Walking Pace, Leisure Time Physical Activity, and Resting Heart Rate in Relation to Disease-Specific Mortality in London: 40 Years Follow-Up of the Original Whitehall Study. An Update of Our Work with Professor Jerry N. Morris (1910–2009)

Purpose

To examine the association of leisure time physical activity, walking pace and resting heart rate with disease-specific mortality in a prospective cohort study by reporting updated analyses of an earlier report we produced with the British epidemiologist, Jerry N. Morris (1910–2009).

Methods

In the original Whitehall study, 19,019 male, nonindustrial, London-based government employees, aged from 40 to 69 years in 1967 and 1970, participated in a medical examination during which data on leisure time physical activity (N = 6715), self-rated walking pace (N = 6729), and resting heart rate (N = 1183) were collected. Cox proportional hazards analyses were used to estimate hazard ratios for the relation between these exposures and disease-specific mortality.

Results

In models adjusted for a range of covariates including socioeconomic status, smoking, and obesity, high resting heart rate was associated with a modestly elevated rate of mortality from all causes (hazard ratio; 95% confidence interval: tertile 3 vs. tertile 1: 1.17; 0.99, 1.37 p[trend]: 0.07) and respiratory disease (1.69; 1.04, 2.76 p[trend]: 0.03). Of the two markers of physical activity, walking pace was inversely related to mortality ascribed to all causes (slow vs. high walking pace 1.71; 1.53, 1.91 p[trend]: <0.001]), coronary heart disease (2.03; 1.68, 2.47 p[trend]: <0.001), and total cancers (1.25; 0.98, 1.59 p[trend]: 0.04). The corresponding associations for leisure time activity were typically weaker. For other mortality endpoints—respiratory disease (walking pace: 1.96; 1.48, 2.60 p[trend]: <0.001]), hematopoietic cancer (walking pace: 1.36; 0.52, 3.51 p[trend]: 0.03), stomach cancer (inactive versus active leisure time: 1.53; 0.88, 2.64 p[trend]: 0.04), and rectal cancer (walking pace: 4.85; 1.70, 13.8 p[trend]: 0.007)—individual activity indices revealed effects, but not both.

Conclusions

Higher levels of physical activity indexed by the various markers herein appeared to confer protection against a range of mortality outcomes.

Introduction

Almost six decades ago, amidst concerns regarding the escalating rates of coronary heart disease (CHD), the first empirical investigation of what was subsequently termed the “exercise hypothesis”—physical activity reduces the occurrence of this condition—was undertaken by Jerry Morris and his colleagues at the Medical Research Council Social Medicine Unit within the London School of Hygiene and Tropical Medicine (1). After typically extended scrutiny and deliberation by Jerry—a practice unacceptable in the current scientific environment of publish or perish—that, remarkably, involved corroborating the results in second investigation study, the novel and contentious findings were finally released as two companion papers in the Lancet(2). They showed lower rates of CHD in bus conductors in comparison to less occupationally active bus drivers, and in postmen relative to deskbound telephonists and other office-based employees (2).

As Jerry Morris would freely and frequently articulate, these studies, precisely because they were seminal, were not without their shortcomings. Statistical methods before the proliferation of personal computers were limited in their capacity to explore the issue of confounding: it was possible that higher levels of overweight, high blood pressure, psychosocial stress, and/or preexisting ischaemia in the less active groups, rather than sedentary behavior itself, were at least partially responsible for the increased risk of CHD. Further, the study focused exclusively on job-orientated activity. Mindful of the diminishing role of occupational physical exertion in modern industrialized societies, Morris et al. (3) and subsequently Paffenbarger et al. (4), also showed physical activity in leisure time to be cardioprotective, an effect that held after a range of covariates were taken into account.

Although still failing to feature in risk prediction algorithms, based on a series of cohort studies 5, 6, 7, 8, 9, 10, 11, 12 and the sporadic randomized controlled trial (13), physical activity and its physiological consequence, such as cardiorespiratory fitness 14, 15, are now widely regarded as being etiologically linked to CHD. Indeed, it is testimony to the robustness of this association that these studies, despite their methodological limitations and with few exception 14, 15 often crude measures of physical exertion, have nonetheless almost universally shown support for Morris' hypothesis. As the prospective cohort studies on which these observations are largely based have matured, investigators have taken the opportunity of exploring the role of physical activity in the occurrence of other important somatic diseases such as stroke and site-specific cancers, an area of physical activity epidemiology that still represents a challenge 16, 17.

In this cohort of British male Civil Servants (government employees)—an extended follow-up of an earlier report that we coauthored with Jerry and with which he, true to form, remained largely unimpressed (18)—we explore the association of leisure time physical activity, walking pace, and resting heart rate with disease-specific causes of death. Doubtless Jerry would have provided penetrating comments, with some mischievous observations. He would typically then decline, the invitation to coauthor—as he did with several of our subsequent articles using this material 19, 20, 21, 22, usually citing his lack of involvement in the design of the original study in the 1960s—before steering the conversation to the latest London stage play or novel on which he would make erudite observations, while causing one to regret that one's own interests and energy levels were a fraction of such an engaging, vital, and now, much missed colleague.