The ACSM and ADA position statement on exercise reported that exercise may slightly reduce SBP and reductions in DBP are less common in persons with T2DM.6
The evidence for this statement was rated category C because of a lack of randomized controlled trials. The key finding in the present randomized controlled trial was no reductions in resting SBP or DBP were achieved among exercisers at 6 months despite a training effect as evidenced by increased fitness, improved glycemic control and improved body composition. Thus, our study provides a higher level of evidence, and corroborates the finding of a recent trial,14
supporting the conclusion of ACSM/ADA regarding lack of efficacy of exercise for reducing BP in this population.
Several factors might explain the lack of change in BP. First, the metabolic abnormalities associated with diabetes impair vascular function, inhibit vasodilation and augment vasoconstriction, which could contribute to arterial structural remodeling and stiffening, leading to raised systolic BP.15
We observed no reduction in aortic stiffness suggesting limited plasticity in diabetic vasculature. One study16
reported no change in SBP or aortic stiffness among men with diabetes, but who were not necessarily hypertensive, after 2 years of exercise training. It is possible that adverse vascular changes in persons with diabetes17
reflects end organ damage that cannot be reversed with exercise alone. Moreover, while ACE inhibitors and diuretics may improve vessel wall structure, beta blockers may have an opposite effect.18,19
Thus, current antihypertensive therapy may differentially affect responses to exercise treatment.
Second, the JNC 7 guidelines9
recommend that physicians consider drug therapy, with exercise as an adjunct treatment for elevated BP in T2DM. Consistent with this recommendation, 70 % of our sample was being treated with BP lowering medications at the time of randomization. A goal of the study was to determine the effects of exercise training above and beyond usual care as practiced in the community. Therefore, we recruited participants who were either treated or untreated with antihypertensive medications. Although scientifically it would be more desirable to study persons with untreated hypertension, this was not ethically possible. Thus, our results may be more generalizable to the broad population of persons with diabetes. The generally well-controlled BPs at baseline may reflect a “floor effect”, thereby limiting the potential beneficial impact of exercise of this intensity and duration. In a separate regression model we found a non-significant trend that participants above the target treatment goal of 130/80 mmHg for diabetes9
at baseline were more likely to experience a reduction in SBP at 6 months, regardless of group assignment or current use of antihypertensive medications. Because of multiple BP checks performed throughout the study, there may have been a regression toward the mean and we were not adequately powered to examine subsets of participants based on race, medication use or whether they were above or below target BP goals.
Third, we observed a modest weight loss of approximately 2.1 % of initial body weight among exercisers. Data from the Action for Health in Diabetes Trial,20
in which the baseline BP of approximately 129/70 mmHg was similar to our study, showed that a diet and exercise intervention produced weight loss of 8.6 % of initial body weight at one year, and reduced SBP and DBP by 5.33 mmHg and 2.92 mmHg, respectively. These data, in contrast to our study with minimal weight loss, suggests that the most effective lifestyle approach for BP reduction in persons with diabetes is one that combines exercise with a weight reducing diet. Of note, in a pooled analysis that included control subjects, a reduction in abdominal subcutaneous fat and total abdominal fat, but not total body weight, were associated with a reduction in SBP, suggesting that metabolic changes that result in abdominal fat changes may impact on blood pressure before marked changes in body weight occur.
Despite the lack of BP reduction with the exercise, there was a modest (0.2 %) reduction in HbA1c in the exercise group. The importance of this finding is underscored by the fact that our cohort had well-controlled diabetes at baseline (HbA1c 6.7 %), which highlights the role of exercise for contributing to a potential reduction in the risk of microvascular complications associated with diabetes. While a recent meta-analysis21
showed no apparent benefits of intensive glucose lowering with pharmacological treatment for preventing microvascular events, exercise training may confer a protective effect associated with increased glycemic control, which may not result from pharmacological treatment of hyperglycemia.22
Exercisers increased aerobic capacity by about 1 metabolic equivalent (MET), a change that is associated with a 15 %-20 % reduction in CVD mortality risk.23
Despite a modest reduction in weight, exercise training reduced the percentage of total body fat, abdominal and subcutaneous fat and increased lean body mass. Yet there was no significant change in abdominal visceral fat, perhaps due to the presence of diabetes, which is associated with disordered fat mobilization from fat storage sites24
or the use of diabetes or antihypertensive medications may limit visceral fat loss. Our results for visceral fat are in apparent contrast to other studies,25,26
which have demonstrated that exercise alone, without weight loss, reduced abdominal visceral fat in individuals with diabetes.
This study had several strengths. The participants underwent a rigorous BP screening and comprehensive body composition and fitness assessments. The sample included both men and women with treated and untreated hypertension, who were representative of the racial distribution of our community. The exercise protocol was guideline driven, being based on those of the ACSM.11
Also, while BP can be influenced by dietary behaviors we observed no changes in diet over the course of the trial. There are also some limitations. We observed a higher than expected dropout rate among exercisers of 24 %. Many participants in the present trial were employed and may have been more susceptible to drop out due to time-constraints. Also, we showed previously27
that persons with T2DM report lower levels of health related quality of life compared to individuals without diabetes, suggesting that they view themselves as being less capable of meeting the demands of the intervention and are therefore more likely to discontinue the program. Though controls received less attention than exercisers, this limitation is less important given there was no BP change in either group. In summary, although BP did not decrease, this finding should not dampen the enthusiasm for exercise since it resulted in several important health benefits including improved fitness body composition, and glycemic control.