This library a list of refereed articles on the topic of adaptive scuba. To be on this list, a paper must have undergone peer-review and been published in a scientific or academic journal.
Scuba diving started as a sport of the exceptionally adventurous and physically fit, but has become a popular recreational activity that attracts both young and old, physically active, as well as sedentary people. All who participate expose themselves to the physical challenges and hazards that are inherent to this activity. The health and fitness requirements required to become certified as a scuba diver vary, but in general appear to have become quite liberal.
The annual incidence of spinal cord injury (SCI) in the United States is approximately 40 cases per million population, or approximately 11 000 new cases each year. The number of people in the United States in 2006 who have SCI has been estimated to be between 225 000 and 296 000 persons. Most injuries occur between the ages of 16 and 30 years. More than half of SCI individuals were employed at the time of injury and many were actively involved in sports. In the post-injury period, many SCI individuals, mostly those with a lower level of injury,1 return to their jobs, lead active lives and some even return to recreation and sports. However, the majority of persons with SCI are inactive and exhibit low levels of cardiovascular fitness,2 which is a major independent risk factor for cardiovascular disease and premature mortality.3 It appears that the ordinary activities of daily living in SCI are not adequate to maintain cardiovascular fitness.2 Historically, individuals with disabilities have been discouraged from pursuing scuba diving by physicians because of both real and perceived risks.
Since the 1990 Americans with Disabilities Act and the 1995 Disability Discrimination Act in Great Britain, dive opportunities for persons with disability have increased. According to a Survey of Scuba Diving for Disabled Divers, over 50% of British dive clubs were involved in the training of disabled divers between 1998 and 2000. Of the 130 survey respondents who described themselves as disabled, 54 had SCI. One-third of them learned to dive before their injury and two-third learned post injury.4
There are concerns that diving may further damage the spinal cord, as there is a rare spinal form of decompression sickness (DCS). Neurological abnormalities are presently the most serious decompression related problem in recreational divers requiring treatment. DCS is purportedly due to gas bubbles that form in body tissues during or after decompression. The amount of inert gas taken up by tissues is influenced by dive depth and duration, as well on regional blood perfusion. Two factors required for bubble formation are gas nuclei and supersaturation. The nature of nuclei is unknown, but they are most likely small, gas-filled bubbles attached to the endothelium of blood vessels. These bubbles eventually lodge in the pulmonary circulation. Recently, several reports have indicated that a single dive to depths regularly taken by recreational divers (∼30 meters of sea water) causes an asymptomatic reduction in cardiovascular function, brachial artery endothelial dysfunction and reduction in right and left ventricle functional indices.5, 6, 7 Some of these changes were reversed by acute pre-dive administration of antioxidants.7 In addition to venous bubble formation during scuba diving, persons with SCI are exposed to other stress factors, such as hypothermia, immersion induced shifts of the peripheral venous blood toward the central vascular compartment, hyperoxia, hemoconcentration and psychological stress.
To date, there is no evidence that the risk of DCS is increased in SCI. The purpose of this study was to compare the occurrence and degree of post-dive venous gas bubbles in divers with disabilities and able-bodied controls.
Recent findings have shown that intracerebroventricular administration of 5-HT3 or 5-HT1b antagonists decrease both LMA and striatal DA increase suggesting that pressure could enhance the serotonin (5-HT) neurotransmission. In this study, for the first time, the striatal levels of DA and 5-HT were simultaneously monitored using microdialysis in free-moving rats exposed to high pressure. Our results show that the striatal 5-HT level increases during pressure exposure.
These data suggest that pressure-induced striatal 5-HT increase could participate in the increasing DA release. Nevertheless, the lack of correlation between striatal DA and 5-HT changes suggests that other processes are involved in the pressure-induced striatal DA increase.
