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Background

The stress response is a critical factor in the training of equine athletes; it is important for performance and for protection of the animal against physio-pathological disorders.

In this study, the molecular mechanisms involved in the response to acute and strenuous exercise were investigated using peripheral blood mononuclear cells (PBMCs).

Results

Quantitative real-time PCR (qRT-PCR) was used to detect modifications in transcription levels of the genes for matrix metalloproteinase-1 (MMP-1) and interleukin 8 (IL-8), which were derived from previous genome-wide expression analysis. Significant up-regulation of these two genes was found in 10 horses that had completed a race of 90–120 km in a time-course experimental design.

Conclusion

These results suggest that MMP-1 and IL-8 are both involved in the exercise-induced stress response, and this represents a starting point from which to understand the adaptive responses to this phenomenon.

Twelve female age-group swimmers and twelve female controls, aged ten to sixteen, performed a pre-training discontinuous maximal cycle ergometer test to determine the capacities of their anaerobic (alactacid and lactacid) and aerobic energy systems. Heart rate and oxygen uptake were determined during rest, exercise, and recovery. Blood samples were collected before and after exercise for determination of blood lactic acid concentrations. Tests were readministered to both groups immediately following the swimmers' competitive season. It was concluded that female swimmers possess significantly superior oxygen transport systems as compared to the untrained controls and that the high level of aerobic fitness is maintained throughout their training programme.

Left ventricle dimensions and wall stress were measured echocardiographically before and immediately after exercise in 14 athletes and 7 control subjects. Our findings suggest that afterload is an important determinant of cardiac performance and wall hypertrophy in athletes. In spite of major changes in heart rate and blood pressure, left ventricular wall stress remains unchanged following submaximal exercise, in trained and untrained hearts. It would appear that the changes in heart size during exercise are to a large extent limited in untrained ventricles, as smaller left ventricular dimensions are required, to "normalise" wall stress. This results in a lower stroke volume for a given stroke dimensional change. Consequently cardiac output is a function of heart rate rather than stroke volume in untrained subjects. The effect of increased muscle mass in athletes, is to permit larger left ventricular dimensions for a given afterload, thus stroke volume can be augmented. The increase h/R ratio suggests that afterload is more important than preload in the development of left ventricular hypertrophy in rowers and swimmers.

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Cytotoxic T lymphocytes are involved in controlling intracellular pathogens in many species, including horses. Particularly, CTL are critical for the control of equine infectious anemia virus (EIAV), a lentivirus that infects horses world-wide. In humans and animal models, CTL clones are valuable for evaluating the fine specificity of epitope recognition, and for adoptive immunotherapy against infectious and neoplastic diseases. Cloned CTL would be equally useful for similar studies in the horse. Here we present the first analysis of a method to generate equine CTL clones. Peripheral blood mononuclear cells were obtained from an EIAV-infected horse and stimulated with the EIAV Rev-QW11 peptide. Sorted CD8+ T cells were cloned by limiting dilution, and expanded without further antigen addition using irradiated PBMC, anti-equine CD3, and human recombinant IL-2. Clones could be frozen and thawed without detrimental effects, and could be subsequently expanded to numbers exceeding 2 × 109 cells. Flow cytometry of expanded clones confirmed the CD3+/CD8+ phenotype, and chromium release assays confirmed CTL activity. Finally, sequencing TCR beta chain genes confirmed clonality. Our results provide a reliable means to generate large numbers of epitope-specific equine CTL clones that are suitable for use in downstream applications, including functional assays and adoptive transfer studies.

Objective

To prove that long-distance running is safe for athletes with pacemaker devices, pacemaker function was evaluated in nine long-distance runners.

Method

Nine runners participated in a nine-month training programme that involved running for 1000 or 2000 km in preparation for either a full or a half marathon. A professional coach, three cardiologists and a technician — all with running experience — conducted the training and medical checkups. Commercial heart rate monitors were used during training to assess heart rates at rest, and during exercise and long-distance running. Sensing and pacing functions of the pacemaker system were tested during training sessions as well as during the race. In addition, the ChampionChip (a time registration device used in competition) and the Polar heart rate monitor (a widely used self-monitoring device) were tested for possible interference with the pacemaker.

Results

All nine athletes completed the Amsterdam 2001 half or full marathon without any pacemaker dysfunction. A short survey after two years showed no pacemaker dysfunction.

Conclusion

Long-distance running is safe for athletes with pacemaker implants. Overall fitness and sufficient endurance training remain the prerequisites for maintaining the condition necessary for successful completion of a marathon regardless of medical status. In our study, it became clear that for patients who had received a pacemaker because of complete heart block, the upper rate of the pacemaker programme needed to be adjusted to 170 to 180 ppm to insure 1:1 atrio-ventricular synchrony during high atrial rates. It is concluded that there is no a priori reason for cardiologists to advise against long-distance running in athletes with pacemakers. Patients with known or suspected structural heart disease should be screened according the recommendations.

Background—A suboptimal haematological status has often been recorded in athletes involved in intensive physical activity. There have even been reports of "sports anaemia" associated with intensive physical exercise. However, studies on the effect of different types of exercise practiced over a long period of time on the red blood cell variables in pubescent athletes are very few.

Aim—To assess the basic red blood cell variables in highly trained pubescent athletes from different sports and to compare the results with those for a control untrained group. Sex related differences in these variables were also assessed.

Methods—876 highly trained athletes (559 boys and 317 girls) were included in the study. Their mean (SEM) age, weight, and duration of training were: 14.01 (0.06) years, 56.24 (0.52) kg, and 3.52 (0.07) years respectively. The control group consisted of 357 untrained subjects (171 boys and 186 girls) with mean (SEM) age and weight of 14.58 (0.09) years and 57.75 (0.67) kg. The group of athletes was divided into seven subgroups according to the sport practiced: athletics (105), swimming (107), rowing (230), wrestling (225), weight lifting (47), various team sports (92), and other sports (67). Venous blood samples were drawn from the cubital vein, and the red blood cell count, packed cell volume, haemoglobin concentration, and mean corpuscular volume were measured. Statistical indices were computed for each group and for each variable, and analysis of variance factorial analysis was performed to evaluate the statistical significance of the differences detected.

Results—The highly trained group was found to have lower red blood cell count, packed cell volume, and haemoglobin concentration (p<0.001) than the control untrained group (4.61 (0.01) x 1012/1 v 4.75 (0.02) x 1012/l, 0.389 (0.001) v 0.404 (0.002) l/l, and 133.01 (0.38) v 139.9 (0.62) g/l respectively). These variables were lower for the boys of the trained group than for the boys of the control group (p<0.001), and similarly for the girls (p<0.001). The lowest red blood cell count, packed cell volume, and haemoglobin concentration were measured in blood samples from the boys of the swimming subgroup (4.54 (0.06) x 1012/l, 0.386 (0.006) l/l, and 129.38 (1.80) g/1 respectively) and the rowing subgroup (4.66 (0.03) x 1012/l, 0.400 (0.003) l/l, and 136.21 (0.94) respectively). The same distribution was found for the girls: lowest in the rowing subgroup (4.32 (0.04) x 1012/1, 0.314 (0.003) l/l, and 124.27 (0.93) g/1) and the swimming subgroup (4.40 (0.05) x 1012/l, 0.375 (0.005) l/l, and 125.90 (1.30) g/1). No differences were found in the mean corpuscular volume.

Conclusions—Continuous (more than one year) high intensity sports training (twice a day/five days a week) results in a decrease in the basic red blood cell variables in pubescent boys and girls, this being most pronounced in the submaximal sports.

Key Words: erythrocytes; haemoglobin; packed cell volume; mean corpuscular volume; pubescence; training

Background:

The aim of this study was to compare post-exercise hypotension after acute sessions of water-walking and land-walking in healthy trained and untrained women.

Methods:

Twenty-three untrained (n = 12) and trained (n = 11) normotensive women performed two walking sessions in water and on land at 40% of peak VO2 for 45 minutes. Systolic and diastolic blood pressure and mean arterial pressure were measured 15, 30, 45, and 60 minutes after the exercise sessions.

Results:

No differences were found between the groups for age and anthropometric parameters, but peak VO2 for the trained women (45 ± 8 mL/kg/minute) was higher than for the untrained women (31 ± 3 mL/kg/minute). No differences were found between the groups with regard to systolic and diastolic blood pressure and mean arterial pressure after water immersion. The heart rate in the trained group (62 ± 3 beats per minute [bpm]) was significantly lower (P < 0.05) than in the untrained group (72 ± 4 bpm) on land, and after water immersion, this difference disappeared (58 ± 5 bpm in the trained women and 66 ± 5 bpm in the untrained women). Sixty minutes after water-walking, systolic blood pressure (108 ± 8 mmHg vs 97 ± 3 mmHg), diastolic blood pressure (69 ± 5 mmHg vs 62 ± 5 mmHg), and mean arterial pressure (82 ± 6 mmHg vs 74 ± 4 mmHg) decreased significantly with rest in the untrained group, and no differences were found after land-walking. In the trained group, significant (P < 0.05) differences were found only for systolic blood pressure (110 ± 9 mmHg vs 100 ± 9 mmHg) after 60 minutes of water-walking; decreases in systolic blood pressure were found after 45 minutes (99 ± 7 mmHg) and 60 minutes (99 ± 6 mmHg) compared with rest (107 ± 5 mmHg) after land-walking.

Conclusion:

Single water-walking and land-walking sessions induced important hypotension following exercise. Additionally, walking performed in chest-deep water has a better effect on exercise-induced hypotension in untrained healthy women than walking at a similar intensity on land.

The purpose of this study was to assess maximal aerobic power (VO2max) in trained and untrained 15-year-old boys. The trained subjects (18) were junior swimmers from a Belgrade swimming team, and the untrained ones (12) were from a Belgrade high school. VO2max was directly measured during progressive cycle ergometer exercise using open circuit spirometry. No significant differences in height, mass, percentage fat and vital capacity were noted between the trained and untrained groups. Maximal aerobic power (overall, relative and in relation to lean body mass) in absolute values, and expressed per kilogram of body mass and lean body mass, was 31.5%, 21.2% and 20.6%, respectively, higher in the trained than in the untrained group (P less than 0.05). These data suggest that physical training significantly increases maximal aerobic power in young subjects.

Objectives—Recent studies have indicated reduced immunity in trained athletes.

Aim—To assess the effects of aerobic and anaerobic exercise on the phagocytic process in 18–26 year old trained female judoka (n = 8) and untrained controls (n = 7).

Methods—Each subject participated randomly in two different testing sessions (aerobic, 20 minutes of treadmill running at 70–80% of maximal heart rate; anaerobic, Wingate anaerobic test). Venous blood samples were drawn before, immediately after, and 24 hours after each session.

Results—There were no significant differences in basal values of net chemotaxis (chemotaxis - random migration), bactericidal activity, and superoxide anion release between the judoka and the untrained women. There was a significant decrease in net chemotaxis 24 hours after the aerobic exercise in both the judoka (from 64 (19) to 39 (13) cells/field, p<0.02) and the untrained controls (from 60 (7) to 47 (12) cells/field, p<0.05). Bactericidal activity and superoxide anion release did not change significantly after aerobic exercise in either group. There were no significant changes in net chemotaxis, bactericidal activity, and superoxide anion release after anaerobic exercise in either the judoka or untrained women.

Conclusions—The decrease in net chemotaxis after aerobic, but not after anaerobic, exercise, suggests that net chemotaxis is affected by the combination of exercise intensity and duration, and not by the exercise intensity itself. Similar effects of both exercise sessions in the judoka and the untrained women suggest that training had no effect on neutrophil function response to aerobic and anaerobic exercises.

Key Words: exercise; aerobic; anaerobic; neutrophil function; female athlete

Aims

We compared the effects of exercise training on neurovascular control and functional capacity in men and women with chronic heart failure (HF).

Methods and results

Forty consecutive HF outpatients from the Heart Institute, University of Sao Paulo, Brazil were divided into the following four groups matched by age: men exercise-trained (n = 12), men untrained (n = 10), women exercise-trained (n = 9), women untrained (n = 9). Maximal exercise capacity was determined from a maximal progressive exercise test on a cycle ergometer. Forearm blood flow was measured by venous occlusion plethysmography. Muscle sympathetic nerve activity (MSNA) was recorded directly using the technique of microneurography. There were no differences between groups in any baseline parameters. Exercise training produced a similar reduction in resting MSNA (P = 0.000002) and forearm vascular resistance (P = 0.0003), in men and women with HF. Peak VO2 was similarly increased in men and women with HF (P = 0.0003) and VE/VCO2 slope was significantly decreased in men and women with HF (P = 0.0007). There were no significant changes in left-ventricular ejection fraction in men and women with HF.

Conclusion

The benefits of exercise training on neurovascular control and functional capacity in patients with HF are independent of gender.

Objectives—To identify physical activity that is beneficial for the maintenance of bone strength with increasing age by examining the relation between bone mineral density (BMD) and chronic endurance training in men. BMD at the proximal femur, its subregions, and the lumbar spine, and serum testosterone were compared between two groups of long distance runners with more than 20 years of training experience and non-athletic controls.

Methods—Runners (n = 12) were divided into (a) high volume runners (n = 7), running 64–80 km a week, and (b) very high volume runners (n = 5), running more than 95 km a week, and compared with non-athletic male controls, exercising in non-endurance oriented activities two to four times a week. BMD (g/cm2) at the total proximal femur, femoral neck, trochanteric region, and lumbar spine was measured by dual energy x ray absorptiometry. Total testosterone (nmol/l) and free testosterone (pmol/l) in serum were measured by radioimmunoassay from single fasting blood samples.

Results—Height, weight, and age (range = 40–55 years) were not significantly different between groups. The high volume runners had significantly higher BMD at the total proximal femur (1.09 (0.17) v 0.94 (0.056)), femoral neck (0.91 (0.16) v 0.78 (0.071)), and trochanteric region (0.85 (0.14) v 0.73 (0.053)) than controls (p<0.05). The differences in BMD for the proximal femur between the very high volume runners and the other two groups were not significant. There was no difference in lumbar spine BMD, total testosterone, or free testosterone between groups. However, there was a significant negative correlation between total testosterone (r = -0.73, p<0.01) and free testosterone (r = -0.79, p<0.005) and running volume in the distance runners.

Conclusions—Long term distance running with training volumes less than 80 km a week had a positive effect on BMD of the proximal femur. With running volumes greater than 64 km a week, training was inversely related to testosterone levels, but levels remained within the normal range.

Key Words: exercise; bone mineral density; male athletes; runners; endurance training; testosterone

Background

The molecular mechanisms underlying the sex differences in human muscle morphology and function remain to be elucidated. The sex differences in the skeletal muscle transcriptome in both the resting state and following anabolic stimuli, such as resistance exercise (RE), might provide insight to the contributors of sexual dimorphism of muscle phenotypes. We used microarrays to profile the transcriptome of the biceps brachii of young men and women who underwent an acute unilateral RE session following 12 weeks of progressive training. Bilateral muscle biopsies were obtained either at an early (4 h post-exercise) or late recovery (24 h post-exercise) time point. Muscle transcription profiles were compared in the resting state between men (n = 6) and women (n = 8), and in response to acute RE in trained exercised vs. untrained non-exercised control muscle for each sex and time point separately (4 h post-exercise, n = 3 males, n = 4 females; 24 h post-exercise, n = 3 males, n = 4 females). A logistic regression-based method (LRpath), following Bayesian moderated t-statistic (IMBT), was used to test gene functional groups and biological pathways enriched with differentially expressed genes.

Results

This investigation identified extensive sex differences present in the muscle transcriptome at baseline and following acute RE. In the resting state, female muscle had a greater transcript abundance of genes involved in fatty acid oxidation and gene transcription/translation processes. After strenuous RE at the same relative intensity, the time course of the transcriptional modulation was sex-dependent. Males experienced prolonged changes while females exhibited a rapid restoration. Most of the biological processes involved in the RE-induced transcriptional regulation were observed in both males and females, but sex specificity was suggested for several signaling pathways including activation of notch signaling and TGF-beta signaling in females. Sex differences in skeletal muscle transcriptional regulation might implicate a mechanism behind disproportional muscle growth in males as compared with female counterparts after RE training at the same relative intensity.

Conclusions

Sex differences exist in skeletal muscle gene transcription both at rest and following acute RE, suggesting that sex is a significant modifier of the transcriptional regulation in skeletal muscle. The findings from the present study provide insight into the molecular mechanisms for sex differences in muscle phenotypes and for muscle transcriptional regulation associated with training adaptations to resistance exercise.

Cytotoxic T lymphocytes (CTL) can control some viral infections and may be important in the control of lentiviruses, including human immunodeficiency virus type 1. Since there is limited evidence for an in vivo role of CTL in control of lentiviruses, dissection of immune mechanisms in animal lentiviral infections may provide needed information. Horses infected with equine infectious anemia virus (EIAV) a lentivirus, have acute plasma viremia which is terminated in immunocompetent horses. Viremic episodes may recur, but most horses ultimately control infection and become asymptomatic carriers. To begin dissection of the immune mechanisms involved in EIAV control, peripheral blood mononuclear cells (PBMC) from infected horses were evaluated for CTL to EIAV-infected cells. By using noninfected and EIAV-infected autologous equine kidney (EK) cells in 51Cr-release assays, EIAV-specific cytotoxic activity was detected in unstimulated PBMC from three infected horses. The EIAV-specific cytotoxic activity was major histocompatibility complex (MHC) restricted, as determined by assaying EIAV-infected heterologous EK targets, and was mediated by CD8+ T lymphocytes, as determined by depleting these cells by a panning procedure with an anti-CD8 monoclonal antibody. MHC-restricted CD8+ CTL in unstimulated PBMC from infected horses caused significant specific lysis of autologous EK cells infected with recombinant vaccinia viruses expressing EIAV genes, either env or gag plus 5' pol. The EIAV-specific MHC-restricted CD8+ CTL were detected in two EIAV-infected horses within a few days after plasma viremia occurred and were present after viremia was terminated. The detection of these immune effector cells in EIAV-infected horses permits further studies to determine their in vivo role.

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Background

Within the animal kingdom, horses are among the most powerful aerobic athletic mammals. Determination of muscle respiratory capacity and control improves our knowledge of mitochondrial physiology in horses and high aerobic performance in general.

Methodology/Principal Findings

We applied high-resolution respirometry and multiple substrate-uncoupler-inhibitor titration protocols to study mitochondrial physiology in small (1.0–2.5 mg) permeabilized muscle fibres sampled from triceps brachii of healthy horses.

Oxidative phosphorylation (OXPHOS) capacity (pmol O2•s−1•mg−1 wet weight) with combined Complex I and II (CI+II) substrate supply (malate+glutamate+succinate) increased from 77±18 in overweight horses to 103±18, 122±15, and 129±12 in untrained, trained and competitive horses (N = 3, 8, 16, and 5, respectively). Similar to human muscle mitochondria, equine OXPHOS capacity was limited by the phosphorylation system to 0.85±0.10 (N = 32) of electron transfer capacity, independent of fitness level. In 15 trained horses, OXPHOS capacity increased from 119±12 to 134±37 when pyruvate was included in the CI+II substrate cocktail. Relative to this maximum OXPHOS capacity, Complex I (CI)-linked OXPHOS capacities were only 50% with glutamate+malate, 64% with pyruvate+malate, and 68% with pyruvate+malate+glutamate, and ∼78% with CII-linked succinate+rotenone. OXPHOS capacity with glutamate+malate increased with fitness relative to CI+II-supported ETS capacity from a flux control ratio of 0.38 to 0.40, 0.41 and 0.46 in overweight to competitive horses, whereas the CII/CI+II substrate control ratio remained constant at 0.70. Therefore, the apparent deficit of the CI- over CII-linked pathway capacity was reduced with physical fitness.

Conclusions/Significance

The scope of mitochondrial density-dependent OXPHOS capacity and the density-independent (qualitative) increase of CI-linked respiratory capacity with increased fitness open up new perspectives of integrative and comparative mitochondrial respiratory physiology.

This study examined the relationship between estimates of alactacid anaerobic power, lactacid anaerobic power and aerobic power in a sample of trained swimmers (age 14.4 yr., n = 8) and a sample of untrained boys (age 13.7 yr., n = 13). The anaerobic power outputs were estimated using a modification of the Wingate Anaerobic Test and aerobic power was estimated using a continuous, incremental cycle ergometer test. In addition to leg power outputs the swimmers' arm power using each energy system was estimated and compared with the corresponding leg value. There was no relationship between the estimates of the power of the three energy systems with either the trained or untrained boys. Furthermore with the trained boys there was no relationship between estimates of the power of the same energy system utilised by different limbs. The data support a specificity hypothesis of energy utilisation during exercise with both trained and untrained adolescent boys.

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Background

Adequate stress response is a critical factor during athlete horses' training and is central to our capacity to obtain better performances while safeguarding animal welfare.

In order to investigate the molecular mechanisms underlying this process, several studies have been conducted that take advantage of microarray and quantitative real-time PCR (qRT-PCR) technologies to analyse the expression of candidate genes involved in the cellular stress response.

Appropriate application of qRT-PCR, however, requires the use of reference genes whose level of expression is not affected by the test, by general physiological conditions or by inter-individual variability.

Results

The expression of nine potential reference genes was evaluated in lymphocytes of ten endurance horses during strenuous exercise. These genes were tested by qRT-PCR and ranked according to the stability of their expression using three different methods (implemented in geNorm, NormFinder and BestKeeper). Succinate dehydrogenase complex subunit A (SDHA) and hypoxanthine phosphoribosyltransferase (HPRT) always ranked as the two most stably expressed genes. On the other hand, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), transferrin receptor (TFRC) and ribosomal protein L32 (RPL32) were constantly classified as the less reliable controls.

Conclusion

This study underlines the importance of a careful selection of reference genes for qRT-PCR studies of exercise induced stress in horses. Our results, based on different algorithms and analytical procedures, clearly indicate SDHA and HPRT as the most stable reference genes of our pool.

This study evaluated the impact of professional training on serum oxidant and antioxidant status in adolescent endurance athletes and compared it with that of untrained individuals. Firstly, serum thiobarbituric-acid-reactive substances (TBARSs), xanthine oxidase (XO), catalase (CAT), reduced glutathione (GSH), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC) were measured in 67 male runners, cyclists, and untrained adolescents. Seven-day dietary intakes were also assessed. Secondly, for age- and Tanner-stage-matched comparison, 36 out of the 67 subjects (12 for each group) were then selected and investigated. In cyclists, XO, GSH, and CAT were higher as compared with runners and controls. The CAT in runners, but not GSH and XO, was also higher than in controls. TBARS, T-AOC, and SOD did not differ among the study populations. Regarding the inter-individual relationships among serum redox statuses and dietary nutrient intakes, significant correlations were noted in CAT versus carbohydrates, protein, magnesium, and manganese; GSH versus carbohydrates, protein, fat, selenium, zinc, iron, and magnesium; XO versus cholesterol; CAT versus GSH. These findings suggest that the resting blood redox balance in the professional adolescent athletes was well maintained partly by the increase of individual antioxidant in adaptation to chronic exercise.

Background and Aims

Exercise-induced iron deficiency is a common finding in endurance athletes. It has been suggested recently that hepcidin may be an important mediator in this process.

Objective

To determine hepcidin levels and markers of iron status during long-term exercise training in female runners with depleted and normal iron stores.

Methods

Fourteen runners were divided into two groups according to iron status. Blood samples were taken during a period of eight weeks at baseline, after training and after ten days’ recovery phase.

Results

Of 14 runners, 7 were iron deficient at baseline and 10 after training. Hepcidin was lower at recovery compared with baseline (p<0.05). The mean cell haemoglobin content, haemoglobin content per reticulocyte and total iron binding capacity all decreased, whereas soluble transferrin receptor and hypochromic red cells increased after training and recovery (p<0.05 for all).

Conclusion

The prevalence of depleted iron stores was 71% at the end of the training phase. Hepcidin and iron stores decreased during long-term running training and did not recover after ten days, regardless of baseline iron status.

Cytokines produced by T helper (Th) cells are important in orchestrating the immune response during health and disease. Recent reports indicated that cytokine mRNA expression in foals is often quantitatively lower than that of adult horses suggesting that foal T cells are not fully mature. Here, peripheral blood mononuclear cells from foals and adult horses were stimulated with phorbol 12-myristate 13-acetate and analyzed for intracellular interferon-gamma (IFN-γ), interleukin-4 (IL-4) and IL-10 production, representing the Th1, Th2 and regulatory TR1 cell phenotypes respectively, by flow cytometry. In agreement with previous reports, all three cytokines were quantitatively reduced in foals compared to adults. However, the balance between Th1 and Th2 cytokines (IFN-γ/IL-4 ratio) showed a clear Th1-biased response in foals by 6 and 12 weeks of life, while similar IFN-γ/IL-10 ratios were found in foals and adult horses. By day 5 after birth, intracellular IFN-γ production by foal CD4+ and CD8+ T cells resembled that in adults. Overall, IL-4 production was low in foals. IL-4+ cells peaked at day 5 of age when IL-4 was mainly produced by IgE+ cells. Relative percentages of IL-4+ Th2 cells were significantly lower in foals at all time points. The data suggested that equine neonates and young foals have an impaired Th2 response, that the immune response of foals is Th1 biased, that IFN-γ production by Th and cytotoxic T cells is qualitatively similar to adult horses, and regulatory IL-10 production by T cells is developmentally mature in foals during the first three months of life.

Background: Soluble transferrin receptor (sTfr) is a new marker of iron status and erythropoietic activity. It has been included in multivariable blood testing models for the detection of performance enhancing erythropoietin misuse in sport.

Objective: To evaluate the effect of different types and volumes of physical activity on sTfr concentration, variables of iron status (ferritin, transferrin, iron, and protein), and haematological indices.

Methods: Thirty nine subjects were divided into three groups: 1, untrained (n = 12); 2, moderately trained (n = 14); 3, highly trained (n = 13, seven men, six women). Groups 1 and 2 carried out two exercise tests: an incremental running test until exhaustion (test A) and a 45 minute constant speed running test at 70% VO2MAX (test B). Group 3 performed three days (women) or four days (men) of prolonged aerobic cycling exercise. The above variables together with haemoglobin and packed cell volume were analysed in venous blood samples before and after exercise. Changes in blood and plasma volume were estimated.

Results: sTfr levels were slightly increased in trained and untrained subjects immediately after test A. Test B and aerobic exercise had no significant effect on sTfr. Ferritin levels were increased after the laboratory tests for trained and untrained subjects and after prolonged aerobic exercise in male cyclists. Transferrin was increased significantly in trained and untrained subjects after both laboratory tests, but remained unchanged after prolonged exercise. Plasma and blood volumes were decreased after the laboratory tests but increased after aerobic exercise. No differences in the variables were observed between trained and untrained subjects with respect to response to exercise.

Conclusion: The changes in sTfr and the variables of iron status can be mainly attributed to exercise induced changes in volume. Taking these limitations into account, sTfr can be recommended as a marker of iron deficiency in athletes.

Background

Different conditions may alter tendon characteristics. Clinical evidence suggests that tendon injuries are more frequent in athletes that change type, intensity and duration of training. Aim of the study was the assessment of training and especially detraining on the patellar tendon (PT) and its enthesis.

Methods

27 male adult Sprague-Dawley rats were divided into 3 groups: 20 rats were trained on a treadmill for 10 weeks. Of these, 10 rats were euthanized immediately after training (trained group), and 10 were caged without exercise for 4 weeks before being euthanized (de-trained group). The remaining 7 rats were used as controls (untrained rats). PT insertion, structure (collagen fiber organization and proteoglycan, PG, content), PT thickness, enthesis area, and subchondral bone volume at the enthesis were measured by histomorphometry and microtomography.

Results

Both PG content and collagen fiber organization were significantly lower in untrained and detrained animals than in trained ones (p < 0.05 and p < 0.0001). In the detrained group, fiber organization and PG content were worse than that of the untrained groups and the untrained group showed a significantly higher score than the detrained group (p < 0.05). In the trained group, the PT was significantly thicker than in untrained group (p < 0.05). No significant differences in the enthesis area and subchondral bone volume among the three groups were seen.

Conclusions

Moderate exercise exerts a protective effect on the PT structure while sudden discontinuation of physical activity has a negative effect on tendons. The present results suggest that after a period of sudden de-training (such as after an injury) physical activity should be restarted with caution and with appropriate rehabilitation programs.

Reduced activation of exercise responsive signalling pathways have been reported in response to acute exercise after training; however little is known about the adaptive responses of the mitochondria. Accordingly, we investigated changes in mitochondrial gene expression and protein abundance in response to the same acute exercise before and after 10-d of intensive cycle training. Nine untrained, healthy participants (mean±SD; VO2peak 44.1±17.6 ml/kg/min) performed a 60 min bout of cycling exercise at 164±18 W (72% of pre-training VO2peak). Muscle biopsies were obtained from the vastus lateralis muscle at rest, immediately and 3 h after exercise. The participants then underwent 10-d of cycle training which included four high-intensity interval training sessions (6×5 min; 90–100% VO2peak) and six prolonged moderate-intensity sessions (45–90 min; 75% VO2peak). Participants repeated the pre-training exercise trial at the same absolute work load (64% of pre-training VO2peak). Muscle PGC1-α mRNA expression was attenuated as it increased by 11- and 4- fold (P<0.001) after exercise pre- and post-training, respectively. PGC1-α protein expression increased 1.5 fold (P<0.05) in response to exercise pre-training with no further increases after the post-training exercise bout. RIP140 protein abundance was responsive to acute exercise only (P<0.01). COXIV mRNA (1.6 fold; P<0.01) and COXIV protein expression (1.5 fold; P<0.05) were increased by training but COXIV protein expression was decreased (20%; P<0.01) by acute exercise pre- and post-training. These findings demonstrate that short-term intensified training promotes increased mitochondrial gene expression and protein abundance. Furthermore, acute indicators of exercise-induced mitochondrial adaptation appear to be blunted in response to exercise at the same absolute intensity following short-term training.

Cigarette smokers experience an exaggerated triglyceride (TAG) and oxidative stress response to high fat feeding. Exercise training may serve to attenuate the rise in these variables, by improving TAG clearance and antioxidant defense. We compared blood TAG, antioxidant capacity, and oxidative stress biomarkers in exercise trained (>2 hrs per wk) and untrained smokers matched for age, in response to a high fat test meal. We report here that low volume exercise training can attenuate postprandial lipid peroxidation, but has little impact on blood TAG and other markers of oxidative stress. Higher volumes of exercise may be needed to allow for clinically meaningful adaptations in postprandial lipemia and oxidative stress.

An exaggerated exercise blood pressure response (EEBPR) may be associated with an increased risk of hypertension. We hypothesized that aerobic exercise training can decrease EEBPR and the risk for hypertension by decreasing arterial resistance. We studied the effects of aerobic training on the submaximal exercise blood pressure (BP) of eight normotensive young adult African-American men with an EEBPR. Subjects were trained on a stationary bicycle at an intensity of 70% peak oxygen uptake (VO2peak) for 30 min, three times per week, for 8 weeks. BP, heart rate, cardiac output (CO), stroke volume (SV) and total peripheral vascular resistance (TPR) were measured at rest and during submaximal exercise at a work intensity of 50% VO2peak. Significance of the training effects were evaluated by comparing the pre- and post-training measures (t-test, p < 0.05). A 15% post-training increase in VO2peak (34.6 ± 1.4 to 40 ± 1.4 ml/kg/min) and a 9.5 ml post-training increase in mean resting stroke volume were found. A 16.2 mmHg decrement in mean systolic BP, an 11.5 mmHg decrement in mean diastolic BP, a 120 dyne/s/cm5 decrement in TPR and a 1.2 l/min increase in CO were detected during the post-training submaximal exercise tests. These results suggest that reductions in TPR may attenuate the EEBPR of normotensive African-American males following an 8-week training regimen of stationary bicycling at 70% VO2peak. Aerobic exercise training may, therefore, reduce the risk of hypertension in normotensive African-American males by the mechanism of a reduction in TPR. Because of the limited number of subjects, the results of this study should be interpreted cautiously pending confirmation by a larger controlled trial.

Background

The purpose of this investigation was to determine the effects of a dietary supplement (Ambrotose AO®) on resting and exercise-induced blood antioxidant capacity and oxidative stress in exercise-trained and untrained men and women.

Methods

25 individuals (7 trained and 5 untrained men; 7 trained and 6 untrained women) received Ambrotose AO® (4 capsules per day = 2 grams per day) or a placebo for 3 weeks in a random order, double blind cross-over design (with a 3 week washout period). Blood samples were collected at rest, and at 0 and 30 minutes following a graded exercise treadmill test (GXT) performed to exhaustion, both before and after each 3 week supplementation period. Samples were analyzed for Trolox Equivalent Antioxidant Capacity (TEAC), Oxygen Radical Absorbance Capacity (ORAC), malondialdehyde (MDA), hydrogen peroxide (H2O2), and nitrate/nitrite (NOx). Quality of life was assessed using the SF-12 form and exercise time to exhaustion was recorded. Resting blood samples were analyzed for complete blood count (CBC), metabolic panel, and lipid panel before and after each 3 week supplementation period. Dietary intake during the week before each exercise test was recorded.

Results

No condition effects were noted for SF-12 data, for GXT time to exhaustion, or for any variable within the CBC, metabolic panel, or lipid panel (p > 0.05). Treatment with Ambrotose AO® resulted in an increase in resting levels of TEAC (p = 0.02) and ORAC (p < 0.0001). No significant change was noted in resting levels of MDA, H2O2, or NOx (p > 0.05). Exercise resulted in an acute increase in TEAC, MDA, and H2O2 (p < 0.05), all which were higher at 0 minutes post exercise compared to pre exercise (p < 0.05). No condition effects were noted for exercise related data (p > 0.05), with the exception of ORAC (p = 0.0005) which was greater at 30 minutes post exercise for Ambrotose AO® compared to placebo.

Conclusion

Ambrotose AO® at a daily dosage of 4 capsules per day increases resting blood antioxidant capacity and may enhance post exercise antioxidant capacity. However, no statistically detected difference is observed in resting or exercise-induced oxidative stress biomarkers, in quality of life, or in GXT time to exhaustion.