"Sleep Apnea in Professional Football Players" ...an explanation
James Michael Howard
jmhoward at arkansas.net
Sat Jan 25 09:40:05 EST 2003
Sleep Apnea and Testosterone. Why Athletes May Have More Sleep Apnea
It has just been found that sleep apnea is more common in pro footballers than
the average population. see "Sleep Apnea in Professional Football Players" at
Well, I suggest this is due to extra testosterone in these individuals. Yes,
testosterone may be a causative agent in sleep apnea, even in women. First,
here is an abstract of research showing there is a direct connection between
testosterone and "better explosive strength and sprint running performances."
My explanation of the relationship of testosterone with sleep apnea follows this
abstract. My article on sleep apnea and testosterone is also at
Clin Physiol 1996 May;16(3):317-22
Relationships between field fitness test and basal serum testosterone and
cortisol levels in soccer players.
Bosco C, Tihanyi J, Viru A
School of Specialization in Sport Medicine, University G D'Annunzio Chieti,
The aim of this study was to investigate the existence of a relationship between
performance capacities and blood levels of testosterone (T) and cortisol (C).
Thirty-two professional soccer players volunteered for the study. Morning levels
of hormones were plotted against results of maximal vertical jump with a
preparatory counter-movement (CMJ), 30 m running, and Cooper's 12-min running
test. The serum T was positively related to both CMJ and average running speed
(r=0.43 and r=0.47, respectively). Serum levels of C and T were in negative
correlation (r= -0.40 and r= -0.49, respectively) with the results of Cooper's
test. It was concluded that athletes with better explosive strength and sprint
running performances have a higher basal level of testosterone. The results
suggest a relationship between testosterone production and development of fast
twitch muscle fibres in athletes.
Testosterone and Sleep: Support for Sleep Theory
Copyright 1997, by James Michael Howard.
This is new addtional support for my sleep theory.
In 1994, it was determined that testosterone makes obstructive sleep apnea
worse. This is the finding of the following research from 1994. Following this
quotation, however, one can see that it is not a simple effect of testosterone
on airway passages.
"Testosterone is thought to play a role in the pathogenesis of obstructive sleep
apnea (OSA), but the mechanism is unclear. We present a case in which
testosterone administration induced or exacerbated OSA in a 13-year-old male. We
demonstrated that exacerbation of OSA by testosterone was associated with an
increase in upper airway collapsibility during sleep, and that this improved
after cessation of hormone administration. Our data strongly suggest that the
mechanism by which testosterone administration may induce or exacerbate OSA is
through an influence on neuromuscular control of upper airway patency during
sleep." (American Journal of Respiratory and Critical Care Medicine 1994; 149:
This report is supported by some earlier reports. However, some reports suggest
that testosterone replacement in hypogonadal men significantly increases "both
apneas and hypoapneas" but that this is a "highly variable event with some
subjects demonstrating large increases in apneas and hypoapneas when androgen
[testosterone] was replaced, whereas others had little change in repiration
during sleep." This report also studied airway dimensions and concluded that
"Upper airway dimensions, on the other hand, were unaffected by testosterone.
These results suggest that testosterone contributes to sleep-disordered
breathing through mechanisms independent of anatomic changes in the upper
airway." (Journal of Applied Physiology 1986; 61: 618)
Another study of testosterone replacement in hypogondal men produced some
similar results, along with some additional information that allows me to apply
my theory of sleep and produce an explanation of the connection of testosterone
and sleep apneas.
"Obstructive sleep apnoea developed in one man and markedly worsened in another
man in association with testosterone administration. Both of these subjects also
exhibited marked decreases in oxygen saturation with the development of cardiac
dysrhythmias during sleep and large increases in haematocrit. The remaining
three hypogonadal men did not demonstrate significant sleep apnoea either on or
off testosterone. The percentage of sleep time spent in REM sleep increased from
14 +/- 3% to 22 +/- 2% when the men were receiving testosterone (P less than
0.01), but the episodes of sleep apnoea tended to occur during non-REM sleep. We
conclude that in some hypogonadal men, replacement dosages of testosterone may
affect ventilatory drives and induce or worsen obstructive sleep apnoea. The
obstructive sleep apnoea syndrome is a potential complication of testosterone
therapy." (Clinical Endocrinology 1985; 22: 713)
Testosterone appears to produce apneas due to collapse of the airway and apneas
that occur without collapse of the airway. I developed a theory of sleep that
may explain this apparent paradox. (For full detail, I invite you to read my
theory of sleep on the web.) It is my hypothesis that the hormone,
dehydroepiandrosterone (DHEA), is necessary for activation of the nervous
system. This has allowed me to produce a theory of sudden infant death syndrome
(SIDS), based on too little DHEA during sleep to maintain functions of the
brainstem. When I was working on my theory of SIDS, it became quite apparent
that infants who produce too much testosterone are more prone to SIDS. This has
allowed me to explain the connection of testosterone with apneas in men.
My theory suggests that all genes use DHEA to function. Testosterone causes the
genes of "testosterone target tissues" to absorb extra DHEA for their functions.
For example, this is why men have larger, more powerful muscles than women. So,
the increased testosterone of men reduces the availability of DHEA, therefore, I
suggest sleep apneas occur more in men because of reduced availability of DHEA
for proper nervous stimulation. According to my theory of DHEA function, all
tissues compete for DHEA. Therefore, in a man of low DHEA, administering
testosterone as in the report above, will cause some tissues to absorb extra
DHEA and reduce already low DHEA. This may cause either the nervous stimulation
of the airways to decline, resulting in a collapsed airway, or it may reduce the
DHEA so low that the brainstem ceases to function momentarily, as in SIDS. This
situation would produce the apnea in which the airways do not collapse. Of
course, the brainstem malfunction and airway collapse could occur
simultaneously. This could explain the variability of effects of administration
of testosterone in the quotation, above. Some of the men may be hypogonadal
because of a poorly functioning pituitary-adrenal-gonadal axis, caused by low
DHEA with low testosterone as a secondary consequence. Some of the men may have
simply not produced much testosterone along with ample amounts of DHEA. This
second group would represent those individuals in whom testosterone
administration had no effect on sleep at all.
I have suggested that testosterone stimulates testosterone target tissues, which
absorb extra DHEA. This effect should stimulate some increase in the production
of DHEA. In my theory of sleep, I suggest that REM sleep is a time when the low
levels of DHEA of night increase slightly to maintain brainstem function.
(Please read my theory of sleep in detail.) This means that testosterone
administration during sleep should increase REM sleep; this in fact is reported
in the quotation above. I have suggested that DHEA is necessary for nervous
system function, so I would expect apneas, caused by too low DHEA, to occur
during non-REM sleep, which is a time of the lowest levels of DHEA, according to
my theory of sleep and SIDS. This is reported above: "...but the episodes of
sleep apnoea tended to occur during non-REM sleep."
I suggest the reason men exhibit more sleep apneas than women, and why
testosterone administration in some individuals induces sleep apneas, is due to
abnormally low DHEA during sleep. This low DHEA can manifest itself as lack of
nervous support of the muscles of the airway, lack of support of brainstem
function, or a combination of both.
Added in Support of Above
Mayo. Clin. Proc. 1998 Mar; 73(3): 246-8
"Obstructive sleep apnea due to endogenous testosterone production in a woman"
Dexter DD, Dovre EJ
Department of Neurology, Midelfort Clinic, Eau Claire, Wisconsin 54701, USA.
"Obstructive sleep apnea (OSA) is a common condition characterized by snoring,
recurrent episodes of cessation of breathing (obstructive apneas), disrupted
sleep, and excessive daytime somnolence. Associated serious complications are
hypertension, increased risk of heart disease, stroke, and increased
susceptibility to industrial and motor vehicle accidents. OSA is considerably
more common in men than in women. In postmenopausal women, the incidence of OSA
increases. These factors suggest that reproductive hormones have a role in the
cause of OSA. Treatment with testosterone has been reported to cause OSA in men,
and exogenous androgen administration has been reported to cause OSA in one
woman. In a review of the English literature, we found no previous reports of
OSA that was induced by endogenous testosterone in women. Herein we describe a
nonobese 70-year old woman with clinically significant OSA and a benign
testosterone-producing ovarian tumor. After successful removal of the tumor, her
OSA resolved, and her testosterone level normalized. This unique case supports
the theory of male hormonal (testosterone) influence in the OSA syndrome.
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