Exercise reduces CVD-related mortality in hypertensives

Williams PT
Hypertension. 2013 Sep;62(3):485-91. doi: 10.1161/HYPERTENSIONAHA.113.01608

Background

Physical activity lowers the risk of all-cause and cardiovascular disease mortality, in normotensives and hypertensives [1]. Many aspects of the beneficial effect of physical activity for hypertensives remain unclear, such as whether a dose-response relationship exists, the effect of intensity and the specific diseases affected. Previous cohorts provided little insight into the optimum exercise dose, because they were set up for general purposes, thus did not include very detailed quantification of activities. None of the studies compared the benefits of moderate versus vigorous exercise.
The National Runners’ and Walkers’ Health Studies [2-10] are the only large prospective cohort designed to specifically assess the health benefits of exercise. Data of over 10000 hypertensive medication users (6973 walkers and 3907 runners) were analysed to investigate the nature of the dose-response relationship between exercise and mortality and whether it affects specific CVD diagnoses, diabetes mellitus and chronic kidney disease (CKD).

Main results

• Hypertensives were at higher risk for all-cause mortality than normotensives (30.5% higher, 95%CI: 21.0-40.8%, P<0.001), as well as for mortality related to CVD (47.5% higher, 95%CI: 33.5-62.8%, P<0.001) (adjusted).
• Meeting the current exercise guidelines (1.07-1.8 METh/d) gave a non-significant risk reduction of all-cause mortality by 9%, as compared to not meeting them (<1.07 METh/d). When guidelines were exceeded 1-2 fold (1.8-3.6 METh/d), all-cause mortality decreased by 29%. Energy expenditure >3.6METh/d did not seem to further reduce all-cause mortality.
• Concerning CVD-related mortality, exercising at 1.8-3.6 METh/d gave a 34% decrease, which persisted at greater energy expenditures. Adjustment for BMI did not change the results.
• Other CVD end points such as cerebrovascular disease-related, heart failure related and dysrhythmia-related mortality showed stronger reductions in risk at >1,8 METh/d than <1.8METh/d. Risk of ischemic heart disease-related mortality per METh/d was less affected by energy expenditure, and hypertensive heart disease-related mortality was unrelated to exercise energy expenditure.
• Each METh/d increment in energy expenditure was associated with 19.1% lower risk for diabetes-mellitus-related mortality, which persisted when adjusted for BMI.
• Risk of CKD-related mortality was also reduced by 25.4% per METh/d.
• Being a runner or a walker did not significantly affect the risk for all CVD-related deaths, at 1.8-3.6 or >3.6 METh/d, neither for individual CVD endpoints. Neither did exercise mode significantly affect the per METh/d declines in diabetes-mellitus-related or CKD-related deaths.
  

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Conclusion

Exercise can reduce the hypertensive’s risk for cerebrovascular disease, heart failure and cardiac dysrhythmias. Risk reductions were larger than those reported before; this could mean that hypertensives profit more from exercise than others, or it could be due to this specialised study design.
These findings suggest that current exercise guidelines are not adequate to significantly reduce CVD mortality. Reduction in mortality was achieved when exercising a bit more, to wit between 1.8 and 3.6 METh/d, at which individuals taking antihypertensive medication are at the same risk level as sedentary nonusers.
Provided the energy expenditure is the same, walking and running yielded similar risk reductions. This means that one must go about twice as far and long to expend the same amount of energy by walking briskly as by running.

References

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