Does breath-holding increase the risk of a thrombotic event?

Platelets (PLT) have been implicated in the pathogenesis of cardiovascular disorders. It has been shown large platelets are metabolically and enzymatically more active than small platelets and produce more thromboxane A2 [1]. On the other hand, the human spleen normally retains about one-third of the body’s platelets in an exchangeable pool, which can be released into circulation by adrenergic stimulation [2, 3]. Schmidt and Rasmussen [4] reported that 98% of the rise in circulating Indium-labelled platelets after exercise could be accounted for by the loss of labeled platelets from the spleen. It was also previously shown that the mean platelet volume (MPV) of splenic platelets was 20% greater than MPV of the circulating platelets [5]. Thus, the spleen could be an important source of large platelets, mobilized by adrenergic stimulation, thereby increasing the risk of sudden coronary incidents. We and others have previously shown that voluntary breath-hold triggers splenic contraction [6, 7]. Our aim was to test the hypothesis that voluntary breathholds are also associated with an increase in MPV. This model of splenic adrenergic stimulation may be important because of its resemblance to periods of breath-halt in obstructive sleep apnea (OSA). This report focuses on the data obtained, but not analysed in our previous study [8]. In that previous report on the impact of breath hold on hematological parameters we failed to analyse the changes in MPV (observing unchanged platelet count). In brief, there were 18 trained apnea divers and 24 subjects without diving experience, six of whom had been splenectomized previously. Each participant performed five maximal breath holds with cold forehead stimulation. The successive apneas were separated by 2 min intervals, allowing for data collection. The venous blood samples were taken before the first apnea and immediately after apneas 1 (A1), 3 (A3) and 5 (A5), as well as after at times 10, 20, 40 and 60 min following the last apnea attempt. Since apnea increases the arterial blood pressure, and thereby induces some loss of water from the vascular blood pool [9], the serum PLT count was corrected for the changes in plasma water, using the changes in total protein concentration as the markers [10]. The results are expressed as mean (SD). The percentage differences between parameters before and after apneas were tested with non-parametric Friedman analysis of variance, followed by post-hoc Wilcoxon signed-rank tests. Splenectomized subjects had higher baseline PLT count (10.5 10/L) than intact subjects (6.7 10/L). No apnea induced change in PLT count was observed in any group of participants. However, MPV increased significantly after breath holds, maximally for 9.3% in trained divers after A3 (P1⁄4 0.02), whereas in intact persons it increased, albeit not significantly, by 3.1% (P1⁄4 0.1) after A2. The increase in MPV in trained divers lasted for 20 min after the last apnea. In splenectomized subjects MPV was unchanged (Figure 1). Thus the series of successive breath-holds with face-immersion in cold water results in fast and sustained increase in MPV in systemic venous blood, both in trained divers and untrained subjects. Since the splenic contraction was observed during the same breath-hold protocol [6] it is likely that breathholding triggered the exchange of platelets between the splenic and circulating blood pools. This hypothesis is substantiated by unchanged MPV in splenectomized persons. Furthermore, since platelet concentration did not change in any of the three studied groups, there must have been the splenic