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The following is the abstract of the article discussed in the subsequent letter:
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ABSTRACT |
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Fuentes, Ricardo M., Markus Perola, Aulikki Nissinen, and Jaako
Tuomilehto. ACE gene and physical activity, blood pressure, and hypertension: a
population study in Finland. J Appl Physiol 92: 2508-2512, 2002.
The study evaluated the association of the insertion/deletion polymorphism of the angiotensin-converting enzyme
gene (ACE I/D) with self-reported moderate-intensity leisure time
physical activity (MILTPA), arterial blood pressure (BP) and history of
hypertension (HT). A representative population-based sample of 721 middle-aged adults (358 women) from two areas of Finland was genotyped
for the ACE I/D. After exclusion criteria were applied, 455 subjects
(288 women) were selected for the analysis. The distribution of the ACE
I/D genotypes did not differ significantly among frequent vs.
nonfrequent MILTPA groups (2 = 2.556; df = 2; P
value = 0.279). The main predictors of BP were male gender, age,
body mass index, and arterial pulse. Additionally, tobacco smoking and
alcohol consumption also had a significant main effect on diastolic BP.
HT was significantly more frequent in subjects with obesity, family
history of cardiovascular disease, or lower educational level. As for
BP, neither ACE I/D nor MILTPA was associated with HT. The study
confirmed recent reports from population-based studies of no
association between ACE I/D and physical fitness. The study
also confirmed a lack of association between ACE I/D and BP or HT.
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To the Editor: We read with interest the recent article on the topic of the angiotensin-converting enzyme (ACE) gene by Fuentes and colleagues (2). We see some value in aspects of their study, for example, as an investigation of the effect of the ACE insertion (I)/deletion (D) polymorphism on blood pressure in a specific population. However, we were disturbed at elements of both the introduction section and the discussion and conclusion.
An introduction section is traditionally used to outline the theoretical basis for the investigation being presented. In this case (2), a major focus of the study was the possible association of the ACE gene with self-reported moderate-intensity leisure time physical activity. The theoretical basis presented for such an association was weak in the extreme, for two reasons.
First, no literature was cited by Fuentes et al. (2) to support the premise that a greater fitness level and/or trainability will encourage greater physical activity in adulthood (regardless of any influences of specific genes). Yet this was the premise underpinning a major part of the study (see Table 2 in Ref. 2).
Second, even if appropriate literature supporting the premise that greater fitness and/or trainability produces greater activity in adulthood had been cited, there are strong reasons why seeking an effect of the ACE gene in this regard is likely to prove fruitless. Specifically, the research on the ACE gene has suggested possible beneficial effects of both alleles on the response to physical training. Growing evidence associates the D allele with the growth of muscle in humans (1, 6, 9) and elite performance in power events (8). Furthermore, evidence from a nonhuman model associates angiotensin II (the product of the action of ACE on angiotensin I) with skeletal muscle growth (4). Thus evidence suggests that the D allele might predispose an individual to successful performance in particular sporting events. Although we acknowledge that there is some important contradictory evidence (10, 11), there is also considerable evidence associating the I allele with certain endurance phenotypes (5, 12, 13) and with elite endurance status (3, 7, 8). Hence, evidence suggests that the I allele, in addition to the D allele, might predispose an individual to successful performance in particular sporting events. Consequently, an effect of the ACE gene on activity in adulthood due to effects on fitness and/or the response to training is highly unlikely.
Even more importantly, the lack of association of the ACE I/D polymorphism with adulthood activity is used (2) to "confirm" reports of no association between ACE I/D and physical fitness in both the concluding paragraph of the article and the abstract. The lack of association reported by Fuentes et al. (2) does not confirm anything of the sort. Single-question self-reported moderate-intensity leisure time physical activity is not a recognized fitness phenotype suitable for investigating gene and gene-environment effects. Thus the data presented by Fuentes et al. add nothing to the debate on the effect of the ACE gene on fitness phenotypes and should not be used to "confirm" results of one sort or another in that field.
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REFERENCES |
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1.
Folland, J,
Leach B,
Little T,
Hawker K,
Myerson S,
Montgomery H,
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Angiotensin-converting enzyme genotype affects the response of human skeletal muscle to functional overload.
Exp Physiol
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2.
Fuentes, RM,
Perola M,
Nissinen A,
and
Tuomilehto J.
ACE gene and physical activity, blood pressure, and hypertension: a population study in Finland.
J Appl Physiol
92:
2508-2512,
2002
3.
Gayagay, G,
Yu B,
Hambly B,
Boston T,
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J Appl Physiol
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Association of angiotensin converting enzyme gene I/D polymorphism with change in left ventricular mass in response to physical training.
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Clarkson P,
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Thomas EL,
Brynes AE,
Saeed N,
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Bell JD,
Prasad K,
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Talmud PJ,
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Myerson, S,
Hemingway H,
Budget R,
Martin J,
Humphries S,
and
Montgomery H.
Human angiotensin I-converting enzyme gene and endurance performance.
J Appl Physiol
87:
1313-1316,
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9.
Myerson, SG,
Montgomery HE,
Whittingham M,
Jubb M,
World MJ,
Humphries SE,
and
Pennell DJ.
Left ventricular hypertrophy with exercise and ACE gene insertion/deletion polymorphism: a randomized controlled trial with losartan.
Circulation
103:
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Rankinen, T,
Perusse L,
Gagnon J,
Chagnon YC,
Leon AS,
Skinner JS,
Wilmore JH,
Rao DC,
and
Bouchard C.
Angiotensin-converting enzyme ID polymorphism and fitness phenotype in the HERITAGE Family Study.
J Appl Physiol
88:
1029-1035,
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11.
Rankinen, T,
Wolfarth B,
Simoneau J-A,
Maier-Lenz D,
Rauramaa R,
Rivera MA,
Boulay MR,
Chagnon YC,
Perusse L,
Keul J,
and
Bouchard C.
No association between the angiotensin-converting enzyme ID polymorphism and elite endurance athlete status.
J Appl Physiol
88:
1571-1575,
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12.
Williams, AG,
Rayson MP,
Jubb M,
World M,
Woods DR,
Hayward M,
Martin J,
Humphries SE,
and
Montgomery HE.
The ACE gene and muscle performance.
Nature
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614,
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13.
Woods, DR,
World M,
Rayson MP,
Williams AG,
Jubb M,
Jamshidi Y,
Hayward M,
Mary DASG,
Humphries SE,
and
Montgomery HE.
Endurance enhancement related to the human angiotensin I-converting enzyme I-D polymorphism is not due to differences in the cardiorespiratory response to training.
Eur J Appl Physiol
86:
240-244,
2002[ISI][Medline].
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Alun G. Williams, Stephen H. Day Human Physiology Research Group Department of Sport, Health and Exercise Staffordshire University Stoke-on-Trent ST4 2DF, United Kingdom E-mail: a.williams{at}staffs.ac.uk | ||||||||||||
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Sukhbir Dhamrait UCL Cardiovascular Genetics Rayne Institute London WC1E 6JJ, United Kingdom |
To the Editor: The aim of our study was to evaluate
the association of the I/D ACE gene polymorphism with regular leisure time physical activity (LTPA) in a representative sample of the Finnish
middle-aged adult population (2). The relevance of the study is
based on the high cardiovasular disease risk associated with low levels
of regular physical activity and on the association of the D allele of
the ACE gene with both coronary heart disease risk and physical
endurance. Both of these aspects are briefly introduced in the
introduction section of the article (2).
Our working hypothesis was that "given an ACE I/D genotype, subjects
might be more likely to become physically active during adulthood"
(2). Our working hypothesis was not that "a greater fitness level
and/or trainability will encourage greater physical activity in
adulthood," as has been suggested. We did not use the I/D ACE gene
polymorphism as a surrogate of fitness and/or trainability, and we do
not see the reason to do that. In a population survey, a subject will
be found to have a certain level of regular physical activity and
physical fitness (supposing it can be measured), and no causal
relationship can be determined between them.
We acknowledge that we did not consider the association of the I allele
of the ACE gene with physical endurance because the evidence for this
association is contradictory.
We used a single question to assess behavior, LTPA, in the Finnish
middle-aged adult population. As discussed in the article, the validity
of few-question or single-question self-assessment of LTPA has been
found acceptable to consider and recommend their use in population
studies (1, 3, 4). We did not use single-question self-reported
moderate-intensity LTPA as a surrogate of fitness.
Our study conclusion "we found no association between ACE I/D and
LTPA in the Finnish middle-aged adult population. Although a
single-question self-assessment of LTPA was used in our study, the
result confirms recent negative reports in which physical fitness has
been assessed more thoroughly" is a general comparative statement
that precisely considers the fact that single-question self-assessment
of LTPA is not a good surrogate of physical fitness (2).
REPLY
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FOOTNOTES |
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10.1152/japplphysiol.00540.2002
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REFERENCES |
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1.
Cardinal, BJ.
Predicting cardiorespiratory fitness without exercise testing in epidemiologic studies: a concurrent validity study.
J Epidemiol
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31-35,
1996[Medline].
2.
Fuentes, RM,
Perola M,
Nissinen A,
and
Tuomilehto J.
ACE gene and physical activity, blood pressure, and hypertension: a population study in Finland.
J Appl Physiol
92:
2508-2512,
2002
3.
Schechtman, KB,
Barzilai B,
and
Fisher EB.
Measuring physical activity with a single question.
Am J Public Health
81:
771-773,
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Washburn, RA,
Adams LL,
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Physical activity assessment for epidemiologic research: the utility of two simplified approaches.
Prev Med
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636-646,
1987[ISI][Medline].
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Ricardo M. Fuentes Department of Public Health and General Practice University of Kuopio FIN-70211 Kuopio, Finland E-mail: ricardo.fuentes{at}messi.uku.fi |
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