The main results from Howden et al., the paper that motivated this blog post. Middle-aged participants who engaged in aerobic training improved VO2max and remaining ventricular end-diastolic volume, both markers for reduced incidence of heart disease, whereas participants who engaged in flexibility and strength training did not. Between ages 21 and 56, my level of exercise was inadequate to non-existent.
Had I waited too much time to restart working out, or had I managed to just squeak under the cable? Could I really anyway believe any of this? Howden et al.1 is the original paper which created the basis for the article in BBC News. Fujimoto et al.2 is the sooner paper from the same group.
The group that released these two papers is a cardiology group. I’ve no experience in cardiology so cannot comment critically with this part of their work, I just have to take the authors at their term. Considering that, my understanding of what they are saying is that one form of heart failure is associated with a decrease in left ventricular end-diastolic volume or LVEDV.
LVEDV decreases with age, but is higher in the elderly who have exercised their whole lives (“master athletes”). The relevant question both documents are asking is, for one of those unfortunates who’ve not exercised, will exercise in life invert the reduction in LVEDV later? The hope is that if exercise can increase LVEDV, this will lead to a lower probability of the development of the one kind of heart failure and thus increase longevity. In addition to LVEDV, the authors of both documents assessed lots of other parameters.
The one which caught my eyesight was VO2max, because VO2potential is probably the most common biomarker for the beneficial ramifications of exercise on durability, one that I’ve talked about frequently on this blog. The authors mentioned their results with VO2max barely, but I will spend significant attention to them. The good reason for considering Howden et al.
- If you have recently added a fitness regimen to help you
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What we take note is that this groups studied is different and that for younger generation, LVEDV raises significantly, whereas for the older age group, the difference is not significant statistically. We also note that Howden et al. I am going to discuss in the next section. Finally, we note that VO2max, the workhorse biomarker used in a large quantity of studies as a proxy for health advantages increased in both studies by similar amounts. 0.0001 for Howden et al. The first number in each column in the above mentioned is the amount of rides of this kind done monthly.
The intensity of the ride is given in the column header. Thus, 15 @ 25 min in the Base Pace column means that 15 trips per month are done at Base Pace, where each ride long is 25 minutes. The fitness plan in Fujimoto et al. Howden et al. that was two years long, but Howden et al. I only show the results of this first ten a few months.
Fujimoto et al. described their exercise process very clearly, such that it was easy for me to put it in to the figure above and I am relatively confident I correctly described it. On the other hand, I found the description of the fitness plan in Howden et al. I am less confident I’ve accurately described it. As noted above, I am not just a cardiologist so cannot comment on the protocols found in both papers to measure cardiac parameters, but to my untrained eye, it seemed that both papers used different protocols. Finally, there are differences between the papers that concern parts of the studies not relevant to this blog post.