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iank

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 #1 

I've recently switched from BSX to Moxy, and some of the results I've been getting have been a little different so I am unsure how to interpret them. 

Firstly is this one, a failure to desaturate on the primary muscle (VL) during a treadmill 5-1 test where the 7th out of 10 stages is the runners 10k pace. From here I work back and the first 5 stages increase by 15 seconds per km pace, and the last 5 by 10 seconds per km.

Screenshots from PeriPedal below, I'll put the data up tomorrow when I have more time. Prim No Desat.png 

Non Prim No Desat.png 
Recreational marathon runner, coming out of injury. I know it's a utilization issue from the lack of desaturation, but what else can I gain from this test? Any zoning info? Do I treat this like a regular utilization limiter or is it a 'super-utilization' ?

Thanks!

Ian


bobbyjobling

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 #2 
Interesting, lot's to look at.

If you look at the first load you were able to disaturate down to around 10%(hard start), so you can disaturate.
Subsequent loads we can see an increase of smO2, this could be due to an increase in CO or/and a gradual change in muscular cordination pattern due to maybe a higher leg speed.

Your HR appears to be stable up to load 4 to 5 so maybe you have good blood redistribution and good Stroke volume increase. Your tHb during each of the first 7 loads appears to be flat and not increasing much during the loads. So maybe vasodilation is not activated that much due to good blood flow and high level of O2.

During each rest period we see a good rebound of thb(VL)and with increasing peak as the load increases, we also see a reduction of thb peaks level in the non involved muscle so maybe some PB control is activated.

After load 7 in the VL, we see a decrease in thb and during each subsequent loads, thb still mostly flat, so the CO2 to O2 ratio is still low. I think capillary density is good or muscle compression is not that high ( is VL still the primary muscle?)

....

Maybe we can limit the change in muscular cordination if we keeped the leg speed constant and instead increase the slope of the treadmill for each new load.

PS. I probably made to many incorrect assumptions by just looking at the graph so treat my post lightly.:)



CraigMahony

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 #3 
@bobbyjobling I do not necessarily agree about being able able to desaturate at the first work load. I have had a runner who had a similar graph. What happened though was that the first work load was too slow and he was very uneconomical. Running at too slow a speed causes a longer ground contact with less reactive (elastic) energy and much more muscular energy contributing to each stride. This can cause compression which can reduce arterial inflow and venous outflow, perhaps causing less total HB in the muscle and some minor pooling causing SmO2 to drop due to being diluted by HHB. You can see that when Heart Rate finishes climbing in the first load that SmO2 starts rising, so blood pressure at this stage is great enough to overcome the extra muscular compresssion from a longer ground contact time. This is conjecture here. What is needed is the raw data to determine the O2Hb and HHb levels.

@iank The tHb is quite different in the lower workloads. What is the difference between what you ran on the first and second graph? The last workload appears to have the SmO2 constantly dropping, even if it does not drop much. This might be your High Intensity Zone. It would be interesting to see if your SmO2 continues to drop if you spend longer in this workload or if it levels out and stabilises,


iank

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 #4 

Thank you for the replies, apologies, I missed out explaining that the second graph was from the same test, on the deltoid. It is a 40 yo female runner also.

 

Data from PeriPedal attached.

 
Attached Files
csv NP.csv (178.44 KB, 2 views)
csv P.csv (186.90 KB, 4 views)

CraigMahony

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 #5 
Here is a graph with the O2Hb and the HHb.
IanK-P.jpg  You can see that at the first load O2Hb supply was reduced and that HHb increased. As I said previously, I believe this is due to muscular compression not desaturation. Cardiac Output would have been low and insufficient to overcome the the muscular compression, particularly when running very slowly which causes a longer ground contact and therefore more muscular effort and less use of elastic energy return. When the warmed up the cardiac output no doubt increased creating higher blood pressure that was more able to overcome the muscular compression. There would have been some vasodilation as well.

Yes there was very little desaturation. Possibly due to not doing much higher intensity running as a marathoner. and having lower mitochondrial density. Another reason, mentioned in other posts, is the possibility that the subject has high levels of myoglobin which has a very different oxygen desaturation curve does not desaturate until very low levels of oxygen partial pressure.

Now that we know the second graph is from a non priority muscle we can say that there are perhaps small signs of blood redistribution away from the non priority muscle at the third / fourth workload, but not much. The main cardiac limitation seems to be in the last workload where both the non priority and the priority muscle had a drop throughout the workload. 

iank

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Posts: 8
 #6 
Many thanks Craig.

If the runner had higher levels of myoglobin would the non-primary graph not also show little desaturation?

Next time I test them I will use a different muscle perhaps, and check their form to see if there are any signs that they do not fully engage the VL.

They are already unhappy that they have to do sprints/higher intensity work - I am guessing that is a sign that they have done very little in the past!

Thanks for your insights everyone!
CraigMahony

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 #7 
Yes iank that is true. However, the non priority muscle only desaturated a few percent. If you look you will see that the scaling on the right is different for both graphs.
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