Morning activity and blood pressure – a cause for concern?

The frequency of important cardiovascular events, such as myocardial infarction, sudden death, ventricular dysrhythmias and stroke, exhibits diurnal variation [1]. Much research has focused on identifying mechanisms responsible for circadian variations in blood pressure and heart rate as two potential haemodynamic ‘triggers’ of these phenomena. Several studies using intra-arterial ambulatory blood pressure monitoring characterized the amplitude and timing of these rhythms, and provided qualitative insight into the impact of arousal and physical activity in mediating these changes, but did not resolve the debate as to the relative importance of endogenous cycles or extrinsic factors in their generation [2–5]. To address this question quantitatively, Leary et al. recorded blood pressure and physical activity over 24 h in 420 patients (of which 212 were women), referred to their clinic for the evaluation of hypertension, as reported in this issue of the journal [6]. These authors had previously reported, in these same patients, positive correlations between daytime blood pressure and heart rate, and activity over the 15 min preceding each measurement [7]. Their objective in the present iteration of these data was to define the influence of physical activity on the magnitude of the morning rise in these variables. Patients were aged 15–81 years. Blood pressure was measured non-invasively, every 20 min, using an ambulatory device with validated accuracy. Activity was quantified by a piezoelectric accelerometer worn on the dominant wrist, which registered and assigned an arbitrary unit scale to any motor activity detected. These patients could be broadly categorized, on the basis of their ambulatory blood pressure, into four groups: (i) normotensive (n = 82); (ii) untreated hypertensive (n = 146); (iii) treated hypertensive, but with poor blood pressure control (n = 137) and (iv) hypertension adequately controlled with treatment (n = 55). The strengths of this analysis therefore include the large number of subjects studied prospectively, a uniform approach to recruitment and analysis, a quantitative estimate of physical activity (rather than reliance on patient diaries) and the use of a well-validated device to determine ambulatory blood pressure. The mean (SD) morning ‘surge’ in blood pressure in these subjects, defined as the difference between mean values encompassing the 4 h after waking, and the 4 h before waking, averaged 23 ± 13 mmHg for systolic and 15 ± 10 mmHg for diastolic. The corresponding rise in heart rate was 17 ± 10 beats/min. The average ‘trough to peak rise', defined as the difference between the peak awake value and the trough asleep value for each subject, was considerably greater (60 ± 18 mmHg for systolic blood pressure). The authors report significant positive relationships between the morning increase in physical activity, and concurrent ‘surges’ in both blood pressure and heart rate (P = 0.0001 for both). Also, there was a significant direct correlation between clinical pressure and the morning increase in blood pressure (P < 0.0005). Men had a significantly greater blood pressure ‘surge’ per unit of physical activity than women, whereas age, body mass index, time of waking, smoking status and the use of blood pressure-lowering medications did not dilute the strength of these relationships. The authors conclude that physical activity should be accounted for when interpreting ambulatory blood pressure data, and caution patients with hypertension or ischaemic heart disease against ‘vigorous physical exercise soon after rising in the morning'. An important corollary, not articulated in the present paper, is that physical activity must also be considered in any discussion of the mechanisms or implications of nocturnal blood pressure ‘dipping’ status. Before reflecting upon the potential clinical implications of these principal observations, certain aspects of this study should be considered in greater detail. The authors’ claim for a significant relationship between daytime activity and ambulatory blood pressure and heart rate rests entirely upon their large sample size. In their study, less than 6% of the morning increase in blood pressure, and less than 10% of the corresponding rise in heart rate could be attributed to concurrent increases in physical activity. Thus, if it were not for the strong probability that the true effect of activity on these cardiovascular variables was underestimated by their study design, these weak correlations might reasonably be discounted as interesting, but without clinical relevance. It appears, from the text, that patients were studied consecutively, as referred to their clinic. If so, the inclusion of individuals with conditions known to increase nocturnal blood pressure (such as certain secondary forms of hypertension, supine hypertension in the setting of autonomic insufficiency and obstructive sleep apnoea) would reduce the magnitude of the morning ‘surge’ and dilute the relationships documented in the results. It should be emphasized that blood pressure was recorded non-invasively, at 20-min intervals, by a device that requires a still arm for accurate measurement. Blood pressure during vigorous activity cannot be established reliably with this method, and is better determined by intra-arterial blood pressure recording [8]. The almost three-fold greater difference between the average ‘trough to peak rise’ and the ‘morning surge’ in systolic blood pressure (60 versus 23 mmHg) suggests considerable underestimation of the true impact of arousal and activity on blood pressure. Data are presented in the aggregate. We are informed that 192 patients (46%) were receiving treatment for hypertension, but there is no information as to the number of these who were prescribed β-adrenoceptor antagonists, or other agents with negative chronotropic effects that might blunt heart rate and blood pressure responses to activity [9]. The authors’ investigation would have been strengthened by exclusion of all treated patients from the primary analysis. Unfortunately, as presented, the data provide no insight into the more important pathophysiological question, namely, the relative impact of activity on blood pressure and heart rate in untreated hypertensive or normotensive subjects. Statistical power may have been inadequate for such subgroup analysis. The selection of such a broad and heterogenous population (one-fifth were classified as normotensive) for study does provide insight into the breadth of activity and blood pressure responses of clinical patients, as a whole, but the authors’ mechanistic hypothesis could have been tested far more efficiently in a small, well-characterized group of patients, using non-invasive or invasive ambulatory blood pressure monitoring. Should patients with hypertension or ischaemic heart disease, or asymptomatic patients at risk for cardiovascular disease, avoid strenuous exercise in the early morning, as the authors suggest? Their own data do not address this issue directly. The average morning blood pressure ‘surge’ detected was within the bounds of normal diurnal variability [10], the variance in blood pressure attributable to activity was trivial, the effect of a standardized exercise protocol or strenuous exercise on awake blood pressure was not determined, and the study design was observational in nature, rather than outcome-driven or interventional. Moreover, the investigators had no means of incorporating the equally potent pressor and chronotropic effects of emotion and conversation into their analysis [8,11]. The beneficial short- and long-term effects of regular rhythmic exercise are well established [12–17], whereas the risk of a cardiovascular event occurring during exercise is extremely low [18]. Circadian variation in haemodynamics and the frequency of important cardiovascular events may be temporally related, but the hypothesis that physical activity represents the fundamental link between these two phenomena remains unproven. Thus, the proscription of morning exercise is premature. The deliberate adoption of an indolent lifestyle for ‘cardioprotection’ is certainly inappropriate, as the sedentary are at greatest risk of suffering a myocardial infarction after strenuous exercise [19,20]. The present data do suggest some sensible cautions. Asymptomatic patients who prefer to exercise in the morning should be encouraged to do so regularly rather than intermittently. Furthermore, they should be prescribed isotonic exercises with modest effects on mean arterial pressure, and be advised to avoid modes of isometric exercise which provoke marked pressor responses, or abrupt decreases in intra-thoracic pressure. Those with exercise-induced ischaemia must be given individual consideration and should undergo appropriate evaluation and supervised testing before embarking on a program of regular prescribed activity [18]. Leary et al. [6] inform us of a significant direct correlation between clinic pressure and the morning increase in blood pressure. This important finding reminds us of the clinician's primary responsibility, which is to ensure the detection and adequate control of hypertension.

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