Pulmonary and Circulatory Adjustment Determining the Limits of Depths in Breath-Hold Diving
Authors: Karl E. Schaefer, Robert D. Allison, James H. Dougherty Jr., Charles R. Carey, Roger Walker, Frank Jost, Donald Parker
DOI / Source: https://doi.org/10.1126/science.162.3857.1020
Date: 05 June 1968
Reading level: Intermediate
Why This Matters for Freedivers
This report supports one of the most important “deep diving realities”: your chest isn’t just an air tank — it can partially refill with blood at depth, which helps protect the lungs and can extend depth beyond what simple lung-volume math predicts. It also reminds us that in some extreme deep dives, the limiting factor may not be “CO₂ got too high” or “O₂ got too low” at the end — other physiological and mechanical limits can take over.
Synopsis
A common old-school idea was that your maximum depth on one breath is mainly limited by a simple squeeze equation: when the air in your lungs gets compressed down to your residual volume (the air you can’t blow out), you’ve hit a “hard limit.” If that were the whole story, the deepest divers shouldn’t be able to go much past the depth predicted by their total lung volume divided by residual volume.
This 1968 Navy report set out to test what actually happens in real deep breath-hold dives, using Robert Croft (a record-setting U.S. Navy diver) and controlled dives in a training tank and the open sea. The researchers did two big things:
1) They measured lung gas pressures at the end of dives (oxygen and carbon dioxide in the alveoli). Surprisingly, after very deep dives (including an open-sea dive to 217.5 ft / ~66 m), Croft’s end-of-dive alveolar oxygen pressure generally stayed around or above ~40 mmHg, and carbon dioxide typically stayed around or below ~40 mmHg. In plain terms: at the end of these dives, the “numbers” didn’t look like a classic CO₂-panic limit or a severe oxygen crash limit. Under these conditions, neither high CO₂ nor low O₂ seemed to explain the depth boundary.
2) They measured “blood shift” into the chest using an impedance plethysmograph (a method that detects changes in thoracic electrical resistance caused by changes in blood vs gas volume). The key finding was direct evidence that, at depth, blood is forced into the thorax. They estimated on the order of ~1 liter of blood being displaced into the chest at depth (reported values include about 1,047 mL at 90 ft and 850 mL at 130 ft, depending on conditions). This supports the idea that as the lungs compress, the body can partially replace “lost” air volume with blood volume in the thorax, which effectively reduces how far the lungs need to collapse and can extend depth beyond what you’d predict from lung volumes alone.
The report uses this to explain a famous freediving mismatch: Croft’s predicted “lung-compression depth limit” (based on his lung volumes) was about 197 ft, yet he reached 217.5 ft. The most likely reason is that the chest can “make room” by shifting blood inward, changing the mechanical limit.
The big message is that deep freediving limits aren’t purely a simple oxygen/CO₂ story, and they aren’t purely a lung-compression math story either. At depth, the body dynamically rearranges blood and air to keep the system working — right up to the edge of what the lungs, circulation, and mechanics can tolerate.
Abstract
This Navy research report investigated what pulmonary gas exchange and circulation changes might set depth limits in extreme breath-hold diving. Data were collected during breath-hold dives in a training tank to 90 ft and in open-water dives to 217.5 ft performed by diver Robert A. Croft. The team measured end-of-dive alveolar oxygen and carbon dioxide tensions and assessed thoracic blood-volume displacement using impedance plethysmography at multiple depths. End-of-dive alveolar oxygen generally remained at or above about 40 mmHg and alveolar CO₂ generally remained at or below about 40 mmHg, suggesting that, in these dives, neither hypoxia nor hypercapnia alone explained the depth limit. Plethysmography provided direct evidence of substantial blood displacement into the thorax at depth (on the order of ~0.85–1.05 L in the reported measurements), supporting the concept of intrathoracic blood pooling (“blood shift”). The authors propose this blood shift as a key mechanism that can extend achievable depth beyond predictions based solely on lung compression to residual volume.