Protective mechanisms in hypobaric decompression

To reduce bubble formation and growth during hypobaric exposures, a denitrogenation or nitrogen "washout" procedure is performed. This procedure consists of prebreathing oxygen fractions as close to one as possible (oxygen prebreathe) prior to depressurization before ascending to the working altitude or low spacesuit pressures. During the NASA prebreathe reduction program (PRP), it was determined that the addition of a light arm exercise to short, individually designed, performance-based heavy exercise (dual cycle ergometry) during an abbreviated 2-h prebreathe (F1O2 - 1.0) reduced the occurrence of decompression sickness (DCS). Heavy-exercise-induced DCS reduction is likely to be related to the enhancement of the tissue nitrogen washout during the oxygen prebreathe. In addition to the heavy-exercise-induced microcirculatory adaptation, we hypothesized that the light exercise would not cause sufficient microcirculatory changes in the limbs to explain alone this further DCS protection. We evaluated microcirculatory changes as minimal by replicating the exercise characteristics of the PRP trials in 13 healthy subjects.

Noninvasive near infrared spectroscopy (NIRS) allowed observation of instantaneous variations of total, oxygenated, and deoxygenated hemoglobin/myoglobin concentrations in the microcirculatory networks (probes facing the vastus lateralis and deltoid muscles) of active limbs during dynamic exercise.

The high-intensity leg exercise alone produced the changes in NIRS parameters; the light arm exercise induced minimal microcirculatory volume changes. However, this coupling appeared to be critical in previous altitude PRP chamber studies by reducing DCS.

With only minimal microcirculatory blood volume changes, it is unlikely that light exercise alone causes significant nitrogen tissue washout. Therefore, our results suggest that in addition to nitrogen tissue washout, another unknown exercise-induced effect may have further enhanced the DCS protection, possibly mediated via the anti-inflammatory effect of exercise, gas micronuclei reduction, NO pathways, or other molecular mechanisms.