Managing ventilatory response and cerebrovascular reactivity to CO2 during immersion

Principal InvestigatorDavid Hostler, PhD

Funding Source: Office of Naval Research

Abstract: During every studied form of physical activity, including swimming and SCUBA diving, the respiratory system is the limiting factor of performance, not the working extremity muscles. Additionally, the stressors associated with diving exacerbate the respiratory system’s limitations. Water immersion per se reduces minute ventilation and contributes to respiratory muscle fatigue (Held and Pendergast 2013; Pendergast et al., 2015). This leads to a mild, but measurable increase in arterial partial pressure of carbon dioxide (PaCO2). Some individuals tolerate this and permit CO2 levels to rise without increasing ventilation (hypo-responders), while others hyperventilate and either prematurely deplete their breathing air supply or panic (hyper-responders). The former is an issue for working divers while the latter results in many individuals prematurely leaving diver training.

Studies in animals and humans have shown that respiratory muscle strength and endurance can be improved through respiratory muscle training (RMT). RMT increases strength and metabolic capacity of the respiratory muscles. At a cellular level, RMT remodels the oxidative components of the respiratory muscles and substantial improvements in whole body endurance exercise occur after RMT. Studies in our lab have shown this for both surface swimming and immersed fin swimming. 

Although not tested, it is often assumed that the benefits of RMT extend beyond improvements in the respiratory system by modulating cerebrovascular control. This would be particularly important for divers, especially when using closed and semi-closed circuit diving rigs. In these scenarios, the oxygen enriched breathing gas and depth of the dive increase the partial pressure of oxygen, which increases the risk of oxygen (O2) toxicity. The normal response of the cerebral vessels in this situation is to constrict and reduce cerebral blood flow. However, increased partial pressure of CO2 from a scrubber failure, skip breathing, or respiratory muscle fatigue promotes cerebral vasodilation. The subsequent increase in cerebral blood flow is believed to expose the brain to more oxygen leading to oxygen toxicity (Arieli et al., 2006a). However, these changes in cerebral blood flow are assumptions made from non-diving studies and have not been tested in a diving scenario that included the increased work of breathing (WOB) from immersion and a SCUBA regulator or elevated CO2. 

Specific Research Tasks for This Proposal: We will describe cerebrovascular responses to immersion before and after RMT. We will measure CO2 sensitivity and cerebral blood flow in response to increased work of breathing and elevated CO2 in neutral, warm, and cold water.