Skip header and navigation

Refine By

38 records – page 1 of 4.

ACTN3 R577X and other polymorphisms are not associated with elite endurance athlete status in the Genathlete study.

https://arctichealth.org/en/permalink/ahliterature140771
Source
J Sports Sci. 2010 Oct;28(12):1355-9
Publication Type
Article
Date
Oct-2010
Author
Frank E Döring
Simone Onur
Ulf Geisen
Marcel R Boulay
Louis Pérusse
Tuomo Rankinen
Rainer Rauramaa
Bernd Wolfahrt
C. Bouchard
Author Affiliation
Institute of Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Kiel, Germany. vgoyrgoy@phyed.duth.gr
Source
J Sports Sci. 2010 Oct;28(12):1355-9
Date
Oct-2010
Language
English
Publication Type
Article
Keywords
Actinin - genetics
Athletes
Athletic Performance
European Continental Ancestry Group - genetics
Finland
Gene Frequency
Genotype
Germany
Homozygote
Humans
Male
North America
Odds Ratio
Physical Endurance - genetics
Polymorphism, Single Nucleotide
Abstract
Homozygosity for a premature stop codon at amino acid position 577 in the alpha-actinin-3 (ACTN3) gene leads to a-actinin-3 deficiency. This genotype is observed in approximately 18% of Caucasians. The ACTN3 R577X polymorphism has been previously associated with indicators of physical performance in several, but not all, studies. We examined the prevalence of R577X (rs1815739) and two additional haplotype tagging single nucleotide polymorphisms (htSNPs) of the ACTN3 gene (rs1791690 and rs2275998) in the Genathlete study comprising 316 male elite endurance athletes (VO2max 79.0+3.5 ml · kg(-1) · min(-1); mean +/- s) from North America, Finland, and Germany and 304 sedentary controls (VO2max 40.1+7.0 ml · kg(-1) · min(-1) matched by country of origin. The distribution of genotype and allele frequencies between the two groups was tested by Pearson chi-square and/or Fischer exact test. The prevalence of the 577X homozygote genotype was similar in endurance athletes and controls (20% and 17.5%, respectively). The resulting odds ratio for endurance performance in 577X homozygotes compared with 577R-allele carriers was 1.24 (95%CI 0.82-1.87, P = 0.3). The genotype distribution of the two htSNPs and haplotype frequencies did not differ significantly between athletes and controls. In conclusion, our findings indicate that ACTN3 R577X and other SNPs in ACTN3 are not genetic determinants of endurance performance in Caucasian males.
PubMed ID
20845221 View in PubMed
Less detail

Adiponectin and adiponectin receptor gene variants in relation to resting metabolic rate, respiratory quotient, and adiposity-related phenotypes in the Quebec Family Study.

https://arctichealth.org/en/permalink/ahliterature165769
Source
Am J Clin Nutr. 2007 Jan;85(1):26-34
Publication Type
Article
Date
Jan-2007
Author
Ruth J F Loos
Stéphanie Ruchat
Tuomo Rankinen
Angelo Tremblay
Louis Pérusse
Claude Bouchard
Author Affiliation
Human Genomics Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA.
Source
Am J Clin Nutr. 2007 Jan;85(1):26-34
Date
Jan-2007
Language
English
Publication Type
Article
Keywords
Adiponectin - genetics - metabolism
Adipose Tissue - metabolism
Adult
Basal Metabolism - genetics - physiology
Body Composition - genetics
Body Fat Distribution
Body mass index
Female
Gene Frequency
Genetic Predisposition to Disease
Genetic Variation
Humans
Longitudinal Studies
Male
Middle Aged
Obesity - genetics - metabolism
Oxygen Consumption - genetics - physiology
Phenotype
Polymorphism, Single Nucleotide
Promoter Regions, Genetic
Quebec
Receptors, Adiponectin
Receptors, Cell Surface - genetics - metabolism
Abstract
Despite adiponectin's presumed role in fatty acid oxidation and energy homeostasis, little is known about the effect of gene variants on substrate oxidation, energy expenditure, and adiposity-related phenotypes.
We examined the effects of genetic variation in adiponectin (ADIPOQ) and adiponectin receptors 1 and 2 (ADIPOR1 and ADIPOR2) on resting metabolic rate, respiratory quotient (RQ), and adiposity-related phenotypes.
We studied the associations of ADIPOQ, ADIPOR1, and ADIPOR2 polymorphisms with resting metabolic rate, RQ, and body mass index, percentage body fat, sum of 6 skinfold thicknesses, waist circumference, and total, subcutaneous, and visceral fat in 759 participants in the Québec Family Study.
The ADIPOQ 45T-->G single-nucleotide polymorphism (SNP) was significantly (P = 0.0002 to 0.04) associated with overall adiposity and abdominal adiposity; the rare homozygotes (G/G) had a leaner phenotype than did the carriers of the common allele. One SNP each in the putative promoter of ADIPOR1 (ie, -3882T-->C) and ADIPOR2 (ie, IVS1 -1352G-->A) was associated with RQ (P = 0.03 and 0.04, respectively), and the association was even stronger in nonobese persons (P = 0.02 and 0.003). Carriers of the common alleles (ADIPOR1 T and ADIPOR2 G alleles) had a lower RQ than did the rare homozygotes. A significant genotype-by-genotype interaction (P = 0.0002 to 0.02) was found between SNPs in the promoters of ADIPOQ (-3971A-->G) and ADIPOR1 (-3882T-->C). Subjects carrying the minor ADIPOQ allele (G allele) who were rare homozygotes (C/C) for the ADIPOR1 SNP had a higher RQ (P = 0.003) and greater overall (P G variant contributes to overall fatness and abdominal obesity are confirmed. Moreover, variants in the promoter region of both ADIPOR genes contribute to substrate oxidation.
Notes
Comment In: Am J Clin Nutr. 2007 Jan;85(1):1-217209169
PubMed ID
17209173 View in PubMed
Less detail

The alpha 2-adrenergic receptor gene and body fat content and distribution: the HERITAGE Family Study.

https://arctichealth.org/en/permalink/ahliterature189645
Source
Mol Med. 2002 Feb;8(2):88-94
Publication Type
Article
Date
Feb-2002
Author
Christophe Garenc
Louis Pérusse
Yvon C Chagnon
Tuomo Rankinen
Jacques Gagnon
Ingrid B Borecki
Arthur S Leon
James S Skinner
Jack H Wilmore
D C Rao
Claude Bouchard
Author Affiliation
Division of Kinesiology, Department of Preventive Medicine, Laval University, Ste-Foy, Québec, Canada.
Source
Mol Med. 2002 Feb;8(2):88-94
Date
Feb-2002
Language
English
Publication Type
Article
Keywords
Adult
African Continental Ancestry Group - genetics
Body Composition - genetics
Body mass index
Canada
European Continental Ancestry Group - genetics
Fats - analysis
Female
Gene Frequency
Genetic Predisposition to Disease
Humans
Male
Phenotype
Polymorphism, Genetic - genetics
Receptors, Adrenergic, alpha-2 - genetics
United States
Abstract
Among adrenergic receptor subtypes that regulate lipid mobilization, the alpha2-adrenergic receptor is involved in the inhibition of fatty acid mobilization from adipose tissue. A C-1291G polymorphism is located in the alpha2-adrenergic receptor gene (ADRA2A) but no association with body fat accumulation has been reported yet.
Body mass index (BMI), fat mass (FAT), percentage body fat (%FAT), trunk-to-extremity skinfold ratio (TER), sum of eight skinfolds (SF8), and abdominal subcutaneous (ASF), visceral (AVF), and total (ATF) fat areas assessed by CT scan have been measured in adult sedentary white (n = 503) and black (n = 276) subjects participating in the HERITAGE Family Study. Association between the C-1291G polymorphism and each phenotype was tested separately in men and women of each race using ANCOVA with the effects of age as covariate in addition to the effects of BMI for TER and of FAT for AVF, ASF, and ATF.
The allele frequencies of the ADRA2A C-1291G polymorphism differed between races. No association was observed in white subjects, except for a moderate effect of the polymorphism accounting for less than 1% of the variance in AVF and ATF in women. In black subjects, however, the G-1291 allele was found to be associated with an increase of TER in men (3.8% of variance accounted for by the polymorphism), while in black women it was associated with a decrease in TER (2.9%) and in AVF (2.5%).
These results suggest a role for the ADRA2A gene in determining the propensity to store fat in the abdominal area, independently of total body fatness.
PubMed ID
12080184 View in PubMed
Less detail

Association between insulin secretion, insulin sensitivity and type 2 diabetes susceptibility variants identified in genome-wide association studies.

https://arctichealth.org/en/permalink/ahliterature153680
Source
Acta Diabetol. 2009 Sep;46(3):217-26
Publication Type
Article
Date
Sep-2009
Author
Stephanie-May Ruchat
Cathy E Elks
Ruth J F Loos
Marie-Claude Vohl
S John Weisnagel
Tuomo Rankinen
Claude Bouchard
Louis Pérusse
Author Affiliation
Department of Preventive Medicine, Laval University, Quebec City, QC, Canada.
Source
Acta Diabetol. 2009 Sep;46(3):217-26
Date
Sep-2009
Language
English
Publication Type
Article
Keywords
Adult
Blood Glucose - metabolism
Diabetes Mellitus, Type 2 - genetics - metabolism
Female
Gene Frequency
Genetic Predisposition to Disease
Genome-Wide Association Study
Glucose Tolerance Test
Humans
Insulin - secretion
Insulin-Secreting Cells - secretion
Male
Middle Aged
Polymorphism, Single Nucleotide
Quebec - epidemiology
Risk factors
Abstract
Several single nucleotide polymorphisms (SNPs) for type 2 diabetes mellitus (T2DM) risk have been identified by genome wide association studies (GWAS). The objective of the present study was to investigate the impact of these SNPs on T2DM intermediate phenotypes in order to clarify the physiological mechanisms through which they exert their effects on disease etiology. We analysed 23 SNPs in 9 T2DM genes (CDKAL1, CDKN2B, HHEX/IDE, IGF2BP2, KCNJ11, SLC30A8, TCF2, TCF7L2 and WFS1) in a maximum of 712 men and women from the Quebec Family Study. The participants underwent a 75 g oral glucose tolerance test (OGTT) and were measured for glucose, insulin and C-peptide levels. Indices of insulin sensitivity and insulin secretion were derived from fasting and OGTT measurements. We confirmed the significant associations of variants in CDKAL1, CDKN2B, HHEX/IDE, KCNJ11 and TCF7L2 with insulin secretion and also found associations of some of these variants with insulin sensitivity and glucose tolerance. IGF2BP2 and SLC30A8 SNPs were not associated with insulin secretion but were with insulin sensitivity and glucose tolerance (0.002
PubMed ID
19082521 View in PubMed
Less detail

Association between mu-opioid receptor-1 102T>C polymorphism and intermediate type 2 diabetes phenotypes: results from the Quebec Family Study (QFS).

https://arctichealth.org/en/permalink/ahliterature156912
Source
Clin Exp Pharmacol Physiol. 2008 Sep;35(9):1018-22
Publication Type
Article
Date
Sep-2008
Author
Stephanie-May Ruchat
Martine Girard
S John Weisnagel
Claude Bouchard
Marie-Claude Vohl
Louis Pérusse
Author Affiliation
Department of Preventive Medicine, Division of Kinesiology, Laval University, Quebec, Canada.
Source
Clin Exp Pharmacol Physiol. 2008 Sep;35(9):1018-22
Date
Sep-2008
Language
English
Publication Type
Article
Keywords
Adult
Diabetes Mellitus, Type 2 - genetics
Female
Gene Frequency
Genetic Linkage
Genetic Predisposition to Disease
Glucose Intolerance - genetics
Glucose Tolerance Test
Humans
Insulin Resistance - genetics
Male
Middle Aged
Phenotype
Polymorphism, Single Nucleotide
Quebec
Receptors, Opioid, mu - genetics
Risk factors
Abstract
It has been suggested recently that molecules expressed both in the pancreas and hypothalamus, such as mu-opioid receptor 1 (OPRM1), could form an integrated brain-liver system, which may sense glucose levels and therefore contribute to the development of type 2 diabetes mellitus (T2DM). In the present study, we tested associations between OPRM1 gene polymorphisms (rs1799971, 102T/C and rs0648007G/A) and indices of glucose tolerance, insulin sensitivity (IS) and insulin secretion derived from plasma measures obtained in a fasting state and following a 75 g oral glucose tolerance test (OGTT) in 749 subjects from the Quebec Family Study (QFS). Polymorphisms were tested for association with glucose tolerance (normal vs IFG and T2DM combined) by calculating a chi(2) statistic and corresponding P values, whereas associations with quantitative measures of glucose tolerance, IS and insulin secretion were tested using mixed linear models implemented in the MIXED procedure of sas (SAS Institute, Cary, NC, USA). Associations were found between 102T/C OPRM1 and indices of glucose tolerance and IS. Compared with T/T homozygotes, carriers of the OPRM1 C-102 variant exhibited a better glucose tolerance with a lower (P = 0.006) glucose area under the curve (AUC) following the OGTT and a better IS with a higher (P = 0.03) value of the Cederholm index, a numerical index of the curve relating glucose uptake to the log(10) plasma insulin levels during the OGTT. The results of the present study reveal that the 102T/C OPRM1 gene polymorphism is associated with a better glucose tolerance and improved IS, both of which suggest a potential protective effect of this variant on T2DM risk.
PubMed ID
18518884 View in PubMed
Less detail

Association between the PPARalpha-L162V polymorphism and components of the metabolic syndrome.

https://arctichealth.org/en/permalink/ahliterature178847
Source
J Hum Genet. 2004;49(9):482-9
Publication Type
Article
Date
2004
Author
Julie Robitaille
Charles Brouillette
Alain Houde
Simone Lemieux
Louis Pérusse
André Tchernof
Daniel Gaudet
Marie-Claude Vohl
Author Affiliation
Lipid Research Center, CHUQ-CHUL Pavilion, 2705 Laurier Blvd, TR-93, G1V 4G2, Ste-Foy, QC, Canada.
Source
J Hum Genet. 2004;49(9):482-9
Date
2004
Language
English
Publication Type
Article
Keywords
Adult
Alcohol Drinking
Apolipoproteins B - blood
Body Weights and Measures
Cholesterol, LDL - blood - genetics
Dietary Fats
Gene Frequency
Genotype
Humans
Hypertriglyceridemia - blood - genetics
Linear Models
Male
Middle Aged
Obesity - blood - genetics
Polymorphism, Genetic
Polymorphism, Restriction Fragment Length
Quebec
Questionnaires
Receptors, Cytoplasmic and Nuclear - genetics
Smoking
Syndrome
Transcription Factors - genetics
Abstract
Genetic factors, alone or in interaction with components of the diet, are thought to be involved in the development of the metabolic syndrome. The objective of our study was first to compare the frequency of the peroxisome proliferator-activated receptor (PPAR)alpha-L162V polymorphism in a sample of men with and without the metabolic syndrome as defined by the National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATPIII) guidelines, and secondly, to evaluate gene-diet interaction effects on features of the metabolic syndrome. The PPARalpha-L162V genotype was determined in a sample of 632 men by a polymerase chain reaction-restriction length polymorphism (PCR-RFLP)-based method; fat as well as saturated fat intakes were evaluated by a dietitian-administered food frequency questionnaire. The frequency of the V162 allele was similar in men with ( n=281) and without ( n=351) the metabolic syndrome ( chi(2)=0.03, p=0.84) but was higher in subjects having simultaneously abdominal obesity, hypertriglyceridemia, and low high-density lipoprotein cholesterol (HDL-C) levels ( chi(2)=3.73, p=0.05). Carriers of the V162 were characterized by higher plasma apolipoprotein B and triglyceride (TG) levels ( p=0.10, p=0.004). In a model including the PPARalpha-L162V polymorphism, fat or saturated fat, its interaction, and covariates (smoking habits, and energy and alcohol intake), the interaction explained a significant percentage of the variance observed in waist circumference ( p
PubMed ID
15309680 View in PubMed
Less detail

Association of LIPA gene polymorphisms with obesity-related metabolic complications among severely obese patients.

https://arctichealth.org/en/permalink/ahliterature126395
Source
Obesity (Silver Spring). 2012 Oct;20(10):2075-82
Publication Type
Article
Date
Oct-2012
Author
Frédéric Guénard
Alain Houde
Luigi Bouchard
André Tchernof
Yves Deshaies
Simon Biron
Odette Lescelleur
Laurent Biertho
Simon Marceau
Louis Pérusse
Marie-Claude Vohl
Author Affiliation
Nutraceuticals and Functional Foods Institute, Laval University, Quebec City, Quebec, Canada.
Source
Obesity (Silver Spring). 2012 Oct;20(10):2075-82
Date
Oct-2012
Language
English
Publication Type
Article
Keywords
Adult
Cardiovascular diseases - blood - epidemiology - genetics
Cohort Studies
Female
Humans
Male
Metabolic Syndrome X - blood - epidemiology - genetics
Obesity, Morbid - blood - epidemiology - genetics
Polymorphism, Genetic
Polymorphism, Single Nucleotide
Quebec - epidemiology
Sequence Analysis, DNA
Sterol Esterase - blood - genetics
Triglycerides - blood
Wolman Disease - epidemiology - genetics
Abstract
The lipase A, lysosomal acid, cholesterol esterase enzyme (LIPA) is involved in the hydrolysis of triglycerides (TGs) and cholesteryl esters (CEs) delivered to lysosomes. LIPA deficiency in human causes two distinct phenotypes characterized by intracellular storage of CE and derangements in the control of cholesterol production, namely the Wolman disease (WD) and the CE storage disease (CESD). To test the potential association of LIPA gene polymorphisms with obesity-related metabolic complications, promoter, exons, and intronic flanking regions of the LIPA gene were first sequenced in 25 individuals. From the 14 common polymorphisms identified, 12 tagging single-nucleotide polymorphisms (tSNPs) were genotyped in a cohort of 1,751 obese individuals. After adjustments for the effect of age, sex, diabetes, and medication, the C allele of SNP rs1051338 was associated with lower blood pressure (BP; systolic (SBP) P = 0.004; diastolic (DBP) P = 0.006). Three of the tested SNPs were associated with modifications of the plasma lipid profile. The G/G genotype of rs2071509 was associated with higher high-density lipoprotein cholesterol (HDL-C) levels (P = 0.009) and minor allele of rs1131706 was also associated with higher HDL-C (P = 0.004) and an association between rs3802656 and total cholesterol (total-C)/HDL-C ratio was identified (P = 0.04). These results thus suggest that LIPA polymorphisms contribute to the interindividual variability observed in obesity-related metabolic complications.
PubMed ID
22395809 View in PubMed
Less detail

Associations between polymorphisms in genes involved in fatty acid metabolism and dietary fat intakes.

https://arctichealth.org/en/permalink/ahliterature126193
Source
J Nutrigenet Nutrigenomics. 2012;5(1):1-12
Publication Type
Article
Date
2012
Author
Annie Bouchard-Mercier
Ann-Marie Paradis
Louis Pérusse
Marie-Claude Vohl
Author Affiliation
Institute of Nutraceuticals and Functional Foods-INAF, Quebec, Que., Canada.
Source
J Nutrigenet Nutrigenomics. 2012;5(1):1-12
Date
2012
Language
English
Publication Type
Article
Keywords
Adult
Dietary Fats - administration & dosage
Fatty Acids - metabolism
Female
Humans
Male
Middle Aged
Polymorphism, Restriction Fragment Length
Polymorphism, Single Nucleotide
Quebec
Questionnaires
Reverse Transcriptase Polymerase Chain Reaction
Abstract
Obesity prevalence is growing in our population. Twin studies have estimated the heritability of dietary intakes to about 30%. The objective of this study was to verify whether polymorphisms in genes involved in fatty acid metabolism are associated with dietary fat intakes.
Seven hundred participants were recruited. A validated food frequency questionnaire was used to assess dietary intakes. PCR-RFLP and TAQMAN methodology were used to genotype PPARa Leu162Val, PPAR? Pro12Ala, PPARd -87T>C, PPARGC1a Gly482Ser, FASN Val1483Ile and SREBF1 c.*619C>G. Statistical analyses were executed with SAS statistical package.
Carriers of the Ala12 allele of PPAR? Pro12Ala polymorphism had higher intakes of total fat (p = 0.04). For FASN Val1483Ile polymorphism, significant gene-sex interaction effects were found for total fat and saturated fat intakes (p = 0.02 and p = 0.002, respectively). No significant difference in fat intakes was observed for PPARa Leu162Val, PPARd -87T>C, PPARGC1a Gly482Ser and SREBF1 c.*619C>G polymorphisms.
Polymorphisms in PPAR? and FASN seem to be associated with dietary fat intakes. Genetic variants are important to take into account when studying dietary intakes.
PubMed ID
22414759 View in PubMed
Less detail

Detection of a major gene effect for LDL peak particle diameter and association with apolipoprotein H gene haplotype.

https://arctichealth.org/en/permalink/ahliterature172896
Source
Atherosclerosis. 2005 Oct;182(2):231-9
Publication Type
Article
Date
Oct-2005
Author
Yohan Bossé
Mary F Feitosa
Jean-Pierre Després
Benoît Lamarche
Treva Rice
D C Rao
Claude Bouchard
Louis Pérusse
Marie-Claude Vohl
Author Affiliation
Lipid Research Center, CHUL Research Center, TR-93, 2705 Laurier Blvd Sainte-Foy, Que., Canada G1V 4G2.
Source
Atherosclerosis. 2005 Oct;182(2):231-9
Date
Oct-2005
Language
English
Publication Type
Article
Keywords
Adult
Aged
Chromosome Segregation
Chromosomes, Human, Pair 17
Coronary Disease - genetics
Female
Genetic Variation
Glycoproteins - genetics
Haplotypes
Humans
Lipoproteins, LDL - chemistry - genetics
Male
Middle Aged
Particle Size
Quantitative Trait Loci
Quebec
beta 2-Glycoprotein I
Abstract
Low-density lipoprotein (LDL) size, a coronary heart disease risk factor, is influenced by both genetic and environmental factors. Results from the Quebec Family Study (QFS) revealed that the LDL peak particle diameter (LDL-PPD) aggregates in families with a heritability coefficient above 50% and is affected by a major quantitative trait locus on chromosome 17q (LOD=6.8). Complex segregation analyses have consistently demonstrated a major gene effect influencing LDL size. In the present study, we report a similar analysis in the QFS cohort, which suggests that a major gene explains 23% of the variance in age-body mass index and triglyceride-adjusted LDL-PPD. The most intuitive positional candidate gene on chromosome 17q is the apolipoprotein H gene. Direct sequencing of the promoter, coding regions, and exon-intron splicing boundaries of this gene revealed the presence of three missense mutations and two polymorphisms in the untranslated regions. Using family-based association tests, none of these variants was individually associated with LDL-PPD. However, analysis of the haplotypes constructed from the three missense mutations, suggested that one particular haplotype (frequency=20.9%) was associated with a significant increase in LDL-PPD trait values (p=0.046). Taken together, these results suggest the presence of a major gene effect influencing LDL-PPD and a positive association with a positional candidate gene located on chromosome 17q. Replication of the association between apolipoprotein H gene haplotype and LDL-PPD is required before reaching firm conclusion.
PubMed ID
16159595 View in PubMed
Less detail

The effect of mere-measurement of cognitions on physical activity behavior: a randomized controlled trial among overweight and obese individuals.

https://arctichealth.org/en/permalink/ahliterature137984
Source
Int J Behav Nutr Phys Act. 2011;8:2
Publication Type
Article
Date
2011
Author
Gaston Godin
Ariane Bélanger-Gravel
Steve Amireault
Marie-Claude Vohl
Louis Pérusse
Author Affiliation
Canada Research Chair on Behavior and Health, Faculty of Nursing, Laval University, Quebec city (Quebec), Canada. Gaston.Godin@fsi.ulaval.ca
Source
Int J Behav Nutr Phys Act. 2011;8:2
Date
2011
Language
English
Publication Type
Article
Keywords
Adult
Behavioral Medicine - methods
Bias (epidemiology)
Cognition
Double-Blind Method
Female
Genetic Predisposition to Disease
Health Behavior
Health Knowledge, Attitudes, Practice
Health Promotion - methods
Humans
Leisure Activities - psychology
Male
Middle Aged
Motor Activity
Obesity - epidemiology - psychology - therapy
Overweight - epidemiology - psychology - therapy
Quebec - epidemiology
Questionnaires
Abstract
The promotion of physical activity among an overweight/obese population is an important challenge for clinical practitioners and researchers. In this regard, completing a questionnaire on cognitions could be a simple and easy strategy to increase levels of physical activity. Thus, the aim of the present study was to test the effect of completing a questionnaire based on the Theory of Planned Behavior (TPB) on the level of physical activity.
Overall, 452 overweight/obese adults were recruited and randomized to the experimental or control group. At baseline, participants completed a questionnaire on cognitions regarding their participation in leisure-time physical activity (experimental condition) versus a questionnaire on fruit and vegetable consumption (control condition). The questionnaires assessed the TPB variables that are beliefs, attitude, norm, perception of control, intention and a few additional variables from other theories. At three-month follow-up, leisure-time physical activity was self-reported by means of a short questionnaire. An analysis of covariance with baseline physical activity level as covariate was used to verify the effect of the intervention.
At follow-up, 373 participants completed the leisure-time physical activity questionnaire. The statistical analysis showed that physical activity participation was greater among participants in the experimental condition than those in the control condition (F(1,370)=6.85, p=.009, d=0.20).
Findings indicate that completing a TPB questionnaire has a significant positive impact on subsequent participation in physical activity. Consequently, asking individuals to complete such a questionnaire is a simple, inexpensive and easy strategy to increase the level of physical activity among overweight/obese adults.
Notes
Cites: J Exp Psychol Appl. 2000 Sep;6(3):195-20611014052
Cites: Obes Rev. 2011 Jun;12(6):430-920331511
Cites: Br J Soc Psychol. 2001 Dec;40(Pt 4):471-9911795063
Cites: J Appl Psychol. 2003 Jun;88(3):423-3112814292
Cites: Psychol Rev. 1977 Mar;84(2):191-215847061
Cites: J Chronic Dis. 1978;31(12):741-55748370
Cites: Can J Public Health. 1986 Sep-Oct;77(5):359-623791117
Cites: J Occup Med. 1989 Dec;31(12):969-732614536
Cites: Am J Health Promot. 1996 Nov-Dec;11(2):87-9810163601
Cites: Med Sci Sports Exerc. 1997 Jun;29(6 Suppl):S1-2059243481
Cites: Cochrane Database Syst Rev. 2005;(1):CD00318015674903
Cites: Psychol Sci. 2006 Mar;17(3):207-1316507060
Cites: J Clin Epidemiol. 2006 Apr;59(4):404-1116549263
Cites: MMWR Morb Mortal Wkly Rep. 2007 Nov 23;56(46):1209-1218030281
Cites: Health Psychol. 2008 Mar;27(2):179-8418377136
Cites: Health Psychol. 2008 May;27(3):379-8718624603
Cites: Obesity (Silver Spring). 2009 Apr;17(4):706-1219148116
Cites: Br J Soc Psychol. 2009 Jun;48(Pt 2):221-3618793492
Cites: J Med Internet Res. 2010;12(1):e420164043
Cites: Psychol Health. 2009 Sep;24(7):777-8920205026
Cites: Br J Health Psychol. 2010 Sep;15(Pt 3):453-6820205982
Cites: Health Psychol. 2010 Nov;29(6):636-4420939639
Cites: CMAJ. 2000 Nov 28;163(11):1435-4011192648
PubMed ID
21223565 View in PubMed
Less detail

38 records – page 1 of 4.