International Journal of Sports Physiology and Performance, 2015, 10, 636 -641 http://dx.doi.org/10.1123/ijspp.2014-0205 © 2015 Human Kinetics, Inc.
ORIGINAL INVESTIGATION
Elimination of Influences of the ACTN3 R577X Variant on Oxygen Uptake by Endurance Training in Healthy Individuals Michelle S.M. Silva, Wladimir Bolani, Cleber R. Alves, Diogo G. Biagi, José R. Lemos Jr, Jeferson L. da Silva, Patrícia A. de Oliveira, Guilherme B. Alves, Edilamar M. de Oliveira, Carlos E. Negrão, José E. Krieger, Rodrigo G. Dias, and Alexandre C. Pereira Aim: To study the relationship between the ACTN3 R577X polymorphism and oxygen uptake (VO2) before and after exercise training. Methods: Police recruits (N = 206, 25 ± 4 y) with RR (n = 75), RX (n = 97), and XX (n = 33) genotypes were selected. After baseline measures, they underwent 18 wk of running endurance training. Peak VO2 was obtained by cardiopulmonary exercise testing. Results: Baseline body weight was not different among genotypes. At baseline, XX individuals displayed higher VO2 at anaerobic threshold, respiratory compensation point, and exercise peak than did RR individuals (P < .003). Endurance training significantly increased VO2 at anaerobic threshold, respiratory compensation point, and exercise peak (P < 2 × 10–6), but the differences between XX and RR were no longer observed. Only relative peak VO2 exercise remained higher in XX than in RR genotype (P = .04). In contrast, the increase in relative peak VO2 was greater in RR than in XX individuals (12% vs 6%; P = .02). Conclusion: ACTN3 R577X polymorphism is associated with VO2. XX individuals have greater aerobic capacity. Endurance training eliminates differences in peak VO2 between XX and RR individuals. These findings suggest a ceiling-effect phenomenon, and, perhaps, trained individuals may not constitute an adequate population to explain associations between phenotypic variability and gene variations. Keywords: oxygen consumption, physical endurance, exercise training, exercise test Peak oxygen uptake (VO2peak) is the maximum capacity of transport and use of oxygen and represents cardiorespiratory, circulatory, and muscular systems’ efficiency to perform under increasing work demands. VO2peak and VO2 at ventilatory thresholds are used to evaluate the ability to endure aerobic exertion (aerobic capacity), which is demanded for improving health and athletic performance. Genetic makeup is a factor with the potential to influence VO2. The vast heterogeneity of VO2peak and individual training adaptation has led many investigators to study the genetic influence on this phenotype in untrained and trained individuals. A common genetic variant R577X in the ACTN3 gene results in synthesis interruption of the sarcomeric protein α-actinin-3, due to a C-to-T transition in exon 16 (rs1815739), which results in the replacement of an arginine (R) with a stop codon (X) at amino acid 577.1 This protein, expressed preferentially in skeletalmuscle type II glycolytic fibers that are responsible for rapid and powerful contractions, is thought to have a specialized role in the structure of these fibers.1 In addition, this protein seems to take part in the regulation of muscle metabolism.2–4 XX genotype carriers are deficient of α-actinin-3 and have been associated with a predominance of oxidative type I fiber.5 This ACTN3 XX genotype characteristic seems to confer a predisposition for endurance, while the RR genotype has been consistently associated with sprint/power Silva, Bolani, Biagi, Lemos, da Silva, Krieger, Dias, and Pereira are with the Laboratory of Genetics and Molecular Cardiology, and P. de Oliveira, G. Alves, and Negrão, the Unit of Cardiac Rehabilitation and Exercise Physiology, University of São Paulo Medical School, São Paulo, Brazil. C. Alves and E. de Oliveira are with the School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil. Address author correspondence to Rodrigo Dias at [email protected]. 636
athletic ability.6,7 Reports have been published of overrepresentation of the XX genotype among endurance athletes,8–11 and the fact that ACTN3 knockout mice have an increased capacity for endurance has been reported.4 However, this is a controversial issue, because some studies have shown no such associations with ACTN3 R577X12–14 or have even shown an inverse association.15 Nonetheless, there has been significant heterogeneity of performance levels reported among many studies,6,7 which could have obscured their results. Moreover, the possible innate advantage bestowed by this polymorphism to the endurance capacity of the general population is less well understood, and its genetic modulation of regular endurance-exercise-training responses is also less well understood. We studied the relationship between the ACTN3 R577X polymorphism and VO2 during a progressive maximal cardiopulmo-nary exercise test in a homogeneous Brazilian police recruit cohort before and after endurance-exercise training.
Methods Participants Since 2005, 40 individuals have been selected per semester to participate in this ongoing research protocol. Of the 317 individuals in our database, 206 underwent a cardiopulmonary exercise test before and after endurance-exercise training and, hence, were included in the current study. There were no genotypic differences between the selected group and the database group. Individuals had a homogene-ous dietary and daily routine and were 100% compliant with exercise training. Despite their similar nutritional routine throughout the research protocol period, we were unable to control their individual intake. They were male, were 19 to 35
ACTN3 R577X’s Influence on Oxygen Uptake 637
years of age, and were recruits joining the São Paulo State Police Department, Brazil. Individuals self-reported nonsmoking, no use of medication, and no engagement in regular physical activity for at least 6 months before joining the police department. Health status was confirmed by screening with a clinical examination, laboratory testing, echocardiography, and car-diopulmonary exercise testing. Caffeine and alcohol ingestion were prohibited 1 day before the cardiopulmonary exercise test, and it was performed at least 3 hours in the postabsorptive state.
Ethics Statement
Downloaded by Alkek Lbry Serials Acq on 11/16/16, Volume 10, Article Number 5
The Human Subject Protection Committees of the Heart Institute (InCor), Clinical Hospital, University of São Paulo Medical School, and the Ethics Committee of the Center for High Studies on Security, São Paulo State Police Department, approved the study protocol, and all participants gave written consent.
Measurements and Procedures DNA Extraction and Genotyping. Genomic DNA was extracted from leukocytes in samples of whole blood using the salting-out technique. This process was done between 2005 and 2012, and genotyping was performed in the Laboratory of Genetics and Molecular Cardiology of the Heart Institute (InCor), São Paulo, Brazil. Primers were designed using the accession number (GenBank: NG_013304.1). Primers for ACTN3 polymorphism amplified a region with only the rs1815739 polymorphism. Genotypes for ACTN3 polymorphisms were determined by HRM (high-resolutionmelting) analysis. Briefly, PCR with a fluorescent DNA-intercalating SYTO9 (Invitrogen, Carlsbad, CA, USA) was performed using the primer sequences 5′-TCAGTTCAAGGCAACACTGC-3′ and 5′-CTTCTGGATCTCACCCTGGA-3′. The PCR cycling conditions were as follows: 1 cycle of 94°C for 5 minutes; 35 cycles of 94°C for 20 seconds, 60° for 20 seconds, 72°C for 20 seconds; and 1 cycle of 72°C for 5 minutes. In the HRM phase, the Rotor Gene 6000 (Qiagen, Courtaboeuf, France) was used to measure the fluorescence in each 0.1°C temperature increase in the range of 70°C to 94°C. Melting curves were generated by the decrease in fluorescence with the increase in the temperature; nucleotide changes resulting from different curve patterns were analyzed and genotyped. Samples of the 3 observed curves were sequenced (ABI 3500XL Sequencer, Applied Biosystems, Foster City, CA, USA) to confirm the genotypes indicated by HRM. Cardiopulmonary Exercise Test. VO2 was measured in a cardio
pulmonary exercise test as previously described.16 Briefly, the test was carried out on a programmable treadmill (Quinton Q65 model 645, Quinton Instruments Co, Bothell, WA, USA) using a ramp protocol with increments in workload until volitional exhaustion. VO2 was determined at ventilatory anaerobic threshold (VO2vat), respiratory compensation point (VO2rcp), and peak exercise (VO2peak).
Exercise-Training Protocol. Exercise training was performed under supervision and consisted of three 80-minute sessions per week for 18 weeks. Sessions consisted of a 5-minute warm-up, followed by a 60-minute run, and 15 minutes of cooldown exercises. The running exercise intensity was individually controlled by heart rate (Polar FS1, Polar Electro Oy, Kempele, Finland) corresponding to ventilatory anaerobic threshold and respiratory compensation point. During the first half of the training protocol period, running intensity was moderate, and heart rate was kept between the ventilatory thresholds. During the second half, heart rate was kept
slightly above the respiratory compensation point. There was no change in diet and daily routine, with respect to academic activities and rest hours, during the entire exercise-training period.
Statistical Analysis Data are presented as mean ± SD. Normality and homogeneity of variance assumptions were checked using Kolmogorov-Smirnov and Levene tests, respectively. Possible confounders such as age, weight, and height were not associated with ACTN3 R577X genotypes. To analyze the effect of endurance training on aerobiccapacity measures, a paired-samples t test or Wilcoxon test was used. Choice of test was made according to violations of normality or homogeneity-of-variance assumptions. Regression analyses with aerobic-capacity measures versus age, weight, and height revealed no associations; therefore, further analyses were performed without adjusting for these covariates. The influence of ACTN3 on aerobiccapacity measures at baseline and after endurance training was tested using univariate 1-way ANOVA or Kruskal-Wallis ANOVA (choice of test made as above). The effect of endurance training on ACTN3 genotypes (training × genotype interaction) was analyzed using 2-way ANOVA with repeated measures. Each measure (at baseline and after training) entered as the within-subject factor, and the ACTN3 genotypes entered as the between-subjects factor. When significance was found, Tukey or Mann-Whitney tests for post hoc comparisons were performed. Hardy-Weinberg equilibrium for the distribution of genotypes was estimated by the χ2 test. All the analyses were performed using SPSS software for Windows 13.0 (SPSS Inc, Chicago, IL, USA), and significance level was set at .05.
Results The distribution of ACTN3 R577X alleles (R 60%, X 40%) and genotypes (RR 37%, RX 47%, XX 16%) was in Hardy-Weinberg equilibrium (χ2 = .03, df = 1, P = .86). Although hormonal variability due to age may occur, in this study there was no statistical difference in VO2 among RR, RX, and XX genotypes according to individual age (age used as covariate).
Baseline Measures The demographic and VO2 measures in all 3 ACTN3 genotypes are shown in Table 1. Age, weight, and body-mass-index variables were not different among genotypes. Absolute and relative VO2 levels at anaerobic threshold, respiratory compensation point, and peak exercise were higher in XX individuals (Table 1).
Effects of Exercise Training Considering the analysis of all 206 individuals together, body weight, and body-mass index did not significantly change with endurance training (Table 2). Endurance training significantly increased absolute and relative VO2 at anaerobic threshold, respiratory compensation point, and peak exercise (Table 2). Considering the genotypic analysis, the differences in absolute VO2 between XX and RR genotypes observed at baseline were no longer found (Table 1, Figure 1). Only relative VO2 at peak exercise remained different among genotypes (Table 1). In addition, there was an evident interaction effect between endurance training and ACTN3 genotypes in the relative VO2 at peak exercise (Pinteraction = .05). RR had a higher gain (Δ%) than the XX genotype (RR = 12% ± 13%, RX = 8% ± 11%, XX = 6% ± 10%, P = .02; Figure 2).
IJSPP Vol. 10, No. 5, 2015
Table 1 Demographic Characteristics and Differences in Oxygen Uptake (VO2) Among ACTN3 R577X Genotypes Before and After the Running-Endurance-Training Program (N = 206) Baseline RR
Post
RX
XX
Pa
RR
RX
XX
76
97
33
26 ± 4
25 ± 4
25 ± 4
Pa
Pint
.20
.13
Demographic measures n
76
97
33
26 ± 4
25 ± 4
25 ± 3
.21
1.75 ± 0.06
1.75 ± 0.06
1.77 ± 0.05
.18
weight (kg)
76.0 ± 9.1
76.0 ± 10.2
73.9 ± 9.4
.53
74.8 ± 8.7
75.1 ± 9.2
73.5 ± 8.8
.67
.54
body-mass index (kg/m2)
24.8 ± 2.8
24.7 ± 3.1
23.5 ± 2.5
.08
24.4 ± 2.6
24.5 ± 2.7
23.3 ± 2.4
.09
.53
age (y) height (m)
VO2 measures
Downloaded by Alkek Lbry Serials Acq on 11/16/16, Volume 10, Article Number 5
Ventilatory anaerobic threshold absolute (L/min)
2.1 ± 0.6
2.3 ± 0.7
2.3 ± 0.5*
.03
2.3 ± 0.5
2.5 ± 0.7
2.5 ± 0.6
.21
.97
relative (mL · kg–1 · min–1)
27.2 ± 7.7
29.9 ± 8.8
31.9 ± 7.5*
.01
30.4 ± 6.2
33.2 ± 8.9
34.3 ± 7.7
.09
.90
Respiratory compensation point absolute (L/min)
3.1 ± 0.6
3.3 ± 0.7
3.5 ± 0.6*
.01
3.5 ± 0.6
3.6 ± 0.6
3.7 ± 0.6
.29
.19
min–1)
41.4 ± 7.9
44.0 ± 8.9
47.9 ± 7.4*
.001
47.3 ± 6.7
48.1 ± 7.4
50.7 ± 5.8
.07
.13
absolute (L/min)
3.6 ± 0.6
3.8 ± 0.6
3.9 ± 0.5*
.001
3.9 ± 0.5
4.0 ± 0.6
4.1 ± 0.5
.23
.11
relative (mL · kg–1 · min–1)
47.2 ± 7.5
49.8 ± 8.1
52.8 ± 6.2*
.002
52.6 ± 5.9
53.2 ± 6.5
56.1 ± 5.6*
.04
.05
relative (mL ·
kg–1
·
Peak exercise
Values of univariate ANOVA with genotypes as fixed factor; italicized P values are from Kruskal-Wallis tests. b Interaction P values between effects of training and genotype on measures (repeated-measures ANOVA). *Versus RR genotype, from Tukey post hoc test.
a
Table 2 Demographic Characteristics and Improvements in Oxygen Uptake (VO2) After an 18-Week RunningEndurance-Training Program for Police Recruits (N = 206) Baseline
After
Pa
Demographic measures age (y) height (m) weight (kg) body-mass index (kg/m2)
25 ± 4 1.76 ± 0.06 75.7 ± 9.7 24.6 ± 2.9
26 ± 4 74.7 ± 8.9 24.2 ± 2.6
.26 .28 .94 .26
VO2 measures VAT abs (L/min) rel (mL · kg–1 · min–1)
2.2 ± 0.6 29.2 ± 8.4
2.4 ± 0.6 32.4 ± 7.9
ORIGINAL INVESTIGATION
Elimination of Influences of the ACTN3 R577X Variant on Oxygen Uptake by Endurance Training in Healthy Individuals Michelle S.M. Silva, Wladimir Bolani, Cleber R. Alves, Diogo G. Biagi, José R. Lemos Jr, Jeferson L. da Silva, Patrícia A. de Oliveira, Guilherme B. Alves, Edilamar M. de Oliveira, Carlos E. Negrão, José E. Krieger, Rodrigo G. Dias, and Alexandre C. Pereira Aim: To study the relationship between the ACTN3 R577X polymorphism and oxygen uptake (VO2) before and after exercise training. Methods: Police recruits (N = 206, 25 ± 4 y) with RR (n = 75), RX (n = 97), and XX (n = 33) genotypes were selected. After baseline measures, they underwent 18 wk of running endurance training. Peak VO2 was obtained by cardiopulmonary exercise testing. Results: Baseline body weight was not different among genotypes. At baseline, XX individuals displayed higher VO2 at anaerobic threshold, respiratory compensation point, and exercise peak than did RR individuals (P < .003). Endurance training significantly increased VO2 at anaerobic threshold, respiratory compensation point, and exercise peak (P < 2 × 10–6), but the differences between XX and RR were no longer observed. Only relative peak VO2 exercise remained higher in XX than in RR genotype (P = .04). In contrast, the increase in relative peak VO2 was greater in RR than in XX individuals (12% vs 6%; P = .02). Conclusion: ACTN3 R577X polymorphism is associated with VO2. XX individuals have greater aerobic capacity. Endurance training eliminates differences in peak VO2 between XX and RR individuals. These findings suggest a ceiling-effect phenomenon, and, perhaps, trained individuals may not constitute an adequate population to explain associations between phenotypic variability and gene variations. Keywords: oxygen consumption, physical endurance, exercise training, exercise test Peak oxygen uptake (VO2peak) is the maximum capacity of transport and use of oxygen and represents cardiorespiratory, circulatory, and muscular systems’ efficiency to perform under increasing work demands. VO2peak and VO2 at ventilatory thresholds are used to evaluate the ability to endure aerobic exertion (aerobic capacity), which is demanded for improving health and athletic performance. Genetic makeup is a factor with the potential to influence VO2. The vast heterogeneity of VO2peak and individual training adaptation has led many investigators to study the genetic influence on this phenotype in untrained and trained individuals. A common genetic variant R577X in the ACTN3 gene results in synthesis interruption of the sarcomeric protein α-actinin-3, due to a C-to-T transition in exon 16 (rs1815739), which results in the replacement of an arginine (R) with a stop codon (X) at amino acid 577.1 This protein, expressed preferentially in skeletalmuscle type II glycolytic fibers that are responsible for rapid and powerful contractions, is thought to have a specialized role in the structure of these fibers.1 In addition, this protein seems to take part in the regulation of muscle metabolism.2–4 XX genotype carriers are deficient of α-actinin-3 and have been associated with a predominance of oxidative type I fiber.5 This ACTN3 XX genotype characteristic seems to confer a predisposition for endurance, while the RR genotype has been consistently associated with sprint/power Silva, Bolani, Biagi, Lemos, da Silva, Krieger, Dias, and Pereira are with the Laboratory of Genetics and Molecular Cardiology, and P. de Oliveira, G. Alves, and Negrão, the Unit of Cardiac Rehabilitation and Exercise Physiology, University of São Paulo Medical School, São Paulo, Brazil. C. Alves and E. de Oliveira are with the School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil. Address author correspondence to Rodrigo Dias at [email protected]. 636
athletic ability.6,7 Reports have been published of overrepresentation of the XX genotype among endurance athletes,8–11 and the fact that ACTN3 knockout mice have an increased capacity for endurance has been reported.4 However, this is a controversial issue, because some studies have shown no such associations with ACTN3 R577X12–14 or have even shown an inverse association.15 Nonetheless, there has been significant heterogeneity of performance levels reported among many studies,6,7 which could have obscured their results. Moreover, the possible innate advantage bestowed by this polymorphism to the endurance capacity of the general population is less well understood, and its genetic modulation of regular endurance-exercise-training responses is also less well understood. We studied the relationship between the ACTN3 R577X polymorphism and VO2 during a progressive maximal cardiopulmo-nary exercise test in a homogeneous Brazilian police recruit cohort before and after endurance-exercise training.
Methods Participants Since 2005, 40 individuals have been selected per semester to participate in this ongoing research protocol. Of the 317 individuals in our database, 206 underwent a cardiopulmonary exercise test before and after endurance-exercise training and, hence, were included in the current study. There were no genotypic differences between the selected group and the database group. Individuals had a homogene-ous dietary and daily routine and were 100% compliant with exercise training. Despite their similar nutritional routine throughout the research protocol period, we were unable to control their individual intake. They were male, were 19 to 35
ACTN3 R577X’s Influence on Oxygen Uptake 637
years of age, and were recruits joining the São Paulo State Police Department, Brazil. Individuals self-reported nonsmoking, no use of medication, and no engagement in regular physical activity for at least 6 months before joining the police department. Health status was confirmed by screening with a clinical examination, laboratory testing, echocardiography, and car-diopulmonary exercise testing. Caffeine and alcohol ingestion were prohibited 1 day before the cardiopulmonary exercise test, and it was performed at least 3 hours in the postabsorptive state.
Ethics Statement
Downloaded by Alkek Lbry Serials Acq on 11/16/16, Volume 10, Article Number 5
The Human Subject Protection Committees of the Heart Institute (InCor), Clinical Hospital, University of São Paulo Medical School, and the Ethics Committee of the Center for High Studies on Security, São Paulo State Police Department, approved the study protocol, and all participants gave written consent.
Measurements and Procedures DNA Extraction and Genotyping. Genomic DNA was extracted from leukocytes in samples of whole blood using the salting-out technique. This process was done between 2005 and 2012, and genotyping was performed in the Laboratory of Genetics and Molecular Cardiology of the Heart Institute (InCor), São Paulo, Brazil. Primers were designed using the accession number (GenBank: NG_013304.1). Primers for ACTN3 polymorphism amplified a region with only the rs1815739 polymorphism. Genotypes for ACTN3 polymorphisms were determined by HRM (high-resolutionmelting) analysis. Briefly, PCR with a fluorescent DNA-intercalating SYTO9 (Invitrogen, Carlsbad, CA, USA) was performed using the primer sequences 5′-TCAGTTCAAGGCAACACTGC-3′ and 5′-CTTCTGGATCTCACCCTGGA-3′. The PCR cycling conditions were as follows: 1 cycle of 94°C for 5 minutes; 35 cycles of 94°C for 20 seconds, 60° for 20 seconds, 72°C for 20 seconds; and 1 cycle of 72°C for 5 minutes. In the HRM phase, the Rotor Gene 6000 (Qiagen, Courtaboeuf, France) was used to measure the fluorescence in each 0.1°C temperature increase in the range of 70°C to 94°C. Melting curves were generated by the decrease in fluorescence with the increase in the temperature; nucleotide changes resulting from different curve patterns were analyzed and genotyped. Samples of the 3 observed curves were sequenced (ABI 3500XL Sequencer, Applied Biosystems, Foster City, CA, USA) to confirm the genotypes indicated by HRM. Cardiopulmonary Exercise Test. VO2 was measured in a cardio
pulmonary exercise test as previously described.16 Briefly, the test was carried out on a programmable treadmill (Quinton Q65 model 645, Quinton Instruments Co, Bothell, WA, USA) using a ramp protocol with increments in workload until volitional exhaustion. VO2 was determined at ventilatory anaerobic threshold (VO2vat), respiratory compensation point (VO2rcp), and peak exercise (VO2peak).
Exercise-Training Protocol. Exercise training was performed under supervision and consisted of three 80-minute sessions per week for 18 weeks. Sessions consisted of a 5-minute warm-up, followed by a 60-minute run, and 15 minutes of cooldown exercises. The running exercise intensity was individually controlled by heart rate (Polar FS1, Polar Electro Oy, Kempele, Finland) corresponding to ventilatory anaerobic threshold and respiratory compensation point. During the first half of the training protocol period, running intensity was moderate, and heart rate was kept between the ventilatory thresholds. During the second half, heart rate was kept
slightly above the respiratory compensation point. There was no change in diet and daily routine, with respect to academic activities and rest hours, during the entire exercise-training period.
Statistical Analysis Data are presented as mean ± SD. Normality and homogeneity of variance assumptions were checked using Kolmogorov-Smirnov and Levene tests, respectively. Possible confounders such as age, weight, and height were not associated with ACTN3 R577X genotypes. To analyze the effect of endurance training on aerobiccapacity measures, a paired-samples t test or Wilcoxon test was used. Choice of test was made according to violations of normality or homogeneity-of-variance assumptions. Regression analyses with aerobic-capacity measures versus age, weight, and height revealed no associations; therefore, further analyses were performed without adjusting for these covariates. The influence of ACTN3 on aerobiccapacity measures at baseline and after endurance training was tested using univariate 1-way ANOVA or Kruskal-Wallis ANOVA (choice of test made as above). The effect of endurance training on ACTN3 genotypes (training × genotype interaction) was analyzed using 2-way ANOVA with repeated measures. Each measure (at baseline and after training) entered as the within-subject factor, and the ACTN3 genotypes entered as the between-subjects factor. When significance was found, Tukey or Mann-Whitney tests for post hoc comparisons were performed. Hardy-Weinberg equilibrium for the distribution of genotypes was estimated by the χ2 test. All the analyses were performed using SPSS software for Windows 13.0 (SPSS Inc, Chicago, IL, USA), and significance level was set at .05.
Results The distribution of ACTN3 R577X alleles (R 60%, X 40%) and genotypes (RR 37%, RX 47%, XX 16%) was in Hardy-Weinberg equilibrium (χ2 = .03, df = 1, P = .86). Although hormonal variability due to age may occur, in this study there was no statistical difference in VO2 among RR, RX, and XX genotypes according to individual age (age used as covariate).
Baseline Measures The demographic and VO2 measures in all 3 ACTN3 genotypes are shown in Table 1. Age, weight, and body-mass-index variables were not different among genotypes. Absolute and relative VO2 levels at anaerobic threshold, respiratory compensation point, and peak exercise were higher in XX individuals (Table 1).
Effects of Exercise Training Considering the analysis of all 206 individuals together, body weight, and body-mass index did not significantly change with endurance training (Table 2). Endurance training significantly increased absolute and relative VO2 at anaerobic threshold, respiratory compensation point, and peak exercise (Table 2). Considering the genotypic analysis, the differences in absolute VO2 between XX and RR genotypes observed at baseline were no longer found (Table 1, Figure 1). Only relative VO2 at peak exercise remained different among genotypes (Table 1). In addition, there was an evident interaction effect between endurance training and ACTN3 genotypes in the relative VO2 at peak exercise (Pinteraction = .05). RR had a higher gain (Δ%) than the XX genotype (RR = 12% ± 13%, RX = 8% ± 11%, XX = 6% ± 10%, P = .02; Figure 2).
IJSPP Vol. 10, No. 5, 2015
Table 1 Demographic Characteristics and Differences in Oxygen Uptake (VO2) Among ACTN3 R577X Genotypes Before and After the Running-Endurance-Training Program (N = 206) Baseline RR
Post
RX
XX
Pa
RR
RX
XX
76
97
33
26 ± 4
25 ± 4
25 ± 4
Pa
Pint
.20
.13
Demographic measures n
76
97
33
26 ± 4
25 ± 4
25 ± 3
.21
1.75 ± 0.06
1.75 ± 0.06
1.77 ± 0.05
.18
weight (kg)
76.0 ± 9.1
76.0 ± 10.2
73.9 ± 9.4
.53
74.8 ± 8.7
75.1 ± 9.2
73.5 ± 8.8
.67
.54
body-mass index (kg/m2)
24.8 ± 2.8
24.7 ± 3.1
23.5 ± 2.5
.08
24.4 ± 2.6
24.5 ± 2.7
23.3 ± 2.4
.09
.53
age (y) height (m)
VO2 measures
Downloaded by Alkek Lbry Serials Acq on 11/16/16, Volume 10, Article Number 5
Ventilatory anaerobic threshold absolute (L/min)
2.1 ± 0.6
2.3 ± 0.7
2.3 ± 0.5*
.03
2.3 ± 0.5
2.5 ± 0.7
2.5 ± 0.6
.21
.97
relative (mL · kg–1 · min–1)
27.2 ± 7.7
29.9 ± 8.8
31.9 ± 7.5*
.01
30.4 ± 6.2
33.2 ± 8.9
34.3 ± 7.7
.09
.90
Respiratory compensation point absolute (L/min)
3.1 ± 0.6
3.3 ± 0.7
3.5 ± 0.6*
.01
3.5 ± 0.6
3.6 ± 0.6
3.7 ± 0.6
.29
.19
min–1)
41.4 ± 7.9
44.0 ± 8.9
47.9 ± 7.4*
.001
47.3 ± 6.7
48.1 ± 7.4
50.7 ± 5.8
.07
.13
absolute (L/min)
3.6 ± 0.6
3.8 ± 0.6
3.9 ± 0.5*
.001
3.9 ± 0.5
4.0 ± 0.6
4.1 ± 0.5
.23
.11
relative (mL · kg–1 · min–1)
47.2 ± 7.5
49.8 ± 8.1
52.8 ± 6.2*
.002
52.6 ± 5.9
53.2 ± 6.5
56.1 ± 5.6*
.04
.05
relative (mL ·
kg–1
·
Peak exercise
Values of univariate ANOVA with genotypes as fixed factor; italicized P values are from Kruskal-Wallis tests. b Interaction P values between effects of training and genotype on measures (repeated-measures ANOVA). *Versus RR genotype, from Tukey post hoc test.
a
Table 2 Demographic Characteristics and Improvements in Oxygen Uptake (VO2) After an 18-Week RunningEndurance-Training Program for Police Recruits (N = 206) Baseline
After
Pa
Demographic measures age (y) height (m) weight (kg) body-mass index (kg/m2)
25 ± 4 1.76 ± 0.06 75.7 ± 9.7 24.6 ± 2.9
26 ± 4 74.7 ± 8.9 24.2 ± 2.6
.26 .28 .94 .26
VO2 measures VAT abs (L/min) rel (mL · kg–1 · min–1)
2.2 ± 0.6 29.2 ± 8.4
2.4 ± 0.6 32.4 ± 7.9
