Results from the present study showed no statistically significant differences of BP response after an acute RT session between different allele carriers of the ACE gene. However, ES showed a moderate magnitude on SBP by comparing the CON versus RT session in homozygotic carriers of the allele D, while allele I carriers presented a small magnitude 30 minutes after exercise. Additionally, homozygotic D carriers presented a large ES on MBP 20 minutes after the RT session. Moreover, HR was higher up to 30 after exercise in the allele I carriers. Whole group analysis, without considering the polymorphism revealed a decrease on SBP 30 minutes after exercise as compared with resting values. In addition to this, DBP and MBP were lower 40 minutes after the acute RT session as compared with the same period of the control session. Therefore, the initial hypothesis was partially confirmed, considering that the ACE polymorphism exerted some effects on the cardiovascular response to an acute RT session in sedentary women. Finally, to the best of our knowledge no previous research has been designed to test this specific hypothesis.
Therefore, two important aspects should be considered: 1) whole group analysis revealed a drop in BP (PEH) and 2) considering the polymorphism, there was no statistically significant PEH, while ES BP values were of higher magnitude in some periods for DD, even with a reduced number of participants in this group as compared with allele I carriers. Thus, ACE gene polymorphism exerted some effect on the acute cardiovascular response to a RT session.
Whelton et al. (2002) found that even less expressive drops in BP, such as 3 to 5 mm·Hg, contribute to a decrease of 8-14% of acute myocardial infarction episodes, 5 to 9% of risk for coronary disease, and 4 to 7% in the general causes of mortality . For example, the drop in SBP 30 minutes after exercise was ~5 mm·Hg for the DD group and ~2.5 mm·Hg for the allele I carriers. The decrease in DBP was ~4.5 mm·Hg for DD carriers versus ~1.5 mm·Hg for the allele I carriers 40 minutes after the acute RT session. These results reinforce the importance of using ES for some biological variables with clinical relevance, especially under situations where conventional statistics reveals no differences.
Busjahn et al. (1997) investigated the influence of ACE gene polymorphism on cardiac dimension and ACE activity in 132 twins, 91 monozygotic and 41 dizygotic. The study revealed that DD carriers presented a higher dimension of posterior cardiac wall and ACE circulating activity, independent of resting BP . Another study showed that, apart from the circulating levels of ACE, the activity of ACE from the heart was higher for DD carriers, while this phenomenon is associated with a higher incidence of cardiovascular disorders . Considering these phenotypic differences between different allele carriers of the ACE gene, it is important to investigate the effect of the ACE polymorphism on the cardiovascular response to exercise.
In response to aerobic exercise, normotensive individuals presented a PEH of 8 to 10 mm·Hg for SBP and 3 to 5 mm·Hg for DBP. Alternatively, in hypertensive individuals this decrease was of 18 to 20 mm·Hg for SBP and of 7 to 9 mm·Hg for DBP . These data reinforce the idea that hypertensive individuals or those with any type of cardiovascular disorder could present a higher magnitude of decrease in BP after exercise as compared with normotensive controls . Thus, the superior magnitude of reduction in BP verified by the ES in the DD group could be associated to the greater prevalence of cardiovascular disorders, inherent to this polymorphism. Similarly, Pescatello et al. (2007) observed a PEH at 40% of VO2max after a cycloergometer exercise session in stage I hypertensive individuals, only in homozygotic allele D carriers . It is important to consider that, similar to the present study, resting values of BP were not different between the distinct alleles.
Alternatively, Santana et al. (2011) found a reduction of BP after a maximal incremental cycloergometer exercise test only for allele I carriers . The differences between studies may be associated with the studied population, considering that Santana and co-workers evaluated elderly individuals. Other factors that could explain the differences include the moment of BP measurement (only after exercise) and the type of exercise used.
Moreover, Hagberg et al. (2001) observed superior values (~10 beats) of HR maximum and cardiac output (~25%) for homozygotic II women compared with ID/DD . However, these results were obtained during treadmill exercise, not after the effort as in the present study. Another possible explanation for the higher HR values after the RT session for the allele I carriers found in the present study, would be an improved autonomic adjustment as compared with allele D carriers . These observations indicate that ACE gene polymorphism may present some influence on the mechanisms responsible for HR regulation.
PEH is a well-documented phenomenon in response to aerobic, resistance and water exercise [28–30]. The involved mechanisms are: a decrease of cardiac output and peripheral vascular resistance due to a lower sympathetic activity, as well as a higher activity of the kallekrein system mediating nitric oxide release [24, 31, 32]. In the present study, without considering the polymorphism, PEH was accompanied by a compensatory increase in HR, possible to maintain the cardiovascular homeostasis.
When evaluating data from the present study it is important to consider the reduced number of participants in each group, lack of a 24h analysis of BP, the analysis of only one gene, considering the multiple gene influence on BP, apart from the lack of other RT intensities. However, some methodological precautions were taken to minimize possible confounding issues, between them, the homogeneity of the anthropometric, cardiovascular and metabolic variables, rigid control of BP measures and RT variables, apart from the estimated sample power fixed at 85%.
Although ACE polymorphism has been associated with cardiovascular, metabolic and functional phenotypes, the discrepancy between the results of association studies with the ACE gene reveals the necessity of caution when trying to respond a macro event, such as BP and HR response to a moderate intensity RT session, especially with the analysis of only one gene, feasible of modulation by several genes. Multiple gene polymorphism analysis, including candidates such as beta 1-adrenergic receptor, angiotensin II (Ang II) Type 1 receptor (ATlR) and endothelial nitric oxide synthase (eNOS) would be of great importance. Moreover, non genetic factors may modulate BP results, such as lifestyle, nutrition, between others, obtaining verisimilitude between its pairs of only carrying the same genotype of ACE.