Slow walking speed in elderly people

People who walk faster are less likely to die than slow walkers, especially from vascular disease. In the linked prospective cohort study (doi:10.1136/bmj.b4460), Dumurgier and colleagues show that this is true for walking speed measured over 6 m in 3208 relatively fit older people, over five years of follow-up.1

Walking speed is determined by physical features such as age, sex, and height, by the presence or absence of diseases, and by physical fitness.

Evidence that exercise is beneficial for health goes back over 50 years, and includes activity during sport and work as well as fitness training. Benefits are primarily in mortality and morbidity from vascular disease, and are seen in middle aged and older people, and those with and without established cardiovascular disease, diabetes, hypertension, or obesity.2 3

Diseases that slow down walking include musculoskeletal, cardiac, respiratory, neurological, and psychiatric disorders. Some of these are associated with excess mortality from vascular disease by virtue of being vascular diseases themselves or via common causal factors, such as smoking. If angina or heart failure cause slow walking, the association between slow walking and vascular mortality is through reverse causation. In epidemiological studies this can be discounted to some extent by excluding people with diagnosed vascular disease at baseline from the analysis, or by excluding events that occur in the first 5-10 years of follow-up, which suggests that the condition was not present at baseline but developed subsequently.

Measures of physical performance are more strongly associated with adverse outcomes than some classic risk factors.3 4 This means that they are more important causally or that they can be measured more precisely. Most studies measure physical activity by using questionnaires. Lack of standardisation and problems with recall or classification of activities present a major challenge for research and weaken the observed association between activity and outcomes. Physical performance is strongly and causally associated with activity and can be measured more precisely. Exercise tolerance on a treadmill, peak oxygen consumption, self reported and measured gait speed, and pulse rate have all been associated with vascular disease in this way. Walking speed may therefore simply be a good way of measuring habitual activity.

Walking speed has been suggested as a new “vital sign” or screening test for people at risk of vascular disease.5 In practice, this approach has two problems. An epidemiologist is more interested in whether walking speed per se is related to outcomes than the effects of confounding and reverse causal factors, and so tries hard to exclude their effects. However, to clinicians, slow walking is slow walking whatever the cause. Moreover, as with classic risk factors, walking speed in isolation is of limited use in defining the likelihood of disease in individual patients. For predicting all cause mortality, the sensitivity and specificity of the lowest third of gait velocity in Dumurgier and colleagues’ study are modest (0.5 and 0.67, respectively).

Preventing vascular disease is important, especially for older people who are well. But as old age progresses, there is a trade off between preventing disease and the burden of polypharmacy, and the priority shifts from preventing mortality to predicting and forestalling transitions to disability.

Walking speed has also been investigated as part of a syndrome of frailty, defined as a state of vulnerability to deterioration in the face of stressors. Frailty is common in older people (about 20% of those over 65) and is associated with falls, disability, and admission to hospital and care homes.6 7 Previously, approaches to defining frailty have included counting diagnoses, disabilities, or vulnerability factors (such as cognitive impairment, poor vision, or a history of falls).8 However, recently a physiological model has been proposed that comprises three or more of the following criteria: unintentional weight loss, self reported exhaustion, weakness (reduced grip strength), slow walking speed, and low physical activity (albeit with a much lower threshold for slow walking than that used by Dumurgier and colleagues—0.65 m/s compared with 1.35-1.5 m/s).9 Frailty by this definition may represent the effects of underlying processes of ageing. It predicts adverse outcomes,7 but being a physiological definition it also suggests interventions that could slow or reverse the process.

Researchers assessing frailty also refer to a “pre-frail” state, where not all of the features of the syndrome exist, or where the severity of features is below the threshold.9 10 If interventions can modify frailty or attenuate its association with poor outcomes, they are likely to be valuable, not just in preventing vascular disease. Interventions may include lifestyle changes such as exercise or diet, but in the future they may include drugs that are anabolic or that modify age associated cellular and metabolic dysfunction.

Showing that these interventions improve outcomes for frail or pre-frail older people has been difficult.10 One notable exception is falls prevention,11 where exercise based treatments reduce clinically important end points. Evidence that this extends to other outcomes (such as death and institutionalisation) is suggestive, but weak.12