Managing ventilatory response and cerebrovascular reactivity to CO2 in divers (ONR White Paper Tracking Number - 23-000005557)
Abstract
Approved for Public Release During every studied form of physical activity, including swimming and diving, the respiratory system is the limiting factor of performance, not the working extremity muscles. In healthy individuals, ventilatory limitations reduce maximal exercise performance. Increased energy expenditure of respiratory muscles during heavy exertion increases blood flow to those muscles at the expense of the locomotor muscles. This has been termed the #steal phenomenon#. The stressors associated with diving exacerbate the respiratory system limitations. Water immersion per se reduces minute ventilation in the water and contributed to respiratory muscle fatigue. This leads to a mild but measurable increase in PETCO2. Some individuals tolerate this and permit CO2 levels to rise without increasing ventilation while others hyperventilate and either prematurely deplete their breathing air supply or panic. The former is an issue for working divers while the latter results in many individuals leaving diver training before completion. Studies in animals and humans, however, 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. The benefits of RMT may extend beyond improvements in the respiratory system by modulating cerebrovascular control. This is 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 may expose the brain to more oxygen leading to oxygen toxicity. However, these changes in cerebral blood flow are assumptions made from normal physiologic responses and have not been tested in a diving scenario that included the increased work of breathing from immersion and a SCUBA regulator. We will measure cerebral blood flow in response to increased work of breathing and elevated CO2 before and after RMT in neutral, cold, and warm water.
Document Details
- Document Type
- DoD Grant Award
- Publication Date
- Dec 15, 2023
- Source ID
- N000142412041
Entities
People
- David Hostler
Organizations
- Office of Naval Research
- Research Foundation for the State University of New York
- United States Navy