Here is my most recent Exercise Physiology paper. Our assignment was to research how much aerobic exercise is too much. I chose to examine marathons. Please do not hear me saying in this paper that marathons are bad. I am just reporting what I found reported in a few studies. It is pretty technical so if you get confused I am sorry.
Introduction
How much aerobic exercise is too much? What must first be defined is your target population. The answer will differ according to the demographic. For example, the answer to that question would look very different for a pregnant person compared to someone preparing for a triathlon. The answer will also vary if you were addressing the needs of an American football player during pre-season compared to someone diagnosed with an immune disorder.
Since 490 BC people have been running marathons (Mohseni et al., 2011). Personally, I have trained several people competing in marathons. In light of that and the fact that over 400,000 people in the United States alone will compete in a marathon this year I have chosen to focus my efforts on marathon runners (Fortescue et al., 2007).
One way to frame the question could be, “Are the cardiovascular (CV) and other physiological effects of running a marathon more harmful than helpful?” We all know aerobic exercise is good for the body but is running 26.2 miles more than the body can safely adapt too?
Marathon Running
Aerobic exercise has been proven to enhance the function of the CV system (Dawson et al., 2008). But is there a point of diminishing returns? Troponin I (CTnI) is a serum marker used to indicate cardiac damage. Clinical levels of CTnI ≥ 0.50 ng/mL results in an acute myocardial infarction (AMI) diagnosis (Fortescue et al., 2007). AMI is also knows as a heart attack. In a study examining 17 recreational runners 11 of these had statistically significant increased levels of CTnI above the threshold for an AMI diagnosis six hours post-marathon completion (O’Hanlon et al., 2010). (Dawson et al., 2008) following 13 runners during the 2007 London Marathon observed that seven of these had CTnI levels above the AMI cut-off. In a study designed to identify the characteristics of a runner more predisposed to elevated troponin levels 55 of the 482 (11%) runners evaluated in the 2002 Boston Marathon had troponin levels above the AMI threshold. This study measured both Troponin T and Troponin I (Fortescue et al., 2007). In relation to the study’s purpose it was concluded that younger runners (≤ 30 years) and those with less marathon experience (≤5) were more likely to have increased troponin levels.
Cardiovascular changes were not the only changes noted.
Mohseni (2011) monitoring 195 marathon and half-marathon participants observed that there was a statistically significant increase in blood urea nitrogen (BUN) levels that clinically would be classified as renal dysfunction. 45.8% of the 83 runners with increased BUN levels would be considered to have moderate to severe renal dysfunction. According to his data he also found men participating in the marathon to be 9x as likely to develop levels classified as moderate renal dysfunction. Vascular function was also discovered to be at risk. Dawson (2008) found a clinically significant decrease in the femoral artery flow-mediated dilation (FMD) response compared to that of the brachial artery.
Conclusion
The findings above indicate CV, renal, and vascular changes to be of concern. However, the clinical significance of these changes is not yet known. More studies need to be conducted and in particular more longitudinal studies. One question to ponder in relation to the cardiac response is- Are the changes pathological in nature or physiological and transient which would lead to enhanced cardiac muscle and function? Other differences that may influence study outcomes include but are not limited to gender, age, the effects of altitude, marathon completion time, and recreational vs. elite athlete.
References
Dawson, E. A., Whyte, G. P., Black, M. A., Jones, H., Hopkins, N., Oxborough, D., Gaze, D., Shave, R. E., Wilson, M., George, K. P., & Green, D. J. (2008). Changes in vascular and cardiac function after prolonged strenuous exercise in humans. Journal Of Applied Physiology, 105(5), 1562-1568.
Fortescue, E., Shin, A., Greenes, D., Mannix, R., Agarwal, S., Feldman, B., Shah, M. I., Rifal, N., Landzberg, M. J., Newburger, J. W., & Almond, C. (2007). Cardiac troponin increases among runners in the Boston Marathon. Annals Of Emergency Medicine, 49(2), 137-143.
Mohseni, M., Silvers, S., McNeil, R., Diehl, N., Vadeboncoeur, T., Taylor, W., Shapiro, S., Roth, J., & Mahoney, S. (2011). Prevalence of Hyponatremia, Renal Dysfunction, and Other Electrolyte Abnormalities Among Runners Before and After Completing a Marathon or Half Marathon. Sports Health: A Multidisciplinary Approach, 3(2), 145-151.
O’Hanlon, R., Wilson, M., Wage, R., Smith, G., Alpendurada, F. D., Wong, J., Dahl, A., Oxborough, D., Godfrey, R., Sharma, S., Roughton, M., George, K., Pennell, D. J., Whyte, G. & Prasad, S. K. (2010). Troponin release following endurance exercise: is inflammation the cause? a cardiovascular magnetic resonance study. Journal Of Cardiovascular Magnetic Resonance, January 2010;12:38-44.






