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Background: For optimal recommendations in cardiovascular training for the general population, knowing the essential parameters for physical fitness is required. Heart rate recovery (HRR) is an easy-to-measure parameter and is discussed to derive the physical fitness of an individual subject. This study evaluates HRR as a potential physical fitness parameter for public health programs, as it is measured in every ergometry., Methods: In this retrospective cross-sectional study, we analyzed HRR regarding physical fitness (W/kg (IAT: individual anaerobic threshold)). In total, we analyzed 1234 performance protocols in cycle ergometry. Significance tests ( p < 0.001) and multiple linear regression were performed., Results: The analysis of HRR and weight-related performance showed a significant correlation with a moderate coefficient of determination (R 2 = 0.250). The coefficient of determination increases from very weak correlation levels at 1 min post-workout towards weak to moderate levels of correlation at 5 min post-workout., Conclusions: In this study HRR and the weight-related performance at the IAT showed a significant correlation with a mean strength. Thus, a prediction or conclusion on physical performance based singularly on HRR decrease is not recommended. However, in preventive medicine, HRR should be measured and observed on a long-term basis, for analysis of vagal activity and to draw to inferences of mortality.

This review of the exercise genomics literature encompasses the highest-quality articles published in 2015 across seven broad topics: physical activity behavior, muscular strength and power, cardiorespiratory fitness and endurance performance, body weight and adiposity, insulin and glucose metabolism, lipid and lipoprotein metabolism, and hemodynamic traits. One study used a quantitative trait locus for wheel running in mice to identify single nucleotide polymorphisms (SNPs) in humans associated with physical activity levels. Two studies examined the association of candidate gene ACTN3 R577X genotype on muscular performance. Several studies examined gene-physical activity interactions on cardiometabolic traits. One study showed that physical inactivity exacerbated the body mass index (BMI)-increasing effect of an FTO SNP but only in individuals of European ancestry, whereas another showed that high-density lipoprotein cholesterol (HDL-C) SNPs from genome-wide association studies exerted a smaller effect in active individuals. Increased levels of moderate-to-vigorous-intensity physical activity were associated with higher Matsuda insulin sensitivity index in PPARG Ala12 carriers but not Pro12 homozygotes. One study combined genome-wide and transcriptome-wide profiling to identify genes and SNPs associated with the response of triglycerides (TG) to exercise training. The genome-wide association study results showed that four SNPs accounted for all of the heritability of △TG, whereas the baseline expression of 11 genes predicted 27% of △TG. A composite SNP score based on the top eight SNPs derived from the genomic and transcriptomic analyses was the strongest predictor of ΔTG, explaining 14% of the variance. The review concludes with a discussion of a conceptual framework defining some of the critical conditions for exercise genomics studies and highlights the importance of the recently launched National Institutes of Health Common Fund program titled "Molecular Transducers of Physical Activity in Humans."

This is the annual review of the exercise genomics literature in which we report on the highest quality papers published in 2014. We identified a number of noteworthy papers across a number of fields. In 70-89 yr olds, only 19% of angiotensin-converting enzyme (ACE) II homozygotes exhibited significant improvement in gait speed in response to a yearlong physical activity program compared to 30% of ACE D-allele carriers. New studies continue to support the notion that the genetic susceptibility to obesity, as evidenced by a genomic risk score (GRS; based on multiple single nucleotide polymorphisms), is attenuated by 40%-50% in individuals who are physically active, compared to those who are sedentary. One study reported that the polygenic risk for hypertriglyceridemia was reduced by 30%-40% in individuals with high cardiorespiratory fitness. One report showed that there was a significant interaction of a type 2 diabetes GRS with physical activity, with active individuals having the lowest risk of developing diabetes. The protective effect of physical activity was most pronounced in the low GRS tertile (hazard ratio, 0.82). The interaction observed with the diabetes GRS seemed to be dependent on a genetic susceptibility to insulin resistance and not insulin secretion. A significant interaction between PPARα sequence variants and physical activity levels on cardiometabolic risk was observed, with higher activity levels associated with lower risk only in carriers of specific genotypes and haplotypes. The review concludes with a discussion of the importance of replication studies when very large population or intervention discovery studies are not feasible or are cost prohibitive.

The most significant and scientifically sound articles in exercise genomics that were published in 2013 are reviewed in this report. No article on the genetic basis of sedentary behavior or physical activity level was identified. A calcineurin- and alpha actinin-2-based mechanism has been identified as the potential molecular basis for the observed lower muscular strength and power in alpha actinin-3-deficient individuals. Although baseline muscle transcriptomic signatures were found to be associated with strength training-induced muscle hypertrophy, no predictive genomic variants could be identified as of yet. One study found no clear evidence that the inverse relation between physical activity level and incident CHD events was influenced by 58 genomic variants clustered into four genetic scores. Lower physical activity level in North American populations may be driving the apparent risk of obesity in fat mass- and obesity-associated gene (FTO)-susceptible individuals compared with more active populations. Two large studies revealed that common genetic variants associated with baseline levels of plasma HDL cholesterol and triglycerides are not clear predictors of changes induced by interventions focused on weight loss, diet, and physical activity behavior. One large study from Japan reported that a higher fitness level attenuated the arterial stiffness-promoting effect of the Ala54 allele at the fatty acid binding protein 2 locus, which is a controversial finding because previous studies have suggested that Thr54 was the risk allele. Using transcriptomics to generate genomic targets in an unbiased manner for subsequent DNA sequence variants studies appears to be a growing trend. Moreover, exercise genomics is rapidly embracing gene and pathway analysis to better define the underlying biology and provide a foundation for the study of human variation.

This review of the exercise genomics literature emphasizes the highest quality articles published in 2011. Given this emphasis on the best publications, only a small number of published articles are reviewed. One study found that physical activity levels were significantly lower in patients with mitochondrial DNA mutations compared with controls. A two-stage fine-mapping follow-up of a previous linkage peak found strong associations between sequence variation in the activin A receptor, type-1B (ACVRIB) gene and knee extensor strength, with rs2854464 emerging as the most promising candidate polymorphism. The association of higher muscular strength with the rs2854464 A allele was confirmed in two separate cohorts. A study using a combination of transcriptomic and genomic data identified a comprehensive map of the transcriptomic features important for aerobic exercise training-induced improvements in maximal oxygen consumption, but no genetic variants derived from candidate transcripts were associated with trainability. A large-scale de novo meta-analysis confirmed that the effect of sequence variation in the fat mass and obesity-associated (FTO) gene on the risk of obesity differs between sedentary and physically active adults. Evidence for gene-physical activity interactions on type 2 diabetes risk was found in two separate studies. A large study of women found that physical activity modified the effect of polymorphisms in the lipoprotein lipase (LPL), hepatic lipase (LIPC), and cholesteryl ester transfer protein (CETP) genes, identified in previous genome-wide association study reports, on HDL cholesterol. We conclude that a strong exercise genomics corpus of evidence would not only translate into powerful genomic predictors but also have a major effect on exercise biology and exercise behavior research.

This review of the exercise genomics literature emphasizes the strongest articles published in 2010 as defined by sample size, quality of phenotype measurements, quality of the exercise program or physical activity exposure, study design, adjustment for multiple testing, quality of genotyping, and other related study characteristics. One study on voluntary running wheel behavior was performed in 448 mice from 41 inbred strains. Several quantitative trait loci for running distance, speed, and duration were identified. Several studies on the alpha-3 actinin (ACTN3) R577X nonsense polymorphism and the angiotensin-converting enzyme (ACE) I/D polymorphism were reported with no clear evidence for a joint effect, but the studies were generally underpowered. Skeletal muscle RNA abundance at baseline for 29 transcripts and 11 single nucleotide polymorphisms (SNPs) were both found to be predictive of the V˙O2max response to exercise training in one report from multiple laboratories. None of the 50 loci associated with adiposity traits are known to influence physical activity behavior. However, physical activity seems to reduce the obesity-promoting effects of at least 12 of these loci. Evidence continues to be strong for a role of gene-exercise interaction effects on the improvement in insulin sensitivity after exposure to regular exercise. SNPs in the cAMP-responsive element binding position 1 (CREB1) gene were associated with training-induced HR response, in the C-reactive protein (CRP) gene with training-induced changes in left ventricular mass, and in the methylenetetrahydrofolate reductase (MTHFR) gene with carotid stiffness in low-fit individuals. We conclude that progress is being made but that high-quality research designs and replication studies with large sample sizes are urgently needed., (© 2011 by the American College of Sports Medicine)

An annual review publication of the most significant articles in exercise, fitness, and performance genomics begins with this article, which covers 2 yr, 2008 and 2009. The review emphasizes the strongest articles as defined by sample size, quality of phenotype measurements, quality of the exercise program or physical activity exposure, study design, adjustment for multiple testing, quality of genotyping, and other related study characteristics. With this avowed focus on the highest quality articles, only a small number of published articles are reviewed. Among the most significant findings reported here are a brief overview of the first genome-wide association study of the genetic differences between exercisers and nonexercisers. In addition, the latest results on the actinin alpha 3 (ACTN3) R577X nonsense polymorphism are reviewed, emphasizing that no definitive conclusion can be reached at this time. Recent studies that have dealt with mitochondrial DNA haplogroups and endurance performance are described. Published reports indicating that physical activity may attenuate the effect of the fat mass and obesity associated (FTO) gene risk allele on body mass index are reviewed. Articles that have tested the contributions of specific genes to the response of glucose and insulin metabolism traits to regular exercise or physical activity level are considered and found to be generally inconclusive at this stage. Studies examining ethnic differences in the response of blood lipids and lipoproteins to exercise training cannot unequivocally relate these to apolipoprotein E (APOE) genotypes. Hemodynamic changes with exercise training were reported to be associated to sequence variation in kinesin heavy chain (KIF5B), but no replication study is available as of yet. We conclude from this first installment that exercise scientists need to prioritize high-quality research designs and that replication studies with large sample sizes are urgently needed.

This update of the human gene map for physical performance and health-related fitness phenotypes covers the research advances reported in 2006 and 2007. The genes and markers with evidence of association or linkage with a performance or a fitness phenotype in sedentary or active people, in responses to acute exercise, or for training-induced adaptations are positioned on the map of all autosomes and sex chromosomes. Negative studies are reviewed, but a gene or a locus must be supported by at least one positive study before being inserted on the map. A brief discussion on the nature of the evidence and on what to look for in assessing human genetic studies of relevance to fitness and performance is offered in the introduction, followed by a review of all studies published in 2006 and 2007. The findings from these new studies are added to the appropriate tables that are designed to serve as the cumulative summary of all publications with positive genetic associations available to date for a given phenotype and study design. The fitness and performance map now includes 214 autosomal gene entries and quantitative trait loci plus seven others on the X chromosome. Moreover, there are 18 mitochondrial genes that have been shown to influence fitness and performance phenotypes. Thus,the map is growing in complexity. Although the map is exhaustive for currently published accounts of genes and exercise associations and linkages, there are undoubtedly many more gene-exercise interaction effects that have not even been considered thus far. Finally, it should be appreciated that most studies reported to date are based on small sample sizes and cannot therefore provide definitive evidence that DNA sequence variants in a given gene are reliably associated with human variation in fitness and performance traits.

The current review presents the 2005 update of the human gene map for physical performance and health-related fitness phenotypes. It is based on peer-reviewed papers published by the end of 2005. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise, or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed, but a gene or locus must be supported by at least one positive study before being inserted on the map. By the end of 2000, in the early version of the gene map, 29 loci were depicted. In contrast, the 2005 human gene map for physical performance and health-related phenotypes includes 165 autosomal gene entries and QTL, plus five others on the X chromosome. Moreover, there are 17 mitochondrial genes in which sequence variants have been shown to influence relevant fitness and performance phenotypes. Thus, the map is growing in complexity. Unfortunately, progress is slow in the field of genetics of fitness and performance, primarily because the number of laboratories and scientists focused on the role of genes and sequence variations in exercise-related traits continues to be quite limited.

We began this series in 2000 with the aim of making available in an easily accessible format all the advances on the genetic basis of a large family of exercise-related traits. The current review presents the 2004 update of the human gene map for physical performance and health-related fitness phenotypes. It is based on peer-reviewed papers published by the end of 2004. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise, or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed but a gene or locus must be supported by at least one positive study before being inserted on the map. One new feature is that we have incorporated the genes whose sequence variants have been associated with either the level of physical activity or indicators of sedentarism. By the end of 2000, in the early version of the gene map, 29 loci were depicted. In contrast, the 2004 human gene map for physical performance and health-related phenotypes includes 140 autosomal gene entries and quantitative trait loci, plus four on the X chromosome. Moreover, there are 16 mitochondrial genes in which sequence variants have been shown to influence relevant fitness and performance phenotypes. Thus, the map is growing in complexity and progress is being made. The number of laboratories and scientists concerned by the role of genes and sequence variations in exercise-related traits is rising. But exercise science and sports medicine is generally lagging behind in terms of utilizing the advances in genetic and genomic technologies.

This review presents the 2003 update of the human gene map for physical performance and health-related fitness phenotypes. It is based on peer-reviewed papers published by the end of 2003 and includes association studies with candidate genes, genome-wide scans with polymorphic markers, and single-gene defects causing exercise intolerance to variable degrees. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise, or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed but a gene or locus must be supported by at least one positive study before being inserted on the map. By the end of 2000, 29 loci were depicted on the first edition of the map. In contrast, the 2003 human gene map for physical performance and health-related phenotypes includes 109 autosomal gene entries and QTL, plus two on the X chromosome. Moreover, there are 15 mitochondrial genes in which sequence variants have been shown to influence relevant fitness and performance phenotypes.

Obesity as well as low physical fitness and inactivity are associated with an increased incidence of cardiovascular risk factors and coronary artery disease (CAD). Increased inflammation has recently been addressed to play an important role for the relationship between obesity and CAD, as adipose tissue expresses and releases pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). As this relationship is less clear in childhood, we investigated 197 children aged 10-15 years assessing obesity, physical fitness, and a metabolic cardiovascular risk profile including markers of inflammation. Obese children had significantly higher concentrations of inflammatory parameters such as fibrinogen, ferritin, IL-6, and TNF-alpha than non-obese subjects (P<0.01). When dividing the children into groups regarding obesity (BMI < 22.5 kg/mz, BMI > or = 22.5 kglm2) and fitness (< 5 MET, > or = 5 MET), we found that obese, unfit children showed the highest systemic inflammation, whereas fit but obese individuals had as low levels as lean and fit children. These data reveal that even in childhood inflammatory parameters are elevated in obesity and that physical fitness counteracts this association.

This review presents the 2002 update of the human gene map for physical performance and health-related phenotypes. It is based on peer-reviewed papers published by the end of 2002 and includes association studies with candidate genes, genome-wide scans with polymorphic markers, and single gene defects causing exercise intolerance to variable degrees. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise, or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed, but a gene or locus must be supported by at least one positive study before being inserted on the map. By the end of 2000, 29 loci were depicted on the map. The 2001 map includes 71 loci on the autosomes and two on the X chromosome. In contrast, the 2002 human gene map for physical performance and health-related phenotypes includes 90 gene entries and QTL, plus two on the X chromosome. To all these loci, one must add 14 mitochondrial genes in which sequence variants have been shown to influence relevant fitness and performance phenotypes.

This review presents the 2001 update of the human gene map for physical performance and health-related phenotypes. It is based on scientific papers published by the end of 2001. Association studies with candidate genes, genome-wide scans with polymorphic markers, and single gene defects causing exercise intolerance to variable degrees are included. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed, but a gene or locus must be supported by at least one positive study before being inserted on the map. By the end of 2000, there were 29 loci depicted on the map. The 2001 map includes 71 loci on the autosomes and two on the X chromosome. Among these genes or markers, 24 are from prior publications on exercise intolerance and four relate to other pathologies. Finally, 13 sequence variants in mitochondrial DNA have been shown to influence relevant fitness and performance phenotypes.

Exercise interventions are nowadays considered as effective add-on treatments in people with schizophrenia but are usually associated with high dropout rates. Therefore, the present study investigated potential predictors of adherence from a large multicenter study, encompassing two types of exercise training, conducted over a 6-month period with individuals with schizophrenia. First, we examined the role of multiple participants' characteristics, including levels of functioning, symptom severity, cognitive performance, quality of life, and physical fitness. Second, we used K-means clustering to identify clinical subgroups of participants that potentially exhibited superior adherence. Last, we explored if adherence could be predicted on the individual level using Random Forest, Logistic Regression, and Ridge Regression. We found that individuals with higher levels of functioning at baseline were more likely to adhere to the exercise interventions, while other factors such as symptom severity, cognitive performance, quality of life or physical fitness seemed to be less influential. Accordingly, the high-functioning group with low symptoms exhibited a greater likelihood of adhering to the interventions compared to the severely ill group. Despite incorporating various algorithms, it was not possible to predict adherence at the individual level. These findings add to the understanding of the factors that influence adherence to exercise interventions. They underscore the predictive importance of daily life functioning while indicating a lack of association between symptom severity and adherence. Future research should focus on developing targeted strategies to improve adherence, particularly for people with schizophrenia who suffer from impairments in daily functioning. Clinical trials registration The study of this manuscript which the manuscript is based was registered in the International Clinical Trials Database, ClinicalTrials.gov (NCT number: NCT03466112, https://clinicaltrials.gov/ct2/show/NCT03466112?term=NCT03466112&draw=2&rank=1) and in the German Clinical Trials Register (DRKS-ID: DRKS00009804. [ABSTRACT FROM AUTHOR]

Purpose: Occupational health programmes have been successfully implemented to improve body composition, physical fitness and cardiovascular risk. However, most programmes have been small and have not included long-term evaluation. Therefore, we evaluated a twelve-month life-style change programme in a German refinery. Methods: We offered a supervised six-week endurance exercise programme (2 × 90 min/week), starting after a two-day life-style seminar. After the active intervention and a half-day refresher seminar, employees were encouraged to continue exercising over one year on their own, with monthly supervised sessions to maintain adherence. Anthropometry, bicycle ergometry, cardio-metabolic risk profile, inflammatory parameters, and vascular function e.g. endothelial function was studied at baseline, after three and after twelve months. Results: Of 550 employees, n = 327 (age 40.8 ± 9.7 years, 88% males) participated in the study. Twelve-month intervention was associated with a reduced waist circumference (92.6 ± 12.2 to 90.8 ± 11.7 cm, 95% confidence interval for the mean change (CI): -2.5 to -1.1 cm) and a gain in maximal exercise capacity (202 ± 39.6 to 210 ± 38.9 Watt; 95% CI: + 5.1 to + 10.9 Watt). Metabolic and inflammatory parameters likewise HbA1c and C-reactive protein improved in central tendency at a local 95% level of confidence. Vascular function e.g. Reactive-Hyperaemia-Index revealed a slight reduction, whereas no statistically robust changes in mean Cardio-Ankle-Vascular-Index and mean Ankle-Brachial-Index were observed. Conclusion: Health education added by a six-week supervised exercise programme was associated with minor long-term twelve-month improvements of body composition as well as physical fitness and a concomitant improvement of inflammatory state. These changes were, however, not clinically relevant and not accompanied by statistically robust improvements of vascular function. Trial registration: ClinTrialsGov: NCT01919632; date of registration: August 9, 2013; retrospectively registered. [ABSTRACT FROM AUTHOR]

This retrospective cross-sectional study aimed to explore interactions between signs of periodontal inflammation and systemic parameters in athletes. Members of German squads with available data on sports medical and oral examination were included. Groups were divided by gingival inflammation (median of papillary bleeding index, PBI ≥ median) and signs of periodontitis (Periodontal Screening Index, PSI ≥ 3). Age, gender, anthropometry, blood parameters, echocardiography, sports performance on ergometer, and maximal aerobic capacity (VO2max) were evaluated. Eighty-five athletes (f = 51%, 20.6 ± 3.5 years) were included (PBI < 0.42: 45%; PSI ≥ 3: 38%). Most associations were not statistically significant. Significant group differences were found for body fat percentage and body mass index. All blood parameters were in reference ranges. Minor differences in hematocrit, hemoglobin, basophils, erythrocyte sedimentation rates, urea, and HDL cholesterol were found for PBI, in uric acid for PSI. Echocardiographic parameters (n = 40) did not show any associations. Athletes with PSI ≥ 3 had lower VO2max values (55.9 ± 6.7 mL/min/kg vs. 59.3 ± 7.0 mL/min/kg; p = 0.03). In exercise tests (n = 30), athletes with PBI < 0.42 achieved higher relative maximal load on the cycling ergometer (5.0 ± 0.5 W/kg vs. 4.4 ± 0.3 W/kg; p = 0.03). Despite the limitations of this study, potential associations between signs of periodontal inflammation and body composition, blood parameters, and performance were identified. Further studies on the systemic impact of oral inflammation in athletes, especially regarding performance, are necessary. [ABSTRACT FROM AUTHOR]

Introduction: The standard 12-lead electrocardiogram (ECG) remains a widely used tool in the basic cardiac evaluation of children and adolescents. With the emergence of inherited arrhythmia syndromes, the period of cardiac repolarization has been the focus of attention. So far, data on cardiac repolarization and its normal variants in healthy children are scarce. This may cause uncertainties in the differentiation between pathologies and normal variants. As abnormal autonomic regulation seems to be a major influencing factor on cardiac repolarization, this study aimed to evaluate the parameters of cardiac repolarization of children in extremely good physical shape to obese children to improve knowledge about cardiac repolarization in these subgroups of pediatric patients that are vastly affected by the alterations of autonomic regulation. Methods: A total of 426 pediatric volunteers (84 lean, healthy controls; 130 obese healthy pediatric volunteers; and 212 elite athletes) were enrolled in the study, and the parameters of cardiac repolarization were determined in 12-lead ECG. Results: Most importantly, there were no pathological findings, neither in the healthy controls nor in the obese or athletes. Athletes showed overall shorter corrected QT intervals than children from the other groups. This is also true if a correction of the QT interval is performed using the Hodges formula to avoid bias due to a tendency to lower heart rates in athletes. Athletes showed the shortest Tpeak-to-end ratios between the groups. The comparison of athletes from primarily strength and power sports versus those from endurance sports showed endurance-trained athletes to have significantly longer QT intervals. Conclusions: This study suggests that neither obesity nor extensive sports seems to result in pathological cardiac repolarization parameters in healthy children. Therefore, pathology has to be assumed if abnormal repolarization parameters are seen and might not be simply attributed to the child's habitus or an excellent level of fitness. [ABSTRACT FROM AUTHOR]

Background: Infection with human immunodeficiency virus (HIV) affects muscle mass, altering independent activities of people living with HIV (PLWH). Resistance training alone (RT) or combined with aerobic exercise (AE) is linked to improved muscle mass and strength maintenance in PLWH. These exercise benefits have been the focus of different meta-analyses, although only a limited number of studies have been identified up to the year 2013/4. An up-to-date systematic review and meta-analysis concerning the effect of RT alone or combined with AE on strength parameters and hormones is of high value, since more and recent studies dealing with these types of exercise in PLWH have been published. Methods: Randomized controlled trials evaluating the effects of RT alone, AE alone or the combination of both (AERT) on PLWH was performed through five web-databases up to December 2017. Risk of bias and study quality was attained using the PEDro scale. Weighted mean difference (WMD) from baseline to post-intervention changes was calculated. The I2 statistics for heterogeneity was calculated. Results: Thirteen studies reported strength outcomes. Eight studies presented a low risk of bias. The overall change in upper body strength was 19.3 Kg (95% CI: 9.8–28.8, p< 0.001) after AERT and 17.5 Kg (95% CI: 16–19.1, p< 0.001) for RT. Lower body change was 29.4 Kg (95% CI: 18.1–40.8, p< 0.001) after RT and 10.2 Kg (95% CI: 6.7–13.8, p< 0.001) for AERT. Changes were higher after controlling for the risk of bias in upper and lower body strength and for supervised exercise in lower body strength. A significant change towards lower levels of IL-6 was found (-2.4 ng/dl (95% CI: -2.6, -2.1, p< 0.001). Conclusion: Both resistance training alone and combined with aerobic exercise showed a positive change when studies with low risk of bias and professional supervision were analyzed, improving upper and, more critically, lower body muscle strength. Also, this study found that exercise had a lowering effect on IL-6 levels in PLWH. [ABSTRACT FROM AUTHOR]

There are strong genetic components to cardiorespiratory fitness and its response to exercise training. It would be useful to understand the differences in the genomic profile of highly trained endurance athletes of world class caliber and sedentary controls. An international consortium (GAMES) was established in order to compare elite endurance athletes and ethnicity-matched controls in a case-control study design. Genome-wide association studies were undertaken on two cohorts of elite endurance athletes and controls (GENATHLETE and Japanese endurance runners), from which a panel of 45 promising markers was identified. These markers were tested for replication in seven additional cohorts of endurance athletes and controls: from Australia, Ethiopia, Japan, Kenya, Poland, Russia and Spain. The study is based on a total of 1520 endurance athletes (835 who took part in endurance events in World Championships and/or Olympic Games) and 2760 controls. We hypothesized that world-class athletes are likely to be characterized by an even higher concentration of endurance performance alleles and we performed separate analyses on this subsample. The meta-analysis of all available studies revealed one statistically significant marker (rs558129 at GALNTL6 locus, p = 0.0002), even after correcting for multiple testing. As shown by the low heterogeneity index (I2 = 0), all eight cohorts showed the same direction of association with rs558129, even though p-values varied across the individual studies. In summary, this study did not identify a panel of genomic variants common to these elite endurance athlete groups. Since GAMES was underpowered to identify alleles with small effect sizes, some of the suggestive leads identified should be explored in expanded comparisons of world-class endurance athletes and sedentary controls and in tightly controlled exercise training studies. Such studies have the potential to illuminate the biology not only of world class endurance performance but also of compromised cardiac functions and cardiometabolic diseases. [ABSTRACT FROM AUTHOR]

The article presents a study which investigates the prevalence of complex aberrant Epstein-Barr virus (EBV) patterns in an athletic endurance population and to determine the athletes' complex serology. The study uses serological testing of 202 advance endurance athletes and avidity determination to differentiate acute, recent, and past infections. The results reveal that athletes show 35 negative, 6 unresolvable, 1 acute, 11 recent, 122 past, and 27 aberrant past while control group shows 31 negative, 4 unresolvable, 1 acute, 1 recent, 135 past, and 28 cases of aberrant past. The study concludes that no evidence found on the susceptibility of endurance athletes to EBV infections compared to general population.

Abstract: The Arg16Gly single nucleotide polymorphism of the human β 2-adrenoceptor (ADRB2) gene was evaluated in a case-control study that included 313 white male elite endurance athletes and 297 white male sedentary controls (SCs) recruited in a multicenter project from North America, Finland, and Germany. The groups were matched by country of origin. The elite endurance athletes were required to have a maximum oxygen uptake ≥75 mL·kg−1·min−1 (mean [SD], 79.0 [3.5]), whereas SC subjects had to be sedentary with a measured maximum oxygen uptake ≤50 mL·kg−1·min−1 (40.1 [7.0]). Polymerase chain reaction technique was used to amplify the single nucleotide polymorphism–containing region in codon 16 of the ADRB2 gene. ADRB2 genotypes were in Hardy-Weinberg equilibrium in both groups. Genotypes did not differ between countries or sports of the athletes. The χ 2 analysis for the genotype distribution showed a significant difference between the 2 cohorts (P = .030), suggesting a positive association between the tested Arg16Gly polymorphism and endurance performance. Comparing carriers vs non-carriers for the 2 alleles, an excess of Gly allele carriers was seen in the SC group (P = .009), indicating an unfavorable effect of the Gly allele with respect to the performance status. In conclusion, we found suggestive evidence that the Arg16Gly polymorphism in the gene encoding for the β 2-adrenergic receptor may associate with endurance performance status in white men. [Copyright &y& Elsevier]

Reviews of several articles on exercise genomics are presented which includes the reports "Exercise and Diet Affect Quantitative Trait Loci for Body Weight and Composition Traits in an Advanced Intercross Population of Mice, by L. J. Leamy, S. A. Kelly, K. Hua, and D. Pomp in a 2012 issue of the journal "Physiological Genomics," "Variation in the Uncoupling Protein 2 and 3 Genes and Human Performance," by S. S. Dhamrait, A. G. Williams, and S. H. Day et al. in a 2012 issue of the "Journal of Applied Physiology," and "Knock-in Mice for the R50X Mutation in the PYGM Gene Present With McArdle Disease," by G. Nogales-Gadea, T. Pinos, and A. Lucia et al. in a 2012 issue of the journal "Brain."