By Aliza Hirsch,


Biological processes that follow a 24-hour cycle are defined as circadian [1] . Specifically in relation to cardiovascular health, previous research has reported a pattern between greater incidence of sudden cardiac death (SCD), which is unexpected death due to loss of heart function, myocardial infarction (MI), also known as a heart attack, and certain periods of the circadian cycle [2,3] . Intense exercise has also been linked to SCD and MI [4]. These two associations have led to the hypothesis that exercise during specific times of day may increase risk of adverse cardiovascular outcomes.

As previously mentioned, the incidence of SCD and MI has been tied to specific times of day. This is crucial considering SCD is one of the leading causes of death globally[5]. In the United States alone, SCD accounts for nearly 400,000 annual deaths [6,7]. Moreover, MI and SCD are related; as a result, patients who have experienced an MI show increased risk for SCD. Notably, previous studies have indicated an increased risk of SCD in the morning and decreased risk in the nighttime [3]. A meta-analysis reviewing nearly 20 studies examining the effects of circadian rhythm on SCD, indicated approximately 30% of SCD events occurred between 6:00 am and 12:00 pm [8] MI follows a similar circadian pattern with an increased report of MI events in the morning (9 am) relative to nighttime (11 pm)[2].

There are several physiological mechanisms that have been shown to mediate the higher incidence of SCD and MI in the morning. One supported theory is that there is an increase in blood platelet aggregation which is likely due to morning postural changes and elevated levels of epinephrine [9] . Blood platelet aggregation is when blood platelets, a type of blood cell, clump together. Although blood platelet aggregation is necessary for many biological processes (i.e. stopping the bleeding when you get a cut), a surplus of this process can lead to a narrowing of arterial walls and thus block proper blood flow to the heart.  Other potential explanations for this circadian-cardiovascular relationship include increases in morning cortisol activity due to anticipatory stress, sympathetic nervous system (SNS) activity, and early morning blood pressure (BP)[3, 9-11]. These explanations are connected since cortisol secretion leads to SNS activation and increased BP.

Combining our current knowledge of the link between circadian rhythm and adverse cardiovascular outcomes as well as the reported effects of intense exercise on these measures, leads to the question of whether or not there is a ’safest’ time to exercise. Studies have shown that patients with coronary artery disease (CAD) exhibit more cardiac ischemia (i.e. restriction of blood flow to the heart tissue) when exercising in the morning than those patients with CAD who decreased their activity before 12:00 pm [13]. Currently, it is unclear whether circardian rhythm has the same effects on MI and SCD for people who exercise regularly at a vigorous level.

SportsCardiologyBC is currently investigating this matter in greater depth with a new research project entitled the ‘Time of Day Study’. The primary goal of this research is twofold as it aims to a) determine whether there is in fact a safest time to exercise and b) whether or not this criterion applies to athletes. Visit our research page if you are interested in participating!




Reference List

  1. Guo, Y. F., & Stein, P. K. (2003). Circadian rhythm in the cardiovascular system: Chronocardiology. American Heart Journal, 145(5), 779–786.
  2. Muller, J. E., Stone, P. H., Turi, Z. G., Rutherford, J. D., Czeisler, C. A., Parker, C., … Robertson, T. (1985). Circadian variation in the frequency of onset of acute myocardial infarction. The New England Journal of Medicine, 313(21), 1315–22.
  3. Muller, J. E., Ludmer, P. L., Willich, S. N., Tofler, G. H., Aylmer, G., Klangos, I., & Stone, P. H. (1987). Circadian variation in the frequency of sudden cardiac death. Circulation, 75(1), 131–138.
  4. Albert, C. M., Mittleman, M. A., Chae, C. U., Lee, I.-M., Hennekens, C. H., & Manson, J. E. (2000). Triggering of Sudden Death from Cardiac Causes by Vigorous Exertion. New England Journal of Medicine, 343(19), 1355–1361.
  5. Zaman, S., & Kovoor, P. (2014). Sudden cardiac death early after myocardial infarction pathogenesis, risk stratification, and primary prevention. Circulation.

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  5. Ohashi, N., Isobe, S., Ishigaki, S., & Yasuda, H. (2016). Circadian rhythm of blood pressure and the renin–angiotensin system in the kidney. Hypertension Research.
  6. Weitzman, E. D., Fukushima, D., Nogeire, C., Roffwarg, H., Gallagher, T. F., & Hellman, L. (1971). Twenty-four hour pattern of the episodic secretion of cortisol in normal subjects. Journal of Clinical Endocrinology and Metabolism, 33(1), 14–22.
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  8. Parker, J. D., Testa, M. A., Jimenez, A. H., Tofler, G. H., Muller, J. E., Parker, J. O., & Stone, P. H. (1994). Morning increase in ambulatory ischemia in patients with stable coronary artery disease. Importance of physical activity and increased cardiac demand. Circulation. Retrieved from