@lymphocyte It is an expiratory phenomena and RR also effects the resistance to air outflow, which I'm sure you'll agree to, is equally important.
I don't understand what you're saying. Dynamic airway compression
limits expiratory air flow. You almost physically can't expire faster. In diseased lungs, this limitation occurs at low expiratory flow rates. That limits exercise capacity, but how does it significantly increase the work of breathing? Expiratory flow is mostly
effort-independent across most lung volumes. (As an aside, DAC is why you get breath stacking on COPDers on the vent if the expiratory time is too short.)
Flow rate people. Flow rate. That explains the important relationship between RR and airflow resistance. Ohm's law is the most helpful way to think about things. But we can also get into a discussion about laminar flow vs Reynold's number.
Edit: You even made me dig out John West's Respiratory Physiology because I felt like I was living in crazy world reading the explanations above. "The higher the breathing rate, the faster the flow rates and the greater amount of work" (pg. 121) I also drew a picture to help explain things. WOB has lots of components, but it's helpful to think of just two: resistive and elastic. Resistive work is from the alveoli and lung parenchyma. (Airflow makes up about 80% of the resistive work, so it's massively important. Tissue makes up about 20%, so it matters if you have crap tissue, like in COPD.) Elastance work is from the intercostal muscles, chest wall, and diaphragm. Where the two intersect, you minimise WOB.
Let's think about the clinical implications:
1. What happens as resistive work decreases (i.e. the resistive curve shifts left) as in the case of COPD? Hint: they tend to breath slower.
2. What happens as elastance work increases (i.e. the elastance curve shifts right) as in people with stiff chests? Hint: they tend to be breath faster.
Both 1 and 2 minimise WOB in pathophysiological states, but cause other problems (remember the PaCO2 equation?). So to compensate, you sometimes have to needle the RR off the ideal point and therefore increase WOB--until you can't anymore, and then you have respiratory failure. Welcome to the nightmare that can be asthma. (Check for understanding: why is a normalising PaCO2 a very worrying sign in a severe asthma exacerbation? Do you see how air-flow limitation, RR, airway resistance, WOB, and PaCO2 all tie in together?)
Edit 2: If you still don't believe, me check out this lecture:
http://www.physiologylectures.net/index.php?id=28