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“Tighter fit” theory—physiologists explain why “higher altitude” and jugular occlusion are unlikely to reduce risks for sports concussion and brain injuries

2016; American Physiological Society; Volume: 122; Issue: 1 Linguagem: Inglês

10.1152/japplphysiol.00661.2016

ISSN

8750-7587

Autores

James M. Smoliga, Gerald S. Zavorsky,

Tópico(s)

Neuroscience of respiration and sleep

Resumo

Viewpoint"Tighter fit" theory—physiologists explain why "higher altitude" and jugular occlusion are unlikely to reduce risks for sports concussion and brain injuriesJames M. Smoliga and Gerald S. ZavorskyJames M. SmoligaDepartment of Physical Therapy, High Point University, High Point, North Carolina; and and Gerald S. ZavorskyDepartment of Respiratory Therapy, Georgia State University, Georgia State University, Atlanta, GeorgiaPublished Online:18 Jan 2017https://doi.org/10.1152/japplphysiol.00661.2016This is the final version - click for previous versionMoreSectionsPDF (275 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat recent studies claim that the incidence of sports-related concussions may be reduced (16, 25) at "higher altitudes." The proposed mechanism of protection is rooted in the "tighter fit" theory, such that altitude exposure causes the brain to swell, which leaves less room for it to "slosh" within the skull (16, 25). However, another study reported decreased incidence of concussion at "higher altitudes," (14), and meta-analysis indicates no effect (32). Despite the underlying weakness of this idea, the idea has received considerable mainstream media attention and inspired protective equipment designed to mimic the supposed protective effects of altitude. As this weakly supported idea persists and drives intervention strategies, physiologists must enter the discussion to clarify the numerous inaccuracies in "tighter fit" hypothesis. This is especially important in an era where politics and conflicts of interest influence concussion research (2, 23).Inappropriate Altitude ClassificationsIn studies linking altitude and concussion, the defining thresholds for "higher altitude" are based on the median altitude at which concussions occurred within the data set (~197 m or 645 ft), rather than the ranges of altitude exposure that yield physiologic effects. For instance, maximal oxygen uptake begins to decline at altitudes >610 m (2,000 ft), and aerobic performance declines are first noticed only at ~1,000 m (~3,300 ft) (5, 13). These declines are most applicable to highly trained endurance athletes and are minimally relevant to American football, which is characterized by short sprints with long rest periods (13). Anaerobic events lasting <2 min are minimally affected up to 2,134 m (7,000 ft) (5), and sprint speed is enhanced because of decreased air resistance (13). Therefore, there are no known data to support any mechanism for altitudes 5× than the arbitrary threshold) to influence concussion rate.With the exception of Denver, NFL stadium elevations range from 1 m (3.3 ft, Mercedes-Benz Superdome) to 327 m (1,070 ft, University of Phoenix Stadium) above sea level, and the upper quintile in the National Collegiate Athletics Association Division 1 Football is 284 m (931 ft). Between 0 and 327 m altitude, the difference in atmospheric pressure is ~30 mmHg,1 producing a ~6 mmHg differential in inspired oxygen pressure. However, atmospheric pressure may have a typical range of ±25 mmHg relative to the mean2, which means that a "low altitude" site could overlap with the atmospheric pressure in most [arbitrarily] classified "high altitude" sites on a given day, with few exceptions (i.e., Mile High in Denver, Folsom Field in Boulder). If small differences in altitude between most stadiums actually influenced concussion risk, typical barometric pressure fluctuation would be just as influential on concussion risk at most stadiums (i.e., 4,000 m (~13,000 ft) (20). Incidentally, the role of brain swelling in these conditions is also known as "tighter fit" and attempts to account for the seemingly random nature of altitude-related illness. This clearly differs from sports-related concussions, which are not random, but a direct consequence of impact.Although true high-altitude exposure may cause a brief, small magnitude increase in intracranial pressure, this is transient, because a number of mechanisms allow for intracranial pressure to quickly return to normal values in most individuals (12). Transient increases in intracranial pressure are rooted in lower atmospheric pressures at truly high altitudes, which decreases the partial pressure of inspired oxygen, which in turn reduces the alveolar oxygen pressure and, consequently, reduces arterial oxygen pressure (PaO2). It is well-established that the threshold for physiologic changes in the cranium, including increased cerebral blood flow and intracranial pressure, occurs at PaO2 ~50–60 mmHg (12), which only occurs at altitudes 10–20 times greater than those considered in these concussion studies (Fig. 1). It must be emphasized that as a threshold, there is not a linear relationship between PaO2and cerebral blood flow or intracranial pressure, but rather these remain essentially unchanged when PaO2 remains above this critical value (12), and thus altitudes less than ~2,000 m should not influence them.Fig. 1.Typical barometric pressure, arterial partial pressure of oxygen (PaO2), and mean arterial oxyhemoglobin saturation (SaO2) at various reference points. Physiologic changes in the cranium do not occur at PaO2>60 mmHg (9), and thus would only be expected >2,134 m (7,000 ft). Mean values for arterial oxygen pressure and arterial oxyhemoglobin at a given atmospheric pressure up to and including 1,609 m were obtained from Crapo et al. (3). At 2,134 m (7,000 ft), arterial oxygen pressure and arterial oxyhemoglobin obtained were from http://www.altitude.org/oxygen_levels.php. At 4,000 m (13,000 ft), arterial oxygen pressure and arterial oxyhemoglobin were from Banchero et al. (1).Download figureDownload PowerPointAccording to the "tighter fit" theory of concussion protection, even a small [~4 ml or 3% of total cranial blood volume (16)] increase in cranial content could protect the brain by decreasing "sloshing" within the head upon impact. Exposure to an equivalent altitude >3,800 m has been shown to induce changes below this standard, with no significant changes in cerebral blood flow, CSF volume (21), or sinus volume (22). In other instances, there are significant decreases in CSF volume (4, 22) and deep cerebral venous volume (22). Minimal changes (0–2.5%) in total brain parenchymal volume are reported (4, 21, 22), with the largest increase in total cerebral volume ~3 mL (4). Because actual hypoxic conditions were insufficient to achieve the proposed target for protection, it seems highly unlikely that the ~197 m altitudes used in concussion studies would do so. Although Denver is the extreme case in the NFL (1,609 m or 5,280 ft), it should elicit PaO2 ~75 mmHg (above the critical threshold for brain changes), and indeed did not have the lowest incidence of concussion in the NFL study, which is counter to what would be expected if altitude influenced concussion rates (16). Furthermore, normal fluctuation in cerebral blood volume within a cardiac cycle is 1.5–2.0 ml, and intracranial pressure can vary from −5 to +10 mmHg during upright posture, depending on tilt angles (which are clearly variable during football) (12). Thus, even if tightness-of-fit could prevent brain "sloshing," the effect could be quite variable, because any theoretic increase in protection brought about by true altitude exposure may be offset if a hit occurs during diastole and / or certain postures.Inducing Tighter Fit Through Jugular Occlusion?It has been proposed that jugular occlusion can mimic the supposed effects of "higher altitude" to protect athletes from concussion (16–18, 24, 25). Woodpeckers are commonly cited as the inspiration for the theorized protective effects of "tighter fit," based on their limited intracranial space (24, 27). However, it seems scientifically implausible for slight increases in cranial fluid volume to functionally mimic woodpeckers' "unique anatomic structure," which includes numerous macroscopic (i.e., brain structure and orientation, skull thickness) and microscopic (i.e., various trabecular and biochemical qualities that influence mechanical properties) anatomic adaptations that collectively create impact-resistance (28). A jugular occlusion study in rats reporting decreased brain damage (24, 27) after a 900 g impact (15) has been used to justify its potential in sports (16, 25). However, typical impacts in football are well below this, with accelerations >100 g considered severe, and concussions occurring at 145 ± 35 g (6).Despite weak justification from animal models and altitude epidemiology, clinical trials have begun to examine brain MRI after use of a jugular occlusion device in athletes (17, 18). However, investigations into the safety of neckwear reveal some concerns for jugular occlusion, and it is unknown if these could be exacerbated with rapid movement and impact. Simulated necktie wear impairs cerebrovascular reactivity (19), and there are conflicting findings regarding the effect of neckties on intraocular pressure (10, 26). Tight neckwear has been demonstrated to decrease visual performance in healthy men (11) and decrease cervical range of motion and increase trapezius muscle activity in office workers (31). Although mild jugular compression may alter selected cephalic blood flow and CSF parameters at some points within the cardiac cycle (with considerable interindividual differences due to vascular anatomical variation), it does not alter brain tissue viscoelastic properties (9). Given its weak physiologic foundation, it is concerning that jugular occlusion is now being suggested for widespread athletic and military applications and for auto safety, including seat belts and child safety seats (18a).ConclusionInput from physiologists is critical to ensure that concussion intervention strategies with weak scientific foundations do not ultimately put athletes at risk. The lack of physiologic rationale for "tighter fit" protection suggests that research on this issue will simply divert time and resources away from more clinically impactful research aimed at identifying modifiable risk factors for concussion, developing scientifically sound technologies that improve athlete safety, and improving acute and chronic management of sports-related head injuries.DISCLOSURESNo conflicts of interest, financial or otherwise, are declared by the author(s).AUTHOR CONTRIBUTIONSJ.M.S. and G.S.Z. conceived and designed research; J.M.S. prepared figures; J.M.S. and G.S.Z. drafted manuscript; J.M.S. and G.S.Z. edited and revised manuscript; J.M.S. and G.S.Z. approved final version of manuscript.FOOTNOTES2As an example, Chicago Midway Airport [near median altitude threshold of aforementioned studies; 189 m (620 ft)] had an air pressure range of 740–779 mmHg, with a mean of 762 mmHg in December 2015 (29). 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Risk of concussion in contact sports at "high" altitude vs sea level: a meta-analysis. JAMA Neurol 73: 1369–1370, 2016. doi:10.1001/jamaneurol.2016.0795. Crossref | PubMed | ISI | Google ScholarAUTHOR NOTES1http://www.altitude.org/air_pressure.php.Address for reprint requests and other correspondence: J. M. Smoliga, Dept. of Physical Therapy, High Point University, One University Parkway, High Point, NC 27268 (e-mail: [email protected]edu). Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByTeam Logo Predicts Concussion RiskEpidemiology, Vol. 28, No. 5Last Word on Viewpoint: All is fair in altitude and concussionsJames M. Smoliga and Gerald S. Zavorsky18 January 2017 | Journal of Applied Physiology, Vol. 122, No. 1Commentaries on Viewpoint: "Tighter fit" theory—physiologists explain why "higher altitude" and jugular occlusion are unlikely to reduce risks for sports concussion and brain injuries18 January 2017 | Journal of Applied Physiology, Vol. 122, No. 1 More from this issue > Volume 122Issue 1January 2017Pages 215-217 Copyright & PermissionsCopyright © 2017 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00661.2016PubMed27609202History Received 25 July 2016 Accepted 5 September 2016 Published online 18 January 2017 Published in print 1 January 2017 Metrics

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