Although you would think blood flow would be awful high during an sort of endurance activity pretty much eliminating the chance of a thrombus forming simply from "thick" blood.

I agree with you but I suspect that clots formed as a result of doping would form the night before the race as a result of damage caused during recon rides.

In effect you cause micro-damage in training running up to the event. Then you take the juice the night before the big race and during the night clots form in the body. Sometime during the next day a clot brakes free and causes a heart attack.

Thanks for sharing the link to the article, Neal. It's easy to lose track of the number of young, seemingly healthy, cyclists who've died from heart-related problems.

At this point, I don't think this problem should be surprising. We could make a similar list of young, apparently healthy, athletes from a variety of sports who've died--or nearly died--from heart problems.

I do wonder, though, about the depth of cardiac screening for professional cyclists and the possible influence of doping.

.

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Larry Creswell
http://www.athletesheart.org, @athletesheart

Hello Icreswell and All,

A young man, 26, that married into our family, while visiting from Australia, who was active and cycled and was active in other sports, said he did not feel well and was going into the kitchen to get a drink. He went in the kitchen and died of a heart attack. The autopsy showed a congenital heart defect.

He had participated in physical exams and did not seem to be aware of any problems.

https://www.ncbi.nlm.nih.gov/...articles/PMC1994446/

https://en.wikipedia.org/...ac_death_of_athletes

I expect that pro cyclists are screened and have regular physical exams ..... but ........

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Cheers, Neal

+1 mph Faster

http://www.theargus.co.uk/...d_during_cycle_race/

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Cheers, Neal

+1 mph Faster

Hello All,

http://www.cyclingweekly.com/...m_term=cyclingweekly

Excerpts:



"Belgian cyclist Jeroen Goeleven, 25, died in his sleep last night from what initial reports suggest was natural causes, happening only two weeks after Michael Goolaerts suffered a heart attack in Paris-Roubaix.

Goeleven, born on July 4, 1992, raced with the continental team Colbra in 2015, but in recent years with smaller teams. Only 10 days ago, he won the Limburg time trial title."

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Cheers, Neal

+1 mph Faster

Very sad. Hopefully these have nothing to do with the string of deaths in the 90s over here attributed to overusage of EPO.

Hello turdburgler and All,

I have bradycardia (slow heart rate) and also now have a pacemaker to provide a ‘floor’ for my heart rate so it will not beat too slowly.



The pacemaker function is transparent to me (I am not aware of it at all) and my heart rate goes up normally during exercise and returns to normal as before ….. but the pacemaker prevents my heart from going too slowly when resting or sleeping.

Could it be that some young highly trained individuals have heart rates that are pumping ‘too’ slowly when sleeping or resting?

https://www.ncbi.nlm.nih.gov/...articles/PMC4024745/

Excerpts:

After lifelong physical endurance training, veteran endurance athletes have a higher incidence of sinus node disease and artificial pacemaker implantation than normal individuals5,6,7, and it is likely that this is a consequence of the marked remodelling of the sinus node shown here.

It may also help explain syncope [fainting] in the young athlete46. Other rhythm disturbances beset the athlete (for example, atrial fibrillation, heart block47,48, bundle branch block48,49 and even sudden cardiac death50,51) and it is likely that they are a consequence of an analogous remodelling of other parts of the heart: the atrial muscle, atrioventricular node, Purkinje fibres and ventricles (perhaps in combination with a pre-existing heart condition in the case of sudden cardiac death). [added or emphasis]

Exercise is undoubtedly beneficial for the cardiovascular system, but at the same time intense endurance training can have harmful effects, and our findings highlight the fundamental changes taking place.

https://www.ncbi.nlm.nih.gov/...articles/PMC4405729/

It is well known that athletes have a low resting heart rate (bradycardia). The bradycardia can be moderate to severe: reports of heart rates of 40–60 beats min−1 in athletes are common (Boyett et al. 2013), and Jensen-Urstad et al. (1997) reported heart rates of <30 beats min−1 in elite athletes at night. Consistent with this, S. Sharma has studied 142 elite cyclists and rowers and observed heart rates over the range 30–70 beats min−1; the distribution of heart rates in the athletes (and for comparison in a normal population) is shown in Fig.​Fig.1.1.

The resting heart rate is easy to measure and it is clear that athletes use the resting heart rate as a measure of fitness and speak of it in terms of pride and bravado. This is despite evidence that veteran athletes are more likely to need an electronic heart pacemaker fitted in later life (Baldesberger et al. 2008). [emphasis added]

The bradycardia is widely believed to be the result of high vagal tone; this is a natural assumption because high vagal tone will reduce the heart rate. However, despite this widespread belief, efferent vagal nerve activity to the heart's pacemaker (the sinus node) has never been recorded. It is not obvious how it could be measured, because the vagus nerve carries afferent as well as efferent nerve fibres. Because of this, the scientific community uses what is assumed to be a surrogate of vagal nerve activity to the sinus node, heart rate variability.

Heart rate variability is a beat-to-beat variability in the heart rate and is assumed to be the result of stochastic fluctuations in autonomic nerve activity to the sinus node and changes in heart rate variability are assumed to represent changes in this. PubMed lists more than 17,000 publications concerned with heart rate variability.

Heart rate variability is higher in athletes (Aubert et al. 2003) and this is taken as evidence of high vagal tone in athletes, and this is then assumed to be responsible for the bradycardia. However, a causative link between autonomic nerve activity and heart rate variability has never been demonstrated (for reasons discussed above). Furthermore, we have recently analysed the biophysics underlying heart rate variability and we have shown that, regardless of whatever is responsible for heart rate variability, heart rate variability is a steep exponential function of heart rate (heart rate variability increases with a decrease in heart rate) and the majority of reported changes in heart rate variability can be explained by the concurrent change in heart rate (Monfredi et al. 2014).

https://www.ncbi.nlm.nih.gov/pubmed/23657540

https://www.ncbi.nlm.nih.gov/pubmed/24886917

https://www.ncbi.nlm.nih.gov/pubmed/18512181

https://www.ncbi.nlm.nih.gov/pubmed/14992127

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Cheers, Neal

+1 mph Faster

Nope. It doesn't appear to have anything to do with an imaginary string of deaths in the 90s. These are actually real.

It would seem to me that while bradycardia may contribute to syncope in young athletes that it would be unlikely to contribute to SCD. I would expect that vagal mediated depression of the SA node and even temporary blockade of the AV node would still allow a sufficient ventricular escape rhythm to maintain life. So absent coexisting structural heart disease or genetic conduction abnormalities I don’t think athletically associated bradycardias could be a cause of sudden death. I would be interested to hear Larry’s thoughts however.

As per the young man who died in his sleep, in addition to SCD other possible causes include psychiatric disease (including accidental or non accidental overdose), cerebral aneurysm, or aortic dissection. One of these is much more stigmatized than the others despite all four being medical diseases. But I digress.