The testing showed that some individuals had a wider difference between cardiac output and VO2:
Note that the VO2 is oxygen consumption at the given power, not VO2 max.
A comparison of baseline characteristics was done as well:
The only baseline feature that was different in high vs low responders was the resting heart rate. This is not surprising in that the high responder theoretically has a larger stroke volume, so pump rate can be less providing the same net output.
Capillary density, type 1 fiber percent was not different. It is interesting that the higher responders did have a superior VO2 max (consumption) despite no change in fiber type and one of the oxidative enzymes measured.
The situation during cycling exercise is shown below. As the intensity increased, so did cardiac output, heart rate and stroke volume. But notice the difference in pattern between low and high responders. There was a very large disparity in stroke volume
In regards to muscle O2, no major change eas seen between groups:
This is of interest to the muscle O2 sensor enthusiast. It does indicate that the active muscle will maintain perfusion/oxygenation even as cardiac output fails to keep up with increasing O2 demand by presumably rerouting vascular assets.
The following is the computed redistribution of cardiac output. As noted, the perfusion of "other tissues" is severely compromised at higher outputs. Besides the obvious negative effects this may have on respiratory function, one wonders what the impact on gastrointestinal nutrient and fluid absorption could be. Speculation on profound impairment in rehydration/carbohydrate influx ultimately causing lower power outputs (depending on the duration of the event) is very reasonable. Athletes without the burden of severe cardiac output redistribution should be at a nutritional advantage on a long event.
Here is a look at indexes of gut perfusion with increasing exercise intensity. As can be seen, there is a substantial effect.
However, look at C, 2 different individual responses- makes one wonder what the stroke volume responder type was of each.
Speaking about nutrition, here is an analogy of the above. Let's say you have a cafeteria full of hungry college students(the muscle + other tissues net O2 consumption) but the kitchen(cardiac output) can only make so many meals per hour. On a regular day there's no difficulty in keeping everyone fed as the kitchen output can handle demand. What about on a day where the football team(locomotor muscles) is practicing hard and gets extra hungry. Well, this being a sports oriented school, the food manager is going to favor the athletes and the regular students may or may not be able to get fed that day. The analogy goes further, is the kitchen limitation related to how quick they can get trays/utensils back(venous return) or is it from lack of personal making the meals(intrinsic cardiac chamber properties). The limitation in stroke volume apparently could be from either decreased cardiac camber properties or reduced venous blood flow return.
In any event, the athletes will be eating their normal portion (no difference in muscle O2 drop, same RPE), but the remaining students will have varying degrees of deprivation. At near maximum football team food consumption on a very active day, the other students will have little to no supply(impairment to respiratory muscle and intestines) and at maximum consumption needs, even the football players will suffer.
Instead of monitoring the state of the football players meals (locomotor muscle O2), one could perhaps get a more accurate read of system capacity/stability by looking at who is not getting fed especially if they are working hard(costal O2).
The authors make several points:
- There is a range of net cardiac output minus O2 consumption. Higher responders will have better stroke volume.
- Whether the stroke volume boost is from enhanced venous return or from intrinsic cardiac factors is not addressed by this study.
- To compensate for lower relative cardiac output in exercise, there is a redistribution of blood flow to the involved muscle and away from non exercising areas.
- Because of this redistribution, active muscle O2 desaturation between high and low responders is about the same.
- Calculated blood flow to the other areas is markedly reduced in low responders.
- O2 monitoring of "other tissues" especially ones that are increasing active at intensity as well as vulnerable to hypoxia induced fatigue/dysfunction (costal muscles) may be more helpful in exercise pacing. Again we are interested in overall integrated system status as well as avoiding respiratory dysfunction.
- Avoidance of levels of effort above the blood redistribution limit may be beneficial in longer events. Here we are concerned with proper gut perfusion to allow carbohydrates and water to be absorbed. There is a range of gut perfusion status at similar exercise intensity as noted above.
- Monitoring of active muscle (locomotor) O2 saturation still has not been shown to be helpful in regards to the above study parameters.