Short- and Long-term exercise induced alterations in haemostasis: a review of the literature.

New Findings

What is the topic of this review?

This review provides an up-to-date assessment of the physiology involved with extreme static dry-land breath holding in trained apneists.


What advances does it highlight?

We specifically highlight the recent findings involved with the cardiovascular, cerebrovascular, and metabolic function during a maximal breath hold in elite apneists.



Abstract
Breath hold related activities have been performed for centuries, but only recently within the last ∼30 years has it emerged as an increasingly popular competitive sport. In apnea sport, people compete in disciplines relating to underwater distances or simply maximal breath hold duration – with the current (oxygen un-supplemented) static breath hold record at 11:35 min. Remarkably, many ultra-elite apneists are able to supress respiratory urges to the point where consciousness fundamentally limits a breath hold duration. Here, arterial oxygen saturations as low as ∼50% have been reported. In such cases, oxygen conservation to maintain cerebral functioning is critical, where responses ascribed to the mammalian dive reflex – e.g., sympathetically mediated peripheral vaconstriction, and vagally mediated bradycardia – are central. In defence of maintaining global cerebral oxygen delivery during prolonged breath holds, the cerebral blood flow may increase by ∼100% from resting values. Interestingly, near the termination of prolonged dry static breath holds, recent studies also indicate that reductions in the cerebral oxidative metabolism can occur, likely attributable to the extreme hypercapnia and irrespective of the hypoxemia. In this review we highlight and discuss the recent data on the cardiovascular, metabolic and particularly cerebrovascular function in competitive apneists performing maximal static breath holds. The physiological adaptation and maladaptation with regular breath hold training are also summarized, and future research areas in this unique physiological field are highlighted, in particular the need to better determine the potential long-term health impacts of extreme breath holding.

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https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/EP086269

Physiology of static breath holding in elite apneists

The human spleen shows a decrease in volume of around 40% early during vigorous exercise and in response to other stressful stimuli such as maximal apnoea and the breathing of hypoxic gas mixtures Contraction seems an active response, mediated by alpha-adrenergic fibres in the splenic nerve Given the relatively small size of the human spleen, the effect upon physical performance is likely to be small; the augmentation of total blood volume is <2%, and even taking account of other causes of haemoconcentration during vigorous exercise, the increase of haematocrit is <10% However, one of two studies suggested that the haemoconcentration may be sufficient to cause errors in the traditional method for calculating exercise-induced changes of plasma volume The spleen also contributes leucocytes and platelets to the general circulation as part of the "fight or flight" reaction to stressors The mobilisation of leucocytes proceeds more slowly than that of the red cells; it depends not only upon an active contraction of the spleen, but also a modulation of leucocyte adhesion molecules Splenectomy impairs exercise performance in horses, but human performance data are lacking; overall health effects seem minimal, and many patients live many years after removal of their spleens

Responses of the human spleen to exercise

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Leukocyte-Expressed β2-Adrenergic Receptors Are Essential for Survival After Acute Myocardial Injury.

The objective of the article is to assess changes in splenic volume in the setting of hypovolemic shock; splenic enhancement in hypovolemic shock is also assessed. 71 consecutive adult patients with the hypovolemic shock complex on computed tomography (CT) were identified. Spleen volume and enhancement were compared to a baseline CT scan (without shock) or to height- and sex-corrected normal values and a control population when a comparison CT was unavailable. Splenic volume was significantly lower in the setting of shock. Average splenic volume in adult patients with shock was 107 ± 63 cm3 compared to 220 ± 164 cm3 in the control population (P < 0.001). All shock patients with a comparison CT (n = 35) had decreased splenic volume in the setting of shock. The area under the receiver operating characteristic (ROC) curve for spleen volume predicting shock was 0.83. Splenic enhancement was also significantly lower in the setting of shock. Mean splenic attenuation value in our shock population was 105 ± 34 HU compared to 134 ± 25 HU in the control population (P < 0.001). Decreased splenic enhancement was present in 25 of 71 shock patients and in none of the control patients (P < 0.001). Decreased splenic volume is a ubiquitous and reliable sign of hypovolemic shock and should be considered a member of the hypovolemic shock complex. It is of particular utility when a prior study is available. Splenic hypoenhancement has high specificity and a high positive predictive value for hypovolemic shock in the correct patient population.

Splenic contraction: a new member of the hypovolemic shock complex

It is generally accepted that the spleen contraction is a consequence of humoral stimulation but recent data suggest a role of neural mechanisms. This study tested the hypothesis that the reduction in spleen size in response to low dose epinephrine infusion is a consequence of neurally mediated unloading of baroreceptors. Continuous ultrasonic measurements of spleen volume in response to intravenous infusion of low doses of epinephrine (0.06 μg/kg/min for 6 minutes, followed 0.12 μg/kg/min for 3 minutes) were performed with simultaneous continuous noninvasive measurements of cardiovascular parameters in thirteen subjects. In subgroup of six subjects we also continuously measured muscle sympathetic nerve activity (MSNA) as an index of peripheral sympathetic activation. Significant spleen contraction (≈30%, p=0.008) was observed early after the onset of epinephrine infusion and was preceded by a decrease in total peripheral resistance (41%, p=0.001) and mean arterial pressure (6.2%, p=0.02) and an increase in heart rate (27%, p=0.001) and total MSNA (120%, p=0.02). Our results demonstrate rapid spleen contraction induced by low-dose epinephrine infusion in conditions of decreased blood pressure and increased MSNA suggesting that the spleen may represent a constitutive part of the sympathetic nervous system under stressful situations.

/pdf/spleen-volume-changes-during-adrenergic-stimulation-with-low-5971rzdeg8.pdf

P Zubin Maslov

Papers

Spleen volume changes during adrenergic stimulation with low doses of epinephrine.