Note: Reading about the structure and execution of a GBI here would go a significant way to enhancing this particular blog post.
The political trepidation behind the very attempt to legislate a guaranteed basic income (GBI) should be quite surprising, but sadly is not. A GBI should be one of the major goals of the progressive movement, but there has been no effort to achieve it, largely based on the notion that a GBI is thought of as “politically unfeasible”. However, what is interesting from a logical and rational perspective is that there is no direct fundamental reason why a vast majority of United State citizens would object to a GBI regardless of their political, religious or other moral leanings.
For example suppose:
You are a Democrat –
A GBI is generally the Holy Grail with respects to eliminating poverty and hunger. With a GBI poor individuals will be able to create a stable savings account and advance their economic position without the significant threat of falling into the poverty trap. In addition all individuals will be able to afford to attend college, if so desired, creating a more educated and creative society. Individuals that have already attended college would have a greater ability to pay off student loan debt in a timely fashion removing the potential of being financially crippled by consistent payments during hard times. Finally no longer would an individual be handicapped and imprisoned by the poor decisions of their parents for regrettably the economic climate of the United States no longer only demands hard work and reasonable intelligence, but social and political connections.
You are a Republican –
A GBI is an effective means to reduce the level of bureaucracy in the Federal government resulting in the simple and transparent consolidation of all government “safety net” programs which include, but are not limited to: unemployment insurance, general welfare, supplemental nutrition assistance program (SNAP a.k.a. food stamps), school meal programs, low-income housing assistance, home energy bill assistance, refundable portions of the Earned Income Tax Credit and Child Tax Credit, supplemental security income, etc.
There is reason to suspect that the supplementary income provided by a GBI will also increase the probability of marriage and strength family bonds in general. One of major reasons why marriage rates have decreased over the last few decades, especially the last decade, is that most younger individuals are holding off marriage because they do not have the necessary financial resources. Some individuals could argue that small-scale studies disprove this benefit, but that argument misinterprets the results of those studies. Based on logic and the existing marriage climate a GBI should increase marriage probability.
Finally a GBI would significantly enhance market efficiency by increasing the available spending and investment capital in the environment. Not only would individuals have more available money to drive the consumption elements of the economy creating more indirect business opportunities and jobs, individuals would have additional capital that could be utilized to establish their own businesses. Basically instead of relying on venture capitalists or harder to acquire bank loans, which creates market inefficiencies by removing money from the general consumer environment, the money acquired from these businesses stays with the company founders and in the general consumer economy. Keeping more money in this part of the economy will accelerate economic growth. However, if bank loans are needed a GBI would increase credit flow from lending institutions due to increased confidence in repayment.
You are a Libertarian –
A GBI significantly enhances personal freedom by reducing the severity of economic obstacles. Instead of being bound to a job one hates and has little skill at solely because one needs the paycheck to eat, an individual can use the GBI to make decisions not bound by the need for a paycheck. The GBI will accomplish a noted goal, reducing the size of the Federal government. Finally a GBI will further the development of a genuine meritocracy, that winners and losers are determined by talent, hard work, drive, intelligence, etc., instead of a somewhat fixed system where an individual can be consistently placed at a significant disadvantage by elements outside of his/her control.
Regardless of one’s political affiliation a GBI would create a dramatic reduction in lost human potential. For example instead of having an individual who is interested and gifted in engineering, psychology, teaching, law enforcement, etc., bound to a low level undesired service job simply to put food on the table or to help his/her family, this individual will now be able to pursue jobs with their valued skill sets and interests. This rejuvenation of human potential will increase economic efficiency and growth as well as increase physical and mental health.
You are an Environmentalist –
An environmentalist may balk at the above mention of economic growth through additional consumption. However, it is important for environmentalists to recall that a vast majority of “environmentally friendly” energy and transport options are significantly more expensive than their less friendly alternatives; with the additional funds from a GBI individuals will be able to more easily support positive environmental changes increasing the probability for continued economic growth while at the same time reducing the damages born from global warming and other pollution factors.
You are a “Insert Religion Here” –
One of the major tenets of every major religion is to help the poor; supporting and creating a GBI is one of the best strategies for helping the poor. In addition a GBI would free up significant charitable donations to various religious organizations from domestic commitments and allow them to be redistributed to global charitable projects, if so desired. Overall anyone who truly believes in the message of their particular religious faith should support a GBI.
You are in the Upper 15% Income Bracket –
Intuitively one might think that rich individuals, make no mistake those in the top 15% income bracket are rich, would be opposed to a GBI because of the small changes it would make to the tax code resulting in a very slightly reduced direct return. However, a GBI would also significantly increase the amount of disposable income to the general public, which would significantly increase the moneymaking opportunities for rich individuals through investment. It stands to reason that intelligent rich individuals would support a GBI because they could identify the worthwhile new business opportunities in which to invest, either directly or indirectly through stocks, thus increasing their overall wealth as well as improving society in general. Therefore, rich individuals should support a GBI as a means to increase their personal wealth, increase the overall prosperity of the country (enhancing international negotiating power) and reduce market uncertainty and inefficiency increasing overall productivity.
With a vast majority of the public falling into one of the above demographics that would logically support a GBI it is rather peculiar that no reasonable effort has been made by the Federal government to establish one. As stated at the beginning of this thought exercise it appears that preconceived notions about a GBI not being “political feasible” has derailed its viability before even identifying whether or not these preconceived notions are accurate. The interesting thing about this philosophy is how can a piece of legislation be defined as “dead on arrival” if no one actually brings the issue up for discussion? Allowing these assumptions to control the actual perception of various ideas prevents the United States from identifying and establishing quality legislation like a GBI. Overall there is little reason to object to a GBI as long as it is operated transparently and is cost effective for it benefits everyone in society even if some individuals may not immediately realize it.
Saturday, September 27, 2014
Tuesday, September 16, 2014
Reducing Concussions in Football?
The awareness and medical implications of concussions in professional sports have increased significantly over the last half-decade, especially in National Football League (NFL). The direct responsibilities of both the NFL and players to manage the concussion question have previously been outlined in the blog here. Unfortunately neither party, especially the players, has administered those responsibilities appropriately. While behavior still needs to be adjusted to reduce concussion probability, there may be biological strategies that can help maximize positive health outcomes for athletes with regards to concussions.
Various concussion research has involved evaluating rugby-based headgear as well as other helmet designs, custom-fitted mouth guards and face shields (in ice hockey).1-4 The general conclusions are that no particular type of headgear, including rugby-based, reduces the probability of acquiring a concussion any more effectively over most other types of helmets and there is no strong evidence that mouth guards or face shields reduce concussions.4,5 In addition significant amounts of research has focused on post-concussion symptoms and recovery. However, less research has been conducted on secondary factors to developing concussions. For example football has changed significantly in many ways since the early professional days in the 50’s and 60’s; one way that could be very relevant to concussion development is the means in which the brain processes and consumes oxygen.
There are two chief theories that attempt to explain the biological origins of a concussion. First, some believe that the first step involves a significant level of at least one type of force, linear, rotational or angular, that is directly or indirectly applied to the head leading to the disruption of cell membranes in various neurons throughout the brain. This disruption creates an influx of potassium ions to the cells resulting in depolarization and the release of neurotransmitters, usually glutamate.6 The release of glutamate creates a cascade of depolarization among various neuronal networks. Sodium-potassium pumps operate at greater than normal capacity to correct the unnatural and uncontrolled potassium influx, which leads to an energy shortage (excessive consumption of ATP and glucose) resulting in excess lactate accumulation.7-9 All of these elements work in consort to generate neurological imbalance and damage.
Some also believe there is a loss of glucose metabolizing efficiency due to excessive metabolization during the initial stages of the concussion. This loss of metabolizing efficiency is due in part to inefficient lactic acid removal after the concussion event, at least in rodents, which leads to reduced blood flow for a number of days after a concussion event.7,10 Interestingly enough this lack of blood flow could explain why an individual has a higher concussion probability rate (vs. baseline) for a number of days after the initial concussion event because there is less cerebral blood flow and greater ability to produce slosh and other forces. Whether or not calcium accumulation results in cell death through a secondary pathway is unclear.11
Second, some believe that rapid acceleration/deceleration of the brain due to forces and collisions create “slosh” (movement of liquid inside containers that are undergoing motion). Slosh occurs in tissues and fluids with differing densities (white matter, skull, spinal fluid, blood, gray matter, etc.) because they accelerate/decelerate at different rates leading to shearing forces and even hydrodynamic cavitation.12,13 Cavitation is the formation of vapor cavities in liquid born from a rapid change to a lower pressure (below saturated vapor pressure of the liquid). After these cavities are formed an increase in pressure results in their implosion creating shockwaves. These shockwaves create damage throughout the brain.14
Whether or not concussions are driven by functional or structural changes is still an open question. While structural damage has been demonstrated in some brains of humans, commonly resulting in a state similar to Alzheimer’s disease, these changes appear to require numerous concussions over a relatively short period of time (decade or less). Overall it is highly likely that concussions are driven by temporary functional changes, which is why the symptoms are only temporary.
An interesting element about concussions is that both rams and woodpeckers can tolerate head impacts much larger than those that are thought to induce concussions in humans. For example typical football impacts generate 25 to 50-g of force whereas rams ramming each other during demonstrations of supremacy generate 500-g and woodpeckers generate 1200-g numerous times a day.15 This ability to experience head trauma without detrimental outcome is thought to be managed by manipulating intracranial volume and pressure. Both animals have different methodologies behind this ability; rams utilize a carbon dioxide-mediated response to altitude and woodpeckers utilize altered jugular outflow.12,15 These methods create efficient brain compacting, which reduces motion and shearing forces. Clearly altering jugular outflow is not reasonable for humans, but it may be possible to incorporate information from an altitude response to reduce the probability of concussions.
Some of the central features that drive a concussion occur within the skull, which is why no helmet can ever clinically claim to reduce concussions because they cannot directly influence forces inside the cranium. However, playing at an increased altitude (venues at or exceeding 644 ft.) appears to decrease the probability of developing a concussion. A recent study of concussion occurrence in the NFL calculated a 30% reduction at higher altitudes.15 Recall from above that one of the elements that is thought to causes concussions is the brain “sloshing” around creating various forces and cavitation. Clearly one of the methods to reduce the probability of concussions is to increase intracranial volume that would allow the brain to reduce “slosh”.15,16
Some have argued that inadequate adjustment to altitude reduces the ability of players to exert maximum effort thus reducing the amount of force applied when running, blocking and tackling thereby reducing the probability of concussions. However, studies in the past have demonstrated that there is no significant enhancement of fatigue at the 644 ft. threshold; therefore, this “reduced force” reasoning should not be applicable. If concussion probability reduction occurred only at higher altitudes like 2000 ft. then it would be more plausible, but that is not the case.
The protective effect of higher altitudes may directly involve the rate of oxygen flow to the brain. The chief change relative to oxygen at higher altitudes is a drop in oxygen partial pressure throughout the body, especially the brain. For example alveolar oxygen partial pressure drops from 103 to 98 when moving from 0 to 1000 ft.17,18 This reduced partial pressure lowers the available oxygen in the blood for consumption by various organs including the brain. With a greater demand for oxygen cerebral blood flow increases, which increases intracranical volume and decreases the probability of concussion. This relationship between oxygen and altitude could also explain why there is not an empirical linear relationship in the above study between altitude and oxygen for after a certain point players become fatigued by the lack of ambient oxygen and resort to supplementing oxygen consumption with outside sources. This supplementation could explain why Denver, the highest altitude playing field in the NFL, did not have the lowest rate of concussion.15
The relationship between oxygen-related blood flow and concussions also can influence the rate of inertial cavitation. The skull can be considered a rigid vessel with a reduced compliance (due to increased intracranial volume) the probability of inertial cavitation decreases because there is less sudden directional changes in near-by fluids reducing the formation of vapor cavities.13,14,19,20 Therefore, increased cerebral blood flow reduces both the force and the cavitation elements associated with potential concussion progression.
So how is cerebral blood flow controlled naturally? The brain has a much higher metabolic requirement for oxygen than other organs and uses approximately 20% of existing oxygen to maintain normal function. Under normal biological operation blood flow to the brain is constant due to vascular resistance provided by large arteries and parenchymal arterioles and tight gap junctions.21,22 Flow is increased through the dilation of upstream vessels avoiding downstream microvascular pressure.23 Overall blood flow rates are controlled by vasodilation of distal to proximal arterial and myogenic mechanism24 maintaining a cerebral blood flow at approximately 50 mL per 100 g per minute as long as cerebral perfusion pressure (CPP) is between 50-60 and 160 mmHg.25
If CPP falls below 50-60 mmHg cerebral ischemia occurs and the body attempts to compensate by increasing oxygen extraction from blood and increasing blood flow to the brain.26,27 Part of the reason blood flow needs to increase is because the partial pressure of oxygen drops hemoglobin saturation from 100% to 50%.28 There is a rather linear relationship between blood flow and CPP below 50-60 mmHg, but there is little change in metabolism regardless of oxygen partial pressure.28 Under these hypoxic conditions cerebral arteries and arterioles reduce vascular resistance increasing vasodilation and smooth muscle hyperpolarization.
An increase in CO2 concentration has a similar effect to reducing oxygen concentration because of a decrease in oxygen partial pressure. In response cerebral blood flow is increased through similar methods as above (cerebral arteries and arterioles dilation).29 The biological effect of CO2 inhalation is rather significant where a solution of 5% CO2 increases cerebral blood flow by 50% and a 7% CO2 solution increases blood flow by 100%.30 The chief mechanism behind hypercapnic vasodilation is the direct influence of extracellular hydrogen on vascular smooth muscle as changes in CO2 partial pressure along does not change cerebral artery diameter.31,32
With the above information it appears that increasing the ratio of CO2/oxygen in the blood will increase the rate of blood flow to the brain, which will decrease the probability that an individual suffers from a concussion. Outside of playing at altitude what are the methods to increase cerebral blood flow? One long term solution could be breathing conditioning where continuous periods of holding one’s breath would increase CO2 concentration in the blood stream over a very short period of time which could lead to the expansion of carotid arteries increasing blood flow to the brain.
However, breathing conditioning is a long-term solution that many individuals may not have the time or the inclination to undertake, so is there a short-term solution that can temporarily increases cerebral blood flow? One possibility that springs to mind is the consumption of a specific carbonic acid beverage (basically a stronger version of soda/pop). Whether or not this method would be viable is unclear as there is almost no empirical information regarding how the consumption of such a beverage would influence cerebral blood flow or other systems and organs.
Another question is whether or not the use of mouth-to-mask ventilation increases concussion risk by temporarily reducing cerebral blood flow. While there appears to be no direct evidence regarding this question, anecdotal evidence involving the drop-off of concussion reduction at very high altitudes (Mile High Stadium in Denver for example) appears to support this idea.
Basically the technical aspect of this question is how does the brain respond with respects to blood flow to a brief (15-30 seconds) inhalation of 50-100% oxygen and what is the residence time of this response? The answer to this question could change the use of mouth-to-mask ventilation to only emergency situations rather than an augmented pick-me-up after a 26-yard run in order to avoid increasing the chance of a concussion in the next play.
There are numerous behavioral methods to reduce the probability of concussions in football including ensuring that defensive players tackle properly (no leading with the head) and proper neurological evaluation after significant head contact. However, another avenue of concussion prevention has remained generally unexplored. Based on some preliminary evidence it appears that devising a strategy to increase cerebral blood flow to act as a “biological helmet” could go a long way to decreasing the probability of concussion development. The one significant caveat to the development of such a method would be determining any long-term detrimental effects associated with multiple temporary increases to cerebral blood flow. Overall it is important to investigate biological methods as well as material methods and behavioral solutions to prevent concussions in sports.
==
Citations –
1. McIntosh, A, et Al. “Does padded headgear prevent head injury in rugby union football?” Med Sci Sports Exerc. 2009. 41:306–13.
2. Benson, B, et Al. “Head and neck injuries among ice hockey players wearing full face shields vs half face shields.” JAMA. 1999. 282:2328–32.
3. Newsome, P, Tran, D, and Cooke, M. “The role of the mouthguard in the prevention of
sports-related dental injuries: a review.” Int J Paediatr Dent. 2001. 11:396–404.
4. Benson, B, et Al. “What are the most effective risk-reduction strategies in sport concussion?” Br. J. Sports Med. 2013. 47:321-326.
5. Benson, B, et Al. “Is protective equipment useful in preventing concussion? A systematic review of the literature.” BJSM. 2009. 43:i56–67.
6. Katayama, Y, et Al. “Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury.” J Neurosurg. 1990. 73(6):889–900.
7. Giza, C, and Hovda, D. “The neurometabolic cascade of concussion.” J Athl Train. 2001. 36(3):228–235.
8. Yoshino, A, et Al. “Dynamic changes in local cerebral glucose utilization following cerebral conclusion in rats: evidence of a hyper- and subsequent hypometabolic state.” Brain Res. 1991. 561(1):106–119
9. Andersen, B, and Marmarou, A. “Functional compartmentalization of energy production in neural tissue.” Brain Res. 1992. 585(1–2):190–195.
10. Maugans, T, et Al. “Pediatric Sports-Related Concussion Produces Cerebral Blood Flow Alterations.” Pediatrics. 2012. 129:28-38.
11. Meehan, W, and Bachur, R. “Sport-Related Concussion.” Pediatrics. 2009. 123;114-123.
12. Smith, D, et Al. “Internal jugular vein compression mitigates traumatic axonal injury in a rat model by reducing the intracranial slosh effect.” Neurosurgery. 2012. 70:740-746.
13. Turner, R, et Al. “Effect of slosh mitigation on histologic markers of traumatic brain injury: laboratory investigation.” J Neurosurg. 2012. 117:1110-1118.
14. Goeller, J, et Al. “Investigation of cavitation as a possible damage mechanism in blast-induced traumatic brain injury.” J Neurotrauma. 2012. 29:1970-1981.
15. Myer, G, et Al. “Rates of concussion are lower in National Football League games played at higher altitudes.” Journal of Orthopaedic & Sports Physical Therapy. 2014. 44(3):164-172.
16. Kurosawa, Y, et al. “Basic study of brain injury mechanism caused by cavitation.” Conf Proc IEEE Eng Med Biol Soc. 2009. 7224-7227.
17. Altitude oxygen calculator. Available at: http://www.altitude.org/oxygen_levels.php.
18. Kraemer, W, et Al. “Resistance training and youth.” Pediatr Exerc Sci. 1989. 1:336-350.
19. Church, C. “A theoretical study of cavitation generated by an extracorporeal shock wave lithotripter.” J Acoust Soc Am. 1989. 86:215-227.
20. Zhong, P, et Al. “Effects of tissue constraint on shock wave-induced bubble expansion in vivo.” J Acoust Soc Am. 1998. 104:3126-3129.
21. Faraci, F, and Heistad, D. “Regulation of large cerebral arteries and cerebral microvascular pressure.” Circ Res. 1990. 66:8–17.
22. Cipolla, M, et Al. “SKCa and IKCa Channels, myogenic tone, and vasodilator responses in middle cerebral arteries and parenchymal arterioles: effect of ischemia and reperfusion.” Stroke. 2009. 40:1451–1457.
23.Kulik, T, et Al. “Regulation of cerebral vasculature in normal and ischemic brain.” Neuropharmacology. 2008. 55:281–288.
24. Iadecola, C, et Al. “Local and propagated vascular responses evoked by focal synaptic activity in cerebellar cortex.” J Neurophysiol. 1997. 78:651–659.
25. Phillips, S, and Whisnant, J. “Hypertension and the brain.” Arch Intern Med. 1992. 152:938–945.
26. Hossmann, K-A. “Viability thresholds and the penumbra of focal ischemia.” Ann Neurol. 1994. 36:557–565.
27. Iadecola, C. Cerebral circulatory dysregulation in ischemia. In Cerebrovascular Diseases, Ginsberg MD, Bogousslavsky J. (Eds.). Cambridge, MA: Blackwell Science, 1998. 319–332.
28. Steiner, L et Al. “Cerebral oxygen vasoreactivity and cerebral tissue oxygen reactivity.” Br J Anaesth. 2003. 90:774–786.
29. Reivich, M. “Arterial PCO2 and cerebral hemodynamics.” Am J Physiol. 1964. 206:25–35.
30. Kety, S, and Schmidt, C. “The effects of altered arterial tensions of carbon dioxide and oxygen on cerebral blood flow and cerebral oxygen consumption of normal young men. J Clin Invest. 1948; 27:484–492.
31. Kontos, H, Raper, A, and Patterson, J. “Analysis of vasoactivity of local pH, PCO2 and bicarbonate on pial vessels.” Stroke. 1977. 8:358–360.
32. Kontos, H, et Al. “Local mechanism of CO2 action of cat pial arterioles.” Stroke. 1977. 8:226–229.
Various concussion research has involved evaluating rugby-based headgear as well as other helmet designs, custom-fitted mouth guards and face shields (in ice hockey).1-4 The general conclusions are that no particular type of headgear, including rugby-based, reduces the probability of acquiring a concussion any more effectively over most other types of helmets and there is no strong evidence that mouth guards or face shields reduce concussions.4,5 In addition significant amounts of research has focused on post-concussion symptoms and recovery. However, less research has been conducted on secondary factors to developing concussions. For example football has changed significantly in many ways since the early professional days in the 50’s and 60’s; one way that could be very relevant to concussion development is the means in which the brain processes and consumes oxygen.
There are two chief theories that attempt to explain the biological origins of a concussion. First, some believe that the first step involves a significant level of at least one type of force, linear, rotational or angular, that is directly or indirectly applied to the head leading to the disruption of cell membranes in various neurons throughout the brain. This disruption creates an influx of potassium ions to the cells resulting in depolarization and the release of neurotransmitters, usually glutamate.6 The release of glutamate creates a cascade of depolarization among various neuronal networks. Sodium-potassium pumps operate at greater than normal capacity to correct the unnatural and uncontrolled potassium influx, which leads to an energy shortage (excessive consumption of ATP and glucose) resulting in excess lactate accumulation.7-9 All of these elements work in consort to generate neurological imbalance and damage.
Some also believe there is a loss of glucose metabolizing efficiency due to excessive metabolization during the initial stages of the concussion. This loss of metabolizing efficiency is due in part to inefficient lactic acid removal after the concussion event, at least in rodents, which leads to reduced blood flow for a number of days after a concussion event.7,10 Interestingly enough this lack of blood flow could explain why an individual has a higher concussion probability rate (vs. baseline) for a number of days after the initial concussion event because there is less cerebral blood flow and greater ability to produce slosh and other forces. Whether or not calcium accumulation results in cell death through a secondary pathway is unclear.11
Second, some believe that rapid acceleration/deceleration of the brain due to forces and collisions create “slosh” (movement of liquid inside containers that are undergoing motion). Slosh occurs in tissues and fluids with differing densities (white matter, skull, spinal fluid, blood, gray matter, etc.) because they accelerate/decelerate at different rates leading to shearing forces and even hydrodynamic cavitation.12,13 Cavitation is the formation of vapor cavities in liquid born from a rapid change to a lower pressure (below saturated vapor pressure of the liquid). After these cavities are formed an increase in pressure results in their implosion creating shockwaves. These shockwaves create damage throughout the brain.14
Whether or not concussions are driven by functional or structural changes is still an open question. While structural damage has been demonstrated in some brains of humans, commonly resulting in a state similar to Alzheimer’s disease, these changes appear to require numerous concussions over a relatively short period of time (decade or less). Overall it is highly likely that concussions are driven by temporary functional changes, which is why the symptoms are only temporary.
An interesting element about concussions is that both rams and woodpeckers can tolerate head impacts much larger than those that are thought to induce concussions in humans. For example typical football impacts generate 25 to 50-g of force whereas rams ramming each other during demonstrations of supremacy generate 500-g and woodpeckers generate 1200-g numerous times a day.15 This ability to experience head trauma without detrimental outcome is thought to be managed by manipulating intracranial volume and pressure. Both animals have different methodologies behind this ability; rams utilize a carbon dioxide-mediated response to altitude and woodpeckers utilize altered jugular outflow.12,15 These methods create efficient brain compacting, which reduces motion and shearing forces. Clearly altering jugular outflow is not reasonable for humans, but it may be possible to incorporate information from an altitude response to reduce the probability of concussions.
Some of the central features that drive a concussion occur within the skull, which is why no helmet can ever clinically claim to reduce concussions because they cannot directly influence forces inside the cranium. However, playing at an increased altitude (venues at or exceeding 644 ft.) appears to decrease the probability of developing a concussion. A recent study of concussion occurrence in the NFL calculated a 30% reduction at higher altitudes.15 Recall from above that one of the elements that is thought to causes concussions is the brain “sloshing” around creating various forces and cavitation. Clearly one of the methods to reduce the probability of concussions is to increase intracranial volume that would allow the brain to reduce “slosh”.15,16
Some have argued that inadequate adjustment to altitude reduces the ability of players to exert maximum effort thus reducing the amount of force applied when running, blocking and tackling thereby reducing the probability of concussions. However, studies in the past have demonstrated that there is no significant enhancement of fatigue at the 644 ft. threshold; therefore, this “reduced force” reasoning should not be applicable. If concussion probability reduction occurred only at higher altitudes like 2000 ft. then it would be more plausible, but that is not the case.
The protective effect of higher altitudes may directly involve the rate of oxygen flow to the brain. The chief change relative to oxygen at higher altitudes is a drop in oxygen partial pressure throughout the body, especially the brain. For example alveolar oxygen partial pressure drops from 103 to 98 when moving from 0 to 1000 ft.17,18 This reduced partial pressure lowers the available oxygen in the blood for consumption by various organs including the brain. With a greater demand for oxygen cerebral blood flow increases, which increases intracranical volume and decreases the probability of concussion. This relationship between oxygen and altitude could also explain why there is not an empirical linear relationship in the above study between altitude and oxygen for after a certain point players become fatigued by the lack of ambient oxygen and resort to supplementing oxygen consumption with outside sources. This supplementation could explain why Denver, the highest altitude playing field in the NFL, did not have the lowest rate of concussion.15
The relationship between oxygen-related blood flow and concussions also can influence the rate of inertial cavitation. The skull can be considered a rigid vessel with a reduced compliance (due to increased intracranial volume) the probability of inertial cavitation decreases because there is less sudden directional changes in near-by fluids reducing the formation of vapor cavities.13,14,19,20 Therefore, increased cerebral blood flow reduces both the force and the cavitation elements associated with potential concussion progression.
So how is cerebral blood flow controlled naturally? The brain has a much higher metabolic requirement for oxygen than other organs and uses approximately 20% of existing oxygen to maintain normal function. Under normal biological operation blood flow to the brain is constant due to vascular resistance provided by large arteries and parenchymal arterioles and tight gap junctions.21,22 Flow is increased through the dilation of upstream vessels avoiding downstream microvascular pressure.23 Overall blood flow rates are controlled by vasodilation of distal to proximal arterial and myogenic mechanism24 maintaining a cerebral blood flow at approximately 50 mL per 100 g per minute as long as cerebral perfusion pressure (CPP) is between 50-60 and 160 mmHg.25
If CPP falls below 50-60 mmHg cerebral ischemia occurs and the body attempts to compensate by increasing oxygen extraction from blood and increasing blood flow to the brain.26,27 Part of the reason blood flow needs to increase is because the partial pressure of oxygen drops hemoglobin saturation from 100% to 50%.28 There is a rather linear relationship between blood flow and CPP below 50-60 mmHg, but there is little change in metabolism regardless of oxygen partial pressure.28 Under these hypoxic conditions cerebral arteries and arterioles reduce vascular resistance increasing vasodilation and smooth muscle hyperpolarization.
An increase in CO2 concentration has a similar effect to reducing oxygen concentration because of a decrease in oxygen partial pressure. In response cerebral blood flow is increased through similar methods as above (cerebral arteries and arterioles dilation).29 The biological effect of CO2 inhalation is rather significant where a solution of 5% CO2 increases cerebral blood flow by 50% and a 7% CO2 solution increases blood flow by 100%.30 The chief mechanism behind hypercapnic vasodilation is the direct influence of extracellular hydrogen on vascular smooth muscle as changes in CO2 partial pressure along does not change cerebral artery diameter.31,32
With the above information it appears that increasing the ratio of CO2/oxygen in the blood will increase the rate of blood flow to the brain, which will decrease the probability that an individual suffers from a concussion. Outside of playing at altitude what are the methods to increase cerebral blood flow? One long term solution could be breathing conditioning where continuous periods of holding one’s breath would increase CO2 concentration in the blood stream over a very short period of time which could lead to the expansion of carotid arteries increasing blood flow to the brain.
However, breathing conditioning is a long-term solution that many individuals may not have the time or the inclination to undertake, so is there a short-term solution that can temporarily increases cerebral blood flow? One possibility that springs to mind is the consumption of a specific carbonic acid beverage (basically a stronger version of soda/pop). Whether or not this method would be viable is unclear as there is almost no empirical information regarding how the consumption of such a beverage would influence cerebral blood flow or other systems and organs.
Another question is whether or not the use of mouth-to-mask ventilation increases concussion risk by temporarily reducing cerebral blood flow. While there appears to be no direct evidence regarding this question, anecdotal evidence involving the drop-off of concussion reduction at very high altitudes (Mile High Stadium in Denver for example) appears to support this idea.
Basically the technical aspect of this question is how does the brain respond with respects to blood flow to a brief (15-30 seconds) inhalation of 50-100% oxygen and what is the residence time of this response? The answer to this question could change the use of mouth-to-mask ventilation to only emergency situations rather than an augmented pick-me-up after a 26-yard run in order to avoid increasing the chance of a concussion in the next play.
There are numerous behavioral methods to reduce the probability of concussions in football including ensuring that defensive players tackle properly (no leading with the head) and proper neurological evaluation after significant head contact. However, another avenue of concussion prevention has remained generally unexplored. Based on some preliminary evidence it appears that devising a strategy to increase cerebral blood flow to act as a “biological helmet” could go a long way to decreasing the probability of concussion development. The one significant caveat to the development of such a method would be determining any long-term detrimental effects associated with multiple temporary increases to cerebral blood flow. Overall it is important to investigate biological methods as well as material methods and behavioral solutions to prevent concussions in sports.
==
Citations –
1. McIntosh, A, et Al. “Does padded headgear prevent head injury in rugby union football?” Med Sci Sports Exerc. 2009. 41:306–13.
2. Benson, B, et Al. “Head and neck injuries among ice hockey players wearing full face shields vs half face shields.” JAMA. 1999. 282:2328–32.
3. Newsome, P, Tran, D, and Cooke, M. “The role of the mouthguard in the prevention of
sports-related dental injuries: a review.” Int J Paediatr Dent. 2001. 11:396–404.
4. Benson, B, et Al. “What are the most effective risk-reduction strategies in sport concussion?” Br. J. Sports Med. 2013. 47:321-326.
5. Benson, B, et Al. “Is protective equipment useful in preventing concussion? A systematic review of the literature.” BJSM. 2009. 43:i56–67.
6. Katayama, Y, et Al. “Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury.” J Neurosurg. 1990. 73(6):889–900.
7. Giza, C, and Hovda, D. “The neurometabolic cascade of concussion.” J Athl Train. 2001. 36(3):228–235.
8. Yoshino, A, et Al. “Dynamic changes in local cerebral glucose utilization following cerebral conclusion in rats: evidence of a hyper- and subsequent hypometabolic state.” Brain Res. 1991. 561(1):106–119
9. Andersen, B, and Marmarou, A. “Functional compartmentalization of energy production in neural tissue.” Brain Res. 1992. 585(1–2):190–195.
10. Maugans, T, et Al. “Pediatric Sports-Related Concussion Produces Cerebral Blood Flow Alterations.” Pediatrics. 2012. 129:28-38.
11. Meehan, W, and Bachur, R. “Sport-Related Concussion.” Pediatrics. 2009. 123;114-123.
12. Smith, D, et Al. “Internal jugular vein compression mitigates traumatic axonal injury in a rat model by reducing the intracranial slosh effect.” Neurosurgery. 2012. 70:740-746.
13. Turner, R, et Al. “Effect of slosh mitigation on histologic markers of traumatic brain injury: laboratory investigation.” J Neurosurg. 2012. 117:1110-1118.
14. Goeller, J, et Al. “Investigation of cavitation as a possible damage mechanism in blast-induced traumatic brain injury.” J Neurotrauma. 2012. 29:1970-1981.
15. Myer, G, et Al. “Rates of concussion are lower in National Football League games played at higher altitudes.” Journal of Orthopaedic & Sports Physical Therapy. 2014. 44(3):164-172.
16. Kurosawa, Y, et al. “Basic study of brain injury mechanism caused by cavitation.” Conf Proc IEEE Eng Med Biol Soc. 2009. 7224-7227.
17. Altitude oxygen calculator. Available at: http://www.altitude.org/oxygen_levels.php.
18. Kraemer, W, et Al. “Resistance training and youth.” Pediatr Exerc Sci. 1989. 1:336-350.
19. Church, C. “A theoretical study of cavitation generated by an extracorporeal shock wave lithotripter.” J Acoust Soc Am. 1989. 86:215-227.
20. Zhong, P, et Al. “Effects of tissue constraint on shock wave-induced bubble expansion in vivo.” J Acoust Soc Am. 1998. 104:3126-3129.
21. Faraci, F, and Heistad, D. “Regulation of large cerebral arteries and cerebral microvascular pressure.” Circ Res. 1990. 66:8–17.
22. Cipolla, M, et Al. “SKCa and IKCa Channels, myogenic tone, and vasodilator responses in middle cerebral arteries and parenchymal arterioles: effect of ischemia and reperfusion.” Stroke. 2009. 40:1451–1457.
23.Kulik, T, et Al. “Regulation of cerebral vasculature in normal and ischemic brain.” Neuropharmacology. 2008. 55:281–288.
24. Iadecola, C, et Al. “Local and propagated vascular responses evoked by focal synaptic activity in cerebellar cortex.” J Neurophysiol. 1997. 78:651–659.
25. Phillips, S, and Whisnant, J. “Hypertension and the brain.” Arch Intern Med. 1992. 152:938–945.
26. Hossmann, K-A. “Viability thresholds and the penumbra of focal ischemia.” Ann Neurol. 1994. 36:557–565.
27. Iadecola, C. Cerebral circulatory dysregulation in ischemia. In Cerebrovascular Diseases, Ginsberg MD, Bogousslavsky J. (Eds.). Cambridge, MA: Blackwell Science, 1998. 319–332.
28. Steiner, L et Al. “Cerebral oxygen vasoreactivity and cerebral tissue oxygen reactivity.” Br J Anaesth. 2003. 90:774–786.
29. Reivich, M. “Arterial PCO2 and cerebral hemodynamics.” Am J Physiol. 1964. 206:25–35.
30. Kety, S, and Schmidt, C. “The effects of altered arterial tensions of carbon dioxide and oxygen on cerebral blood flow and cerebral oxygen consumption of normal young men. J Clin Invest. 1948; 27:484–492.
31. Kontos, H, Raper, A, and Patterson, J. “Analysis of vasoactivity of local pH, PCO2 and bicarbonate on pial vessels.” Stroke. 1977. 8:358–360.
32. Kontos, H, et Al. “Local mechanism of CO2 action of cat pial arterioles.” Stroke. 1977. 8:226–229.
Subscribe to:
Posts (Atom)