©ALL CONTENT OF THIS WEBSITE IS COPYRIGHTED AND CANNOT BE REPRODUCED WITHOUT THE ADMINISTRATORS CONSENT 2002-2024
.gif "IP Gear")
Who's got Sleep Apnea
- Thread starter GoneForever
- Start date
- Joined
- Apr 4, 2003
- Messages
- 1,948
I have it. I would venture you have no more drastic health problem in your life than this and this one is life threatening. I think it contribute to my heart failure in a big way. Wear the mask, get the machine, change your life.
If you are older or married certainly you have the maturity to deal with how others view the machine. If you are a young "player" you can pass it off as part of your "cyborg" bodybuilder training. You don't look like other humans and your require forced oxygen to support your physique.
If you are older or married certainly you have the maturity to deal with how others view the machine. If you are a young "player" you can pass it off as part of your "cyborg" bodybuilder training. You don't look like other humans and your require forced oxygen to support your physique.
- Joined
- Feb 13, 2004
- Messages
- 4,373
I have obstructive sleep apnea and have slept with a CPAP for a year now.
The only way to tell is if you get a sleep study done-you can't diagnose it yourself.
Weight can be a factor as well but NOT always I got a sleep study done in 2001 @310 and they told me it was very mild, and to sleep more on my side. It really suprised me since I also was told years ago I had a sightly deviated septum and allergies. Perhaps getting my tonsils out years before that helped.
Surgery WOULD not be an option for me as whenI got my tonsills taken out I was out for a month ...I can't imagine them going in and shaving and freezing off tissue now..
Lots of risks associated with it and for the guys that juice and bulk on here who already are stessing their CV systems etc, Apnea is like a time bomb...
Sleep apnea is characterized by
snoring,
daytime sleepiness,
repeated interruptions (partial or complete) of breathing during sleep
arousal from sleep
possibly morning headaches
Long-term sufferers may experience symptoms of
fatigue,
mood swings,
obesity,
low sex drive and
poor concentration.
high blood pressure
increased risk of heart attack
and stroke
diabetes
insulin resistance.
The exact association of diabetes and insulin resistance with sleep apnea has not yet been determined, but it may be related to an elevation of stress hormones while sleeping, associated with the disrupted air flow.
Individuals who snore or have sleep apnea may be unaware of their condition. They may deny or minimize their sleep-disordered breathing because of embarrassment.
get help now if you have it...it has killed many and wrecked the health of 100's of thousands as well.
The only way to tell is if you get a sleep study done-you can't diagnose it yourself.
Weight can be a factor as well but NOT always I got a sleep study done in 2001 @310 and they told me it was very mild, and to sleep more on my side. It really suprised me since I also was told years ago I had a sightly deviated septum and allergies. Perhaps getting my tonsils out years before that helped.
Surgery WOULD not be an option for me as whenI got my tonsills taken out I was out for a month ...I can't imagine them going in and shaving and freezing off tissue now..
Lots of risks associated with it and for the guys that juice and bulk on here who already are stessing their CV systems etc, Apnea is like a time bomb...
Sleep apnea is characterized by
snoring,
daytime sleepiness,
repeated interruptions (partial or complete) of breathing during sleep
arousal from sleep
possibly morning headaches
Long-term sufferers may experience symptoms of
fatigue,
mood swings,
obesity,
low sex drive and
poor concentration.
high blood pressure
increased risk of heart attack
and stroke
diabetes
insulin resistance.
The exact association of diabetes and insulin resistance with sleep apnea has not yet been determined, but it may be related to an elevation of stress hormones while sleeping, associated with the disrupted air flow.
Individuals who snore or have sleep apnea may be unaware of their condition. They may deny or minimize their sleep-disordered breathing because of embarrassment.
get help now if you have it...it has killed many and wrecked the health of 100's of thousands as well.
There's a new (er) technique where they put this little carbon fiber(type) rods in under the skin in the roof of your mouth. Somehow this keeps the airway open by making the soft tissue in your mouth more rigid. It looks pretty good... No downtime, relatively cheap, effective, etc. Anyone try this?
- Joined
- Sep 25, 2002
- Messages
- 5,878
Obstructive Sleep Apnea
Implications for Cardiac and Vascular Disease
Abu S. M. Shamsuzzaman, MBBS, PhD; Bernard J. Gersh, MBChB, DPhil; Virend K. Somers, MD, DPhil
JAMA. 2003;290:1906-1914.
Context Obstructive sleep apnea (OSA) has been increasingly implicated in the initiation and progression of cardiovascular diseases.
Objective To systematically review the interactions of OSA with cardiovascular pathophysiology and diseases.
Data Sources and Study Selection The MEDLINE database from January 1966 to March 2003 was searched using the Medical Subject Headings sleep, sleep apnea, obesity, hypertension, heart failure, cardiac arrhythmia, coronary artery disease, stroke, sympathetic activity, endothelium, inflammation, and continuous positive airway pressure (CPAP) to identify peer-reviewed studies of OSA. Priority was given to large prospective cohort studies and to randomized controlled trials.
Data Extraction We identified 154 original investigations and reviews of sleep-related breathing disorders. Data from these studies were examined for relevance and extracted by one of the authors.
Data Synthesis Approximately 1 in 5 adults has at least mild OSA (apnea-hypopnea index [ie, the number of apneic and hypopneic events per hour], 5-15), and 1 in 15 adults has at least moderate OSA (apnea-hypopnea index, 15-30). Repetitive apneic events disrupt the normal physiologic interactions between sleep and the cardiovascular system. Such sleep fragmentation, as well as abnormalities evident in patients with OSA (eg, increased sympathetic activation, vascular endothelial dysfunction, increased oxidative stress, inflammation, increased platelet aggregability, metabolic dysregulation), may be implicated in the initiation and progression of cardiac and vascular disease. Persuasive data implicate OSA in the development of hypertension, and OSA also may contribute to cardiac ischemia, congestive heart failure, cardiac arrhythmias, and perhaps also to cerebrovascular disease and stroke.
Conclusions Obstructive sleep apnea is common, readily diagnosed, and usually treatable. It frequently coexists undiagnosed in patients with cardiovascular disease, activates disease mechanisms known to elicit cardiac and vascular damage, and may be implicated in progression of cardiovascular disease and resistance to conventional therapeutic strategies. In the absence of definitive evidence from large-scale trials and a better understanding of potential cost-effectiveness, the likely benefits of diagnosis and treatment of OSA are presently best appraised on an individualized patient basis..
- Joined
- Sep 25, 2002
- Messages
- 5,878
Upper Airway Myopathy is Important in the Pathophysiology of Obstructive Sleep Apnea
R. John Kimoff, M.D.
Respiratory Division and Sleep Laboratory, McGill University Health Centre and Meakins-Christie Laboratories, McGill University, Montreal, Canada
Address correspondence to: Dr J. Kimoff, Respiratory Division, Room L4.08, McGill University Health Centre, 687 Pine Ave. W, Montreal, Quebec, Canada, H3A 1A1, Phone: (514) 934-1934, Ext: 36117, Fax: (514) 843-1695, Email: [email protected]
Received October 2007; Accepted October 2007.
Top
REFERENCES
In this article, the term “myopathy” will encompass any process which adversely impacts on upper airway muscle force generation and resultant tissue displacement. Key evidence which supports a role for upper airway myopathy in the pathophysiology of OSA will be highlighted.
OSA is associated with changes in contractile function of upper airway dilator muscles. In order to adapt to increased contractile demands, skeletal muscle fiber phenotype can undergo modification from a shift from oxidative slow-twitch, fatigue resistant Type I, to glycolytic fast-twitch Type II fibers, which generate increased force but are more prone to fatigue. Several groups have evaluated upper airway muscle histological, biochemical and in vitro contractile properties in OSA. Series et al 1–3 studied musculus uvulae and found an increased proportion of fast-twitch type IIa fibers along with augmented levels of enzymes associated with anaerobic metabolism in OSA patients vs. snorers1. An increase in type IIa fiber prevalence was also found in the genioglossus muscle of OSA patients2. Contractile characteristics of musculus uvulae but not genioglossus were studied in vitro1–3. Force generation was slightly higher for musculus uvulae in OSA than control1,3 but muscle fatigability showed a nonsignificant tendency to be greater in OSA patients1. Smirne et al4 also reported a type IIa fiber shift. Carrera et al5,6 studied the characteristics of genioglossus in OSA patients vs controls and reported a type II fiber shift, and showed preserved tetanic force generation, but in nonobese OSA patients, clearly increased muscle fatigability.
Changes similar to those in humans have been reported in animal models. Petrof et al7 reported Type II fiber shifts in the sternohyoid and geniohyoid muscles in the English bulldog, a spontaneous model of OSA. In the rat, both short- and longer-term intermittent hypoxia8,9 have been reported to produce type II fiber shifts, preserved contractility, but increased fatigability of geniohyoid and sternohyoid muscles.
Thus a theme emerges that upper airway muscle loading and/or hypoxia in OSA leads to shifts to fast-twitch but more fatigue-prone fiber types, and that in vitro muscle contractility is preserved or even slightly increased but at the cost of increased fatigability, i.e. a reduced ability to sustain force generation with repeated stimulation. While these changes likely represent an adaptive response to increased upper airway loading,10 there is a high likelihood that in vivo, the increased susceptibility to fatigue could lead to a progressive loss of force generation, muscle shortening and tissue displacement by upper airway dilators during the repeated high-level activation required to restore airway patency7,10. Indeed, in vivo changes in muscle function with recurrent apneas could be a contributing factor to the progression of OSA severity across the night that we have previously reported11,12.
There is evidence for dysfunctional mechanical coupling of upper airway muscles in OSA, which attenuates the tissue displacement resulting from dilator muscle contraction. In an important study, Series and colleagues3 measured the elastance of uvular tissue (which incorporated the musculus uvulae). They found that uvular elastance was increased in OSA patients, such that the degree of shortening of intact uvular tissue specimens for a given force of stimulated muscle contraction was significantly less than for nonapneic controls. They subsequently dissected out the musculus uvulae and demonstrated that muscle force generation per se was again slightly greater for OSA than control1,3. Thus even if the force generating capacity of the upper airway dilator muscles is preserved, the effects of muscle activation on tissue displacement in OSA are significantly reduced, likely due to connective tissue alterations3. This would therefore be expected to attenuate the effects on upper airway patency of dilator muscle activation.
There is strong evidence for upper airway dilator muscle denervation in OSA patients, which would impair muscle contractile function in vivo. We have described an oropharyngeal sensory impairment in OSA13–15 which has been confirmed by others16,17 and which is partially reversible with CPAP13. We have also identified a similar impairment at the laryngeal level which correlates with OSA severity.14,15 Woodson et al18 described nerve demyelination in upper airway tissue, and Friberg et al19 reported changes in upper airway mucosal nerve endings consistent with a pattern of injury and repair. These findings support the presence of an upper airway sensory neuropathy in OSA, which is proposed to be due to mechanical trauma associated with snoring and apneas (vibration, tissue traction, etc.) during obstructive events, oxidative stress related to hypoxia-reoxygenation, and inflammation related to both of these factors.13–15,20–22
There is every reason to believe that this neuropathic process would not be isolated to sensory nerves, but would also affect motor nerves, and thereby lead to muscle denervation. Indeed, there is growing morphologic and physiologic evidence for upper airway muscle denervation in OSA. Immunohistochemical studies from several groups have demonstrated classic findings of muscle denervation including characteristic fiber type grouping, grouped atrophy, and increased fiber size variability (fiber atrophy and hypertrophy),20,23–25 particularly in palatal muscle specimens obtained from OSA patients as compared with control. Our laboratory has provided further immunohistochemical evidence for ongoing, active denervation in OSA palatal muscle in that we identified increased expression of Neural Cell Adhesion Molecule, a subsarcolemmal protein which is transiently expressed in denervated muscle cells.21 There is also physiologic evidence for upper airway muscle denervation in OSA. Svanborg has described a high prevalence of characteristic denervation potentials in palatal muscles of OSA patients.20 More recently, an increase has been observed in OSA patients vs. controls in the area and duration of single motor unit action potentials recorded in genioglossus during quiet breathing (Gandevia, Saboisky, and colleagues, unpublished observations). These findings are characteristic for denervation. There is therefore compelling morphologic and physiologic evidence for denervation changes in key upper airway dilator muscles in OSA.
The issue of denervation myopathy is of considerable potential importance with respect to in vivo upper airway contractile function. The in vitro human studies of Series et al1–3 and Carrera et al,5,6 which assessed contractility of musculus uvulae and genioglossus, did so using standard protocols of stimulation via wire electrodes of muscle strips in a bath. This approach will activate all muscle fibers, whether innervated or denervated. While electrically stimulated force generation was found to be similar in OSA and control muscle, the situation in vivo could be very different. In vivo, muscle contraction would be dependent on endogenous neurogenic activation—i.e., activation by the diseased nerves supplying the muscle rather than stimulating electrodes—which would be expected to be much less efficient in the presence of motor neuropathy, and in particular would preclude activation of denervated muscle fibers. Thus the in vitro contractility studies referred to above cannot be taken as conclusive evidence for normal muscle force generation by upper airway dilator muscles in vivo. The observations concerning denervation myopathy, together with the evidence for increased fatigability and dysfunctional mechanical coupling of upper airway dilators discussed above, provide compelling support for the concept of impaired in vivo upper airway dilator muscle contractile function in OSA.
There is histologic evidence for other upper airway myopathic changes in OSA. Petrof et al7 reported abnormal fiber morphology (central nucleation, fissured and moth-eaten appearance), inflammatory cell infiltrates, and increased connective tissue in sternohyoid and geniohyoid in the English bulldog. These changes were attributed to muscle overuse and injury due to upper airway loading,7,10 as well as to eccentric contraction which may occur during airway occlusion.26 Findings in human tissue studies have been discrepant, with some authors reporting grossly normal muscle histology1,2,5 while others have described changes similar to those in the bulldog.18,21,24,27 These disparate findings likely stem from differences in the muscles sampled, pathologic techniques, and patient characteristics, but also suggest that the extent of myopathic change varies between individuals. However, when present, pathologic changes of the nature described are undoubtedly associated with impaired force generation.
OSA is known to occur in clinical conditions involving pharyngeal neuromuscular dysfunction. Examples of this include the high prevalence of sleep apnea reported in Charcot-Marie-Tooth disease, a condition characterized by peripheral sensory and motor neuropathy.28 OSA severity was correlated with the severity of changes in motor nerve conduction, suggesting that neurogenic upper airway myopathy may contribute to OSA. More recently, oculopharyngeal muscular dystrophy, which selectively affects the extraocular and pharyngeal muscles, was reported to be associated with OSA in the absence of obesity or abnormal upper airway morphology.29 These observations suggest that a clinically identified myopathy can be associated with upper airway collapse which occurs uniquely during sleep, resulting in OSA.
The concept of an upper airway myopathy is entirely consistent with other current data on OSA pathophysiology. A fundamental observation is that, while upper airway dimensions are reduced during wakefulness in OSA, complete upper airway closure occurs only during sleep. Upper airway muscle EMG activity is increased during wakefulness in OSA, which is interpreted as indicating increased drive to, and force generation by, upper airway dilators to compensate for reduced anatomic dimensions.30,31 When loss of waking tonic and phasic respiratory drive and attenuation of protective airway reflexes occurs at sleep onset, this is believed to result in inadequate dilator muscle compensation for reduced airway size, and complete collapse ensues.31
The concept of upper airway muscle dysfunction is entirely consistent with the other aspects of this schema. It is well established that EMG amplitude cannot necessarily be equated with muscle force generation, shortening, or tissue displacement.32,33 Changes in excitation-contraction coupling can occur such that EMG amplitude can be maintained or even increase as force generation wanes in fatiguing or myopathic muscle.32,33 Therefore, the augmented EMG activity described during wakefulness in OSA may reflect increased drive to upper airway muscles but does not necessarily indicate commensurately increased muscle force generation. Indeed, the fact that despite increased EMG activity, upper airway dimensions remain reduced during wakefulness in OSA strongly suggests inefficient muscle force generation (i.e., is consistent with myopathy).
With sleep onset, the reduction in drive to upper airway muscles could result in airway collapse, in part due to the fact that the inefficient force generation and tissue displacement by myopathic muscles are no longer adequate at the reduced level of drive to compensate for airway size and collapsibility. Through this mechanism, therefore, an upper airway myopathy could contribute to complete airway collapse, which occurs only during sleep. Consistent with this, at least one study34 indicates that in mild forms of OSA, upper airway muscle training may reduce the number of respiratory events during sleep. Thus an increase in overall muscle force generating capacity and/or endurance due to training during wakefulness may lead to a beneficial impact on preservation of upper airway patency during sleep.
In summary, there is considerable evidence pointing to altered upper airway muscle contractile function in OSA and its role in the pathophysiology of this disorder. On the basis of the arguments presented here, we believe that to fail to pursue further investigation in this area, would be to ignore an important disease mechanism and perhaps even an eventual therapeutic target in this condition.
R. John Kimoff, M.D.
Respiratory Division and Sleep Laboratory, McGill University Health Centre and Meakins-Christie Laboratories, McGill University, Montreal, Canada
Address correspondence to: Dr J. Kimoff, Respiratory Division, Room L4.08, McGill University Health Centre, 687 Pine Ave. W, Montreal, Quebec, Canada, H3A 1A1, Phone: (514) 934-1934, Ext: 36117, Fax: (514) 843-1695, Email: [email protected]
Received October 2007; Accepted October 2007.
Top
REFERENCES
In this article, the term “myopathy” will encompass any process which adversely impacts on upper airway muscle force generation and resultant tissue displacement. Key evidence which supports a role for upper airway myopathy in the pathophysiology of OSA will be highlighted.
OSA is associated with changes in contractile function of upper airway dilator muscles. In order to adapt to increased contractile demands, skeletal muscle fiber phenotype can undergo modification from a shift from oxidative slow-twitch, fatigue resistant Type I, to glycolytic fast-twitch Type II fibers, which generate increased force but are more prone to fatigue. Several groups have evaluated upper airway muscle histological, biochemical and in vitro contractile properties in OSA. Series et al 1–3 studied musculus uvulae and found an increased proportion of fast-twitch type IIa fibers along with augmented levels of enzymes associated with anaerobic metabolism in OSA patients vs. snorers1. An increase in type IIa fiber prevalence was also found in the genioglossus muscle of OSA patients2. Contractile characteristics of musculus uvulae but not genioglossus were studied in vitro1–3. Force generation was slightly higher for musculus uvulae in OSA than control1,3 but muscle fatigability showed a nonsignificant tendency to be greater in OSA patients1. Smirne et al4 also reported a type IIa fiber shift. Carrera et al5,6 studied the characteristics of genioglossus in OSA patients vs controls and reported a type II fiber shift, and showed preserved tetanic force generation, but in nonobese OSA patients, clearly increased muscle fatigability.
Changes similar to those in humans have been reported in animal models. Petrof et al7 reported Type II fiber shifts in the sternohyoid and geniohyoid muscles in the English bulldog, a spontaneous model of OSA. In the rat, both short- and longer-term intermittent hypoxia8,9 have been reported to produce type II fiber shifts, preserved contractility, but increased fatigability of geniohyoid and sternohyoid muscles.
Thus a theme emerges that upper airway muscle loading and/or hypoxia in OSA leads to shifts to fast-twitch but more fatigue-prone fiber types, and that in vitro muscle contractility is preserved or even slightly increased but at the cost of increased fatigability, i.e. a reduced ability to sustain force generation with repeated stimulation. While these changes likely represent an adaptive response to increased upper airway loading,10 there is a high likelihood that in vivo, the increased susceptibility to fatigue could lead to a progressive loss of force generation, muscle shortening and tissue displacement by upper airway dilators during the repeated high-level activation required to restore airway patency7,10. Indeed, in vivo changes in muscle function with recurrent apneas could be a contributing factor to the progression of OSA severity across the night that we have previously reported11,12.
There is evidence for dysfunctional mechanical coupling of upper airway muscles in OSA, which attenuates the tissue displacement resulting from dilator muscle contraction. In an important study, Series and colleagues3 measured the elastance of uvular tissue (which incorporated the musculus uvulae). They found that uvular elastance was increased in OSA patients, such that the degree of shortening of intact uvular tissue specimens for a given force of stimulated muscle contraction was significantly less than for nonapneic controls. They subsequently dissected out the musculus uvulae and demonstrated that muscle force generation per se was again slightly greater for OSA than control1,3. Thus even if the force generating capacity of the upper airway dilator muscles is preserved, the effects of muscle activation on tissue displacement in OSA are significantly reduced, likely due to connective tissue alterations3. This would therefore be expected to attenuate the effects on upper airway patency of dilator muscle activation.
There is strong evidence for upper airway dilator muscle denervation in OSA patients, which would impair muscle contractile function in vivo. We have described an oropharyngeal sensory impairment in OSA13–15 which has been confirmed by others16,17 and which is partially reversible with CPAP13. We have also identified a similar impairment at the laryngeal level which correlates with OSA severity.14,15 Woodson et al18 described nerve demyelination in upper airway tissue, and Friberg et al19 reported changes in upper airway mucosal nerve endings consistent with a pattern of injury and repair. These findings support the presence of an upper airway sensory neuropathy in OSA, which is proposed to be due to mechanical trauma associated with snoring and apneas (vibration, tissue traction, etc.) during obstructive events, oxidative stress related to hypoxia-reoxygenation, and inflammation related to both of these factors.13–15,20–22
There is every reason to believe that this neuropathic process would not be isolated to sensory nerves, but would also affect motor nerves, and thereby lead to muscle denervation. Indeed, there is growing morphologic and physiologic evidence for upper airway muscle denervation in OSA. Immunohistochemical studies from several groups have demonstrated classic findings of muscle denervation including characteristic fiber type grouping, grouped atrophy, and increased fiber size variability (fiber atrophy and hypertrophy),20,23–25 particularly in palatal muscle specimens obtained from OSA patients as compared with control. Our laboratory has provided further immunohistochemical evidence for ongoing, active denervation in OSA palatal muscle in that we identified increased expression of Neural Cell Adhesion Molecule, a subsarcolemmal protein which is transiently expressed in denervated muscle cells.21 There is also physiologic evidence for upper airway muscle denervation in OSA. Svanborg has described a high prevalence of characteristic denervation potentials in palatal muscles of OSA patients.20 More recently, an increase has been observed in OSA patients vs. controls in the area and duration of single motor unit action potentials recorded in genioglossus during quiet breathing (Gandevia, Saboisky, and colleagues, unpublished observations). These findings are characteristic for denervation. There is therefore compelling morphologic and physiologic evidence for denervation changes in key upper airway dilator muscles in OSA.
The issue of denervation myopathy is of considerable potential importance with respect to in vivo upper airway contractile function. The in vitro human studies of Series et al1–3 and Carrera et al,5,6 which assessed contractility of musculus uvulae and genioglossus, did so using standard protocols of stimulation via wire electrodes of muscle strips in a bath. This approach will activate all muscle fibers, whether innervated or denervated. While electrically stimulated force generation was found to be similar in OSA and control muscle, the situation in vivo could be very different. In vivo, muscle contraction would be dependent on endogenous neurogenic activation—i.e., activation by the diseased nerves supplying the muscle rather than stimulating electrodes—which would be expected to be much less efficient in the presence of motor neuropathy, and in particular would preclude activation of denervated muscle fibers. Thus the in vitro contractility studies referred to above cannot be taken as conclusive evidence for normal muscle force generation by upper airway dilator muscles in vivo. The observations concerning denervation myopathy, together with the evidence for increased fatigability and dysfunctional mechanical coupling of upper airway dilators discussed above, provide compelling support for the concept of impaired in vivo upper airway dilator muscle contractile function in OSA.
There is histologic evidence for other upper airway myopathic changes in OSA. Petrof et al7 reported abnormal fiber morphology (central nucleation, fissured and moth-eaten appearance), inflammatory cell infiltrates, and increased connective tissue in sternohyoid and geniohyoid in the English bulldog. These changes were attributed to muscle overuse and injury due to upper airway loading,7,10 as well as to eccentric contraction which may occur during airway occlusion.26 Findings in human tissue studies have been discrepant, with some authors reporting grossly normal muscle histology1,2,5 while others have described changes similar to those in the bulldog.18,21,24,27 These disparate findings likely stem from differences in the muscles sampled, pathologic techniques, and patient characteristics, but also suggest that the extent of myopathic change varies between individuals. However, when present, pathologic changes of the nature described are undoubtedly associated with impaired force generation.
OSA is known to occur in clinical conditions involving pharyngeal neuromuscular dysfunction. Examples of this include the high prevalence of sleep apnea reported in Charcot-Marie-Tooth disease, a condition characterized by peripheral sensory and motor neuropathy.28 OSA severity was correlated with the severity of changes in motor nerve conduction, suggesting that neurogenic upper airway myopathy may contribute to OSA. More recently, oculopharyngeal muscular dystrophy, which selectively affects the extraocular and pharyngeal muscles, was reported to be associated with OSA in the absence of obesity or abnormal upper airway morphology.29 These observations suggest that a clinically identified myopathy can be associated with upper airway collapse which occurs uniquely during sleep, resulting in OSA.
The concept of an upper airway myopathy is entirely consistent with other current data on OSA pathophysiology. A fundamental observation is that, while upper airway dimensions are reduced during wakefulness in OSA, complete upper airway closure occurs only during sleep. Upper airway muscle EMG activity is increased during wakefulness in OSA, which is interpreted as indicating increased drive to, and force generation by, upper airway dilators to compensate for reduced anatomic dimensions.30,31 When loss of waking tonic and phasic respiratory drive and attenuation of protective airway reflexes occurs at sleep onset, this is believed to result in inadequate dilator muscle compensation for reduced airway size, and complete collapse ensues.31
The concept of upper airway muscle dysfunction is entirely consistent with the other aspects of this schema. It is well established that EMG amplitude cannot necessarily be equated with muscle force generation, shortening, or tissue displacement.32,33 Changes in excitation-contraction coupling can occur such that EMG amplitude can be maintained or even increase as force generation wanes in fatiguing or myopathic muscle.32,33 Therefore, the augmented EMG activity described during wakefulness in OSA may reflect increased drive to upper airway muscles but does not necessarily indicate commensurately increased muscle force generation. Indeed, the fact that despite increased EMG activity, upper airway dimensions remain reduced during wakefulness in OSA strongly suggests inefficient muscle force generation (i.e., is consistent with myopathy).
With sleep onset, the reduction in drive to upper airway muscles could result in airway collapse, in part due to the fact that the inefficient force generation and tissue displacement by myopathic muscles are no longer adequate at the reduced level of drive to compensate for airway size and collapsibility. Through this mechanism, therefore, an upper airway myopathy could contribute to complete airway collapse, which occurs only during sleep. Consistent with this, at least one study34 indicates that in mild forms of OSA, upper airway muscle training may reduce the number of respiratory events during sleep. Thus an increase in overall muscle force generating capacity and/or endurance due to training during wakefulness may lead to a beneficial impact on preservation of upper airway patency during sleep.
In summary, there is considerable evidence pointing to altered upper airway muscle contractile function in OSA and its role in the pathophysiology of this disorder. On the basis of the arguments presented here, we believe that to fail to pursue further investigation in this area, would be to ignore an important disease mechanism and perhaps even an eventual therapeutic target in this condition.
Last edited:
- Joined
- Sep 25, 2002
- Messages
- 5,878
Physiological basis for a causal relationship of obstructive sleep apnea to hypertension.
WEISS JW, LIU Y, HUANG J.
Exp Physiol 2006 Nov 23;[epub ahead of print].
Beth Israel Deaconess Medical Center
Abstract:
Obstructive sleep apnea (OSA) is causally related to systemic hypertension through sustained sympathoexcitation. The causes of this sympathoexcitation remain uncertain, however, substantial animal and human data suggest cyclic intermittent hypoxia (CIH), as is experienced at night by patients with OSA provides the causal link between upper airway obstruction during sleep and sympathetic activation during waking. Direct and indirect evidence indicates that CIH leads to sympathoexcitation by two mechanisms: 1) augmentation of peripheral chemoreflex sensitivity (hypoxic acclimatization); and, 2) by direct effects on sites of central sympathetic regulation such as the subfornical organ and the paraventricular nucleus of the hypothalamus. Initial reports suggest that the molecular mechanisms influencing peripheral chemoreflex sensitivity and central sympathetic gain may be the same, involving such neuromodulators as angiotensin II, endothelin, and nitric oxide.
WEISS JW, LIU Y, HUANG J.
Exp Physiol 2006 Nov 23;[epub ahead of print].
Beth Israel Deaconess Medical Center
Abstract:
Obstructive sleep apnea (OSA) is causally related to systemic hypertension through sustained sympathoexcitation. The causes of this sympathoexcitation remain uncertain, however, substantial animal and human data suggest cyclic intermittent hypoxia (CIH), as is experienced at night by patients with OSA provides the causal link between upper airway obstruction during sleep and sympathetic activation during waking. Direct and indirect evidence indicates that CIH leads to sympathoexcitation by two mechanisms: 1) augmentation of peripheral chemoreflex sensitivity (hypoxic acclimatization); and, 2) by direct effects on sites of central sympathetic regulation such as the subfornical organ and the paraventricular nucleus of the hypothalamus. Initial reports suggest that the molecular mechanisms influencing peripheral chemoreflex sensitivity and central sympathetic gain may be the same, involving such neuromodulators as angiotensin II, endothelin, and nitric oxide.
- Joined
- Feb 22, 2006
- Messages
- 194
I have it and have for years, have had the bipap and Cpap machines from Resperonics...have done so much for me. Everything to obviously sleeping better, attitude, lost weight, more energy just a better life.
GoneForever
Banned
- Joined
- Jan 1, 1970
- Messages
- 4
well maybe I dont have it. When I was 260lbs I would wake up more frequently gasping and stuff. Im now 235lbs and leaner and it hardly happens as much. Its def linked with my weight. I say I wake up about 2x per night that I can remember. Maybe 3. I go in monday the 20th so I guess they will have to diagnose to see if its really what I have.
On a side note, my father is a dentist, i wonder if he can make everything I need.
On a side note, my father is a dentist, i wonder if he can make everything I need.
- Joined
- Apr 16, 2007
- Messages
- 521
It is called the Pillar procedure and yes I have had it done. It actually worked very well for me. I have not had a sleep study done since I had the procedure but my snoring has been significantly reduced and I sleep much better. If I remember correctly it cost me $1500 for the procedure. It can be done in one office visit and is done under local anesthetic. It worked very well for me so I would recommend it.
You can also use this in conjunction with a mouthpiece. I tried one of the do it yourself mouthpieces and it eliminated all snoring. The mouthpiece was not very good though so I stopped using it. I want to have one made by a professional though because it definitely helped even more then just the Pillar procedure.
- Joined
- Oct 6, 2008
- Messages
- 39
Diesal Right ON !!
Diesal is so right !
I have sleep apnea an had no idea until my now ex wife told me I stopped breathing all night.
Got tested they said I woke up about 100 X's a night and never went past level 2 sleep let alone REM.
Started with CPAP now use Bi-Level machine BiPap by resperonics.
Love IT !!!
Diesal is so right !
I have sleep apnea an had no idea until my now ex wife told me I stopped breathing all night.
Got tested they said I woke up about 100 X's a night and never went past level 2 sleep let alone REM.
Started with CPAP now use Bi-Level machine BiPap by resperonics.
Love IT !!!
- Joined
- Jul 21, 2002
- Messages
- 11,810
Ive not been diagnosed 100% for sure but my doctor is almost certain. I have no such time for a sleep study,,,so I wont know for sure for awhile.
I hear the CPAP machines can make a great difference on how you sleep and feel if you do indeed have sleep apnea.
- Joined
- Sep 25, 2002
- Messages
- 5,878
This what I'm trying to do, but can't stay asleep with the CPAP. I'm around 265-270 and want to desperately get down to below 220. I started hitting gym hard and finally able to do cardio body is changing, weight is not.
Had bodyfat measured etc. and even if I get below 10% bodyfat I will still be 220.
Get a CPAP. When you look at the thing, you think holly shit how can I sleep with that? Within a week I was where I forgot I had it on about 3 minutes after I put it on and turned off the light. Helped my wife and our relationship(not to mention sex life) too. I snored so bad before I got the CPAP she couldn't sleep, and was always poking me in the ribs in the middle of the night. My apnea (and snoring) didn't really get bad until last few years. That surgery sounds godawful - my doc says it is an option, but doesn't always work. CPAP is the way t go! Keep trying Dragonfire - I have a couple of buddies who have them also, and one had to keep at it for awhile before he got used to it. I think this is a much more common problem (mostly with guys) then people realize. And if you are big, like a lot of us on this board, that can make a difference, but I thought it was more due to BF than muscle. Most everybody on here is big because that have muscle, not BF.
(Got to say I joined the Army at 17 - many moons ago. Was an Army grunt, ended up on a recon team - luckily I didn't snore or have the apnea then. Can't imagine the shit the other guys would have done to me, and of course damned sure couldn't be on a LRP team if you snore (not that we ever slept much in the bush anyway!).
(Got to say I joined the Army at 17 - many moons ago. Was an Army grunt, ended up on a recon team - luckily I didn't snore or have the apnea then. Can't imagine the shit the other guys would have done to me, and of course damned sure couldn't be on a LRP team if you snore (not that we ever slept much in the bush anyway!).
- Joined
- Sep 25, 2002
- Messages
- 5,878
New studies show its not just people who gain fat, but who are large in general and also that it may have to do with upper airway myopathy, see above studies and article.
I have had my machine for at least 3 years and have all types of mask. I still try every weekend to give a could go. If I do in middle of week I won't sleep at all and have work. My sleep studies show sleeping on my side or stomach improve my breathing by about 25%, which is an improvement, but still bad in my case.
- Joined
- Jul 25, 2008
- Messages
- 1,700
This what I'm trying to do, but can't stay asleep with the CPAP. I'm around 265-270 and want to desperately get down to below 220. I started hitting gym hard and finally able to do cardio body is changing, weight is not.
Had bodyfat measured etc. and even if I get below 10% bodyfat I will still be 220.
GHRP-6 & CJC will put you in a coma sleep. GHRP-6 by itself as well.
Put that CPAP on w/ those peps in your system and you will increase slow wave sleep. You will be more rested and you will learn or program yourself to sleep w/ the CPAP.
If you really want to get to 220 you need to think of Vince Gironda & Steve Reeves. Reeves is your new body shape model and Vince Gironda's preaching proportions and sleeker legs, less weight on the diaphragm & smaller neck.
No studies including the one's you cut-and-pasted show that being "large in general" is associated with greater risk of OSA. Where in the abstracts of the studies you posted does it make any reference to fat-free mass?
Upper airway myopathy (i.e. muscle disease not attributable to nerve disease) has been implicated in OSA as have a narrow airway and a mishaped airway but there are no studies that indicate that people with a high BMI that aren't fat have a greater risk of OSA.
So point us to this study.
Similar threads
Members online
- JJT
- DIRECT
- aHarness
- URODA
- grammo13
- Khazad
- Durro
- Onidus
- luki7788
- SABAGOY
- kilsong
- Nicky_Slim24
- Musclebound94
- Linc0ln
- angus62
- Zokim
- Drax
- btails
- mexicanhombre
- Js118
- Bigtwinjc
- Hulk69
- Vmv004
- willie02
- seventhlttd
- Kirbynator
- squatster
- traininsane11
- blackjack
- Gunsmith
- Therealjakejawo
- DetroitDawg
- phani
- pesty4077
- rAJJIN
- Biohazard
- Klime
- Palifter
- hevi-head
- Brahma
- lawman
- qbkilla
- Ranchhand
- GenericAsia
- SAVAGEPMHNP
- whollopa
- slesh
- Blueballs
- COASTAL
- xyz14
Forum statistics
