Age and the cardiovascular system
Sport, exercise and physical activity hold different significance and meaning to every individual, whether it is a part of your daily life, something you watch from a distance or something all-consuming that defines who you are. Maintaining a regular routine of exercise is frequently cited as being highly effective for prevention and treatment of many chronic diseases and unequivocally improves cardiovascular health (Sharkey and Gaskill, 2007). However, with ever growing participation in ultra-endurance events all over the world research has started to look in more detail at the impact this type of exercise has on the human body (IAU Ultra Marathon, 2013). Ultra-endurance is the term given to events that last for over 6 hours, with the term ultra-running being applied to distances over a marathon distance of 26.2 miles (Wortley and Islas, 2011). People seem to seek out these ultra-type events in order to test themselves, with Hinton (2016) a former double ironman competitor reporting ‘Ironman didn’t break me, mentally or physically. I wanted to know my limits’ and while this form of challenge carries with it a huge sense of achievement and success, is there a downside to it all?
When older athletes compete in really tough ultra-endurance events, like Gordon Ramsey does, there is always a concern whether it is safe for them to push themselves as hard as the younger competitors do. The reason for this concern is down to the fact as the human body ages there are many physiological changes that happen, most of which decrease the body’s ability to perform. This sub-section of the blog will discuss the cardiovascular system in depth and explain how Gordon can train to reduce his risk of injury as well as improve his performance.
How the cardiovascular system changes with age
Researchers looking at long distance races have cautioned that as well as inhibiting the immune system this form of exercise may lead to overload of the heart atria and right ventricle which could ultimately make someone more prone to unfavorable heart arrhythmias later in life (O’Keefe, et al, 2012).
More masters athletes than ever before are now participating in ultra-endurance events across the globe. With that comes a rising concern on the health status of these people. Heart health is a particular concern amongst these athletes as these people are all over the age of 35. Although many of these people are deemed to be fit and healthy, the strenuosity of the event is of major interest to doctors, trainers and the athletes themselves. The Ironman Triathlon is one of the most popular ultra-endurance events and participation has increased at both amateur and elite level.
Because of the influence of cardiorespiratory fitness on functional independence, quality of life, and cardiovascular disease, tremendous interest has been directed towards describing the age-related change in maximal oxygen consumption (V̇O2max). There is a study conducted by A. Hawkins and A. Wiswell stating that current evidence supports a 10% per decade decline in V̇O2max in men and women regardless of activity level. High-intensity exercise may reduce this loss by up to 50% in young and middle-aged men, but not older men, if maintained long term. Middle-aged and older women do not appear to be able to reduce loss rates in V̇O2max to less than 10% per decade, which may be related to estrogenic status but there is inconclusive evidence. (A. Hawkins and A. Wiswell, 2012).
The factors limiting the ability to maintain high-intensity training are not completely known but aging most likely plays a role as studies have demonstrated that training maintenance becomes more difficult with advancing age. Age-related loss of V̇O2max seems to occur in a non-linear fashion in association with declines in physical activity. Recommendations for exercise training should include aerobic activities utilising guidelines established by the American College of Sports Medicine for improving CV fitness and health. Because of how strenuous the Ironman events are, it is a concern for masters athletes who train over these guidelines, which most of them do because they are competing to win. (A. Hawkins and A. Wiswell, 2012).
There is also evidence that ultra-endurance exercise causes myocardial injury. The extent and duration of these changes remains unresolved. Recent reports have speculated that structural adaptations to exercise, particularly of the right ventricle, may predispose to tachyarrhythmias and sudden cardiac death (La Gerche et al., 2007). The study composed found that myocardial damage occurs during intense ultra-endurance exercise and, in particular, there is a significant reduction in RV function. The Important piece of information found in this study is that almost all abnormalities resolve within 1 week. So the evidence on reduction in RV dysfunction doesn’t really have a strong impact on long term heart health of aging ultra-endurance athlete (La Gerche et al., 2007) and Gordon is safe to remain on his intense training programme based on this information alone.
On older study form 1999 constructed by P. Whyte et al., 1999 also states similar information.
The purpose of the study was to: Recent echocardiographic studies have reported cardiac dysfunction following ultra-endurance exercise in trained individuals. The duration of exercise required to elicit cardiac dysfunction and the mechanisms underlying this phenomenon have not been fully elucidated. The aim of the present study was to examine the presence of cardiac dysfunction following a half–Ironman and Ironman triathlon in trained individuals (P. Whyte et al., 1999).
They followed the following methods: 14 male triathletes (age: 32 5 yr; height: 180 8 cm; body mass: 75 9 kg) completed a half-Ironman triathlon. Following a 4-wk period, 10 of the original 14 triathletes completed an Ironman triathlon. All triathletes were assessed using ECG, echocardiography, and blood analysis pre-, immediately post-, and 48 h postrace for both distances (P. Whyte et al., 1999).
And they got these results: Echocardiographic results indicated diastolic and systolic left ventricular dysfunction, for both race distances, which were associated with altered relaxation characteristics and a reduced inotropic contractility, respectively. Following 48-h recovery, all echocardiographic measures were similar to resting values. Creatine kinase MB (CKMB) was significantly elevated immediately postrace for both distances; however, it accounted for less than 5% of the total CK value and in the presence of an elevated total CK and CKMM implied that the elevated CKMB was noncardiac in origin. Troponin-T, however, was significantly elevated immediately postrace for both distances and returned to normal following 48-h recovery indicating myocardial damage (P. Whyte et al., 1999).
From this study they found that Echocardiographic results indicated diastolic and systolic left ventricular dysfunction, for both race distances, which were associated with altered relaxation characteristics and a reduced inotropic contractility, respectively. Following 48-h recovery, all echocardiographic measures were similar to resting values. Creatine kinase MB (CKMB) was significantly elevated immediately postrace for both distances; however, it accounted for less than 5% of the total CK value and in the presence of an elevated total CK and CKMM implied that the elevated CKMB was noncardiac in origin. Troponin-T, however, was significantly elevated immediately postrace for both distances and returned to normal following 48-h recovery indicating myocardial damage (P. Whyte et al., 1999).
Although the cardiovascular benefits of exercise are well established, it is recognized that the risk of death is transiently increased during an acute exercise bout in individuals with underlying pathology. Recent echocardiographic studies, however, have reported cardiac dysfunction following endurance exercise in the absence of underlying cardiovascular diseases, which has been attributed to “cardiac fatigue”. Previous echocardiographic studies have reported left ventricular diastolic an systolic dysfunction following ultra-endurance exercise in trained individuals (P. Whyte et al., 1999). This study is from 1999 but still displays similar findings in conjunction with more recent studies. They both state that that exercise is good for the heart, but that too much intense endurance exercise can cause disease. This study by (La Gerche et al; 2007) however states that the damage during intense ultra-endurance exercise there is a significant reduction in the right ventricle and but the earlier study by P. Whyte et al., 1999 finds that the left ventricle has some dysfunction also. Following data conducted from both of these studies both Gordon, his trainer and his Medical team should all be aware of these risks when training to complete his ironman in less than 12 hours.
The oxidative system is also an important part of the body, which is required to perform at an intense level. At least 30 minutes of moderate-intensity physical activity accumulated on most, preferably all days is considered the minimum level necessary to reduce the risk of developing cardiovascular disease. Despite an unclear explanation, some epidemiological data paradoxically suggest that a very high volume of exercise is associated with a decrease in cardiovascular health. Although ultra-endurance exercise training has been shown to increase antioxidant defences (and therefore confer a protective effect against oxidative stress), an increase in oxidative stress may contribute to the development of atherosclerosis via oxidative modification of low-density lipoprotein (LDL). Research has also shown that ultra-endurance exercise is associated with acute cardiac dysfunction and injury, and these may also be related to an increase in free radical production. Longitudinal studies are needed to assess whether antioxidant defences are adequate to prevent LDL oxidation that may occur as a result of increased free radical production during very high volumes of exercise. In addition, this work will assist in understanding the accrued effect of repeated ultra-endurance exercise-induced myocardial damage. (L. Knez, S. Coombes, and D. Jenkins, 2012)
Following information gathered from all of these studies both Gordon, his trainer and his Medical team should all be aware of these risks when training to complete his ironman in less than 12 hours.
References
Hinton, L. (2016) Personal Communication. 24th February 2016.
IAU Ultra Marathon. (2013), available at http://iau-ultramarathon.org. accessed 1st March 2016
O’Keefe, J.H., Patil, H.R., Lavie, C.J. et al. (2012). Potential adverse cardiovascular effects from excessive endurance exercise. Mayo Clinic Proceedings, 87(6), 587-595.
Sharkey, B.J. and Gaskill, S.E. (2007) Fitness and Health. Champaign. Human Kinetics
Wortley, G. and Islas, A.A. (2011). The problem with ultra-endurance athletes. British Journal of Sports Medicine. 45 (14), 1085.
- Hawkins, S. and A. Wiswell, R. (2012) ‘Rate and Mechanism of Maximal Oxygen Consumption Decline with Aging’, Sports Medicine, 33(12), pp. 877–888.
La Gerche, A., A Connelly, K., J Mooney, D. and I MacIsaac, A. (2007) ‘Biochemical and functional abnormalities of left and right ventricular function after ultra-endurance exercise’, Heart, 94(7), pp. 860–866.
(1999) ‘Cardiac fatigue following prolonged endurance exercise of differing distances’, MEDICINE & SCIENCE IN SPORTS & EXERCISE, 32(6), pp. 1067–1072.
- Knez, W., S. Coombes, J. and D. Jenkins, D. (2012) ‘Ultra-Endurance Exercise and Oxidative Damage’, Sports Medicine, 36(5), pp. 429–441.