Study finds no threshold for association between physical activity and lower CVD risk

There is no disputing the fact that exercise is good for your heart — and it turns out the potential benefits may be limitless, according to results from an analysis of the U.K. Biobank cohort that found more physical activity (PA) leads to greater reductions in risk of cardiovascular disease (CVD), with no apparent limit to the association, researchers reported.

“In this large population-based cohort, higher levels of moderate-intensity and vigorous-intensity PAs as well as total volume were inversely associated with risk of incident CVD with no evidence for a threshold effect,” Terence Dwyer, AO, MBBS, MD, FAFPHM, and colleagues at the University of Oxford in Oxford, U.K., reported in PLOS Medicine. “The finding of no threshold effect aligns with the recommendation of the U.K. Chief Medical Officer’s report on PA that ’some physical activity is good but more is better.’”

“The results of this study enhance confidence that physical activity is likely to be an important way of preventing cardiovascular disease,” Dwyer noted in a press release on the findings. “The potential risk reduction estimated in those engaging in relatively high levels of activity is substantial and justifies a greater emphasis on measures to increase levels of physical activity in the community.”

In order to determine the strength of the association between PA and CVD, Dwyer and colleagues delved into data from the U.K. Biobank, a large population-based cohort study that recruited over 500,000 U.K. participants ages 40-69 years from 2006 to 2010 in order to study genetic and non-genetic risk factors for diseases in middle and old age. For their analysis, they created a subsample of 103,687 participants without prior of concurrent CVS who wore an Axivity AX3 triaxial accelerometer on their dominant wrist over a 7-day period in 2013-2015. Participants with less than 72 hours of PA data, implausibly high activity values (average vector magnitude scores of >100 mg), or >1% clipped values (sensor’s dynamic range of ±8 g is exceeded before or after calibration) were excluded.

The final study cohort consisted of 90,211 participants with complete data for PA, age, sex, ethnicity, age completed full time education, Townsend Deprivation Index, smoking, and alcohol consumption — of these, 3,617 were later diagnosed with CVD (3,305 nonfatal and 312 fatal; 2,220 men, 1,397 women) over the course of 440,004 person-years of follow-up (median [IQR]: 5.2 [1.2] years). Participants were divided into four categories of total PA according to total accelerometer-measured volume of activity — ≤22.7 mg, 22.8-27.3 mg, 27.4-32.7 mg, and >32.7 mg.

Dwyer and colleagues found that participants in the lowest category of total PA (≤22.7 mg) smoked more, had higher body mass index and C-reactive protein, and were diagnosed with hypertension.

“We found a linear dose-response relationship between moderate and vigorous PAs and risk of incident CVD,” they found. “The findings for total PA were very similar.” Compared with the lowest category of moderate-intensity PA (≤22.7 mg), the hazard ratios (HRs) and 95% confidence intervals (CIs) for incident CVD were 0.71 (0.65, 0.77) for the 22.8-27.3 mg range, 0.59 (0.54, 0.65) for the 27.4-32.7 mg range, and 0.46 (0.41, 0.51) for the >32.7 mg range; the corresponding values for vigorous activity were 0.70 (0.64, 0.77), 0.54 (0.49, 0.59), and 0.41 (0.37, 0.46). The study authors found similar trends in HRs for total PA and incident CVD — and, they added, there was no threshold effect for this association.

Dwyer and colleagues noted that, while the protective effect reported by questionnaire based studies is “about 26% for total PA, 20% to 25% for moderate volume/intensity of PA, and 30% to 35% for high amounts/intensity of PA,” the results of the current study “concur with the findings from a harmonized meta-analysis with mortality as the outcome that found the protective effect of accelerometer-measured PA to be much greater than that reported in the literature for questionnaire-based studies.” Also, while there were minimal differences between sexes in risk of CVD for moderate and total volume PA, “for vigorous PA, compared with men, a stronger inverse association was observed for women (Pinteraction <0.001),” they wrote.

“This is the largest ever study of exquisite device-measured physical activity and cardiovascular disease,” Aiden Doherty, PhD, study coauthor and associate professor at Oxford University, said in a statement. “It shows that physical activity is probably even more important for the prevention of cardiovascular disease than we previously thought. Our findings lend further weight to the new WHO guidelines on physical activity which recommend at least 150 to 300 minutes of moderate to vigorous aerobic activity per week for all adults.”

Rema Ramakrishnan, MPH, PhD, also of Oxford University and study first author, added that they are “confident about the study findings because physical activity was objectively assessed by a more valid tool that can capture frequency, intensity, and duration of physical activity rather than self-reported by the participants.”

Dwyer and colleagues noted potential limitations to their study, including a lack of robust evidence that a 7-day measurement is representative of habitual PA, as well as the potential for “reverse causality where incipient CVD, not yet detected clinically, might lead to reduced PA because it makes it more difficult for an individual to undertake PA.”

  1. A large population-based cohort study found that higher levels of moderate-intensity and vigorous-intensity physical activity were inversely associated with lower risk of incident CVD, with no evidence for a threshold effect.

  2. These findings suggest that the potential risk reduction estimated in those engaging in relatively high levels of activity is substantial and justifies a greater emphasis on measures to increase levels of physical activity in the community.

John McKenna, Associate Editor, BreakingMED™

Study co-author Rahimi reported receiving personal fees as the associate editor for PLOS Medicine and is in receipt of personal fees as associate editor for BMJ Heart; coauthor Woodward is a consultant for Amen and Kirin; coauthor Walmsley is supported by a Medical Research Council Industrial Strategy Studentship (grant number MR/S502509) — the Medical Research Council had no role in the current study.

Cat ID: 914

Topic ID: 74,914,730,914,192,48,925