Deep Breath
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2021 ◽  
Vol 12 ◽  
Kay Tetzlaff ◽  
Frederic Lemaitre ◽  
Christof Burgstahler ◽  
Julian A. Luetkens ◽  
Lars Eichhorn

Breath-hold diving involves environmental challenges, such as water immersion, hydrostatic pressure, and asphyxia, that put the respiratory system under stress. While training and inherent individual factors may increase tolerance to these challenges, the limits of human respiratory physiology will be reached quickly during deep breath-hold dives. Nonetheless, world records in deep breath-hold diving of more than 214 m of seawater have considerably exceeded predictions from human physiology. Investigations of elite breath-hold divers and their achievements revised our understanding of possible physiological adaptations in humans and revealed techniques such as glossopharyngeal breathing as being essential to achieve extremes in breath-hold diving performance. These techniques allow elite athletes to increase total lung capacity and minimize residual volume, thereby reducing thoracic squeeze. However, the inability of human lungs to collapse early during descent enables respiratory gas exchange to continue at greater depths, forcing nitrogen (N2) out of the alveolar space to dissolve in body tissues. This will increase risk of N2 narcosis and decompression stress. Clinical cases of stroke-like syndromes after single deep breath-hold dives point to possible mechanisms of decompression stress, caused by N2 entering the vasculature upon ascent from these deep dives. Mechanisms of neurological injury and inert gas narcosis during deep breath-hold dives are still incompletely understood. This review addresses possible hypotheses and elucidates factors that may contribute to pathophysiology of deep freediving accidents. Awareness of the unique challenges to pulmonary physiology at depth is paramount to assess medical risks of deep breath-hold diving.

2021 ◽  
Vol 12 ◽  
Alexander Patrician ◽  
Željko Dujić ◽  
Boris Spajić ◽  
Ivan Drviš ◽  
Philip N. Ainslie

Breath-hold diving involves highly integrative physiology and extreme responses to both exercise and asphyxia during progressive elevations in hydrostatic pressure. With astonishing depth records exceeding 100 m, and up to 214 m on a single breath, the human capacity for deep breath-hold diving continues to refute expectations. The physiological challenges and responses occurring during a deep dive highlight the coordinated interplay of oxygen conservation, exercise economy, and hyperbaric management. In this review, the physiology of deep diving is portrayed as it occurs across the phases of a dive: the first 20 m; passive descent; maximal depth; ascent; last 10 m, and surfacing. The acute risks of diving (i.e., pulmonary barotrauma, nitrogen narcosis, and decompression sickness) and the potential long-term medical consequences to breath-hold diving are summarized, and an emphasis on future areas of research of this unique field of physiological adaptation are provided.

2021 ◽  
pp. 153575972110042
Peter Widdess-Walsh

[Box: see text]

2021 ◽  
Vol 9 ◽  
Erica Patterson ◽  
Emily Katheryn Brown ◽  
Christine Ruminski ◽  
Tamara Beth Miller

The way you sit or stand during everyday activities can have a big impact on your health. Poor posture can make certain muscles weak, can cause pain, and can even make it harder to take a deep breath! Maintaining good posture can be difficult, especially while using handheld electronics, such as cell phones and tablets. Many students like you and even adults, spend several hours every day looking down at a screen to read books, play games, or watch movies. Looking down at a screen can put a lot of stress on the neck muscles, which can lead to pain and other health problems in the future. In this article we describe good and poor posture, and we discuss how electronic devices can affect posture. But do not fear! We also provide tips on how to adjust your posture and stay healthy while using your electronics.

Guido Ferretti

This article discusses the limits of deep breath-hold diving in humans. After a short historical introduction and a discussion of the evolution of depth records, the classical theories of breath-hold diving limits are presented and discussed, namely that of the ratio between total lung capacity and residual volume and that of blood shift, implying an increase in central blood volume. Then the current vision is introduced, based on the principles of the energetics of muscular exercise. The new vision has turned the classical vision upside down, moving the discussion to a different level. A direct consequence of the new theory is the importance of having large lung volumes at the start of a dive, in order to increase body oxygen stores. I finally discuss the role of anaerobic lactic metabolism as a possible mechanism of oxygen preservation, thus prolonging breath-hold duration.

2021 ◽  
pp. 195-203
Richard E. Moon ◽  
Simon J. Mitchell ◽  

Hyperbaric oxygen for decompression sickness: 2021 update Decompression sickness (DCS, “bends”) is caused by the formation of bubbles in tissues and/or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation). This may occur when ambient pressure is reduced during: ascent from a dive; rapid ascent to altitude in an unpressurized aircraft or hypobaric chamber; loss of cabin pressure in an aircraft [2]; and during space walks. In diving, compressed-gas breathing is usually necessary, although occasionally DCS has occurred after either repetitive or very deep breath-hold dives

CytoJournal ◽  
2021 ◽  
Vol 18 ◽  
pp. 3
Neeraja Yerrapotu ◽  
Abid Rahman ◽  
Ali Gabali ◽  
Vinod B Shidham

A 51-year-old male with a history of chronic myelomonocytic leukemia-2 (CMML-2) presented with fatigue, night sweats, dyspnea, and right-sided chest pain exacerbated by deep breath. Computed tomography scan demonstrated right-sided pleural effusion with atelectasis. Pleural fluid cytology showed reactive mesothelial cells mixed with atypical cells [Figure 1]. The immunostains are performed using the SCIP approach.[1] The atypical cells were immunoreactive for vimentin, CD68, and CD163, while non-immunoreactive for cytokeratin, calretinin, BerEP4, and MOC31.

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