliorate this deficit. Approximately 22-wk-old rats (generation 22) were studied. In untrained rats, the abundance of mitochondrial respiratory complexes I-V, citrate synthase (CS), and PGC-1 was similar for both phenotypes, although CS activity was greater than 50% in HCR (P = 0.09). Exercise training increased CS activity in both phenotypes but did not alter mitochondrial protein content. Training increased the expression and phosphorylation of proteins with roles in β-adrenergic signaling, including β3-adrenergic receptor (16% increase in LCR; P < 0.05), NOR1 (24% decrease in LCR, 21% decrease in HCR; P < 0.05), phospho-ATGL (25% increase in HCR; P < 0.05), perilipin (25% increase in HCR; P < 0.05), CGI-58 (15% increase in LCR; P < 0.05), and GLUT4 (16% increase in HCR; P < 0.0001). A training effect was also observed for phospho-p38 MAPK (12% decrease in LCR, 20% decrease in HCR; P < 0.05) and phospho-JNK (29% increase in LCR, 20% increase in HCR; P < 0.05). We conclude that in the LCR-HCR model system, mitochondrial protein expression in WAT is not affected by intrinsic running capacity or exercise training. However, training does induce alterations in the activity and expression of several proteins that are essential to the intracellular regulation of WAT metabolism.

Anaerobic running capacity determined from the critical velocity model is not significantly associated with maximal accumulated oxygen deficit in army runners

The aim of this study was to verify whether there is an association between anaerobic running capacity (ARC) values, estimated from two-parameter models, and maximal accumulated oxygen deficit (MAOD) in army runners. Eleven, trained, middle distance runners who are members of the armed forces were recruited for the study (20 ± 1 years). They performed a critical velocity test (CV) for ARC estimation using three mathematical models and an MAOD test, both tests were applied on a motorized treadmill. The MAOD was 61.6 ± 5.2 mL/kg (4.1 ± 0.3 L). The ARC values were 240.4 ± 18.6 m from the linear velocity–inverse time model, 254.0 ± 13.0 m from the linear distance–time model, and 275.2 ± 9.1 m from the hyperbolic time–velocity relationship (nonlinear 2-parameter model), whereas critical velocity values were 3.91 ± 0.07 m/s, 3.86 ± 0.08 m/s and 3.80 ± 0.09 m/s, respectively. There were differences ( P < 0.05) for both the ARC and the CV values when compared between velocity–inverse time linear and nonlinear 2-parameter mathematical models. The different values of ARC did not significantly correlate with MAOD. In conclusion, estimated ARC did not correlate with MAOD, and should not be considered as an anaerobic measure of capacity for treadmill running. Le but de cette étude est de vérifier s’il existe une relation entre les valeurs de la capacité anaérobie en course à pied (CACP) estimées à partir de modèles à deux paramètres et le déficit maximal d’oxygène accumulé (DMOA) chez les coureurs de l’armée. Onze coureurs de demi-fond des forces armées ont été recrutés pour cette étude (20 ± 1 ans). Un test de vitesse critique (VC) a été réalisé afin d’estimer la CACP à l’aide de trois modèles mathématiques et d’un test DMOA, réalisé sur un tapis roulant motorisé. Les valeurs du DMOA test ont été de 61,6 ± 5,2 mL/kg (4,1 ± 0,3 L). Les valeurs de CDA estimées à partir du modèle linéaire vitesse-temps inverse ont été de 240,4 ± 18,6 m, pour le modèle linéaire distance-temps les valeurs ont été de 254,0 ± 13,0 m et pour la relation hyperbolique temps-vitesse (modèle non linéaire à deux paramètres) la valeur a été de 275,2 ± 9,1 m, tandis que les valeurs de vitesse critique étaient respectivement de 3,91 ± 0,07 m/s, 3,86 ± 0,08 m/s et 3,80 ± 0,09 m/s. Des différences ( p < 0,05) ont été constatées pour les valeurs de CACP et VC comparées entre le modèle linéaire vitesse-temps inverse et les modèles mathématiques non linéaires à deux paramètres. Aucune corrélation significative n’a été notée entre les différentes valeurs de la CACP et le DMOA.

Resveratrol Attenuates Exercise-Induced Adaptive Responses in Rats Selectively Bred for Low Running Performance

Low capacity runner (LCR) rats have been developed by divergent artificial selection for treadmill endurance capacity to explore an aerobic biology-disease connection. The beneficial effects of resveratrol supplementation have been demonstrated in endurance running. In this study it was examined whether 12 weeks of treadmill exercise training and/or resveratrol can retrieve the low running performance of the LCR and impact mitochondrial biogenesis and quality control. Resveratrol regressed running performance in trained LCR (p<0.05). Surprisingly, exercise and resveratrol treatments significantly decreased pAMPK/AMPK, SIRT1, SIRT4, forkhead transcription factor 1 (FOXO1) and mitochondrial transcription factor A (TFAM) levels in these animals (p<0.05). Mitochondrial fusion protein, HSP78 and polynucleotide phosphorylase were significantly induced in LCR-trained, LCR-resveratrol treated, LCR-trained and resveratol treated groups compared to LCR-controls. The data indicate that the AMPK-SIRT1-NAMPT-FOXO1 axis could be important to the limited aerobic endurance capacity of low running capacity rats. Resveratrol supplementation was not beneficial in terms of aerobic endurance performance, mitochondrial biogenesis, or quality control.

Surgery Results in Exaggerated and Persistent Cognitive Decline in a Rat Model of the Metabolic Syndrome

Postoperative cognitive decline can be reproduced in animal models. In a well-validated rat model of the Metabolic Syndrome, we sought to investigate whether surgery induced a more severe and persistent form of cognitive decline similar to that noted in preliminary clinical studies. In rats that had been selectively bred for low and high exercise endurance, the low capacity runners (LCR) exhibited features of Metabolic Syndrome (obesity, dyslipidemia, insulin resistance, and hypertension). Tibial fracture surgery was performed under isoflurane anesthesia in LCR and high capacity runner (HCR) rats and cognitive function was assessed postoperatively in a trace-fear conditioning paradigm and Morris Water Maze; non-operated rats were exposed to anesthesia and analgesia (sham). Group sizes were n = 6. On postoperative D7, LCR rats had shorter freezing times than postoperative HCR rats. Five months postoperatively, LCR rats had a flatter learning trajectory and took longer to locate the submerged platform than postoperative HCR rats; dwell-time in the target quadrant in a probe trial was shorter in the postoperative LCR compared to HCR rats. LCR and HCR sham rats did not differ in any test. Postoperatively, LCR rats diverged from HCR rats exhibiting a greater decline in memory, acutely, with persistent learning and memory decline, remotely; this could not be attributed to changes in locomotor or swimming performance. This Metabolic Syndrome animal model of surgery-induced cognitive decline corroborates, with high fidelity, preliminary findings of postoperative cognitive dysfunction in Metabolic Syndrome patients.

Disconnecting Mitochondrial Content from Respiratory Chain Capacity in PGC-1-Deficient Skeletal Muscle

The transcriptional coactivators PGC-1α and PGC-1β are widely thought to be required for mitochondrial biogenesis and fiber typing in skeletal muscle. Here, we show that mice lacking both PGC-1s in myocytes do indeed have profoundly deficient mitochondrial respiration but, surprisingly, have preserved mitochondrial content, isolated muscle contraction capacity, fiber-type composition, in-cage ambulation, and voluntary running capacity. Most of these findings are recapitulated in cell culture and, thus, are cell autonomous. Functional electron microscopy reveals normal cristae density with decreased cytochrome oxidase activity. These data lead to the following surprising conclusions: (1) PGC-1s are in fact dispensable for baseline muscle function, mitochondrial content, and fiber typing, (2) endurance fatigue at low workloads is not limited by muscle mitochondrial capacity, and (3) mitochondrial content and cristae density can be dissociated from respiratory capacity.

Living Without Creatine

Rationale: Creatine is thought to be involved in the spatial and temporal buffering of ATP in energetic organs such as heart and skeletal muscle. Creatine depletion affects force generation during maximal stimulation, while reduced levels of myocardial creatine are a hallmark of the failing heart, leading to the widely held view that creatine is important at high workloads and under conditions of pathological stress. Objective: We therefore hypothesised that the consequences of creatine-deficiency in mice would be impaired running capacity, and exacerbation of heart failure following myocardial infarction. Methods and Results: Surprisingly, mice with whole-body creatine deficiency due to knockout of the biosynthetic enzyme (guanidinoacetate N-methyltransferase [GAMT]) voluntarily ran just as fast and as far as controls (&gt;10 km/night) and performed the same level of work when tested to exhaustion on a treadmill. Furthermore, survival following myocardial infarction was not altered, nor was subsequent left ventricular (LV) remodelling and development of chronic heart failure exacerbated, as measured by 3D-echocardiography and invasive hemodynamics. These findings could not be accounted for by compensatory adaptations, with no differences detected between WT and GAMT −/− proteomes. Alternative phosphotransfer mechanisms were explored; adenylate kinase activity was unaltered, and although GAMT −/− hearts accumulated the creatine precursor guanidinoacetate, this had negligible energy-transfer activity, while mitochondria retained near normal function. Conclusions: Creatine-deficient mice show unaltered maximal exercise capacity and response to chronic myocardial infarction, and no obvious metabolic adaptations. Our results question the paradigm that creatine is essential for high workload and chronic stress responses in heart and skeletal muscle.

Resveratrol enhances exercise training responses in rats selectively bred for high running performance

High Capacity Runner (HCR) rats have been developed by divergent artificial selection for treadmill endurance running capacity to explore an aerobic biology-disease connection. The beneficial effects of resveratrol supplementation have been demonstrated in endurance running and the antioxidant capacity of resveratrol is also demonstrated. In this study we examine whether 12 weeks of treadmill exercise training and/or resveratrol can enhance performance in HCR. Indeed, resveratrol increased aerobic performance and strength of upper limbs of these rats. Moreover, we have found that resveratrol activated the AMP-activated protein kinase, SIRT1, and mitochondrial transcription factor A (p<0.05). The changes in mitochondrial fission/fusion and Lon protease/HSP78 levels suggest that exercise training does not significantly induce damage of proteins. Moreover, neither exercise training nor resveratrol supplementation altered the content of protein carbonyls. Changes in the levels of forkhead transcription factor 1 and SIRT4 could suggest increased fat utilization and improved insulin sensitivity. These data indicate, that resveratrol supplementation enhances aerobic performance due to the activation of the AMPK-SIRT1-PGC-1α pathway.

(-)-Epicatechin is associated with increased angiogenic and mitochondrial signalling in the hindlimb of rats selectively bred for innate low running capacity.

Alternative approaches to reduce congenital muscle dysfunction are needed in cases where the ability to exercise is limited. (-)-Epicatechin is found in cocoa and may stimulate capillarity and mitochondrial proliferation in skeletal muscle. A total of 21 male rats bred for LCR (low running capacity) from generation 28 were randomized into three groups: vehicle for 30 days (control); (-)-epicatechin for 30 days; and (-)-epicatechin for 30 days followed by 15 days without (-)-epicatechin. Groups 2 and 3 received 1.0 mg of (-)-epicatechin/kg of body mass twice daily, whereas water was given to the control group. The plantaris muscle was harvested for protein and morphometric analyses. In addition, in vitro experiments were conducted to examine the role of (-)-epicatechin on mitochondrial respiratory kinetics at different incubation periods. Treatment for 30 days with (-)-epicatechin increased capillarity (P<0.001) and was associated with increases in protein expression of VEGF (vascular endothelial growth factor)-A with a concomitant decrease in TSP-1 (thrombospondin-1) and its receptor, which remained after 15 days of (-)-epicatechin cessation. Analyses of the p38 MAPK (mitogen-activated protein kinase) signalling pathway indicated an associated increase in phosphorylation of MKK3/6 (MAPK kinase 3/6) and p38 and increased protein expression of MEF2A (myocyte enhancer factor 2A). In addition, we observed significant increases in protein expression of PGC-1α (peroxisome-proliferator-activated receptor γ co-activator 1α), PGC-1β, Tfam and cristae abundance. Interestingly, these increases associated with (-)-epicatechin treatment remained after 15 days of cessation. Lastly, in vitro experiments indicated that acute exposure of LCR muscle to (-)-epicatechin incubation was not sufficient to increase mitochondrial respiration. The results suggest that increases in skeletal muscle capillarity and mitochondrial biogenesis are associated with 30 days of (-)-epicatechin treatment and sustained for 15 days following cessation of treatment. Clinically, the use of this natural compound may have potential application in populations that experience muscle fatigue and are unable to perform endurance exercise.

Gene expression profiling of gastrocnemius of “minimuscle” mice

Few studies have investigated heterogeneity of selection response in replicate lines subjected to equivalent selection. We developed four replicate lines of mice based on high levels of voluntary wheel running (high runner or HR lines) while also maintaining four nonselected control lines. This led to the unexpected discovery of the HR minimuscle (HRmini) phenotype, recognized by a 50% reduction in hindlimb muscle mass, which became fixed in 1 of the four HR selected lines. Here, we report genome-wide expression profiling describing transcriptome differences between HRnormal and HRmini medial gastrocnemius. Consistent with the known reduction of type IIB fibers in HRmini, Myh4 gene expression was -8.82-fold less (P = 0.0001) in HRmini, which was closely associated with differences in the "calcium signaling" canonical pathway, including structural genes (e.g., Mef2c, twofold greater in HRmini, P = 0.0003) and myogenic factors (e.g., Myog, 3.8-fold greater in HRmini, P = 0.0026) associated with slow-type myofibers. The gene that determines the HRmini phenotype is known to reside in a 2.6335-Mb interval on mouse chromosome 11 and 7 genes (Myh10, Chrnb1, Acadvl, Senp3, Gabarap, Eif5a, and Clec10a) from this region were differentially expressed. Verification by real-time PCR confirmed 1.5-fold greater (P < 0.05) expression of very long chain acyl-CoA dehydrogenase (Acadvl) in HRmini. Ten other genes associated with fatty acid metabolism were also upregulated in HRmini, suggesting differences in the ability to metabolize fatty acids in HRnormal and HRmini muscles. This work provides a resource for understanding differences in muscle phenotypes in populations exhibiting high running capacity.

Anthropometric and Physical Characteristics of Tunisians Young Soccer Players

The aim of this investigation was to provide anthropometric, physical and physiological performance characteristics of Tunisian young soccer players and to examine the relationship between selected parameters according to their playing standard position. One hundred under 13 years old (U-13) male soccer players were tested. They were classified according to their playing standard positions (goalkeeper: GK, defender: DF, midfield: MF, and forward: FW). Testing consisted of anthropometric measurements including weight, height, and body mass index, and performance measures of speed (5, 15, and 20 m), agility run (Agility-15 m and Ball-15 m), vertical jumping, ball shooting, and aerobic capacity (Hoff Dribble Test and Yo-Yo intermittent Endurance Run, YYIER). GK were taller and heavier than other players. Significant differences of playing positions for the majority of the physical tests include 20 m sprint, Agility-15 m and Ball-15 m times (all p p p p p p < .01). Multiple regression analyses showed that weight and height were the most significant predictors of 20 m sprint time and the YYIER distance, respectively. In conclusion, performance abilities between positions in young soccer players appear to be different. Anthropometry can discriminate physical capacities and soccer skills providing a scientific rational behind the coaches’ practice of selecting young soccer players.

Low intrinsic exercise capacity in rats predisposes to age-dependent cardiac remodeling independent of macrovascular function

Rats selectively bred for low (LCR) or high (HCR) intrinsic running capacity simultaneously present with contrasting risk factors for cardiovascular and metabolic disease. However, the impact of these phenotypes on left ventricular (LV) morphology and microvascular function, and their progression with aging, remains unresolved. We tested the hypothesis that the LCR phenotype induces progressive age-dependent LV remodeling and impairments in microvascular function, glucose utilization, and β-adrenergic responsiveness, compared with HCR. Hearts and vessels isolated from female LCR (n = 22) or HCR (n = 26) were studied at 12 and 35 wk. Nonselected N:NIH founder rats (11 wk) were also investigated (n = 12). LCR had impaired glucose tolerance and elevated plasma insulin (but not glucose) and body-mass at 12 wk compared with HCR, with early LV remodeling. By 35 wk, LV prohypertrophic and glucose transporter GLUT4 gene expression were up- and downregulated, respectively. No differences in LV β-adrenoceptor expression or cAMP content between phenotypes were observed. Macrovascular endothelial function was predominantly nitric oxide (NO)-mediated in both phenotypes and remained intact in LCR for both age-groups. In contrast, mesenteric arteries microvascular endothelial function, which was impaired in LCR rats regardless of age. At 35 wk, endothelial-derived hyperpolarizing factor-mediated relaxation was impaired whereas the NO contribution to relaxation is intact. Furthermore, there was reduced β2-adrenoceptor responsiveness in both aorta and mesenteric LCR arteries. In conclusion, diminished intrinsic exercise capacity impairs systemic glucose tolerance and is accompanied by progressive development of LV remodeling. Impaired microvascular perfusion is a likely contributing factor to the cardiac phenotype.