Journal of Hypertension:
Activity, environment and blood pressure
Gatzka, Christoph D
University of Melbourne, Victoria, Australia
Correspondence and requests for reprints to Dr Christoph Gatzka, Ballarat Health Services, 1 Drummond Street North, Ballarat, Victoria, 3350, Australia Tel: +61 3 5320 4026; fax: +61 3 5320 6500; e-mail: firstname.lastname@example.org
Following the inception of simple, non-invasive blood pressure measurements in the late nineteenth century , it was realized that blood pressure is highly variable, responding to a wide variety of physiological and non-physiological stimuli and interventions [2–4]. This variability and control of blood pressure is of great research interest. However, at the same time, it is an obstacle when attempting to evaluate or improve the accuracy of the measurement itself. More importantly, it reduces the power of a single blood pressure measurement to predict cardiovascular morbidity and mortality [5,6]. In an attempt to improve prediction, guidelines and protocols are specific both on how and in which situation and position should blood pressure be measured when used for risk prediction purposes. They further specify that blood pressure has to be measured multiple times on multiple occasions [7,8].
When portable automated blood pressure monitors became affordable to physicians and acceptable to patients a century later, a similar learning process ensued. The wealth of data, and the relative ease with which it can be obtained, stimulated new research into the variability of blood pressure throughout the day . At the same time, the question arose as to which parameters obtained from ambulatory blood pressure monitoring best predict left-ventricular load , target organ damage  or cardiovascular morbidity and mortality . Similar to using multiple ‘office’ blood pressure readings to best predict risk, averages appear to be the most robust and strongest predictors , whether they be 24-h, day or night, awake or asleep [10,15–17], or a combination of blood pressure and heart rate . Whether the accuracy gained in predicting future risk justifies the additional cost is a subject of great debate. Economic modelling and payers in first-world countries have each taken very different and entirely opposite approaches to this dilemma .
The most obvious observation of blood pressure variability in ambulatory monitoring throughout 24 h is the reduction of blood pressure at night . The question then arises as to the mechanism responsible for this observation; theoretically, a number of possibilities exist. For example, this might just be a simple hydrostatic difference: the cuff during recumbence with the body in the lateral position might be on the arm above and hence simply above heart level. Hydrostatic blood pressure differences introduced by cuff position are measured only in research devices, and this was found not to be the case . Further mechanistic insights came from a number of different, but complimentary approaches: (i) studying night-shift workers demonstrated a reversal of the rhythm ; (ii) ‘asleep’ (as judged by the patient) blood pressure is lower than ‘night’ (as judged by time of day) ; (iii) when also measuring activity with an accelerometer, nocturnal activity is the best correlate of a decrease in blood pressure ; and (iv) studies in sleep laboratories demonstrate consistent blood pressure responses to the ‘lights-out’ and the different stages of sleep . Armed with this knowledge, it can be concluded that the observed nocturnal reduction in blood pressure is related to the reduction of activity in the generally diurnal human species.
In this issue of the journal, Perez-Lloret et al.  report on seasonal differences in blood pressure in Buenos Aires. They found that, when taking a non-random selection of patients presenting for the evaluation of possible hypertension, awake, but not asleep blood pressure is higher during winter than during summer. When evaluated carefully, many biological variables that are sometimes held as constant are found to differ between summer and winter: even though activity is higher during the winter months , body weight increases each winter, decreasing again, but not quite back to baseline, the next summer . Perez-Lloret et al.  evaluated a predominantly urban population. City dwellers, more so white-collar workers, spend most of the day sheltered from the environment . Hence, the quite marked differences in outdoor climate usually translate into much smaller differences in indoor temperatures . If temperature is the determining factor in seasonal blood pressure differences, then it is conceivable that the effect may be considerably larger during parts of the day and on certain days than is suggested by relating large outdoor temperature differences to small differences in awake blood pressure.
How confident can we be that temperature caused this observed difference? There are numerous other factors known to be different between seasons, all of which may contribute to explaining the difference: activity , weight [24,25], selection bias, prevalence of depression , duration of daylight hours, humidity , to name but a few. Similar to the diurnal differences, suggestive evidence for the mechanism is provided by other, complimentary studies: By contrast to the cross-sectional approach of Perez-Lloret et al. , Goodwin et al.  studied a few, but the same individuals multiple times over 3 years, recording indoor temperature, body temperature, activity by accelerometer and weight. Outdoor temperature, indoor temperature, and also interestingly body temperature, even through the night, were all lower in winter than in summer. This was accompanied by increased activity levels, a longer time of nocturnal recumbence, and increased body weight in winter. Activity levels and blood pressure in summer and winter were the same when asleep, despite differences in body core temperature.
The nocturnal data indicating an identical asleep blood pressure during summer and winter , as supported by Perez-Lloret et al.  and the similar findings of others , are particularly important. They show that both weight and core temperature may play little role in the raised blood pressure observed during winter. It has been suggested that increased vasodilatation during warm periods is responsible for the seasonal difference . However, this explanation would be inconsistent with the findings obtained at night. Instead, increased activity, as measured by an accelerometer during the daytime, may be the main driving force for an increase in blood pressure. Further supporting evidence was obtained in blue-collar workers in Israel by Kristal-Boneh et al. [30,31]. Seasonal differences were maximal when at work, presumably with high levels of activity, but yet in a sheltered environment rather than outdoors. Workplaces with greater seasonal variation in indoor temperature were associated with greater seasonal variation in blood pressure. Data from the PAMELA study  again affirm this observation indicating that, despite smaller seasonal indoor than outdoor temperature changes, seasonal differences were greater in ‘office’ and ‘home’ measurements rather than daytime averages. Contrary to the previous three studies, PAMELA also found seasonal differences in night-time systolic, but not diastolic blood pressure. This may reflect the use of fixed night time in PAMELA rather than sleep readings in the study by Perez-Lloret et al. . In light of changed levels of activity being involved in seasonal differences, it is worthy of note that heart rate did not show any seasonal difference in PAMELA. Indeed, if the level of activity plays a crucial role in determining seasonal differences in blood pressure, then it would be consistent with activity playing a crucial role in determining diurnal differences.
Another important aspect of seasonal variation is the incidence of symptomatic cardiovascular disease, which peaks in winter [33–35]. Clinicians have long known that, in some patients with chronic stable angina due to coronary artery disease, attacks can be provoked by cold exposure . Improvements in central indoor heating are not consistently associated with a reduction in seasonal differences in mortality from cardiovascular disease [37–39]. An analysis of worldwide populations demonstrated an almost linear relationship between seasonal variation in temperatures and coronary events . On a similar note, there is a diurnal variation in the incidence of myocardial infarction, with a peak in the early morning hours . There is also a surge in blood pressure associated with waking and rising in the morning . Whether this is causative or coincidental remains actively debated.
Is it conceivable that the small absolute seasonal difference in daytime blood pressure of 3/2 mmHg found by Perez-Lloret et al. , which is larger in other studies [24,29,41], could account for all of the seasonal difference in coronary events? When examined in more detail, the excess cardiovascular deaths attributable to cold periods apparently occur during the first week of a transition from warm to cold . If a blood pressure increase occurred early during this transition phase, similar to the early morning rise in blood pressure, then it would be conceivable that changes in blood pressure at least contribute to this observed excess mortality. Of note is the larger observed change in blood pressure when considering published studies of individuals over long periods [29,41], as opposed to cross-sectional studies such as that of Perez-Lloret et al. . Cholesterol levels show seasonal variation , and a number of thrombogenic factors are both acutely and chronically, adversely affected by exposure to cold. All might contribute together with temperature-related changes in blood pressure to cause excess mortality and morbidity [33,44,45].
In conclusion, the study by Perez-Lloret et al.  contributes further supporting evidence that seasonal differences in blood pressure do exist, but are largely confined to the daytime. Causative mechanisms, the time course of increases in blood pressure in response to changes in ambient temperature, the involvement of changes in activity levels, individual differences and the potential impact on excess cardiovascular mortality during winter all require further study.
1 Riva R. Un nuovo sfigmomanometro. Gaz Med Lomb 1896; 55:497.
2 Stegemann J. Die fortlaufende, unblutige Blutdruckregistrierung unter Verwendung eines mechanisch-elektrischen Transducers. Pflügers Arch 1956; 262:419–424.
3 Shaw BS, Knapp MS, Davies DH. Variations of blood-pressure in hypertensives during sleep. Lancet 1963; 1:797–799.
4 Armitage P, Rose GA. The variability of measurements of casual blood pressure. I. A laboratory study. Clin Sci 1966; 30:325–335.
5 Gatzka CD. Diagnostic certainty in hypertension. J Hypertens 2006; 24:803–805.
6 Chiu Y-H, Wu S-C, Tseng C-D, Yen M-F, Chen TH-H. Progression of pre-hypertension, stage 1 and 2 hypertension (JNC 7): a population-based study in Keelung, Taiwan (Keelung Community-based Integrated Screening no. 9). J Hypertens 2006; 24:821–828.
7 2003 European Society of Hypertension – European Society of Cardiology guidelines for the management of arterial hypertension. J Hypertens
8 US Department of Health and Human Services. The seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure
. National Institutes of Health, Publication no. 04-5230. Bethesda, Maryland: NIH; 2004.
9 Parati G. Assessing circadian blood pressure and heart rate changes: advantages and limitations of different methods of mathematical modelling. J Hypertens 2004; 22:2061–2064.
10 Verdecchia P, Schillaci G, Guerrieri M, Gatteschi C, Benemio G, Boldrini F, Porcellati C. Circadian blood pressure changes and left ventricular hypertrophy in essential hypertension. Circulation 1990; 81:528–536.
11 Gatzka CD, Reid CM, Lux A, Dart AM, Jennings GL, for the Hypertension Diagnostic Service Investigators. Left ventricular mass and microalbuminuria: relation to ambulatory blood pressure. Clin Exp Pharmacol Physiol 1999; 26:514–516.
12 Perloff D, Sokolow M, Cowan R. The prognostic value of ambulatory blood pressures. JAMA 1983; 249:2792–2798.
13 Verdecchia P. Prognostic value of ambulatory blood pressure: current evidence and clinical implications. Hypertension 2000; 35:844–851.
14 Gatzka CD, Schmieder RE, Schobel HP, Klingbeil AU, Weihprecht H. Improved prediction of left ventricular mass from ambulatory blood pressure monitoring using average tension-time-index. J Hypertens Suppl 1993; 11:98–99.
15 Clement DL, De Buyzere ML, De Bacquer DA, de Leeuw PW, Duprez DA, Fagard RH, et al
. Prognostic value of ambulatory blood-pressure recordings in patients with treated hypertension. N Engl J Med 2003; 348:2407–2415.
16 Amar J, Vernier I, Rossignol E, Bongard V, Arnaud C, Conte JJ, et al
. Nocturnal blood pressure and 24-hour pulse pressure are potent indicators of mortality in hemodialysis patients. Kidney Int 2000; 57:2485–2491.
17 Ohkubo T, Imai Y, Tsuji I, Nagai K, Ito S, Satoh H, Hisamichi S. Reference values for 24-hour ambulatory blood pressure monitoring based on a prognostic criterion: the Ohasama study. Hypertension 1998; 32:255–259.
18 Imholz BPM, Langewouters GJ, van Montfrans GA, Parati G, van Goudoever J, Wesseling KH, et al
. Feasibility of ambulatory, continuous 24-hour finger arterial pressure recording. Hypertension 1993; 21:65–73.
19 Mallion JM, de Gaudemaris R, Monzie A, Battistella P, Siche JP. Pression arterielle et activites de travail poste. Arch Mal Coeur Vaiss 1987; 80:897–904.
20 Gatzka CD, Schmieder RE. Improved classification of dippers by individualized analysis of ambulatory blood pressure profiles. Am J Hypertens 1995; 8:666–671.
21 Eissa MA, Yetman RJ, Poffenbarger T, Portman RJ. Comparison of arbitrary definitions of circadian time periods with those determined by wrist actigraphy in analysis of ABPM data. J Hum Hypertens 1999; 13:759–763.
22 Carrington MJ, Barbieri R, Colrain IM, Crowley KE, Kim Y, Trinder J. Changes in cardiovascular function during the sleep onset period in young adults. J Appl Physiol 2005; 98:468–476.
23 Perez-Lloret S, Toblli JE, Vigo DE, Cardinali DP, Milei J. Infradian daytime and nighttime systolic and diastolic blood pressure rhythms in humans. J Hypertens 2006; 24:1273–1279.
24 Goodwin J, Pearce VR, Taylor RS, Read KL, Powers SJ. Seasonal cold and circadian changes in blood pressure and physical activity in young and elderly people. Age Ageing 2001; 30:311–317.
25 Yanovski JA, Yanovski SZ, Sovik KN, Nguyen TT, O'Neil PM, Sebring NG. A prospective study of holiday weight gain. N Engl J Med 2000; 342:861–867.
26 Rastad C, Sjöden PO, Ulfberg J. High prevalence of self-reported winter depression in a Swedish county. Psychiatry Clin Neurosci 2005; 59:666–675.
27 Capon A, Demeurisse G, Zheng L. Seasonal variation of cerebral hemorrhage in 236 consecutive cases in Brussels. Stroke 1992; 23:24–27.
28 Nakajima J, Kawamura M, Fujiwara T, Hiramori K. Body height is a determinant of seasonal blood pressure variation in patients with essential hypertension. Hypertens Res 2000; 23:587–592.
29 Brennan PJ, Greenberg G, Miall WE, Thompson SG. Seasonal variation in arterial blood pressure. Br Med J (Clin Res Ed) 1982; 285:919–923.
30 Kristal-Boneh E, Harari G, Green MS, Ribak J. Seasonal changes in ambulatory blood pressure in employees under different indoor temperatures. Occup Environ Med 1995; 52:715–721.
31 Kristal-Boneh E, Harari G, Green MS, Ribak J. Summer-winter variation in 24 h ambulatory blood pressure. Blood Press Monit 1996; 1:87–94.
32 Sega R, Cesana G, Bombelli M, Grassi G, Stella ML, Zanchetti A, Mancia G. Seasonal variations in home and ambulatory blood pressure in the PAMELA population. J Hypertens 1998; 16:1585–1592.
33 Keatinge WR, Coleshaw SR, Easton JC, Cotter F, Mattock MB, Chelliah R. Increased platelet and red cell counts, blood viscosity, and plasma cholesterol levels during heat stress, and mortality from coronary and cerebral thrombosis. Am J Med 1986; 81:795–800.
34 Donaldson GC, Keatinge WR. Mortality related to cold weather in elderly people in southeast England, 1979–94. BMJ 1997; 315:1055–1056.
35 Donaldson GC, Keatinge WR. Early increases in ischaemic heart disease mortality dissociated from and later changes associated with respiratory mortality after cold weather in south east England. J Epidemiol Commun Health 1997; 51:643–648.
36 Marchant B, Donaldson G, Mridha K, Scarborough M, Timmis AD. Mechanisms of cold intolerance in patients with angina. J Am Coll Cardiol 1994; 23:630–636.
37 Barnett AG, Dobson AJ, McElduff P, Salomaa V, Kuulasmaa K, Sans S. Cold periods and coronary events: an analysis of populations worldwide. J Epidemiol Commun Health 2005; 59:551–557.
38 Keatinge WR, Coleshaw SR, Holmes J. Changes in seasonal mortalities with improvement in home heating in England and Wales from 1964 to 1984. Int J Biometeorol 1989; 33:71–76.
39 Wilkinson P, Pattenden S, Armstrong B, Fletcher A, Kovats RS, Mangtani P, McMichael AJ. Vulnerability to winter mortality in elderly people in Britain: population based study. BMJ 2004; 329:647.
40 Muller JE, Stone PH, Turi ZG, Rutherford JD, Czeisler CA, Parker C, et al
. Circadian variation in the frequency of onset of acute myocardial infarction. N Engl J Med 1985; 313:1315–1322.
41 Argilés À, Mourad G, Mion C. Seasonal changes in blood pressure in patients with end-stage renal disease treated with hemodialysis. N Engl J Med 1998; 339:1364–1370.
42 Kunst AE, Looman CW, Mackenbach JP. Outdoor air temperature and mortality in The Netherlands: a time-series analysis. Am J Epidemiol 1993; 137:331–341.
43 Ockene IS, Chiriboga DE, Stanek EJ III, Harmatz MG, Nicolosi R, Saperia G, et al
. Seasonal variation in serum cholesterol levels: treatment implications and possible mechanisms. Arch Intern Med 2004; 164:863–870.
44 Woodhouse PR, Khaw KT, Plummer M, Foley A, Meade TW. Seasonal variations of plasma fibrinogen and factor VII activity in the elderly: winter infections and death from cardiovascular disease. Lancet 1994; 343:435–439.
45 Mercer JB, Osterud B, Tveita T. The effect of short-term cold exposure on risk factors for cardiovascular disease. Thromb Res 1999; 95:93–104.
© 2006 Lippincott Williams & Wilkins, Inc.