In this meta-analysis, we examined the quantitative relation between meat consumption or avoidance, depression, and anxiety.
In June 2020, we searched 5 online databases for primary studies examining differences in depression and anxiety between meat abstainers and meat consumers that offered a clear (dichotomous) distinction between these groups. 20 studies met the selection criteria representing 171,802 participants with 157,778 meat consumers and 13,259 meat abstainers. We calculated the magnitude of the effect between meat consumers and meat abstainers with bias correction (Hedges’s geffect size) where higher and positive scores reflect better outcomes for meat consumers.
Meat consumption was associated with lower depression (Hedges’s g = 0.216, 95% CI [0.14 to 0.30], p < 0.001) and lower anxiety (g = 0.17, 95% CI [0.03 to 0.31], p = 0.02) compared to meat abstention. Compared to vegans, meat consumers experienced both lower depression (g = 0.26, 95% CI [0.01 to 0.51], p = 0.041) and anxiety (g = 0.15, 95% CI [−0.40 to 0.69], p = 0.598). Sex did not modify these relations. Study quality explained 58% and 76% of between-studies heterogeneity in depression and anxiety, respectively. The analysis also showed that the more rigorous the study, the more positive and consistent the relation between meat consumption and better mental health.
The current body of evidence precludes causal and temporal inferences.
In recent years, evidence has accumulated with regard to the ubiquity of pleiotropy across the genome, and shared genetic etiology is thought to play a large role in the widespread comorbidity among psychiatric disorders and risk factors.
Recent methods investigate pleiotropy by estimating genetic correlation from genome-wide association summary statistics. More comprehensive estimates can be derived from the known relatedness between genetic relatives. Analysis of extended twin pedigree data allows for the estimation of genetic correlation for additive and non-additive genetic effects, as well as a shared household effect.
Here we conduct a series of bivariate genetic analyses in extended twin pedigreedata on lifetime major depressive disorder (MDD) and 3 indicators of lifestyle, namely smoking behavior, physical inactivity, and obesity, decomposing phenotypic variance and covariance into genetic and environmental components. We analyze lifetime MDD and lifestyle data in a large multigenerational dataset of 19,496 individuals by variance component analysis in the ‘Mendel’ software.
We find genetic correlationsfor MDD and smoking behavior (rg = 0.249), physical inactivity (rg = 0.161), body-mass index (rg = 0.081), and obesity (rg = 0.155), which were primarily driven by additive genetic effects.
These outcomes provide evidence in favor of a shared genetic etiology between MDD and the lifestyle factors.
“Energy compensation and adiposity in humans”, Vincent Careau, Lewis G. Halsey, Herman Pontzer, Philip N. Ainslie, Lene F. Andersen, Liam J. Anderson, Lenore Arab, Issad Baddou, Kweku Bedu-Addo, Ellen E. Blaak, Stephane Blanc, Alberto G. Bonomi, Carlijn V.C. Bouten, Maciej S. Buchowski, Nancy F. Butte, Stefan G.J.A. Camps, Graeme L. Close, Jamie A. Cooper, Sai Krupa Das, Richard Cooper, Lara R. Dugas, Simon D. Eaton, Ulf Ekelund, Sonja Entringer, Terrence Forrester, Barry W. Fudge, Annelies H. Goris, Michael Gurven, Catherine Hambly, Asmaa El Hamdouchi, Marije B. Hoos, Sumei Hu, Noorjehan Joonas, Annemiek M. Joosen, Peter Katzmarzyk, Kitty P. Kempen, Misaka Kimura, William E. Kraus, Robert F. Kushner, Estelle V. Lambert, William R. Leonard, Nader Lessan, Corby K. Martin, Anine C. Medin, Erwin P. Meijer, James C. Morehen, James P. Morton, Marian L. Neuhouser, Theresa A. Nicklas, Robert M. Ojiambo, Kirsi H. Pietiläinen, Yannis P. Pitsiladis, Jacob Plange-Rhule, Guy Plasqui, Ross L. Prentice, Roberto A. Rabinovich, Susan B. Racette, David A. Raichlen, Eric Ravussin, John J. Reilly, Rebecca M. Reynolds, Susan B. Roberts, Albertine J. Schuit, Anders M. Sjödin, Eric Stice, Samuel S. Urlacher, Giulio Valenti, Ludo M. Van Etten, Edgar A. Van Mil, Jonathan C.K. Wells, George Wilson, Brian M. Wood, Jack Yanovski, Tsukasa Yoshida, Xueying Zhang, Alexia J. Murphy-Alford, Cornelia U. Loechl, Amy H. Luke, Jennifer Rood, Hiroyuki Sagayama, Dale A. Schoeller, William W. Wong, Yosuke Yamada, John R. Speakman, IAEADLW database group (2021-08-27; biology, psychology):
Degree of energy compensation varied between people of different body composition
Understanding the impacts of activity on energy balance is crucial. Increasing levels of activity may bring diminishing returns in energy expenditure because of compensatory responses in non-activity energy expenditures. This suggestion has profound implications for both the evolution of metabolism and human health. It implies that a long-term increase in activity does not directly translate into an increase in total energy expenditure (TEE) because other components of TEE may decrease in response—energy compensation.
We used the largest dataset compiled on adult TEE and basal energyexpenditure (BEE) (n = 1,754) of people living normal lives to find that energy compensation by a typical human averages 28% due to reduced BEE; this suggests that only 72% of the extra calories we burn from additional activity translates into extra calories burned that day. Moreover, the degree of energy compensation varied considerably between people of different body compositions. This association between compensation and adiposity could be due to among-individual differences in compensation: people who compensate more may be more likely to accumulate body fat. Alternatively, the process might occur within individuals: as we get fatter, our body might compensate more strongly for the calories burned during activity, making losing fat progressively more difficult.
Determining the causality of the relationship between energy compensation and adiposity will be key to improving public health strategies regarding obesity.
[Keywords: activity, basal metabolic rate, daily energy expenditure, energy management models, exercise, Homo sapiens, trade-offs, weight loss, energy compensation]
…To further illustrate the compensation occurring at the within-individual level, we ran a second bivariate mixed model with AEE and BEE as the dependent variables. In this model, the within-individual covariance was statistically-significantly negative (Table S2B). The within-individual correlation (±SE) between AEEand BEE was r = −0.58 ± 0.08 (Figure 4B). Hence, during extended periods when the studied cohort expended more energy on activity, they compensated by reducing energy expended on basal processes (but individuals with higher-than-average AEE do not necessarily have alower-than-average BEE). The within-individual slope in these peopleindicates particularly strong energy compensation between AEE and BEE (Figure 4B). That is, in this sample of people, the calories they burn during bouts of activity are almost entirely compensated for by reducing energy expended on other processes such that variation in activity had little impact on TEE.
Prior research has described women’s experiences with exercise-induced orgasm (EIO). However, little is known aboutmen’s experiences with EIO, the population prevalence of EIO, or theassociation of EIO with other kinds of orgasm. Using U.S. probability survey data, the objectives of the present research were to:
describe the lifetime prevalence of exercise-induced orgasm (EIO) and sleep orgasm;
assess respondents’ age at first experience of EIO as well as thetype of exercise connected with their first EIO;
examine associations between lifetime EIO experience and orgasm at respondents’ most recent partnered sexual event; and
examine associations between lifetime EIO experience and sleep orgasms.
Data were from the 2014 National Survey of Sexual Health and Behavior (1,012 men and 1,083 women, ages 14 years and older).
About 9% of respondents reported having ever experienced exercise-induced orgasm. More men than women reported having experienced orgasm during sleep at least once in their lifetime (66.3% men, 41.8% women). The mean age for women’s first EIO was statistically-significantly older than men (22.8 years women, 16.8 years men). Respondents described a wide range of exercises as associated with their first EIO (i.e., climbing ropes, abdominalexercise, yoga). Lifetime EIO experience was associated with lifetime sleep orgasms but not with event-level orgasm during partnered sex.
Implications related to understanding orgasm and recommendations for clinicians and sex educators are discussed.
…Exercise-Induced Orgasm: In their reports of interviews with thousands of people living in the United States, Kinsey et al. (1948, 1953) ventured that about 5% of people had experienced orgasms from physical exercise or muscular tension. However, questions about orgasms during exercise were not standardized in their interviews, and thus their estimate was based largely on information volunteered by respondents.
To our knowledge, there has been only one systematic study of exercise-induced orgasm (EIO) (Herbenick & Fortenberry, 2011). That study used an online convenience survey that specifically recruited women who had prior experience with sexual arousal or orgasm from exercise. Thus, the study design was not situated to estimate a population-based prevalence of EIO. Also, the researchers surveyed only women, leaving men’s experience with exercise orgasms unexamined. In their convenience survey, Herbenick and Fortenberry found that women reported an average age of 19 years at first EIO experience and that the kinds of exercise participants recalled as most often associated with their first EIO were traditional abdominal exercises (e.g., sit-ups, crunches, Roman’s chair leg raises), climbing ropes or poles, and lifting weights—all of which engage the core musculature as part of strength training or stabilization (e.g., Oliva-Lozano & Muyor, 2020). This finding was consistent with descriptions of EIO in popular media, where the term “coregasm” was first coined by editors at Men’s Health magazine to reflect correspondence they had received from their readers about unexpectedly experiencing orgasms during exercises that engage core abdominal musculature, whether for strength or for stability (Men’s Health, 2007).
Most women in the Herbenick and Fortenberry (2011) survey indicated that they didn’t fantasize sexually in connection with experiencing EIO; also, most generally felt happy about their experience. However, the survey did not assess any aspects of respondents’ orgasm experiences outside of the exercise context, even though doing so might have helped to situate EIO within broader experiences of genitalresponse and orgasm. For example, it is not known to what extent EIO is an idiosyncratic experience—a bodily quirk, even—or if it reflects something larger about how a person’s body and orgasmic response are organized. The present research extends the limited literature on EIO by—in a U.S. nationally representativesample—assessing participants’ age at first EIO experience,examining EIO among men as well as adolescents, and exploringrelationships between EIO and other kinds or orgasm, including orgasms that occur during sleep.
[Keywords: exercise-induced orgasm, orgasm, sleep orgasm, nocturnal emission, probability sample]
Observational, cross-sectional and longitudinal studies showed that physical activity and sedentary behaviour are associated with adiposity-related traits, apparently in a bidirectional manner. Physical activity is also suggested to suppress the genetic risk of adiposity.
Since phenotypic associations with genetic variants are not subject to reverse causation or confounding, they may be used as tools to shed light on cause and effect in this complex interdependency. We review the evidence for shared genetics of physical activity and adiposity-related traits and for gene-by-physical activity interactions on adiposity-related traits in human studies. We outline limitations, challenges and opportunities in studying and understanding of these relationships.
In summary, physical activity and sedentary behaviour are genetically correlated with body mass index and fat percentage but may not be correlated with lean body mass. Mendelian randomisation analyses show that physical activity and sedentary behaviour have bidirectional relationships with adiposity. Several studies suggest that physical activity suppresses genetic risk of adiposity. No studies have yet tested whether adiposity enhances genetic predisposition to sedentariness.
The complexity of the comprehensive causal model makes the assessment of the single or combined components challenging. Substantial progress in this field may need long-term intervention studies.
Triangulation across the results from genetically informative designs supports the existence of causal effects of exercise on mental health as well as residual confounding by genetic factors that independently influence participation in regular exercise and mental health outcomes.
A model explaining the heritability of voluntary exercise behaviour in terms of genetic moderation of its positive mental health effects can explain how causal effects co-exist with genetic pleiotropy.
The model calls for further research with strategies that use genomic information to improve the success of interventions on regular exercise behaviour.
Regular exercise is associated with mental health throughout the life course but the chain-of-causality underlying this association remains contested. I review results from genetically informative designs that examine causality, including the discordant monozygotic twin design, multivariate genetic models, Mendelian Randomization, and stratification on polygenic risk scores. Triangulation across the results from these and the standard designs for causal inference (RCT, prospective studies) in the extant literature supports the existence of causal effects of exercise on mental health as well as residual confounding by genetic factors that independently influence participation in regular exercise and mental health outcomes. I present an update of our earlier model for the genetic determinants of voluntary exercise behaviour. The model allows causal effects of regular exercise on mental health to co-exist with genetic pleiotropy through differences in the genetic sensitivity to the mental health benefits of exercise. The model encourages research on strategies that use genomic information to improve the success of interventions on regular exercise behaviour.
Question: Do vitamin D, omega-3, and a strength-training exercise program alone or in combination prevent 6 health outcomes among relatively healthy adults aged 70 years or older?
Findings: In this randomized trial that included 2157 adults aged 70 years or older, 3-year treatment with vitamin D3 (2000 IU/d), with omega-3 fatty acids (1 g/d), or with a strength-training exercise program did not result in statistically-significant differences in improvement in systolic or diastolic blood pressure, nonvertebral fractures, physical performance, infection rate, or cognition.
Meaning: These findings do not support the use of vitamin D, omega-3, or a strength-training exercise program for these clinical outcomes among relatively healthy older adults. Abstract
Importance: The benefits of vitamin D, omega-3 fatty acids, and exercise in disease prevention remain unclear.
Objective: To test whether vitamin D, omega-3s, and a strength-training exercise program, alone or in combination, improved 6 health outcomes among older adults.
Design, Setting, and Participants: Double-blind, placebo-controlled, 2 × 2 × 2 factorial randomized clinical trial among 2157 adults aged 70 years or older who had no major health events in the 5 years prior to enrollment and had sufficient mobility and good cognitive status. Patients were recruited between December 2012 and November 2014, and final follow-up was in November 2017.
Interventions: Participants were randomized to 3 years of intervention in 1 of the following 8 groups: 2000 IU/d of vitamin D3, 1 g/d of omega-3s, and a strength-training exercise program (n = 264); vitamin D3 and omega-3s (n = 265); vitamin D3 and exercise (n = 275); vitamin D3 alone (n = 272); omega-3s and exercise (n = 275); omega-3s alone (n = 269); exercise alone (n = 267); or placebo (n = 270).
Main Outcomes and Measures: The 6 primary outcomes were change in systolic and diastolic blood pressure (BP), Short Physical Performance Battery (SPPB), Montreal Cognitive Assessment (MoCA), and incidence rates (IRs) of nonvertebral fractures and infections over 3 years. Based on multiple comparisons of 6 primary end points, 99% confidence intervals are presented and p < 0.01 was required for statistical-significance.
Results: Among 2157 randomized participants (mean age, 74.9 years; 61.7% women), 1900 (88%) completed the study. Median follow-up was 2.99 years. Overall, there were no statistically-significant benefits of any intervention individually or in combination for the 6 end points at 3 years. For instance, the differences in mean change in systolic BP with vitamin D vs no vitamin D and with omega-3s vs no omega-3s were both −0.8 (99% CI, –2.1 to 0.5) mm Hg, with p < 0.13 and p < 0.11, respectively; the difference in mean change in diastolic BP with omega-3s vs no omega-3s was –0.5 (99% CI, –1.2 to 0.2) mm Hg; p = 0.06); and the difference in mean change in IR of infections with omega-3s vs no omega-3s was –0.13 (99% CI, –0.23 to –0.03), with an IR ratio of 0.89 (99% CI, 0.78–1.01; p = 0.02). No effects were found on the outcomes of SPPB, MoCA, and incidence of nonvertebral fractures). A total of 25 deaths were reported, with similar numbers in all treatment groups.
Conclusions and Relevance: Among adults without major comorbidities aged 70 years or older, treatment with vitamin D3, omega-3s, or a strength-training exercise program did not result in statistically-significant differences in improvement in systolic or diastolic blood pressure, nonvertebral fractures, physical performance, infection rates, or cognitive function. These findings do not support the effectiveness of these 3 interventions for these clinical outcomes.
Objective:: Efforts to prevent depression, the leading cause of disability worldwide, have focused on a limited number of candidate factors. Using phenotypic and genomic data from over 100,000 UK Biobank participants, the authors sought to systematically screen and validate a wide range of potential modifiable factors for depression.
Methods:: Baseline data were extracted for 106 modifiable factors, including lifestyle (eg., exercise, sleep, media, diet), social (eg., support, engagement), and environmental (eg., green space, pollution) variables. Incident depression was defined as minimal depressive symptoms at baseline and clinically-significant depression at follow-up. At-risk individuals for incident depression were identified by polygenic risk scores or by reported traumatic life events. An exposure-wide association scan was conducted to identify factors associated with incident depression in the full sample and among at-risk individuals. Two-sample Mendelian randomization was then used to validate potentially causal relationships between identified factors and depression.
Results:: Numerous factors across social, sleep, media, dietary, and exercise-related domains were prospectively associated with depression, even among at-risk individuals. However, only a subset of factors was supported by Mendelian randomization evidence, including confiding in others (odds ratio = 0.76, 95% CI = 0.67, 0.86), television watching time (odds ratio = 1.09, 95% CI = 1.05–1.13), and daytime napping (odds ratio = 1.34, 95% CI = 1.17–1.53).
Conclusions:: Using a two-stage approach, this study validates several actionable targets for preventing depression. It also demonstrates that not all factors associated with depression in observational research may translate into robust targets for prevention. A large-scale exposure-wide approach combined with genetically informed methods for causal inference may help prioritize strategies for multimodal prevention in psychiatry.
Background: Recently we provided evidence for a leptin-independent homeostatic regulation, the gravitostat, of body weight in rodents. The aim of the present translational proof of concept study was to test the gravitostat hypothesis in humans.
Methods: We conducted a randomized controlled single center trial (ClinicalTrial.gov number, NCT03672903), to evaluate the efficacy of artificially increased weight loading on body weight in subjects with mild obesity (BMI 30–35 kg/m2). Subjects were either treated with a heavy ( = high load; 11% of body weight) or light ( = low load; 1% of body weight) weight vest for eight hours per day for three weeks. The primary outcome was change in body weight. Secondary outcomes included change in body fat mass and fat-free mass as measured using bioelectrical impedance analysis.
Findings: In total 72 participants underwent randomization and 69 (36 high load and 33 low load) completed the study for the primary outcome. High load treatment resulted in a more pronounced relative body weight loss compared to low load treatment (mean difference −1.37%, 95% confidence interval (CI), −1.96 to −0.79; p = 1.5 × 10−5). High load treatment reduced fat mass (−4.04%, 95% CI, −6,53 to −1.55; p = 1.9 × 10−3) but not fat free mass (0.43%, 95% CI, −1.47 to 2.34; p = 0.65) compared to low load treatment.
Interpretation: Increased weight loading reduces body weight and fat mass in obese subjects in a similar way as previously shown in obese rodents. These findings demonstrate that there is weight loading dependent homeostatic regulation of body weight, the gravitostat, also in humans.
The use of music during training represents a special paradigm for trainers to stimulate people undertaking different types of exercise. However, the relationship between the tempo of music and perception of effort during different metabolic demands is still unclear. Therefore, the aim of this research was to determine whether high intensity exercise is more sensitive to the beneficial effects of music than endurance exercise. This study assessed 19 active women (age 26.4 ± 2.6 years) during endurance (walking for 10′ at 6.5 km/h on a treadmill) and high intensity (80% on 1-RM) exercise under four different randomly assigned conditions: no music (NM), with music at 90–110 bpm (LOW), with music at 130–150 bpm (MED), and with music at170–190 bpm (HIGH). During each trial, heart rate (HR) and the ratingof perceived exertion (RPE) were assessed. Repeated analysis of variance measures was used to detect any differences between the four conditions during high intensity and low intensity exercise. RPE showed more substantial changes during the endurance exercises (11%), than during high intensity exercise (6.5%), between HIGH and NM conditions. The metabolic demand during the walking exercise increased between NM and HIGH bpm conditions. This study indicates the benefits of music under stress conditions as well as during endurance and high intensity training. The results demonstrate that the beneficial effects of music are more likely to be seen in endurance exercise. Consequently, music may be considered an important tool to stimulate people engaging in low intensity physical exercise.
Objective: To determine the implications of car ownership for physical activity and weight in a global city.
Design: Quasi-experimental cross sectional study.
Setting: Beijing, China, 2011-15.
Participants: People aged 18 and older from a random sample of households who had entered a permit lottery to purchase a vehicle between January 2011 and November 2015.
Interventions: Permit allowing purchase of a vehicle within six months of permit issuance.
Main outcome measures: Transit use (number of subway and bus rides each week), physical activity (minutes of walking or bicycling each day), and weight, measured once in early 2016.
Results: Of 937 people analysed in total, 180 had won a permit to purchase a new vehicle. Winning the permit lottery resulted in the purchase of an additional vehicle 91% of the time (95% confidence interval 89% to 94%; p < 0.001). About five years after winning, winners took statistically-significantly fewer weekly transit rides (−2.9 rides (−5.1 to −0.7); p = 0.01) and walked and cycled statistically-significantly less (−24.2 minutes (−40.3 to −8.1); p = 0.003) than those who did not win the lottery. Average weight did not change statistically-significantly between lottery winners and losers. Among those aged 50 and older, however, winners’ weight had increased relative to that of losers (10.3 kg (0.5 to 20.2); p = 0.04) 5.1 years after winning.
Conclusions: These data indicate that vehicle ownership in a rapidly growing global city led to long term reductions in physical activity and increase in weight. Continuing increases in car use and ownership in developing and middle income countries could adversely affect physical health and obesity rates.
Metformin is sometimes proposed to be an “anti-aging” drug, based on preclinical experiments with lower-order organisms and numerous retrospective data on beneficial health outcomes for type 2 diabetics. Large prospective, placebo-controlled trials are planned, in pilot stage or running, to find a new use (or indication) for an aging population. As one of the metformin trials has “frailty” as its endpoint, similar to a trial with a plant-derived senolytic, the latter class of novel anti-aging drugs is briefly discussed. Concerns exist not only for vitamin B12 and B6 deficiencies, but also about whether there are adverse effects of metformin on individuals who try to remain healthy by maintaining cardiovascular fitness via exercise.
…Conclusions, Recommendations, and Perspectives: The rationale for the ongoing or planned metformin trials is almost exclusively based on observations (associations) of potential benefits in a diabetic (or prediabetic) population. Its efficacy even in an at-risk cohort of aged people has not yet been proven. Metformin is associated with a higher risk of vitamin B12 and vitamin B6 deficiency, which may result in an increased risk of cognitive dysfunction . Supplementation is strongly recommended to metformin users.
Of greater concern are the results of small trials in which the effects of metformin on metabolic responses to exercise or on cardiorespiratory fitness were tested. In a placebo-controlled, double-blind, crossover trial with healthy young subjects, metformin caused a small but statistically-significant decline in maximal aerobic capacity . A double-blind, placebo-controlled landmark trial with older adults with one risk factor for T2D investigated the effects of metformin and 12 weeks of aerobic exercise . Contrary to expectations—namely, that the effects of exercise and the drug would be additive–“metformin attenuated the increase in whole-body insulin sensitivity and abrogated the exercise-mediated increase in skeletal muscle mitochondrial respiration.” The results of the (repurposing) MASTERS trial (NCT02308228;Metformin to Augment Strength Training Effective Response in Seniors)  will be instructive. MASTERS is testing the hypothesis that older individuals’ long-term treatment with metformin augments the effects of resistance exercise, especially in the “nonresponder” aging population.
There is evidence from human twin and family studies as well as mouse and rat selection experiments that there are considerable interindividual differences in the response of cardiorespiratory fitness (CRF) and other cardiometabolic traits to a given exercise programme dose. We developed this consensus statement on exercise response variability following a symposium dedicated to this topic. There is strong evidence from both animal and human studies that exercise training doses lead to variable responses. A genetic component contributes to exercise training response variability.
In this consensus statement, we (1) briefly review the literature on exercise response variability and the various sources of variations in CRF response to an exercise programme, (2) introduce the key research designs and corresponding statistical models with an emphasis on randomised controlled designs with or without multiple pretests and post-tests, crossover designs and repeated measures designs, (3) discuss advantages and disadvantages of multiple methods of categorizing exercise response levels-a topic that is of particular interest for personalized exercise medicine and (4) outline approaches that may identify determinants and modifiers of CRF exercise response. We also summarise gaps in knowledge and recommend future research to better understand exercise response variability.
…Human studies designed to investigate CRF response variability: The vast majority of studies on the effects of chronic exercise on CRF focus on main effects and group differences and ignore interindividual CRF response variability. Studies specifically designed to determine the variability of response to exercise report an extraordinary heterogeneity in CRF response. There is variability in improvement to a standardised dose of exercise ranging from no gain in VO2max to about 1 L improvement of O2 uptake.
Here we summarise the findings of selected studies that examined individual variability in CRF (VO2max) response to endurance-type exercise training. The selection criteria used to identify suitable trials included: (1) recruitment of previously sedentary adults, (2) exercise interventions were standardised and supervised, (3) intervention duration was 12 weeks or greater, (4) study examined variability in CRF response and (5) included aerobic/endurance-type exercise. Combination (endurance and resistance) and resistance-only exercise were not considered. 8 studies met the inclusion criteria, with all but 2 having sample sizes of at least 30 participants (range 18–720). Table 1 provides a description of the study designs, exercise programmes, study population and mean change in CRF.
The Chinese National Twin Registry (CNTR) currently includes data from 61 566 twin pair from 11 provinces or cities in China. Of these, 31 705, 15 060 and 13 531 pairs are monozygotic, same-sex dizygotic and opposite-sex dizygotic pairs, respectively, determined by opposite sex or intrapair similarity. Since its establishment in 2001, the CNTR has provided an important resource for analysing genetic and environmental influences on chronic diseases especially cardiovascular diseases. Recently, the CNTR has focused on collecting biologic specimens from disease-concordant or disease-discordant twin pairs or from twin pairs reared apart. More than 8000 pairs of these twins have been registered, and blood samples have been collected from more than 1500 pairs.
In this review, we summarize the main findings from univariate and multivariate genetic effects analyses, gene-environment interaction studies, omics studies exploring DNA methylation and metabolomic markers associated with phenotypes. There remains further scope for CNTR research and data mining. The plan for future development of theCNTR is described. The CNTR welcomes worldwide collaboration.
Both fibroblast growth factors (FGFs), by binding to FGF receptors(FGFRs), and activation of the gravitostat, by artificial loading, decrease the body weight (BW). Previous studies demonstrate that both the FGF system and loading have the capacity to regulate BW independently of leptin. The aim of the current study was to determine the possible interactions between the effect of increased loading and the FGF system for the regulation of BW. We observed that the BW-reducing effect of increased loading was abolished in mice treated with a monoclonal antibody directed against FGFR1c, suggesting interactions between the two systems. As serum levels of endocrine FGF21 and hepatic FGF21mRNA were increased in the loaded mice compared with the control mice, we first evaluated the loading response in FGF21 over expressing mice with constant high FGF21 levels. Leptin treatment, but not increased loading, decreased the BW in the FGF21-overexpressing mice, demonstrating that specifically the loading effect is attenuated in the presence of high activity in the FGF system. However, as FGF21 knockout mice displayed a normal loadingresponse on BW, FGF21 is neither mediating nor essential for the loading response. In conclusion, the BW-reducing effect of increased loading but not of leptin treatment is blocked by high activity in the FGF system. We propose that both the gravitostat and the FGF system regulate BW independently of leptin and that pharmacologically enhanced activity in the FGF system reduces the sensitivity of the gravitostat.
The heritability of exercise behavior (EB) in young adults is substantial (60%–81%).
Several parameters measured in adolescence were correlated with adult EB.
These correlates showed statistically-significant genetic associations with adult EB.
A large part of the covariation between EB and the correlates was due to genetic causes.
Objectives: To improve the success of interventions aimed to increase moderate to vigorous physical activity, we need to better understand the correlates of the extensive individual differences in voluntary exercise activities. Starting in adolescence, genetic effects become a dominant factor in explaining individual differences in voluntary exercise behavior. Here we aim to establish the prospective contribution of potential correlates of voluntary exercise behavior to its heritability.
Design: In a sample of adolescent and young adult twins, data on potential correlates of exercise behavior were collected using surveys (time point 1, n = 373) and a laboratory study (time point 2, n = 499). Information on personality, perceived barriers & benefits, subjective and objective exercise ability and the affective response to exercise were collected in a set of healthy adolescent twin pairs (16–18y) and their non-twin siblings (12–25y). Almost 3 years later, the subjects were sent an online follow-up survey on their current exercise status (time point 3, n = 423).
Methods: In bivariate models, the phenotypic (co)variance in these correlates and exercise behavior at all time points were decomposed in sources of genetic (co)variance and environmental (co)variance. The correlates that were statistically-significant associated with exercise behavior at time point 1 or 2 and showed statistically-significant genetic correlations to exercise behavior at time point 3 were used in 2 further analyses: Multiple regression analysis to predict exercise behavior at time point 3, and a genetic analysis in a common 2-factor model, that tested the overlap in genetic factors influencing these correlates and exercise behavior.
Results: Personality (Extraversion), perceived benefits and barriers, exercise-induced affective response (Energy measured after the cycling test), and subjective and objective exercise ability (VO2max) showed statistically-significant phenotypic and genetic association with exercise behavior at time point 3. The genetic correlation between the 2 latent factors in the common 2-factor model was 0.51, indicating that part of the heritability in exercise behavior derives from genetic variants that also influence these correlates.
Conclusions: Given their shared genetic basis and predictive power we assert that individual differences in extraversion, perceived benefits and barriers, exercise-induced feelings of energy, and subjective and objective exercise ability can be used to develop stratified interventions for adolescent and young adult exercise behavior. In addition, our results provide the first clues on ‘where to look’ for specific genetic variants for voluntary exercise behavior.
Leptin has been the only known homeostatic regulator of fat mass, but we recently found evidence for a second one, named the gravitostat. In the current study, we compared the effects of leptin and increased loading (gravitostat stimulation) on fat mass in mice with different levels of body weight (lean, overweight, and obese). Leptin infusion suppressed body weight and fat mass in lean mice given normal chow but not in overweight or obese mice given a high-fat diet for 4 and 8 weeks, respectively. The maximum effect of leptin on body weight and fat mass was obtained already at <44 ng/mL of serum leptin. Increased loading using intraperitoneal capsules with different weights decreased body weight in overweight and obese mice. Although the implantation of an empty capsule reduced the body weight in lean mice, only a nonsignificant tendency of a specific effect of increased loading was observed in the lean mice. These findings demonstrate that the gravitostat regulates fat mass in obese mice, whereas leptin regulates fat mass only in lean mice with low endogenous serum leptin levels. We propose that activation of the gravitostat primarily protects against obesity, whereas low levels of leptin protect against undernutrition.
In Iran, she was known as Green Nasim, a social media star with followings on YouTube, on Instagram and elsewhere. · In the United States, she cast a very different profile, a proponent of vegan diets, animal rights and home exercise who had increasingly become agitated by one of the tech companies that helped give her a platform… · The police said Ms. Aghdam’s anger over what she believed to be unfair treatment by YouTube had set her on a 500-mile drive from her home near San Diego to YouTube’s offices on the northern edge of Silicon Valley. · “People like me are not good for big business, like for animal business, medicine business and for many other businesses. That’s why they are discriminating and censoring us”, she said in a video posted online last year criticizing YouTube. “This is what they are doing to vegan activists and many other people who try to promote healthy, humane and smart living.”
…Ms. Aghdam was in her late 30s. In several of her videos, she said she was born in Iran, in the city of Urmia, where most people also speak Turkish, as she does in some of her videos. Ms. Aghdam had YouTube pages in Persian, Turkish and English. She explained that she and her family were members of the Baha’i faith, which faces persecution in Iran, a country with a Muslim majority. · Several of her colorful—and sometimes bizarre—videos had gone viral in Iran. Her website, which said it was quoting Western news outlets, identified her as “the first Persian female vegan bodybuilder.” · “Now the media will be faced with a new type of Iranian female which does not fit within any of their usual categorizations”, a Twitter user named Katayoon said Wednesday. · “This was shocking and saddening”, one Iranian, Bahare, wrote on Twitter of Ms. Aghdam. “We laughed so much but now it turns out all those videos were so serious for herself.” · Ms. Aghdam became especially famous for one clip in which she wears a revealing purple dress, showing cleavage, and begins to slowly strip off her clothes to reveal a pair of fake plastic breasts. “Don’t trust your eyes”, read a caption in English on the clip.
…Her personal website and videos posted to YouTube and elsewhere were filled with complaints about YouTube. “When searching for my website in google, at top of link they add ‘an error occurred’ but there is no error!” a website under Ms. Aghdam’s name, NasimeSabz.com, said in February 2016. “They add it to keep you from my visiting my site.” · Life in the United States had not been good, she said in one video from March 30. “There they kill you by ax”, she said of Iran. “Here they kill you with cotton”, referring to an Iranian expression meaning dying by something that you do not know is dangerous. · In another video, she responded to viewers who had begun to wonder if she was mentally ill: “I don’t have any special mental or physical disease, but I live on a planet filled with disease, disorders, perversions and injustices.” · The American dream appeared to be tarnished for her after she began to face hurdles in the United States. · “If you are superficial, you will think it is heaven here, that you can go naked outside and have sex left and right like other animals without any morality”, she said in one video in Persian. “But if you enter the system, you will see that it is worse than Iran”, she said. “Those who want to inform people against the system and big companies get censored.”
[Rebuttal letter: the gravitostat is supported by hypergravity; astronaut microgravity experiments are only weak counterevidence because microgravity and space travel badly damages health in many ways, hiding any potential weight gain. The gravitostat may fit in the two-systems model of weight, in which case a testable prediction is that it should have different effects in rodents with different weight/leptin combinations.]
Significance: The only known homeostatic regulator of fat mass is the leptin system. We hypothesized that there is a second homeostat regulating body weight with an impact on fat mass. In this study we have added and removed weight loads from experimental animals and measured the effects on the biological body weight. The results demonstrate that there is a body weight homeostat that regulates fat mass independently of leptin. As the body weight-reducing effect of increased loading was dependent on osteocytes, we propose that there is a sensor for body weight in the long bones of the lower extremities acting as “body scales.” This is part of a body weight homeostat, “gravitostat”, that keeps body weight and body fat mass constant.
Subjects spending much time sitting have increased risk of obesity but the mechanism for the antiobesity effect of standing is unknown. We hypothesized that there is a homeostatic regulation of body weight. We demonstrate that increased loading of rodents, achieved using capsules with different weights implanted in the abdomen or s.c. on the back, reversibly decreases the biological body weight via reduced food intake. Importantly, loading relieves diet-induced obesity and improves glucose tolerance. The identified homeostat for body weight regulates body fat mass independently of fat-derived leptin, revealing two independent negative feedback systems for fat mass regulation. It is known that osteocytes can sense changes in bone strain. In this study, the body weight-reducing effect of increased loading was lost in mice depleted of osteocytes. We propose that increased body weight activates a sensor dependent on osteocytes of the weight-bearing bones. This induces an afferent signal, which reduces body weight. These findings demonstrate a leptin-independent body weight homeostat (“gravitostat”) that regulates fat mass.
Background: Symptomatic relief is the primary goal of percutaneous coronary intervention (PCI) in stable angina and is commonly observed clinically. However, there is no evidence from blinded, placebo-controlled randomised trials to show its efficacy.
Methods: ORBITA is a blinded, multicentre randomised trial of PCI versus a placebo procedure for angina relief that was done at five study sites in the UK. We enrolled patients with severe (≥70%) single-vessel stenoses. After enrolment, patients received 6 weeks of medication optimisation. Patients then had pre-randomisation assessments with cardiopulmonary exercise testing, symptom questionnaires, and dobutamine stress echocardiography. Patients were randomised 1:1 to undergo PCI or a placebo procedure by use of an automated online randomisation tool. After 6 weeks of follow-up, the assessments done before randomisation were repeated at the final assessment. The primary endpoint was difference in exercise time increment between groups. All analyses were based on the intention-to-treat principle and the study population contained all participants who underwent randomisation. This study is registered with ClinicalTrials.gov, number NCT02062593.
Findings: ORBITA enrolled 230 patients with ischaemic symptoms. After the medication optimisation phase and between Jan 6, 2014, and Aug 11, 2017, 200 patients underwent randomisation, with 105 patients assigned PCI and 95 assigned the placebo procedure. Lesions had mean area stenosis of 84.4% (SD 10.2), fractional flow reserve of 0.69 (0.16), and instantaneous wave-free ratio of 0.76 (0.22). There was no statistically-significant difference in the primary endpoint of exercise time increment between groups (PCI minus placebo 16.6 s, 95% CI −8.9 to 42.0, p = 0.200). There were no deaths. Serious adverse events included four pressure-wire related complications in the placebo group, which required PCI, and five major bleeding events,including two in the PCI group and three in the placebo group.
Interpretation: In patients with medically treated angina and severe coronary stenosis, PCI did not increase exercise time by more than the effect of a placebo procedure. The efficacy of invasive procedures can be assessed with a placebo control, as is standard for pharmacotherapy.
“Genome-wide meta-analysis associates HLA-DQA1/DRB1 and LPA and lifestyle factors with human longevity”, Peter K. Joshi, Nicola Pirastu, Katherine A. Kentistou, Krista Fischer, Edith Hofer, Katharina E. Schraut, David W. Clark, Teresa Nutile, Catriona L. K. Barnes, Paul R. H. J. Timmers, Xia Shen, Ilaria Gandin, Aaron F. McDaid, Thomas Folkmann Hansen, Scott D. Gordon, Franco Giulianini, Thibaud S. Boutin, Abdel Abdellaoui, Wei Zhao, Carolina Medina-Gomez, Traci M. Bartz, Stella Trompet, Leslie A. Lange, Laura Raffield, Ashley van der Spek, Tessel E. Galesloot, Petroula Proitsi, Lisa R. Yanek, Lawrence F. Bielak, Antony Payton, Federico Murgia, Maria Pina Concas, Ginevra Biino, Salman M. Tajuddin, Ilkka Seppälä, Najaf Amin, Eric Boerwinkle, Anders D. Børglum, Archie Campbell, Ellen W. Demerath, Ilja Demuth, Jessica D. Faul, Ian Ford, Alessandro Gialluisi, Martin Gögele, MariaElisa Graff, Aroon Hingorani, Jouke-Jan Hottenga, David M. Hougaard, Mikko A. Hurme, M. Arfan Ikram, Marja Jylhä, Diana Kuh, Lannie Ligthart, Christina M. Lill, Ulman Lindenberger, Thomas Lumley, Reedik Mägi, Pedro Marques-Vidal, Sarah E. Medland, Lili Milani, Reka Nagy, William E. R. Ollier, Patricia A. Peyser, Peter P. Pramstaller, Paul M. Ridker, Fernando Rivadeneira, Daniela Ruggiero, Yasaman Saba, Reinhold Schmidt, Helena Schmidt, P. Eline Slagboom, Blair H. Smith, Jennifer A. Smith, Nona Sotoodehnia, Elisabeth Steinhagen-Thiessen, Frank J. A. van Rooij, André L. Verbeek, Sita H. Vermeulen, Peter Vollenweider, Yunpeng Wang, Thomas Werge, John B. Whitfield, Alan B. Zonderman, Terho Lehtimäki, Michele K. Evans, Mario Pirastu, Christian Fuchsberger, Lars Bertram, Neil Pendleton, Sharon L. R. Kardia, Marina Ciullo, Diane M. Becker, Andrew Wong, Bruce M. Psaty, Cornelia M. van Duijn, James G. Wilson, J. Wouter Jukema, Lambertus Kiemeney, André G. Uitterlinden, Nora Franceschini, Kari E. North, David R. Weir, Andres Metspalu, Dorret I. Boomsma, Caroline Hayward, Daniel Chasman, Nicholas G. Martin, Naveed Sattar, Harry Campbell, Tōnu Esko, Zoltán Kutalik & James F. Wilson (2017-10-13; statistics / causality, genetics / heritable, statistics / survival-analysis; backlinks):
Genomic analysis of longevity offers the potential to illuminate the biology of human aging. Here, using genome-wide association meta-analysis of 606,059 parents’ survival, we discover two regions associated with longevity (HLA-DQA1/DRB1 and LPA). We also validate previous suggestions that APOE, CHRNA3/5, CDKN2A/B, SH2B3 and FOXO3A influence longevity. Next we show that giving up smoking, educational attainment, openness to new experience and high-density lipoprotein (HDL) cholesterol levels are most positively genetically correlated with lifespan while susceptibility to coronary artery disease (CAD), cigarettes smoked per day, lung cancer, insulin resistance and body fat are most negatively correlated. We suggest that the effect of education on lifespan is principally mediated through smoking while the effect of obesity appears to act via CAD. Using instrumental variables, we suggest that an increase of one body mass index unit reduces lifespan by 7 months while 1 year of education adds 11 months to expected lifespan.
Background: Hand grip strength, a simple indicator of muscular strength, has been associated with a range of health conditions, including fractures, disability, cardiovascular disease and premature death risk. Twin studies have suggested a high (50-60%) heritability, but genetic determinants are largely unknown.
In this study, our aim was to study genetic variation associated with muscular strength in a large sample of 334,925 individuals of European descent from the UK Biobank, and to evaluate shared genetic aetiology with and causal effects of grip strength on physical and cognitive health.
Methods and Results
In our discovery analysis of 223,315 individuals, we identified 101 loci associated with grip strength at genome-wide statistical-significance (P<5×10−8). Of these, 64 were associated (P<0.01 and consistent direction) also in the replication dataset (n = 111,610). Many of the lead SNPs were located in or near genes known to have a function in developmental disorders (FTO, SLC39A8, TFAP2B, TGFA, CELF1, TCF4, BDNF, FOXP1, KIF1B, ANTXR2), and one of the most significant genes based on a gene-based analysis (ATP2A1) encodes SERCA1, the critical enzyme in calcium uptake to the sarcoplasmic reticulum, which plays a major role in muscle contraction and relaxation. Further, we demonstrated a significant enrichment of gene expression in brain-related transcripts among grip strength associations. Finally, we observed inverse genetic correlations of grip strength with cardiometabolic traits, and positive correlation with parents’ age of death and education; and showed that grip strength was causally related to fitness, physical activity and other indicators of frailty, including cognitive performance scores.
Conclusion: In our study of over 330,000 individuals from the general population, the genetic findings for hand grip strength suggest an important role of the central nervous system in strength performance. Further, our results indicate that maintaining good muscular strength is important for physical and cognitive performance and healthy aging.
Loss of adult olfactory neurons protects against diet-induced obesity
Loss of smell after obesity also reduces fat mass and insulin resistance
Loss of IGF1 receptors in olfactory sensory neurons (OSNs) improves olfaction
Loss of IGF1R in OSNs increases adiposity and insulin resistance
Olfactory inputs help coordinate food appreciation and selection, but their role in systemic physiology and energy balance is poorly understood. Here we demonstrate that mice upon conditional ablation of mature olfactory sensory neurons (OSNs) are resistant to diet-induced obesity accompanied by increased thermogenesis in brown and inguinal fat depots. Acute loss of smell perception after obesity onset not only abrogated further weight gain but also improved fat mass and insulin resistance. Reduced olfactory input stimulates sympathetic nerve activity, resulting in activation of β-adrenergic receptors on white and brown adipocytes to promote lipolysis. Conversely, conditional ablation of the IGF1 receptor in OSNs enhances olfactory performance in mice and leads to increased adiposity and insulin resistance. These findings unravel a new bidirectional function for the olfactory system in controlling energy homeostasis in response to sensory and hormonal signals.
Our sense of smell is key to the enjoyment of food, so it may be no surprise that in experiments at the University of California, Berkeley, obese mice who lost their sense of smell also lost weight.
What’s weird, however, is that these slimmed-down but smell-deficient mice ate the same amount of fatty food as mice that retained their sense of smell and ballooned to twice their normal weight.
In addition, mice with a boosted sense of smell—super-smellers—got even fatter on a high-fat diet than did mice with normal smell.
The findings suggest that the odor of what we eat may play an important role in how the body deals with calories. If you can’t smell your food, you may burn it rather than store it.
These results point to a key connection between the olfactory or smell system and regions of the brain that regulate metabolism, in particular the hypothalamus, though the neural circuits are still unknown.
“This paper is one of the first studies that really shows if we manipulate olfactory inputs we can actually alter how the brain perceives energy balance, and how the brain regulates energy balance”, said Céline Riera, a former UC Berkeley postdoctoral fellow now at Cedars-Sinai Medical Center in Los Angeles.
…“Sensory systems play a role in metabolism. Weight gain isn’t purely a measure of the calories taken in; it’s also related to how those calories are perceived”, said senior author Andrew Dillin, the Thomas and Stacey Siebel Distinguished Chair in Stem Cell Research, professor of molecular and cell biology and Howard Hughes Medical Institute Investigator. “If we can validate this in humans, perhaps we can actually make a drug that doesn’t interfere with smell but still blocks that metabolic circuitry. That would be amazing.”
Significance: Chimpanzee “super strength” has been widely reported since the 1920s although a critical review of the available data suggests that the chimpanzee-human muscular performance differential is only ~1.5×. Some hypothesize that this differential reflects underlying differences in muscle mechanics. Here, we present direct measurements of chimpanzee skeletal muscle properties in comparison with those of humans and other terrestrial mammals. Our results show that chimpanzee muscle exceeds human muscle in maximum dynamic force and power output by ~1.35×. This is primarily due to the chimpanzee’s higher fast-twitch fiber content, rather than exceptional maximum isometric force or maximum shortening velocities. We suggest that muscular performance capabilities declined during hominin evolution in response to selection for repetitive, low-cost contractile behavior.
Since at least the 1920s, it has been reported that common chimpanzees (Pan troglodytes) differ from humans in being capable of exceptional feats of “super strength”, both in the wild and in captive environments. A mix of anecdotal and more controlled studies provides some support for this view; however, a critical review of available data suggests that chimpanzee mass-specific muscular performance is a more modest 1.5× greater than humans on average. Hypotheses for the muscular basis of this performance differential have included greater isometric force-generating capabilities, faster maximum shortening velocities, and/or a difference in myosin heavy chain (MHC) isoform content in chimpanzee relative to human skeletal muscle. Here, we show that chimpanzee muscle is similar to human muscle in its single-fiber contractile properties, but exhibits a much higher fraction of MHC II isoforms. Unlike humans, chimpanzee muscle is composed of ~67% fast-twitch fibers (MHC IIa+IId). Computer simulations of species-specific whole-muscle models indicate that maximum dynamic force and power output is 1.35 times higher in a chimpanzee muscle than a human muscle of similar size. Thus, the superior mass-specific muscular performance of chimpanzees does not stem from differences in isometric force-generating capabilities or maximum shortening velocities—as has long been suggested—but rather is due in part to differences in MHC isoform content and fiber length. We propose that the hominin lineage experienced a decline in maximum dynamic force and power output during the past 7–8 million years in response to selection for repetitive, low-cost contractile behavior.
[Keywords: chimpanzee, human, muscle, myosin heavy chain, muscle modeling]
Background: Exercise is inversely related with cardiovascular disease (CVD), but large-scale studies of incident CVD events are lacking. Moreover, little is known about genetic determinants of fitness and physical activity, and modifiable effects of exercise in individuals with elevated genetic risk of CVD. Finally, causal analyses of exercise traits are limited.
Methods: We estimated associations of grip strength, physical activity, and cardiorespiratory fitness with CVD and all-cause death in up to 502,635 individuals from the UK Biobank. We also examined these associations in individuals with different genetic burden on coronary heart disease (CHD) and atrial fibrillation (AF). Finally, we performed genome-wide association study (GWAS) of grip strength and physical activity, as well as Mendelian randomization analysis to assess the causal role of grip strength in CHD.
Grip strength, physical activity, and cardiorespiratory fitness showed strong inverse associations with incident cardiovascular events and all-cause death (for composite CVD; HR, 0.78, 95%CI, 0.77–0.80; HR, 0.94, 95% CI, 0.93–0.95, and HR, 0.67, 95% CI, 0.63–0.71, per SD change, respectively). We observed stronger associations of grip strength with CHD and AF for individuals in the lowest tertile of genetic risk (pinteraction = 0.006, pinteraction = 0.03, respectively), but the inverse associations were present in each category of genetic risk. We report 27 novel genetic loci associated with grip strength and 2 loci with physical activity, with the strongest associations in FTO (rs56094641, p = 3.8×10−24) and SMIM2 (rs9316077, p = 1.4×10−8), respectively. By use of Mendelian randomization, we provide evidence that grip strength is causally related to CHD.
Maintaining physical strength is likely to prevent future cardiovascular events, also in individuals with elevated genetic risk for CVD.
National Institutes of Health (1 R01 HL135313–01), Knut and Alice Wallenberg Foundation (2013.0126), and the Finnish Cultural Foundation.
It has long been discussed whether fitness or fatness is a more important determinant of health status. If the same genetic factors that promote body fat percentage (body fat%) are related to cardiorespiratory fitness (CRF), part of the concurrent associations with health outcomes could reflect a common genetic origin. In this study we aimed to 1) examine genetic correlations between body fat% and CRF; 2) determine whether CRF can be attributed to a genetic risk score (GRS) based on known body fat% increasing loci; and 3) examine whether the fat mass and obesity associated (FTO) locus associates with CRF.
Genetic correlations based on pedigree information were examined in a family based cohort (n = 230 from 55 families). For the genetic association analyses, we examined two Danish population-based cohorts (ntotal = 3206). The body fat% GRS was created by summing the alleles of twelve independent risk variants known to associate with body fat%. We assessed CRF as maximal oxygen uptake expressed in millilitres of oxygen uptake per kg of body mass (VO2max), per kg fat-free mass (VO2maxFFM), or per kg fat mass (VO2maxFM). All analyses were adjusted for age and sex, and when relevant, for body composition.
We found a significant negative genetic correlation between VO2max and body fat% (ρG = −0.72 (SE ±0.13)). The body fat% GRS associated with decreased VO2max (β = −0.15 mL/kg/min per allele, p = 0.0034, age and sex adjusted). The body fat%-increasing FTO allele was associated with a 0.42 mL/kg/min unit decrease in VO2max per allele (p = 0.0092, age and sex adjusted). Both associations were abolished after additional adjustment for body fat%. The fat% increasing GRS and FTO risk allele were associated with decreased VO2maxFM but not with VO2maxFFM.
Our findings suggest a shared genetic etiology between whole body fat% and CRF.
The production of heat, ie., thermogenesis, is a substantial component of the metabolic rate, which in turn affects weight gain and health. Thermogenesis is linked to physical activity (PA) level. However, it is not known whether intrinsic exercise capacity, aging, and long-term voluntary running affect core body temperature.
Here we use rat models selectively bred to differ in maximal treadmill endurance running capacity (Low capacity runners, LCR and Highcapacity Runners, HCR), that as adults are divergent for aerobic exercise capacity, aging, and metabolic disease risk to study the connection between PA and body temperature.
10 high capacity runner (HCR) and 10 low capacity runner (LCR) female rats were studied between 9 and 21 months of age. Rectal body temperature of HCR and LCR rats was measured before and after 1-year voluntary running/control intervention to explore the effects of aging and PA. Also, we determined whether injected glucose and spontaneous activity affect the body temperature differently between LCR and HCRrats at 9 vs. 21 months of age. HCRs had on average 1.3°C higher bodytemperature than LCRs (p < 0.001). Aging decreased the body temperature level of HCRs to similar levels with LCRs. The opportunity to run voluntarily had a statistically-significant impact on the body temperature of HCRs (p < 0.001) allowing them to maintain body temperature at a similar level as when at younger age. Compared to LCRs, HCRs were spontaneously more active, had higher relativegastrocnemius muscle mass and higher UCP2, PGC-1α, cytochrome c, andOXPHOS levels in the skeletal muscle (p < 0.050).
These results suggest that higher PA level together with greater relative muscle mass and higher mitochondrial content/function contribute to the accumulation of heat in the HCRs. Interestingly, neither aging nor voluntary training had a statistically-significant impact on core body temperature of LCRs. However, glucose injectionresulted in a lowering of the body temperature of LCRs (p < 0.050), but not that of HCRs.
In conclusion, rats born with high intrinsic capacity for aerobic exercise and better health have higher body temperature compared to rats born with low exercise capacity and disease risk. Voluntary running allowed HCRs to maintain high body temperature during aging, which suggests that high PA level was crucial in maintaining the high body temperature of HCRs.
Obesity and metabolic disorders have become a notable world-wide epidemic. The pathogenesis of metabolic diseases, such as metabolic syndrome and type 2 diabetes, has begun to negatively affect life expectancy of current generations. Low aerobic capacity has shown to be a strong predictor of mortality both in rodents and humans. Exercise is known to increase an individual’s aerobic capacity; interestingly, recent studies have suggested that genetic background may play a substantial role in the physical activity level of an individual. The purpose of this study was to investigate the role of genetic background and physical activity on skeletal muscle properties, metabolism and lifespan.
The study consisted of three parts:
a cross-sectional voluntary running intervention in high-capacity runner (HCR) and low-capacity runner (LCR) rats,
a longitudinal voluntary running intervention in HCR and LCR rats, and
a long-term follow-up study with physical activity discordant human twins.
Our study showed that low intrinsic aerobic capacity is associated with fast muscular fatigue and slow metabolic recovery after maximal muscle contractions. At the whole-body level, low intrinsic aerobic capacity was linked to low body temperature, which may play a role in the onset of gaining extra weight and, thus, developing metabolic disorders. High intrinsic aerobic capacity in turn was associated with elevated SIRT3 protein level in skeletal muscle, which is possibly linked to increased lifespan. Nevertheless, vigorous physical activity commenced at adult age did not reduce mortality or increase lifespan in rodents. High long-term participation in vigorous leisure-time physical activity did predict statistically-significantly reduced mortality in dizygotic twins; however, there was no difference in the lifespan of monozygotic twins that are genetically identical. HCRs were more physically active both in control and voluntary running groups when compared to corresponding LCR groups. Also, the persistent discordances in participation of vigorous physical activity were statistically-significantly more common in dizygotic twin pairs than in monozygotic pairs stating that genes have an influence on the persistent voluntary participation in vigorous leisure-time physical activity.
Our results indicated that genetic predisposition plays a substantial role in exercise participation, hence, genetic pleiotropy may partly explain the associations observed previously between high physical activity and mortality.
Observational studies report a strong inverse relationship between leisure-time physical activity and all-cause mortality. Despite suggestive evidence from population-based associations, scientists have not been able to show a beneficial effect of physical activity on the risk of death in controlled intervention studies among individuals who have been healthy at baseline. On the other hand, high cardiorespiratory fitness is known to be a strong predictor of reduced mortality, even more robust than physical activity level itself.
Here, in both animals and/or human twins, we show that the same genetic factors influence physical activity levels, cardiorespiratory fitness and risk of death. Previous observational follow-up studies in humans suggest that increasing fitness through physical activity levels could prolong life; however, our controlled interventional study with laboratory rats bred for low and high intrinsic fitness contrast with these findings. Also, we find no evidence for the suggested association using pairwise analysis among monozygotic twin pairs who are discordant in their physical activity levels.
Based on both our animal and human findings, we propose that genetic pleiotropy might partly explain the frequently observed associations between high baseline physical activity and later reduced mortality in humans.
Purpose: The main aim of the present study (FITFATTWIN) was to investigate how physical activity level is associated with body composition, glucose homeostasis, and brain morphology in young adult male monozygotic twin pairs discordant for physical activity.
Methods: From a population-based twin cohort, we systematically selected 10 young adult male monozygotic twin pairs (age range, 32–36 yr) discordant for leisure time physical activity during the past 3 yr. On the basis of interviews, we calculated a mean sum index for leisure time and commuting activity during the past 3 yr (3-yr LTMETindex expressed as MET-hours per day). We conducted extensive measurements on body composition (including fat percentage measured by dual-energy x-ray absorptiometry), glucose homeostasis including homeostatic model assessment index and insulin sensitivity index (Matsuda index, calculated from glucose and insulin values from an oral glucose tolerance test), and whole brain magnetic resonance imaging for regional volumetric analyses.
Results: According to pairwise analysis, the active twins had lower body fat percentage (p = 0.029) and homeostatic model assessment index (p = 0.031) and higher Matsuda index (p = 0.021) compared with their inactive co-twins. Striatal and prefrontal cortex (subgyral and inferior frontal gyrus) brain gray matter volumes were larger in the nondominant hemisphere in active twins compared with those in inactive co-twins, with a statistical threshold of p < 0.001.
Conclusions: Among healthy adult male twins in their mid-30s, a greater level of physical activity is associated with improved glucose homeostasis and modulation of striatum and prefrontal cortex gray matter volume, independent of genetic background. The findings may contribute to later reduced risk of type 2 diabetes and mobility limitations.
Evolutionary explanations regarding the differential preference for particular traits hold that preferences arose due to traits’ association with increased potential for reproductive fitness. Assessments of physical attractiveness have been shown to be related to perceived and measured levels of health, an important fitness-related trait.
Despite the robust association between physical attractiveness and health observed in the extant literature, a number of theoretical and methodological concerns remain. Specifically, the research in this area possesses a lack of specificity in terms of measures of health, a reliance on artificial social interactions in assessing physical attractiveness, and a relatively infrequent use of non-student samples and leaves unaddressed the confounding effects of raters of attractiveness.
Using these concerns as a springboard, the current study employed data from the National Longitudinal Study for Adolescent Health (n ≈ 15,000; aged 25 to 34 years) to assess the relationship between physical attractiveness and various specific and overall measures of health. Logistic and OLS regression models illustrated a robust association between physical attractiveness and various measures of health, controlling for a variety of confounding factors.
In sum, the more attractive a respondent was rated, the less likely he or she was to report being diagnosed with a wide range of chronic diseases and neuropsychological disorders. Importantly, this finding was observed for both sexes. These analyses provide further support for physical attractiveness as a phenotypic marker of health.
The findings are discussed in reference to evolutionary theory, and the limitations of the study and future research suggestions are also addressed.
If you are concerned with American obesity rates and turn to the cross sectional data to try and figure out what is going on, it is easy to reach a flawed conclusion. The correlation between education and obesity, for example, seems quite clear. The poorer and less educated an American is, the more likely he or she is to be obese. Looking at this data it seems reasonable to suggest that something about poverty is making people more obese—perhaps cruddy processed food is the only thing America’’s poor and less educated can afford to buy, or maybe the poor live in urban areas where people do not exercise. These hypotheses are plausible… until you look at the time series. It then becomes apparent that the rich and educated are gaining weight at the same rate as the poor. Poverty cannot explain this.
It is very difficult to make meaningful claims about causation—or even correlation!—on the basis of cross section data alone. Often times seemingly perfect, statistically-significant correlations disappear when the same variables are viewed over a longer stretch of time. In other cases—as in this one—time series data reveals that the real story isn’’t about variance between two groups at all, but about the rate at which each group is changing. It is all too easy to be fooled by the Cross Section Illusion.
Recent studies have indicated that antioxidant supplementation may blunt adaptations to exercise, such as mitochondrial biogenesis induced by endurance training. However, studies in humans are sparse and results are conflicting.
Isolated vitamin C and E supplements are widely used, and unravelling the interference of these vitamins in cellular and physiological adaptations to exercise is of interest to those who exercise for health purposes and to athletes.
Our results show that vitamin C and E supplements blunted the endurance training-induced increase of mitochondrial proteins (COX4), which is important for improving muscular endurance.
Training-induced increases in VO2max and running performance were not detectably affected by the supplementation.
The present study contributes to understanding of how antioxidants may interfere with adaptations to exercise in humans, and the results indicate that high dosages of vitamins C and E should be used with caution.
In this double-blind, randomised, controlled trial, we investigated the effects of vitamin C and E supplementation on endurance training adaptations in humans. Fifty-four young men and women were randomly allocated to receive either 1000 mg of vitamin C and 235 mg of vitamin E or a placebo daily for 11 weeks. During supplementation, the participants completed an endurance training programme consisting of three to four sessions per week (primarily of running), divided into high-intensity interval sessions [4–6 × 4–6 min; >90% of maximal heart rate (HRmax)] and steady state continuous sessions (30–60 min; 70–90% of HRmax). Maximal oxygen uptake (VO2max), submaximal running and a 20 m shuttle run test were assessed and blood samples and muscle biopsies were collected, before and after the intervention. Participants in the vitamin C and E group increased their VO2max (mean ± s.d.: 8 ± 5%) and performance in the 20 m shuttle test (10 ± 11%) to the same degree as those in the placebo group (mean ± s.d.: 8 ± 5% and 14 ± 17%, respectively). However, the mitochondrial marker cytochrome c oxidase subunit IV (COX4) and cytosolic peroxisomeproliferator-activated receptor-γ coactivator 1 α (PGC-1α) increased in the m. vastus lateralis in the placebo group by 59 ± 97% and 19 ± 51%, respectively, but not in the vitamin C and E group (COX4: −13 ±54%; PGC-1α: −13 ± 29%; p ≤ 0.03, between groups). Furthermore, mRNAlevels of CDC42 and mitogen-activated protein kinase 1 (MAPK1) in the trained muscle were lower in the vitamin C and E group than in the placebo group (p ≤ 0.05). Daily vitamin C and E supplementation attenuated increases in markers of mitochondrial biogenesis following endurance training. However, no clear interactions were detected for improvements in VO2max and running performance. Consequently, vitamin C and E supplementation hampered cellular adaptations in the exercised muscles, and although this did not translate to the performance tests applied in this study, we advocate caution when considering antioxidant supplementation combined with endurance exercise.
Social cognitive models of health behavior propose that individual differences in leisure time exercise behavior are influenced by the attitudes towards exercise. At the same time, large scale twin-family studies show a large influence of genetic factors on regular exercise behavior.
This twin-sibling study aimed to unite these findings by demonstrating that exercise attitudes can be heritable themselves. Secondly, the genetic and environmental cross-trait correlations and the monozygotic (MZ) twin intrapair differences model were used to test whether the association between exercise attitudes and exercise behavior can be causal. Survey data were obtained from 5,095 twins and siblings (18–50 years).
A genetic contribution was found for exercise behavior (50% in males, 43% in females) and for the 6 exercise attitude components derived from principal component analysis: perceived benefits (21, 27%), lack of skills, support and/or resources (45, 48%), time constraints (25, 30%), lack of energy (34, 44%), lack of enjoyment (47, 44%), and embarrassment (42, 49%). These components were predictive of leisure time exercise behavior (R2 = 28%). Bivariate modeling further showed that all the genetic (0.36 < |rA| < 0.80) and all but 2 unique environmental (0.00 < |rE| < 0.27) correlations between exercise attitudes and exercise behavior were statistically-significantly different from zero, which is a necessary condition for the existence of a causal effect driving the association. The correlations between the MZ twins’ difference scores were in line with this finding.
It is concluded that exercise attitudes and exercise behavior are heritable, that attitudes and behavior are partly correlated through pleiotropic genetic effects, but that the data are compatible with a causal association between exercise attitudes and behavior.
After the conquests of Alexander the Great and during the reign of his numerous successors, the tradition of combat sports games became institutionalized by the elite of an Hellenized warlike aristocracy in Asia. The heroic cult of the Greeks was perpetuated as far as Central Asia, improving the local traditions by building a gymnasium in every new city of the colonies. The various technical aspects of ancient Greek combat sports were transmitted as well in order to improve effectiveness in close-combat fighting.
To trace back these technical features, a detailed description of wrestling, boxing and pankration as developed in ancient Greece are compared together with their East-Asian counterparts.
…Eurydamas from Cyrene is said to have lost his teeth during his fight and swallowed them so as not to give satisfaction to his adversary, according to the Roman author Aelian.52 The boxers used head protection and leather bands, called imantes or sphaira, around their fists in the place of gloves.53 In Roman times, boxers also wore iron rings called caestus54 on their fists, for the amusement of the Roman spectators during gladiatorial contests. Philostratus, a Greek living in the Roman Empire in the third century A.D., describes clearly how the bands of leather were tightened around the boxers’ fists and why pigskin was prohibited in boxing competitions.55 Unlike modern boxing, pygmachia also used various open-hand strikes, as indicated by various sources. In Homer’s verses, Apollo came down to earth to kill Patroclus with an “open-palm strike to his back”56 and Damoxenos pierced the internal organs of Kreugas with a finger strike (plate 2).57 Vase paintings also depicted ancient boxing practices, as in the case of the pseudo-Panathenaic amphora from Exarchos in Locrid by the painter Eucharides (~500 B.C.), which shows a palm strike and a forearm block (plate 3).
The painting of Eucharides also shows the unusual “distended” abdomen of the athletes, as if filled with air, a characteristic that is seen today in China among the adepts of traditional combat sports. The use of the principles of pneuma together with other concepts from Greek medicine led to training in various breathing techniques that were later lost in the West because of the mind/body split introduced by the Catholic Church. Indeed there is no trace of this practice in the Western world today. The explanation of Pausanias concerning the fight of Damoxenos, that “with the sharpness of his nails and the force of blow he drove his hand into his adversary, caught his bowels, and tore them out”,58 is incomplete in my opinion.
Pausanias, a second-century A.D. traveler and geographer, must have had a superficial understanding of what he heard, since he had no practical knowledge of ancient pygmachia training. To pierce the human body with one’s bare hands requires strengthening of the fingers together with explosive power developed through breathing exercises, allowing one to apply the muscular strength of one’s whole body instantaneously when striking (plate 4). Standing without changing position, and breathing techniques such as those used by Melankomas or those described by Oreibasius,59 were an integral part of a boxer’s training to fill his body with pneuma. Today in China, the best traditional boxers60 are those who apply the notion of an inner vital breath or energy. Oreibasius called this type of exercise “side therapy” or apotherapia, techniques which developed the athlete’s strength through inner breathing exercises or massage to activate the pneuma within their bodies. He advised combat-sports athletes to breathe from the lower abdomen, and to push the pneuma down using other types of breathing exercises, and also to speak with a deep voice, in order to open and fill the “empty spaces of the body.”
…Pythagoras himself is said to have been crowned in boxing, according to Eusebios of Cesarea (A.D. 265–339). During the 48h Olympiad (588 B.C.), Glycon of Croton won the stadion race. Pythagoras of Samos was excluded from boxing in the junior category because of his effeminate appearance, but he was still able to participate in the adult contest and beat all his adversaries.70Diogenes Laerce also writes that, having been expelled from the junior category, Pythagoras went on to participate in the adult contest and beat all his adversaries.71
Some of the boxers had such excellent technique that they were never hit by their opponents. They were called “the untouchables” (atravmatisti), and included famous boxers such as Kleoxenos of Alexandria (240 B.C.; one-hundred thirty-fifth Olympiad), Melankomas of Caria,72 and Hippomachos. Hippomachos, son of Moschion, sustained no blows or injuries from his 3 successive opponents in the games.73Julius Africanus (A.D. ~200) wrote that Kleoxenos had never been injured in any of his fights, and that he won all the Panhellenic games without being hurt. Melankomas was particularly well versed in standing positions, which are practiced today in China,74 but have been lost to the Western world.75 He could remain standing for 2 days with his 2 hands raised,76 a practice far removed from modern boxing. Being so skilful at his art, he was never beaten by his opponents and neither did he hurt them. He just let them exhaust themselves. Dio Chrysostom (A.D. 30–117) wrote that he had perfect control over his mind and body:
The most fantastic thing is that he was not only undefeated by his adversaries, but also by hard training in the heat, avoiding hunger, and sexual desires. The men who wish to be superior to their adversaries should not be defeated by these things. If Melankomas did not have control of himself (enkrateo),77 I doubt that he would be superior in strength, even if he was naturally strong.78
An influential book written by A. Mosso in the late nineteenth century proposed that fatigue that “at first sight might appear an imperfection of our body, is on the contrary one of its most marvelous perfections. The fatigue increasing more rapidly than the amount of work done saves us from the injury which lesser sensibility would involve for the organism” so that “muscular fatigue also is at bottom an exhaustion of the nervous system.” It has taken more than a century to confirm Mosso’s idea that both the brain and the muscles alter their function during exercise and that fatigue is predominantly an emotion, part of a complex regulation, the goal of which is to protect the body from harm. Mosso’s ideas were supplanted in the English literature by those of A. V. Hill who believed that fatigue was the result of biochemical changes in the exercising limb muscles–“peripheral fatigue”–to which the central nervous system makes no contribution. The past decade has witnessed the growing realization that this brainless model cannot explain exercise performance. This article traces the evolution of our modern understanding of how the CNS regulates exercise specifically to insure that each exercise bout terminates whilst homeostasis is retained in all bodily systems. The brain uses the symptoms of fatigue as key regulators to insure that the exercise is completed before harm develops. These sensations of fatigue are unique to each individual and are illusory since their generation is largely independent of the real biological state of the athlete at the time they develop. The model predicts that attempts to understand fatigue and to explain superior human athletic performance purely on the basis of the body’s known physiological and metabolic responses to exercise must fail since subconscious and conscious mental decisions made by winners and losers, in both training and competition, are the ultimate determinants of both fatigue and athletic performance.
Introduction: The aim of this study was to investigate the relative influence of genetic and environmental factors on children’s leisure time exercise behavior through the classic twin design.
Methods: Data were taken from The Netherlands Twin Register. The twins were 7 (n = 3966 subjects), 10 (n = 3562), and 12-yr-olds (n = 8687), with longitudinal data for 27% of the sample. Parents were asked to indicate the children’s regular participation in leisure time exercise activities, including frequency and duration. Resemblance between monozygotic and dizygotic twins for weekly MET-hours spent on exercise activities was analyzed as a function of their genetic relatedness.
Results: Average weekly MET-hours increased with age for both boys (age 7 yr: 14.0 (SD = 11.8); age 10 yr: 22.6 (SD = 18.7); age 12 yr: 28.4 (SD = 24.9)) and girls (age 7 yr: 9.7 (SD = 9.5); age 10 yr: 15.3 (SD = 15.1); age 12 yr: 19.3 (SD = 19.8)). Around 13% of boys and girls across all age groups did not participate in any regular leisure time exercise activities. Tracking of exercise behavior from age 7 to 12 yr was modest (0.168 < r < 0.534). For boys, genetic effects accounted for 24% (confidence interval, 18%-30%) of the variance at age 7 yr, 66% (53%-81%) at age 10 yr, and 38% (32%-46%) at age 12 yr. For girls, this was 22% (15%-30%), 16% (9%-24%), and 36% (30%-43%), respectively. Environmental influences shared by children from the same family explained 71%, 25%, and 50% of the variance in boys (age 7, 10, and 12 yr) and 67%, 72%, and 53% in girls. The shared environment influencing exercise behavior was partially different between boys and girls.
Conclusion: Our results stress the important role of shared environment for exercise behavior in young children.
Individual differences in adolescent exercise behavior are to a large extent explained by shared environmental factors. The aim of this study was to explore to what extent this shared environment represents effects of cultural transmission of parents to their offspring, generation specific environmental effects or assortative mating. Survey data on leisure-time exercise behavior were available from 3,525 adolescent twins and their siblings (13–18 years) and 3,138 parents from 1,736 families registered at the Netherlands Twin Registry. Data were also available from 5,471 adult twins, their siblings and spouses similar in age to the parents. Exercise participation (No/Yes, using a cut-off criterion of 4 metabolic equivalents and 60 min weekly) was based on questions on type, frequency and duration of exercise. A model to analyze dichotomous data from twins, siblings and parents including differences in variance decomposition across sex and generation was developed. Data from adult twins and their spouses were used to investigate the causes of assortative mating (correlation between spouses = 0.41, due to phenotypic assortment). The heritability of exercise in the adult generation was estimated at 42%. The shared environment for exercise behavior in adolescents mainly represents generation specific shared environmental influences that seem somewhat more important in explaining familial clustering in girls than in boys (52 versus 41%). A small effect of vertical cultural transmission was found for boys only (3%). The remaining familial clustering for exercise behavior was explained by additive genetic factors (42% in boys and 36% in girls). Future studies on adolescent exercise behavior should focus on identification of the generation specific environmental factors.
Background: Twin studies offer a ‘natural experiment’ that can estimate the magnitude of environmental and genetic effects on a target phenotype. We hypothesised that fidgetiness and enjoyment of activity would be heritable but that objectively-measured daily activity would show a strong shared environmental effect.
Methodology/Principal Findings: In a sample of 9–12 year-old same-sex twin pairs (234 individuals; 57 MZ, 60 DZ pairs) we assessed three dimensions of physical activity: (1) objectively-measured physical activity using accelerometry, (2) ‘fidgetiness’ using a standard psychometric scale, and (3) enjoyment of physical activity from both parent ratings and children’s self-reports. Shared environment effects explained the majority (73%) of the variance in objectively-measured total physical activity (95% confidence intervals (CI): 0.63–0.81) with a smaller unshared environmental effect (27%; CI: 0.19–0.37) and no statistically-significant genetic effect. In contrast, fidgetiness was primarily under genetic control, with additive genetic effects explaining 75% (CI: 62–84%) of the variance, as was parent’s report of children’s enjoyment of low 74% (CI: 61–82%), medium 80% (CI: 71–86%), and high impact activity (85%; CI: 78–90%), and children’s expressed activity preferences (60%, CI: 42–72%).
Conclusions: Consistent with our hypothesis, the shared environment was the dominant influence on children’s day-to-day activity levels. This finding gives a strong impetus to research into the specific environmental characteristics influencing children’s activity, and supports the value of interventions focused on home or school environments.
The purpose of this study was to examine changes in the contribution of genetic and environmental influences to leisure time physical activity among male and female twins over a 6-year follow-up. At baseline the sample comprised 4,280 monozygotic and 9,276 dizygotic twin individuals, and at follow-up 4,383 monozygotic and 9,439 dizygotic twin individuals. Participants were aged 18–54 years at baseline. Genetic modeling results showed that genetic influences on leisure time physical activity declined from baseline (44%) to follow-up (34%). Most of the genetic influences identified at baseline were present at followup (rg= 0.72). Specific environmental influences increased from baseline (56%) to follow-up (66%) while at follow-up new environmental time-specific influences were observed (re= 0.23). The model with sex differences showed a higher estimate of genetic influences for men than women both at baseline (men 47% vs. women 42%) and at follow-up (men 38% vs. women 31%). The additive genetic correlation for this phenotype was greater for men (rg= 0.79) than women (rg= 0.64). The specific environmental influences were corresponding; at baseline men 53% and women 56% and at follow-up men 62% and women 69%. The environmental correlations between the two time points were similar for men (re= 0.21) and for women (re= 0.24). In conclusion, in a sample of healthy twins most of the genetic influences on leisure time physical activity expressed at baseline were present at 6 years of follow-up. New specific environmental factors underlying follow-up leisure time physical activity were observed.
Background: The health benefits of regular physical activity are well established. However, the relative contribution of heritable and environmental factors to physical activity participation remains controversial. Using a cut-point of 60 minutes of total activity per week, data from the GenomEUtwin project revealed consistent genetic influence on physical activity participation in 37,051 twin pairs from seven countries. We hypothesized that the heritability of physical activity participation would be attenuated using the CDC/ACSM recommended minimum threshold of 150 minutes of moderate intensity activity per week.
Methods: Data were obtained from 1,389 twin pairs from the community-based University of Washington Twin Registry. Twin similarity in physical activity participation using both cut-points was analyzed using tetrachoric correlations and structural equation modeling in all same-sex pairs.
Results: Correlations were higher in monozygotic (rMZ = 0.43, 95% CI = 0.33–0.54) than dizygotic pairs (rDZ = 0.30, 95% CI = 0.12–0.47) using the 60 minute cut-point. However, differences were attenuated using the 150 minute standard (rMZ = 0.30, 95% CI = 0.20–0.40; rDZ = 0.25, 95% CI = 0.07–0.42). Using the lower cut-point, the best fitting model of twin resemblance only included additive genetics and unique environment, with a heritability of 45%. In contrast, using the higher threshold, the best fitting model included the common and unique environment, with the unique environment contributing 72% of the variance.
Conclusion: Unique environment factors provide the strongest influence on physical activity participation at levels recommended for health benefits.
Background: A sedentary lifestyle remains a major threat to health in contemporary societies. To get more insight in the relative contribution of genetic and environmental influences on individual differences in exercise participation, twin samples from seven countries participating in the GenomEUtwin project were used.
Methodology: Self-reported data on leisure time exercise behavior from Australia, Denmark, Finland, Norway, the Netherlands, Sweden and United Kingdom were used to create a comparable index of exercise participation in each country (60 minutes weekly at a minimum intensity of four metabolic equivalents).
Principal Findings: Modest geographical variation in exercise participation was revealed in 85,198 subjects, aged 19–40 years. Modeling of monozygotic and dizygotic twin resemblance showed that genetic effects play an important role in explaining individual differences in exercise participation in each country. Shared environmental effects played no role except for Norwegian males. Heritability of exercise participation in males and females was similar and ranged from 48% to 71% (excluding Norwegian males).
Conclusions: Genetic variation is important in individual exercise behavior and may involve genes influencing the acute mood effects of exercise, high exercise ability, high weight loss ability, and personality. This collaborative study suggests that attempts to find genes influencing exercise participation can pool exercise data across multiple countries and different instruments.
Objectives: To determine the effectiveness of vitamin D and home-based quadriceps resistance exercise on reducing falls and improving the physical health of frail older people after hospital discharge.
Design: Multicenter, randomized, controlled trial with a factorial design.
Setting: Five hospitals in Auckland, New Zealand, and Sydney, Australia.
Participants: Two hundred forty-three frail older people.
Interventions: Patients were randomized to receive a single dose of vitamin D (calciferol, 300,000 IU) or placebo tablets and 10 weeks of high-intensity home-based quadriceps resistance exercise or frequency-matched visits.
Measurements: The primary endpoints were physical health according to the short-form health survey at 3 months and falls over 6 months. Physical performance and self-rated function were secondary endpoints. Assessments took place in the participants’ homes at 3 and 6 months after randomization and were performed by blinded assessors.
Results: There was no effect of either intervention on physical health or falls, but patients in the exercise group were at increased risk of musculoskeletal injury (risk ratio = 3.6, 95% confidence interval = 1.5–8.0). Vitamin D supplementation did not improve physical performance, even in those who were vitamin D deficient (<12 ng/mL) at baseline.
Conclusion: Neither vitamin D supplementation nor a home-based program of high-intensity quadriceps resistance exercise improved rehabilitation outcomes in frail older people after hospitalization. There was no effect of vitamin D on physical performance, and the exercises increased the risk of musculoskeletal injury. These findings do not support the routine use of these interventions at these dosages in the rehabilitation of frail older people.
Background: Substantial interindividual variation is observed in sports participation and physical activity levels in youth. This study aimed to (1) estimate the relative contribution of genes, along with shared and nonshared environmental factors, to variation in sports participation index (SPI) and leisure-time physical activity (LTPA); and (2) test differences in those factors in males and females.
Methods: The sample was comprised of 411 Portuguese twin pairs of different zygosity aged 12 to 25 years. The SPI and LTPA were assessed with the Baecke questionnaire. Quantitative genetic modeling was used to test alternative models for the presence of additive gene effects (a2), common or shared environment within the family (c2), and unique environmental factors (e2).
Results: The best-fitting models showed sex-specific effects for the two phenotypes. Variance componentsfor SPI in males were a2 = 68.4%, c2 = 20%, and e2 = 11.6%; and in females, a2 = 39.8%, c2 = 28.4%, and e2 = 31.8%. For variation in LTPA, genetic factors in males explained 63%, common environment was not statistically-significant, and unique environment explained 37%. In females, contributing factors were a2 = 32%, c2 = 38%, and e2 = 30%.
Conclusions: Genetic effects explained a considerable amount of variation in SPI and LTPA, which were greater in males than in females. The relevance of shared environmental factors (family and peers) and nonshared environmental factors in SPI and LTPA is particularly evident in females.
Purpose: The beneficial effects of exercise on bone mass and strength can be attributed to the sensitivity of bone cells to mechanical stimuli. However, bone cells lose mechanosensitivity soon after they are stimulated. We investigated whether the osteogenic response to a simulated high-impact exercise program lasting 4 months could be enhanced by dividing the daily protocol into brief sessions of loading, separated by recovery periods.
Methods: The right forelimbs of adult rats were subjected to 360 load cycles · d-1, 3 d·wk-1, for 16 wk. On each loading day, one group received all 360 cycles in a single, uninterrupted bout (360×1); the other group received 4 bouts of 90 cycles/bout (90×4), with each bout separated by 3 h. After sacrifice, bone mineral content (BMC),and areal bone mineral density (aBMD) were measured in the loaded(right) and non-loaded control (left) ulnae using DXA. Volumetric BMD(vBMD) and cross-sectional area (CSA) were measured at midshaft andthe olecranon by using pQCT. Maximum and minimum second moments of area (IMAX and IMIN) were measured from the midshaft tomographs.
Results: After 16 wk of loading, BMC, aBMD, vBMD, midshaft CSA, IMAX, and IMIN were statistically-significantly greater in right (loaded) ulnae compared with left (non-loaded) ulnae in the 2 loaded groups. When the daily loading regimen was broken into 4 sessions per day (90×4), BMC, aBMD, midshaft CSA, and I(MIN) improved statistically-significantly over the loading schedule that applied the daily stimulus in a single, uninterrupted session (360×1).
Conclusion: Human exercise programs aimed at maintaining or improving bone mass might achieve greater success if the daily exercise regime is broken down into smaller sessions separated by recovery periods.
[Keywords: mechanical loading, bone adaptation, recovery, exercise, osteoporosis, BMD]
Purpose: The purpose of this review was to address the question of interindividual variation in responsiveness to regular exercise training and to define the contributions of age, sex, race, and pretraining phenotype level to this variability.
Methods: A literature review was conducted of the studies reporting interindividual variation in responsiveness to standardized and controlled exercise-training programs, and included an analysis of the contribution of age, sex, race, and initial phenotype values to the heterogeneity in VO2max, high-density lipoprotein (HDL)-C and submaximal exercise, heart rate (HR), and systolic blood pressure (SBP) training responses in subjects from the HERITAGE Family Study.
Results: Several studies have shown marked individual differences in responsiveness to exercise training. For example, VO2max responses to standardized training programs have ranged from almost no gain up to 100% increase in large groups of sedentary individuals. A similar pattern of heterogeneity has been observed for other phenotypes. Data from the HERITAGE Family Study show that age, sex, and race have little impact on interindividual differences in training responses. On the other hand, the initial level of a phenotype is a major determinant of training response for some traits, such as submaximal exercise heart rate and blood pressure (BP) but has only a minor effect on others (eg., VO2max, HDL-C). The contribution of familial factors (shared environment and genetic factors) is supported by data on substantial familial aggregation of training response phenotypes.
Conclusions: There is strong evidence for considerable heterogeneity in the responsiveness to regular physical activity. Age, sex, and ethnic origin are not major determinants of human responses to regular physical activity, whereas the pretraining level of a phenotype has a considerable impact in some cases. Familial factors also contribute substantially to variability in training response.
It has long been recognized that both smoking and sports participation tend to cluster in families. In this chapter, we first describe the current status of smoking and sports participation as cardiovascular risk factors. After an outline of the principles of the quantitative genetic approaches to the analysis of individual differences in behaviour, we will review the literature on genetic and environmental determinants of smoking and sports participation. In the second half of this chapter, results from the Dutch Twin/Family Study of Health-Related Behavior are presented.