• Something seems strange on the 1st step at the 3rd load - the load seems shorter and the recovery longer - what happened here?

• In general priority muscles are not showing much desaturation - almost looks as though it could be a normal step test rather than a 5-1-5.
• Unexpectedly the deltoid is actually the muscle showing the most desaturation, and it shows it on rest. Was there perhaps something going on (e.g. a shift in position during recovery periods?)
• Lack of desaturation might be due to the muscle chosen - in general my preference is to use RF for well trained cyclists but in this case VL muscle might show more insightful information?

• Similar reactions across all three muscles, except in load where the left RF rebounds more significantly - this most likely simply because left leg in 6 o clock position on rest?
• In general tHb trends upwards during loads, however the reactions on recovery do not look like venous occlusion. The trend seems to follow HR quite closely so probably just CO overcoming muscle tension.
• There is a suggestion of overshoots of tHb on recovery in the later loads, probably due to C02 build up (particularly looking at deltoid).

• Strange heart rate reactions on recovery  at end of 1st load at 2nd step and last step? Why did heart rate increase for a while on recovery?
• On first load of 2nd step, heart rate increases steadily but on the next load at the same step heart rate flat - is this indicative of stroke volume to rise?
• Quite a low heart rate overall
• Heart rate recoveries hardly ever get down to the same level

Stuart, first keep in mind I am no expert either, everything here is just what I have learnt (or think I have learnt!) following the forum over a year or two. In other words, don't take anything i say with any level of authority!

I am also going to answer your questions in a way that will hopefully illuminate the thinking process, rather than necessarily provide clear cut answers. This is not intended to be patronising or opaque – please don’t interpret that way if that is how it comes across. I am simply trying to respect the culture Juerg has tried to instill on the forum of each person coming to their own thinking conclusion, and so that the threads serve as a source of a thinking process to future readers too rather than a set of “cookbook” answers (as Juerg would put it). 

However, if it still is not clear then ask further questions about what is not clear as this helps to further highlight how people are thinking about this.

However the reactions on recovery do not look like venous occlusion

A venous occlusion would occur when the compression of the muscle due to the load actually blocks outflow of the blood – what would happen if the "exit" for the blood at the muscle is blocked?  Next, think about how the mix of oxygenated vs dexoygenated blood might change if the venous outflow is blocked. Now think what trend tHb and Sm02 would show during the load, and then think what would happen on the release of the load when the occlusion is released?   

Once you have it clear in your mind – have a look at what we see here on the female athlete,  does it look like what you would expect a venous occlusion to look like? Also go have a look at your world’s race file, where Juerg circled certain periods of interest. It was suggested by some that there might be a venous occlusion although there was debate about this, and it has still not been settled yet – but form your own view why or why not could it be a venous occlusion?

Then go have a look at the case studies section, I recently shared a picture of what I thought was a trend of venous occlusions – what are the similarities and/or differences?

Going a step further,  if we do see a venous occlusion what might that tell us about the athlete?

There is a suggestion of overshoots of tHb on recovery in the later loads, probably due to C02 build up (particularly looking at deltoid)

The deltoid muscle will be a “non-priority” muscle during cycling activity – so looking at the trends of this muscle will often tell you a lot more about systemic reactions, than “priority” muscles (e.g. the legs) which show the result of reactions taking place at the muscle itself (i.e. local reactions) due to the load as well as broader systemic reactions. Now if you look at the peaks that tHb reaches on recovery of the deltoid muscle in the female athlete and how these change through the assessment? What do you see? Now you need to think what is causing this, on the one hand it could simply be cardiac output has increased on the other it could be vasodilation (i.e. widening of blood vessels). One of the things that stimulates vasodilation is C02? Now why might there be more C02 around at the later loads, and what could this possibly indicate?

Cheers
Ryan