5-1-5 assessments can be used to estimate the system that is most limiting to an athlete’s performance. These systems include 1) pulmonary, the lung’s ability to uptake, and transfer oxygen to the blood 2) cardiac, the heart’s ability to deliver oxygen rich blood to the muscle and get rid of metabolites and 3) skeletal muscle, the mitochondria’s ability to utilize oxygen in the working muscle Whole-body exercise requires multifaceted integration of biological systems in order to sustain locomotion, if one of these systems is inadequate then fatigue is imminent. In this post, I want to take a deeper dive into what could be responsible for a pulmonary limitation and what could be leading to fatigue in athletes with this limitation, a few papers are cited but the main one spurring this post is by Dempsey et al. 2006.
The start of exercise is accompanied by increases in heart rate and mean arterial pressure (MAP). These increases are due to decreased parasympathetic (rest and digest) and increased sympathetic (fight or flight) output (O’Leary 1993). This large increase in central nervous system (CNS) activation is primarily due to increases in mechanical and chemical signals originating from the contracting skeletal muscle deemed the metaboreflex. These signals are integrated via messenger neurons (type III and IV afferents) relayed to the brain resulting in a release of stimulatory hormones, epinephrine (E) and norepinephrine (NE).
The release of E and NE typically lead to a vasoconstriction (blood vessel constriction) response (Joyner et al. 2010). Remember, one important aspect to maintaining high intensity during prolonged exercise duration is proper loading, delivery, and utilization of oxygen to contracting skeletal muscle. In this context, CNS stimulation seems oxymoronic. If exercise results in higher CNS activation and higher CNS activation results in vasoconstriction then less oxygenated blood would be delivered to the working muscle. Luckily, the local environment of the skeletal muscle is able to override increases in sympathetic vasoconstriction (functional sympatholysis) in order to maintain adequate blood flow. This allows for specific continued perfusion of skeletal muscle even during high intensity exercise.
However, since there is a limited amount of blood in circulation, eventually the demand for oxygen outstrips the supply, resulting in a net negative oxygen balance at the working muscle. Simply, there isn’t enough blood to go around. In the case of some pulmonary limitations, respiratory muscles are demanding so much blood that they limit the perfusion of other working muscles. Dempsey et al. 2006 surmise that inspiratory muscles could be a MAJOR contributor to fatigue through repartitioning of blood flow away from locomotor muscles to respiratory muscles. This is because the inspiratory muscle metaboreflex increases global CNS activity resulting in a CNS signal that is too high for functional sympatholysis to overcome causing vasoconstriction decreasing blood flow to the working muscles.
In summary, the skeletal muscle is generally very good at locally overriding vasoconstriction in order to keep blood flow and oxygen delivery high during maximal exercise. However, in some pulmonary limited athletes, when exercise intensity gets too high, the inspiratory muscles (I.e. the diaphragm) are working so hard that their metaboreflex triggers further increases in CNS activity resulting in vasoconstriction in the working muscle. Note: From an applied standpoint it would be expected that during maximal exercise SmO2 would continue to decrease, while THb would show signs of a pulmonary limitation with a STEEP drop off in THb towards the very end of exercise (indicating a shunting of blood away from the working muscle).