My iBike power meter died last week when the wired speed sensor started to fail and the completely crapped out. It needed recalibrating again too after some wet rides, and the data has been unreliable at best and crazy at worst for the last couple of weeks. I’ve kind of had enough of recalibrating and second guessing it, worrying about it warming up in the sun and skewing the wind speed sensor, or wondering what the hell its doing after a big descent. It’s a great introduction to biking with power, but after almost 2 years I want a more reliable, more accurate power meter. Time to upgrade but I’m skint. It will cost me more than £100 to buy a new wireless mount (they don’t do the cheaper wired mount any more) and get it shipped from the USA to me in Wales.
So I took the iBike off, retired it to its box (I wonder if anyone will want it on eBay without a working speed sensor) and put the bracket for my ever reliable Garmin 305 back on the bars.
Hill reps this morning started off quite nice not having to calibrate, worry about, and recalibrate the iBike. These are habits I have got into with each ride, so not doing it was a bit weird. I didn’t mind losing the wind and slope data. It was annoying not having the power data.
On the 3 minute work reps up the east side of Cefn Bryn it wasn’t so great. Heart rate is way too slow to be a useful metric other than as a maximum HR target for the top of the hill, so the effort is all based on perceived exertion. As I’ve been training with a power meter on these intervals for months my perceived exertion in this case is probably pretty good, but not being able to see my power output in the early part of the climb felt like I was probably taking it a little easy there as I got tired.
The effort put into the work rep is kind of rewarded (or punished) by seeing the power output for the 3 minute climb. Without seeing my power output I didn’t get the feelings of, “wooo! 400W over the top – I crushed it!” or “aaargh! I can’t squeeze 300W out of my legs – they’re trashed!”
I’ve still got a lot of training to do this season, but I may have to leave training with power again until the winter. The most annoying thing is that my TSS for a ride is lower if based on heart rate instead of on power, so my TSB (training stress balance) is dipping erroneously. It’s mucking up my graphs!
Three and a half weeks after ripping up my calf at the Pembrokeshire Coast Triathlon (yes, I still need to write up a race report for that) I finally got to see he-who-looks-after-my-legs for some work on my legs. The poor bloke twisted his own knee the same week and has had to have surgery to trim the meniscus and clean out the joint, so my little calf injury was put into perspective. I’m glad my knees are still strong!
He quickly found other sore bits in my calves with his thumbs that I hadn’t noticed and caused much pain. I’m hoping that tomorrow they’ll be feeling looser as the right flexor hallucis longus muscle was very tight again for this morning’s run. Golf with dad and Nick on Saturday won’t have helped this, but it was worth it.
More work from him in 7 days on both my calves, and more work from me daily with stretching and strengthening work. It was definitely a good job that I skipped the Gower Triathlon. I went to watch in full waterproofs, so I’ve got it in mind for next year.
I’m looking forward to running again on Thursday.
I had a headache for 4 or 5 days that was probably caused by a blocked maxillary sinus after a recent snotty virus. I had some jaw & tooth pain too but assumed that was linked. It now seems that I’ve been grinding my teeth, which for me is a sure sign of high stress levels.
I feel ok; that is, I don’t feel under undue stress. I’m just getting on with what I need to get on with. I think I’m getting a bit salmon-like again and I’d better watch out for it.
I guess I need a holiday. I don’t see one coming up though. Hmmm.
Chatting with physioDave last night helped me decide not to race tomorrow at the Gower Triathlon.
My right calf is getting better, and feeling pretty good after yesterday’s massage, but the flexor hallucis longus muscle really isn’t back to full strength or race fitness. My rule in training if I’m not sure how tired or sore I am is: “get out of the door, then see how you feel”. Racing needs to be different I think. Even if I plan to drop out after the bike if I get myself into a top 3 position on the bike am I still going to pull aside? After putting in a lot of pain and effort I tend to be inclined to see it through to the end. If I do that I’m going to tear up this muscle again, and then I’ll be back to where I was 2 weeks ago, or worse.
PhysioDave points out that a DNS meant you were sensible. A DNF, not so much.
This is only a training race, and my last A race of the season is 8 weeks away. 8 weeks of consistent rehab and running would be really helpful in seeing me meet my goals. Another 3 weeks off running and only 5 weeks of rehab might make my cycling and swimming really good, but I’ll be let down by the third discipline. Blending has been the key to my success this season.
I think I’ll get up early, don my waterproofs, grab my camera and go and cheer on my club mates. And see how the winner does it. I might stick my wetsuit and a towel in the car boot, but no running shoes.
The sunny, windless weather we’ve been enjoying this week is predicted to be replaced by rain and strong winds just in time for the Gower Triathlon on Saturday morning. We’ve had one race this year with good weather, and the rest have all been chilly, damp, blowy mornings.
So I still can’t run after the Pembrokeshire Coast Triathlon (must write a race report for that – I wanted to get the cardiovascular thing up first), the race starts at 7am which means I have to get out of bed at 5, it’ll be wet and windy, and the family won’t be there. It sounds like I should stay in bed.
I’ve got my fingers crossed for my right flexor hallucis longus muscle recovering super rapidly over the next 36 hours after today’s massage.
I think I’ll turn up though. I might have to walk up the beach and DNF after the bike, but I reckon I’ll show my face.
On Monday I gave a double lecture. The first part was about cardiovascular embryology, and the heart in particular, and the second part was about the changes to the cardiovascular system that occur with birth and the baby’s first breath. The second part is normally delivered by Dr Geraint Morris, a consultant paediatrician and neonatologist far more able to talk about these things and their clinical relevance and examples than me, but unfortunately a scheduling snafu meant he was unable to be there.
I think Rhi and I have written 4 short chapters about the development of blood vessels and the heart, but I won’t try to reproduce that here. Probably the most relevant and important parts for medical students to understand are how the heart is formed and split into chambers, and how well oxygenated blood from the placenta bypasses the foetal lungs and gets to the developing brain instead.
I talked about the differences between vasculogenesis and angiogenesis, the former being important in the early embryo (from around day 19) and the latter occurring during development, repair, in the endometrium during the menstrual cycle, and in tumour growth. Anti-angiogenic drugs have been developed to target the growth of tumours.
Vasculogenesis describes the appearance of new blood cells and blood vessels as if by magic; from out of thin air. Of course what really happens is that mesoderm cells differentiate into a “haemangioblast”, or if you prefer, into haemoblasts and angioblasts. Angioblasts will form new blood vessels.
Angiogenesis is defined as the formation of new blood vessels from existing ones. The term intussusception is often used here, and describes the splitting of a blood vessels into two.
So if we’re going to talk about how the heart develops, we first need to bring together these little pockets of new blood vessels that are forming in a horseshoe shape around the head end of the early, flat embryo.
The embryo folds laterally and along its length, rolling up to form the body wall and bringing some of those early blood cysts together to form the early heart tube, which lies a little inferior to the head. At an early stage this simple tube receives blood from 3 pairs of veins at a sinus venosus, squeezes it through an early atrium, ventricle, bulbus cordis and out through a truncus arteriosus into the early arteries of the neck and into paired dorsal aortae.
The next phase must include splitting the heart up into the four chambers that we recognise in the adult heart, and the processes that do this pretty much all run at the same time. We’ll talk about them separately though, and will start with the splitting of the atrium from the ventricle.
The heart tube folds to bring the atrium posterior (dorsal) to the ventricle. At the junction between the atrium and ventricle the endocardium in the walls starts to plump up, and the atrioventricular canal starts to narrow. These “endocardial cushions” thicken, and the ventral and dorsal cushions grow towards each other and meet, splitting the atrioventricular canal into two.
The single atrium is split into two at the same time but in a slightly more complex manner, and this may be a story you’re aware of. Failure of this process can leave an atrial septal defect, which is different to a patent foramen ovale. You’ve probably seen the fossa ovalis in the adult heart. So what normally happens?
From the roof of the single atrium a wedge of endocardium begins to grow down towards the endocardial cushions. Think of it as a thin, curved, extending wedge. This is the septum primum (the first fence). It splits the atrium into two atria, but before it meets the endocardial cushions and completes this, a hole forms high up in the septum primum. This is the ostium primum (the first hole). In this way the left atrium remains connected to the right atrium.
Next, a second, curved wedge of endocardium descends from the roof of the right atrium, beside the septum primum. This is the septum secundum. This wedge of endocardium will never quite reach the endocardial cushions. The hole that remains beneath it is called the septum secundum.
In the foetus pressure within the right atrium is higher than in the left atrium. The blood entering the right atrium is returning from the systemic circulation and from the placenta, whereas blood entering the left atrium is returning from the developing lungs. At this time resistance to blood flow through the lungs is high.
The well-oxygenated blood entering the right atrium of the heart (from the placenta) rushes across into the left atrium through the foramen ovale. The foramen ovale has formed from the flap of the septum primum flapping against the septum secundum that acts as the doorstop. So blood in the right atrium pushes open the flap of the foramen ovale. The eustachian valve of the inferior vena cava (labelled as “valve of inf. vena cava in the Gray’s Anatomy illustration below) entering the right atrium helps direct the flow of blood through the foramen ovale. By avoiding the lungs, well-oxygenated blood can pass through the left atrium, left ventricle, and out of the heart and up into the carotid arteries to get to the developing brain with only a small loss in oxygen and nutrient content.
At birth, when the lungs begin to work, the resistance to blood flow through the lungs drops. Blood flows through the lungs and back into the left atrium. The blood pressure in the left atrium is then higher than in the right atrium, and the flap (septum primum) of the foramen ovale is pushed closed against the septum secundum. From this point onwards blood will no longer normally flow from the right atrium to the left atrium through this valve, although changes in thoracic pressure with coughing or sneezing may cause this. A little while after birth the edges of the foramen ovale become sealed and fixed, and it becomes the fossa ovalis.
The next time you look into the right atrium of a heart model or prosection have a look for the fossa ovalis and the curve of the eustachian valve.
The single ventricle is split into two ventricles by two structures. The myocardium from the floor of the ventricle grows up towards the endocardial cushions, starting to split the chamber into left and right ventricles. It never quite reaches the endocardial cushions though. This is the muscular interventricular septum.
The conotruncal outflow tract (it has conus arteriosus and truncus arteriosus sections) is the single outflow tract of the early heart. Rather like the endocardial cushions, two ridges of endocardium grow along the length of the conotruncal tube, within it, opposite one another, but in a spiral (or helical) manner. They grow towards each other, meet as the conotruncal septum, and split the conotruncal outflow tract into the two great vessels: the aorta and pulmonary trunk (or artery).
The conotruncal septum also meets with the muscular interventricular septum, finishing the splitting of the ventricles into left and right and connecting the aorta to the left ventricle and the pulmonary trunk to the right ventricle. This is the membranous interventricular septum. If this all doesn’t come together quite right there maybe an interventricular defect, or the aorta and pulmonary trunk may be connected to the wrong sides of the heart.
By the way, that spiralling of the conotruncal septum can be seen in the adult heart, as the aorta and pulmonary trunk spiral around each other.
There’s a little shortcut vessel in the foetus, between the pulmonary trunk and the aorta, called the ductus arteriosus. This is another route by which blood can avoid going through the lungs, and blood in the pulmonary trunk will pass through the ductus arteriosus and into the aorta, rather than into the lungs.
With birth the constricted blood vessels of the lungs dilate, reducing resistance to flow. Blood passing through the pulmonary circulation becomes rich in oxygen, and passes into the left side of the heart and the aorta. Backflow of this oxygen-rich blood into the ductus arteriosus from the aorta triggers the smooth muscle of the ductus arteriosus to constrict (along with other, more complex mechanisms). It closes up, and in the adult this is called the ligamentum arteriosum.
Similarly, the umbilical vessels also constrict, pushing blood back into the foetus, and become ligamentous strands in the adult.
You can review all this with some of the links below. The YouTube video I showed in the lecture. Dr Morris couldn’t teach this year so I covered his lecture, and there is a podcast below covering similar stuff.
The domain name for this website is supposed to remind me (and you) to avoid the stresses of the salmon’s life, and not end up like that fish. I’ve been a bit salmony this week.
I raced hard on Saturday, and very hard during the run fighting for a good placing. We were camping with the kids too, for the first time, which was both stressful and fun. Annabel had a little bit of a snotty nose and some croup, something my immune system would have normally shrugged off with me barely noticing.
Probably because of the physical stresses of the race, the high cortisol levels and the inability to wash my hands as often as I normally would, I picked up Annabel’s bug and it hit me hard. I spent the whole of yesterday off training, off work and on the sofa catching up with Stargate Universe. I felt crap in the water on Monday, and I felt awful on the bike this morning, cutting any serious training sessions down to “just get out there and see how it goes”.
The lesson? You can’t hit it that hard every day. Some days are worth it though.