Now that I have gone back to powerlifting and approaching it from low rep, high weight standpoint, I have noticed an effect on my sleep on days that I lift heavy.
I work out in the afternoon-early evening and I am usually plenty tired by 10PM or so and fall asleep easily. However, I wake up frequently through the night, every couple of hours, sometimes feeling as though it must be morning even though its the middle of the night.
What's the cause of this and how do I counter it? I've tried high dose ascorbic acid, tryptophan, melatonin, valerian, etc. to no avail. The only thing I have found to work consistently is 12.5mg of doxylamine but I suspect this is as much a sleep architecture rapist as diphenhydramine so I don't see this as a viable solution long term.
Full Version: Heavy Lifting...
No idea as to the questions raised but I do know that trazadone increases REM sleep.That said, the systematic rape and pillaging of sleep architecture most sleep inducers sport is absent,for the most part.
The hangover from traz however,really just sucks.I've staved it off via nootropics and caffiene upon waking to some degree.Frangible's post indicating that St-John's Wort,taken in the morning only,fully knocks out the hangover (something to do with 5HT) is dead on the money.
The hangover from traz however,really just sucks.I've staved it off via nootropics and caffiene upon waking to some degree.Frangible's post indicating that St-John's Wort,taken in the morning only,fully knocks out the hangover (something to do with 5HT) is dead on the money.
QUOTE(Colin @ Dec 19 2007, 05:29 PM) [snapback]443716[/snapback]
That said, the systematic rape and pillaging I do really helps me rest well as soon as my head hits the pillow!!
Fixed.
Heh. I used to use and recommend diphenhydramine but I gave it up years ago. Out of curiousity what does it do to sleep?
Well clearly you're putting a lot of demands on your body with that style lifting...perhaps taxing the nervous system would be the way to look at it.
1. Anything come to mind TCM wise e.g. herbs that you could take to calm the nervous system, restore things.
2. Look up my second article and try the great restorer advanced version for 10 or better yet 20 minutes sometime before bed--I know you've secretly been dieing to try yoga ;-)
Well clearly you're putting a lot of demands on your body with that style lifting...perhaps taxing the nervous system would be the way to look at it.
1. Anything come to mind TCM wise e.g. herbs that you could take to calm the nervous system, restore things.
2. Look up my second article and try the great restorer advanced version for 10 or better yet 20 minutes sometime before bed--I know you've secretly been dieing to try yoga ;-)
When I read this title, I thought of heavy_lifter and it was a log.
Benson I too have problems with sleep when I bust out a heavy workout. In terms of supplemental assistance I have not found the key. I have had too many variables placed upon me to make a suggestion. All I find it that the harder I do workout, the worse it is. After a hard one I don't actually feel really tired as I doze of and sort of have to force myself to sleep, I wake up periodically during the night, and when I do wake up I am not tired. I however, know I should go back to sleep and do, but I feel burnt out the next day, as if the sleep did not revitalise me as it should.
Recently, I have developed a lingering cold which really did not grasp me hard, just gave me sore soft palate, and need to clear sinuses. I am not training at all, but I have a problem where I wake up too early and not able to get back to sleep.
Benson I too have problems with sleep when I bust out a heavy workout. In terms of supplemental assistance I have not found the key. I have had too many variables placed upon me to make a suggestion. All I find it that the harder I do workout, the worse it is. After a hard one I don't actually feel really tired as I doze of and sort of have to force myself to sleep, I wake up periodically during the night, and when I do wake up I am not tired. I however, know I should go back to sleep and do, but I feel burnt out the next day, as if the sleep did not revitalise me as it should.
Recently, I have developed a lingering cold which really did not grasp me hard, just gave me sore soft palate, and need to clear sinuses. I am not training at all, but I have a problem where I wake up too early and not able to get back to sleep.
QUOTE(ScottL @ Dec 19 2007, 09:04 PM) [snapback]443719[/snapback]
Heh. I used to use and recommend diphenhydramine but I gave it up years ago. Out of curiousity what does it do to sleep?
Apparently cuts into REM sleep time and changes the amount of time you spend in various stages of sleep.
QUOTE
1. Anything come to mind TCM wise e.g. herbs that you could take to calm the nervous system, restore things.
There are herbal sedatives...jujubee is commonly used. MRM Relax-All, which is good stuff and combines jujubee with phenibut does nothing for this.
QUOTE
2. Look up my second article and try the great restorer advanced version for 10 or better yet 20 minutes sometime before bed--I know you've secretly been dieing to try yoga ;-)
I'll give it a look...again though, I don't have trouble falling asleep, just remaining asleep...I don't even have trouble falling back asleep when I wake up but its still annoying.
I'm going to assume that you already considered this and for whatever reason cant do it, but it doesn't hurt to check.. could you just do the lifting in the morning?
QUOTE(geigertube @ Dec 19 2007, 10:18 PM) [snapback]443733[/snapback]
I'm going to assume that you already considered this and for whatever reason cant do it, but it doesn't hurt to check.. could you just do the lifting in the morning?
Doesn't fit my schedule well...and, when I have lifted in the AM, on the weekends for example, I feel noticiably weaker.
I think it's hormone related...anyone else think that's true? Benson and I were discussing this last night, I guess right before he posted it, but I think it's probably the same reason you don't have DBol, TBol, Winny, anavar and such right before bed...messes up your sleep...any thoughts on that?
Give high dose taurine a whirl. Seems to help me. Also, a semi-cold shower after training will help relax you.
Trazadone INCREASES REM sleep and the daytime residual side effects can be mitigated with a dose of St.John's Wort upon waking.
Edit:
Trazadone shown to NOT effect REM (apparently my memory was off but I was partially right via SWS) but to signifigantly improve SWS I.E. slow wave sleep.I'll dig up more and yeah,25mg(not to exceed50) is a good dose for insomnia,the studies show 50-100mg,which I'm guessing is the dose used for depression.
Another advantage traz has is its price,the generic is ridiculously cheap.
"A comparison of the effectiveness of two hypnotic agents for the treatment of insomnia".
Schwartz T, Nihalani N, Virk S, Jindal S, Costello A, Muldoon R, Azhar N, Hussein J, Tirmazi S.
SUNY Upstate Medical University, Department of Psychiatry, 750 East Adams Street, Syracuse, NY 13210, USA.
OBJECTIVE: To compare the effectiveness and tolerability of two hypnotic agents, trazadone (Desyrel) and zaleplon (Sonata) on psychiatric inpatients with insomnia. METHODS: Fifteen patients who were psychiatric inpatients were assigned openly and randomly to receive either trazodone (50-100 mg) or zaleplon (10-20 mg) doses on an "as-needed basis" and followed throughout their hospital stay. Efficacy and side effect profile were subsequently assessed. CONCLUSION: This pilot study suggests that trazodone may be a better agent to promote longer, deeper subjective quality sleep for psychiatric inpatients with insomnia in terms of effectiveness. However, tolerability was much better with zaleplon as daytime residual side effects were less.
PMID: 15468607 [PubMed - indexed for MEDLINE]
1: Ann Clin Psychiatry. 2006 Jan-Mar;18(1):49-56.Click here to read Links
Comment in:
Ann Clin Psychiatry. 2007 Jan-Mar;19(1):53-4.
Sleep maintenance insomnia: strengths and weaknesses of current pharmacologic therapies.
Rosenberg RP.
Northside Hospital Sleep Medicine Institute, Atlanta, GA, USA. rosenberg@mindspring.com
BACKGROUND: Although insomnia is highly prevalent, sleep disturbances often go unrecognized and untreated. When insomnia is recognized, considerable emphasis has been placed on improving sleep onset; however, there is growing evidence that improving sleep maintenance is an equally important treatment goal. METHODS: A MEDLINE literature search was performed using the search parameters "insomnia," "zolpidem," "zaleplon," "flurazepam," "estazolam," "quazepam," "triazolam," and "temazepam," as these agents are FDA-approved for the treatment of insomnia. Per reviewer comments, the search criteria was later expanded to include lorazepam. A literature search using the terms "trazodone" and "insomnia" was also performed, as this is the second-most commonly prescribed agent for treating insomnia. Sleep efficacy endpoints from randomized, placebo-controlled clinical trials in adult populations and key review articles published between 1975 and 2004 were included in this review. As only one randomized placebo-controlled trial evaluated trazodone use in primary insomnia, the trazodone search was expanded to include all clinical trials that evaluated trazodone use in insomnia. Relevant texts and other articles that evaluated side effect profiles of these agents were also included, one of which was published in January of 2005. In all publications, impact of treatment on sleep maintenance parameters (wake time after sleep onset, number of awakenings) and measures of next-day functioning were evaluated, in addition to sleep onset parameters (sleep latency, time to sleep onset/induction) and sleep duration data (total sleep time). RESULTS: Many of the currently available agents used to treat insomnia, including the antidepressant trazodone, the non-benzodiazepine hypnotics zolpidem and zaleplon, and some of the benzodiazepines, have not consistently demonstrated effectiveness in promoting sleep maintenance. Furthermore, the benzodiazepines with established sleep maintenance efficacy are associated with next-day sedation, the risk of tolerance and dependence, or both. CONCLUSIONS: New agents that offer relief of sleep maintenance insomnia without residual next day impairment while improving next day function are needed. Several compounds currently under development may offer clinicians a more effective and safer treatment for this common disorder.
PMID: 16517453 [PubMed - indexed for MEDLINE]
Effects of trazodone and imipramine on the biological rhythm: an analysis of sleep EEG and body core temperature.
Suzuki H, Yamadera H, Nakamura S, Endo S.
Department of Neuropsychiatry, Nippon Medical School, Japan.
Depression commonly involves abnormalities of the sleep-wake rhythm, the temperature rhythm, and other biological rhythms. The changes of these biological rhythms are caused in remission by medications. However, it has yet to be clarified whether the biological rhythms are changed as a result of recovery from depression or from the direct pharmacological effects of the antidepressants. Therefore, we have undertaken a study on the direct effects of the antidepressants trazodone and imipramine on the biological rhythms of healthy volunteers.The study involved 12 healthy male volunteers (ages 21 approximately 28 years, mean age 23.9+/-1.7 years) who had given written informed consent. Placebo, trazodone, and imipramine were each administered in a single blind manner four times a day, during the three-day study period. The total daily dosage of trazodone was 100 mg (50 mg in one subject), and of imipramine 40 mg (20 mg in one subject). Subjects were submitted to polysomnography (PSG) and body core temperature (rectal temperature) measurements during the study period. We compared the data concerning the antidepressants to those of the placebo.The results show that, with regard to the sleep rhythm, trazodone significantly increased slow wave sleep (SWS), but no changes were observed in REM (rapid eye movement) sleep. Imipramine significantly decreased REM sleep and prolonged the REM cycle. With regard to the temperature rhythm, trazodone showed a tendency to advance the appearance time of the minimal temperature. Imipramine significantly lowered the maximal temperature and decreased the difference between the maximal and the minimal temperature, but no changes in the phases were observed. Neither antidepressant had any effect on the temperature cycle.Trazodone and imipramine showed different effects on PSG. Furthermore, they had different effects on the temperature rhythm. The changes of the sleep-wake rhythm were greater than those of the temperature rhythm. Although the two antidepressants had different mechanisms of action, it is worthy of note that both directly influenced the biological rhythms of healthy volunteers.
PMID: 12187365 [PubMed - indexed for MEDLINE]
Edit:
Trazadone shown to NOT effect REM (apparently my memory was off but I was partially right via SWS) but to signifigantly improve SWS I.E. slow wave sleep.I'll dig up more and yeah,25mg(not to exceed50) is a good dose for insomnia,the studies show 50-100mg,which I'm guessing is the dose used for depression.
Another advantage traz has is its price,the generic is ridiculously cheap.
"A comparison of the effectiveness of two hypnotic agents for the treatment of insomnia".
Schwartz T, Nihalani N, Virk S, Jindal S, Costello A, Muldoon R, Azhar N, Hussein J, Tirmazi S.
SUNY Upstate Medical University, Department of Psychiatry, 750 East Adams Street, Syracuse, NY 13210, USA.
OBJECTIVE: To compare the effectiveness and tolerability of two hypnotic agents, trazadone (Desyrel) and zaleplon (Sonata) on psychiatric inpatients with insomnia. METHODS: Fifteen patients who were psychiatric inpatients were assigned openly and randomly to receive either trazodone (50-100 mg) or zaleplon (10-20 mg) doses on an "as-needed basis" and followed throughout their hospital stay. Efficacy and side effect profile were subsequently assessed. CONCLUSION: This pilot study suggests that trazodone may be a better agent to promote longer, deeper subjective quality sleep for psychiatric inpatients with insomnia in terms of effectiveness. However, tolerability was much better with zaleplon as daytime residual side effects were less.
PMID: 15468607 [PubMed - indexed for MEDLINE]
1: Ann Clin Psychiatry. 2006 Jan-Mar;18(1):49-56.Click here to read Links
Comment in:
Ann Clin Psychiatry. 2007 Jan-Mar;19(1):53-4.
Sleep maintenance insomnia: strengths and weaknesses of current pharmacologic therapies.
Rosenberg RP.
Northside Hospital Sleep Medicine Institute, Atlanta, GA, USA. rosenberg@mindspring.com
BACKGROUND: Although insomnia is highly prevalent, sleep disturbances often go unrecognized and untreated. When insomnia is recognized, considerable emphasis has been placed on improving sleep onset; however, there is growing evidence that improving sleep maintenance is an equally important treatment goal. METHODS: A MEDLINE literature search was performed using the search parameters "insomnia," "zolpidem," "zaleplon," "flurazepam," "estazolam," "quazepam," "triazolam," and "temazepam," as these agents are FDA-approved for the treatment of insomnia. Per reviewer comments, the search criteria was later expanded to include lorazepam. A literature search using the terms "trazodone" and "insomnia" was also performed, as this is the second-most commonly prescribed agent for treating insomnia. Sleep efficacy endpoints from randomized, placebo-controlled clinical trials in adult populations and key review articles published between 1975 and 2004 were included in this review. As only one randomized placebo-controlled trial evaluated trazodone use in primary insomnia, the trazodone search was expanded to include all clinical trials that evaluated trazodone use in insomnia. Relevant texts and other articles that evaluated side effect profiles of these agents were also included, one of which was published in January of 2005. In all publications, impact of treatment on sleep maintenance parameters (wake time after sleep onset, number of awakenings) and measures of next-day functioning were evaluated, in addition to sleep onset parameters (sleep latency, time to sleep onset/induction) and sleep duration data (total sleep time). RESULTS: Many of the currently available agents used to treat insomnia, including the antidepressant trazodone, the non-benzodiazepine hypnotics zolpidem and zaleplon, and some of the benzodiazepines, have not consistently demonstrated effectiveness in promoting sleep maintenance. Furthermore, the benzodiazepines with established sleep maintenance efficacy are associated with next-day sedation, the risk of tolerance and dependence, or both. CONCLUSIONS: New agents that offer relief of sleep maintenance insomnia without residual next day impairment while improving next day function are needed. Several compounds currently under development may offer clinicians a more effective and safer treatment for this common disorder.
PMID: 16517453 [PubMed - indexed for MEDLINE]
Effects of trazodone and imipramine on the biological rhythm: an analysis of sleep EEG and body core temperature.
Suzuki H, Yamadera H, Nakamura S, Endo S.
Department of Neuropsychiatry, Nippon Medical School, Japan.
Depression commonly involves abnormalities of the sleep-wake rhythm, the temperature rhythm, and other biological rhythms. The changes of these biological rhythms are caused in remission by medications. However, it has yet to be clarified whether the biological rhythms are changed as a result of recovery from depression or from the direct pharmacological effects of the antidepressants. Therefore, we have undertaken a study on the direct effects of the antidepressants trazodone and imipramine on the biological rhythms of healthy volunteers.The study involved 12 healthy male volunteers (ages 21 approximately 28 years, mean age 23.9+/-1.7 years) who had given written informed consent. Placebo, trazodone, and imipramine were each administered in a single blind manner four times a day, during the three-day study period. The total daily dosage of trazodone was 100 mg (50 mg in one subject), and of imipramine 40 mg (20 mg in one subject). Subjects were submitted to polysomnography (PSG) and body core temperature (rectal temperature) measurements during the study period. We compared the data concerning the antidepressants to those of the placebo.The results show that, with regard to the sleep rhythm, trazodone significantly increased slow wave sleep (SWS), but no changes were observed in REM (rapid eye movement) sleep. Imipramine significantly decreased REM sleep and prolonged the REM cycle. With regard to the temperature rhythm, trazodone showed a tendency to advance the appearance time of the minimal temperature. Imipramine significantly lowered the maximal temperature and decreased the difference between the maximal and the minimal temperature, but no changes in the phases were observed. Neither antidepressant had any effect on the temperature cycle.Trazodone and imipramine showed different effects on PSG. Furthermore, they had different effects on the temperature rhythm. The changes of the sleep-wake rhythm were greater than those of the temperature rhythm. Although the two antidepressants had different mechanisms of action, it is worthy of note that both directly influenced the biological rhythms of healthy volunteers.
PMID: 12187365 [PubMed - indexed for MEDLINE]
There's 19 studies on trazadone on Pubmed and after reading over the bulk of them,apparently trazadone doesn't increase REM sleep.
I do remember a poster on this board (may have been Sanction,not sure) posting a study indicating that trazadone did in fact increase REM sleep.I'll PM him to see what's up.
Motherfucker...that's all I've got to add now,after my Pubmed whoring.
Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.
Yamadera H, Nakamura S, Suzuki H, Endo S.
Department of Neuropsychiatry, Nippon Medical School, Tokyo, Japan.
Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.
PMID: 9766695 [PubMed - indexed for MEDLINE]
Chronobiological research on antidepressant drugs: the effect of the antidepressant drugs, trazodone and imipramine on the circadian rhythm using electroencephalography in healthy volunteers]
[Article in Japanese]
Nakamura S, Yamadera H, Suzuki H, Endo S.
Department of Neuropsychiatry, Nippon Medical School, Japan. dada-syuichi@rio.odn.ne.jp
The effects of the antidepressant drugs trazodone and imipramine on the circadian rhythm were studied by means of the sleep propensity test (SPT; sleep latency was examined by 35-minute EEG records at 09:00, 11:00, 13:00, 15:00, 17:00). The subjects were 11 healthy male volunteers (mean age, 23.6 years old). The drugs were administered 4 times a day with single blind trials using an inactive placebo as a control. The dosages of the drugs were trazodone 50-100 mg/day and imipramine 20-40 mg/day. We discussed the circadian rhythm referring to previous polysomnograhy (PSG) studies using the same drugs and dosages with most of the same subjects. As a result, the mean sleep latency of SPT was the shortest at 09:00 (p<0.1) with a placebo, at 11:00 (p<0.05) with trazodone and at 13: 00 (not significantly) with imipramine administration. These results suggested that neither drug affected sleepiness. They affected the circadian rhythm during the daytime (=the day rhythm). They delayed the day rhythm. Delay of the day rhythm was due to trazodone and have been caused by not only trazodon administration itself, but also by the increase of slow-wave sleep obtained in the previous night's PSG study. And the day-rhythm delay was due to imipramine and might have been caused by not only imipramine administration itself, but also by the decrease in the percentage of slow-wave sleep and REM sleep, and an increase in REM latency obtained in the previous night's PSG study. Therefore, we concluded that neither drug affected the tendency toward sleepiness, but did affect the day rhythm in healthy subjects.
PMID: 12068317 [PubMed - indexed for MEDLINE]
Effects of trazodone and imipramine on the biological rhythm: an analysis of sleep EEG and body core temperature.
Suzuki H, Yamadera H, Nakamura S, Endo S.
Department of Neuropsychiatry, Nippon Medical School, Japan.
Depression commonly involves abnormalities of the sleep-wake rhythm, the temperature rhythm, and other biological rhythms. The changes of these biological rhythms are caused in remission by medications. However, it has yet to be clarified whether the biological rhythms are changed as a result of recovery from depression or from the direct pharmacological effects of the antidepressants. Therefore, we have undertaken a study on the direct effects of the antidepressants trazodone and imipramine on the biological rhythms of healthy volunteers.The study involved 12 healthy male volunteers (ages 21 approximately 28 years, mean age 23.9+/-1.7 years) who had given written informed consent. Placebo, trazodone, and imipramine were each administered in a single blind manner four times a day, during the three-day study period. The total daily dosage of trazodone was 100 mg (50 mg in one subject), and of imipramine 40 mg (20 mg in one subject). Subjects were submitted to polysomnography (PSG) and body core temperature (rectal temperature) measurements during the study period. We compared the data concerning the antidepressants to those of the placebo.The results show that, with regard to the sleep rhythm, trazodone significantly increased slow wave sleep (SWS), but no changes were observed in REM (rapid eye movement) sleep. Imipramine significantly decreased REM sleep and prolonged the REM cycle. With regard to the temperature rhythm, trazodone showed a tendency to advance the appearance time of the minimal temperature. Imipramine significantly lowered the maximal temperature and decreased the difference between the maximal and the minimal temperature, but no changes in the phases were observed. Neither antidepressant had any effect on the temperature cycle.Trazodone and imipramine showed different effects on PSG. Furthermore, they had different effects on the temperature rhythm. The changes of the sleep-wake rhythm were greater than those of the temperature rhythm. Although the two antidepressants had different mechanisms of action, it is worthy of note that both directly influenced the biological rhythms of healthy volunteers.
PMID: 12187365 [PubMed - indexed for MEDLINE]
Trazadone,bupropion,prolactin and 5-HTP:
1: Acta Psychiatr Scand Suppl. 1981;290:100-21.Links
Effect of antidepressants, lithium and electroconvulsive treatment on rat serum prolactin levels.
Meltzer HY, Simonovic M, Sturgeon RD, Fang VS.
The ability of antidepressant drugs, electroconvulsive treatment (ECT), or lithium chloride (LiCl), to modify prolactin secretion in the rat was studied. Chlorimipramine, citalopram, fluoxetine, imipramine and zimelidine potentiated the low dose 5-hydroxytryptophan (5-HTP)-induced increase in prolactin secretion, suggesting inhibition of serotonin (5-HT) uptake by these drugs. Amitriptyline, doxepin, iprindole, mianserin and trazadone inhibited the prolactin stimulating effects of high doses of 5-HTP and quipazine, suggesting that these drugs have 5-HT receptor blocking properties. Tandamine inhibited only 5-HTP-induced increase in prolactin secretion. Chronic administration of imipramine, potentiated the effect of low dose 5-HTP significantly more than an acute dose. Amitriptyline, produced similar inhibition of the 5-HTP-induced increase in prolactin secretion after both acute and chronic administration. The ability of bupropion and mazindol to inhibit alpha-methylparatyrosine-induced prolactin secretion, and of nomifensine to inhibit reserpine-induced prolactin secretion, is consistent with other evidence that these agents are indirect dopamine (DA) agonists. Desipramine, acutely, had no effect on any of the above paradigms but after chronic administration, potentiated the effect of low dose 5-HTP on prolactin secretion. Nortriptyline had no effect on prolactin secretion after acute or chronic treatment. ECT for 10 days did not affect the ability of a 5-HT agonist or d-amphetamine to modify prolactin secretion. However, chronic, but not acute, treatment with LiCl markedly enhanced the prolactin response to 5-HT agonists and reserpine while shifting the dose response curve for d-amphetamine and apomorphine to the right. These results are discussed in light of current theories of the role of 5-HT and DA in depression.
PMID: 6971560 [PubMed - indexed for MEDLINE]
Not good news for those with wrist pain(especially of interest to myself as I can't lift due to wrist pain ATM):
1: Hear Res. 2007 Apr;226(1-2):221-31. Epub 2006 Sep 14.Click here to read Links
Antidepressant therapy in tinnitus.
Robinson SK, Viirre ES, Stein MB.
Department of Psychiatry, University of California, San Diego School of Medicine, Veterans Administration San Diego Healthcare System, 3350 La Jolla Village Dr., Mail Code 116A, La Jolla, CA 92161, USA. skrobinson@ucsd.edu
OBJECTIVE: Review the literature on the co-morbidity of depression and anxiety with tinnitus. Briefly consider proposed mechanisms by which antidepressants might be helpful for tinnitus, including treatment of co-morbid depression and anxiety and a more direct serotonergic mechanism of tinnitus. Survey the literature on antidepressants and tinnitus including tinnitus reported as a side effect of antidepressants (phenelzine, amitriptyline, protriptyline, doxepin, imipramine, fluoxetine, trazadone, bupropion, venlafaxine), tinnitus associated with withdrawal of antidepressants (venlafaxine and sertraline) and antidepressants as a treatment for tinnitus (case reports--fluoxetine and paroxetine, retrospective reviews--imipramine and selective serotonin reuptake inhibitors, single blind trials of amitriptyline and double blind placebo controlled trials of trimipramine, nortriptyline, paroxetine and sertraline). Provide suggestions on future directions, specifically replication of prior studies and a dose finding study of paroxetine for the treatment of tinnitus.
PMID: 16973315 [PubMed - indexed for MEDLINE]
I do remember a poster on this board (may have been Sanction,not sure) posting a study indicating that trazadone did in fact increase REM sleep.I'll PM him to see what's up.
Motherfucker...that's all I've got to add now,after my Pubmed whoring.
Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.
Yamadera H, Nakamura S, Suzuki H, Endo S.
Department of Neuropsychiatry, Nippon Medical School, Tokyo, Japan.
Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.
PMID: 9766695 [PubMed - indexed for MEDLINE]
Chronobiological research on antidepressant drugs: the effect of the antidepressant drugs, trazodone and imipramine on the circadian rhythm using electroencephalography in healthy volunteers]
[Article in Japanese]
Nakamura S, Yamadera H, Suzuki H, Endo S.
Department of Neuropsychiatry, Nippon Medical School, Japan. dada-syuichi@rio.odn.ne.jp
The effects of the antidepressant drugs trazodone and imipramine on the circadian rhythm were studied by means of the sleep propensity test (SPT; sleep latency was examined by 35-minute EEG records at 09:00, 11:00, 13:00, 15:00, 17:00). The subjects were 11 healthy male volunteers (mean age, 23.6 years old). The drugs were administered 4 times a day with single blind trials using an inactive placebo as a control. The dosages of the drugs were trazodone 50-100 mg/day and imipramine 20-40 mg/day. We discussed the circadian rhythm referring to previous polysomnograhy (PSG) studies using the same drugs and dosages with most of the same subjects. As a result, the mean sleep latency of SPT was the shortest at 09:00 (p<0.1) with a placebo, at 11:00 (p<0.05) with trazodone and at 13: 00 (not significantly) with imipramine administration. These results suggested that neither drug affected sleepiness. They affected the circadian rhythm during the daytime (=the day rhythm). They delayed the day rhythm. Delay of the day rhythm was due to trazodone and have been caused by not only trazodon administration itself, but also by the increase of slow-wave sleep obtained in the previous night's PSG study. And the day-rhythm delay was due to imipramine and might have been caused by not only imipramine administration itself, but also by the decrease in the percentage of slow-wave sleep and REM sleep, and an increase in REM latency obtained in the previous night's PSG study. Therefore, we concluded that neither drug affected the tendency toward sleepiness, but did affect the day rhythm in healthy subjects.
PMID: 12068317 [PubMed - indexed for MEDLINE]
Effects of trazodone and imipramine on the biological rhythm: an analysis of sleep EEG and body core temperature.
Suzuki H, Yamadera H, Nakamura S, Endo S.
Department of Neuropsychiatry, Nippon Medical School, Japan.
Depression commonly involves abnormalities of the sleep-wake rhythm, the temperature rhythm, and other biological rhythms. The changes of these biological rhythms are caused in remission by medications. However, it has yet to be clarified whether the biological rhythms are changed as a result of recovery from depression or from the direct pharmacological effects of the antidepressants. Therefore, we have undertaken a study on the direct effects of the antidepressants trazodone and imipramine on the biological rhythms of healthy volunteers.The study involved 12 healthy male volunteers (ages 21 approximately 28 years, mean age 23.9+/-1.7 years) who had given written informed consent. Placebo, trazodone, and imipramine were each administered in a single blind manner four times a day, during the three-day study period. The total daily dosage of trazodone was 100 mg (50 mg in one subject), and of imipramine 40 mg (20 mg in one subject). Subjects were submitted to polysomnography (PSG) and body core temperature (rectal temperature) measurements during the study period. We compared the data concerning the antidepressants to those of the placebo.The results show that, with regard to the sleep rhythm, trazodone significantly increased slow wave sleep (SWS), but no changes were observed in REM (rapid eye movement) sleep. Imipramine significantly decreased REM sleep and prolonged the REM cycle. With regard to the temperature rhythm, trazodone showed a tendency to advance the appearance time of the minimal temperature. Imipramine significantly lowered the maximal temperature and decreased the difference between the maximal and the minimal temperature, but no changes in the phases were observed. Neither antidepressant had any effect on the temperature cycle.Trazodone and imipramine showed different effects on PSG. Furthermore, they had different effects on the temperature rhythm. The changes of the sleep-wake rhythm were greater than those of the temperature rhythm. Although the two antidepressants had different mechanisms of action, it is worthy of note that both directly influenced the biological rhythms of healthy volunteers.
PMID: 12187365 [PubMed - indexed for MEDLINE]
Trazadone,bupropion,prolactin and 5-HTP:
1: Acta Psychiatr Scand Suppl. 1981;290:100-21.Links
Effect of antidepressants, lithium and electroconvulsive treatment on rat serum prolactin levels.
Meltzer HY, Simonovic M, Sturgeon RD, Fang VS.
The ability of antidepressant drugs, electroconvulsive treatment (ECT), or lithium chloride (LiCl), to modify prolactin secretion in the rat was studied. Chlorimipramine, citalopram, fluoxetine, imipramine and zimelidine potentiated the low dose 5-hydroxytryptophan (5-HTP)-induced increase in prolactin secretion, suggesting inhibition of serotonin (5-HT) uptake by these drugs. Amitriptyline, doxepin, iprindole, mianserin and trazadone inhibited the prolactin stimulating effects of high doses of 5-HTP and quipazine, suggesting that these drugs have 5-HT receptor blocking properties. Tandamine inhibited only 5-HTP-induced increase in prolactin secretion. Chronic administration of imipramine, potentiated the effect of low dose 5-HTP significantly more than an acute dose. Amitriptyline, produced similar inhibition of the 5-HTP-induced increase in prolactin secretion after both acute and chronic administration. The ability of bupropion and mazindol to inhibit alpha-methylparatyrosine-induced prolactin secretion, and of nomifensine to inhibit reserpine-induced prolactin secretion, is consistent with other evidence that these agents are indirect dopamine (DA) agonists. Desipramine, acutely, had no effect on any of the above paradigms but after chronic administration, potentiated the effect of low dose 5-HTP on prolactin secretion. Nortriptyline had no effect on prolactin secretion after acute or chronic treatment. ECT for 10 days did not affect the ability of a 5-HT agonist or d-amphetamine to modify prolactin secretion. However, chronic, but not acute, treatment with LiCl markedly enhanced the prolactin response to 5-HT agonists and reserpine while shifting the dose response curve for d-amphetamine and apomorphine to the right. These results are discussed in light of current theories of the role of 5-HT and DA in depression.
PMID: 6971560 [PubMed - indexed for MEDLINE]
Not good news for those with wrist pain(especially of interest to myself as I can't lift due to wrist pain ATM):
1: Hear Res. 2007 Apr;226(1-2):221-31. Epub 2006 Sep 14.Click here to read Links
Antidepressant therapy in tinnitus.
Robinson SK, Viirre ES, Stein MB.
Department of Psychiatry, University of California, San Diego School of Medicine, Veterans Administration San Diego Healthcare System, 3350 La Jolla Village Dr., Mail Code 116A, La Jolla, CA 92161, USA. skrobinson@ucsd.edu
OBJECTIVE: Review the literature on the co-morbidity of depression and anxiety with tinnitus. Briefly consider proposed mechanisms by which antidepressants might be helpful for tinnitus, including treatment of co-morbid depression and anxiety and a more direct serotonergic mechanism of tinnitus. Survey the literature on antidepressants and tinnitus including tinnitus reported as a side effect of antidepressants (phenelzine, amitriptyline, protriptyline, doxepin, imipramine, fluoxetine, trazadone, bupropion, venlafaxine), tinnitus associated with withdrawal of antidepressants (venlafaxine and sertraline) and antidepressants as a treatment for tinnitus (case reports--fluoxetine and paroxetine, retrospective reviews--imipramine and selective serotonin reuptake inhibitors, single blind trials of amitriptyline and double blind placebo controlled trials of trimipramine, nortriptyline, paroxetine and sertraline). Provide suggestions on future directions, specifically replication of prior studies and a dose finding study of paroxetine for the treatment of tinnitus.
PMID: 16973315 [PubMed - indexed for MEDLINE]
The other obvious question is:
"Now that I have gone back to powerlifting and approaching it from low rep, high weight standpoint"
was your change in lifting habits/weights abrupt? Perhaps you need to change your lifting habits in a more gradual way to allow your body time to adjust.
Taking some prescription drug to mask a symptom strikes me as doing violence to your body (not that docs don't do it all the time).
"Now that I have gone back to powerlifting and approaching it from low rep, high weight standpoint"
was your change in lifting habits/weights abrupt? Perhaps you need to change your lifting habits in a more gradual way to allow your body time to adjust.
Taking some prescription drug to mask a symptom strikes me as doing violence to your body (not that docs don't do it all the time).
What time do you go to sleep on days you don't lift? Could the problem being you're sleeping too early? Does your evening routine differ?
Also, do you feel excessively stimulated / anxious / stressed or anything that day?
Colin: I'm not sure if a morning dose of SJW helps or not (haven't tried it), I just thought an evening dose was a good idea as SJW is a CYP3A4 inducer and would reduce trazodone's T1/2.
Also, do you feel excessively stimulated / anxious / stressed or anything that day?
Colin: I'm not sure if a morning dose of SJW helps or not (haven't tried it), I just thought an evening dose was a good idea as SJW is a CYP3A4 inducer and would reduce trazodone's T1/2.
QUOTE(Frangible @ Dec 20 2007, 05:10 PM) [snapback]443855[/snapback]
What time do you go to sleep on days you don't lift? Could the problem being you're sleeping too early? Does your evening routine differ?
I go to sleep ~10PM every night and get up around 530AM.
@Scott, the intensity is a lot higher so the abruptness of the change may be a factor. I have no intention of taking trazadone to deal with this problem.
try some ZMA
QUOTE(Benson @ Dec 19 2007, 07:59 PM) [snapback]443711[/snapback]
Now that I have gone back to powerlifting and approaching it from low rep, high weight standpoint, I have noticed an effect on my sleep on days that I lift heavy.
I work out in the afternoon-early evening and I am usually plenty tired by 10PM or so and fall asleep easily. However, I wake up frequently through the night, every couple of hours, sometimes feeling as though it must be morning even though its the middle of the night.
What's the cause of this and how do I counter it? I've tried high dose ascorbic acid, tryptophan, melatonin, valerian, etc. to no avail. The only thing I have found to work consistently is 12.5mg of doxylamine but I suspect this is as much a sleep architecture rapist as diphenhydramine so I don't see this as a viable solution long term.
I work out in the afternoon-early evening and I am usually plenty tired by 10PM or so and fall asleep easily. However, I wake up frequently through the night, every couple of hours, sometimes feeling as though it must be morning even though its the middle of the night.
What's the cause of this and how do I counter it? I've tried high dose ascorbic acid, tryptophan, melatonin, valerian, etc. to no avail. The only thing I have found to work consistently is 12.5mg of doxylamine but I suspect this is as much a sleep architecture rapist as diphenhydramine so I don't see this as a viable solution long term.
I lift heavy 2 nights a week, and go light weight / high volume 2 nights. I do abs / lower back / core / cardio the other 3. I wake up frequently throughout the night pretty much every night, sometimes without being able to get back to sleep. I've had this problem for years, though, and it doesn't seem to be affected by working out or not working out on any particular evening.
I've tried tons and tons of things over the years to help me get to sleep and stay asleep through the night. Right now the best thing seems to be zopiclone (Imovane or Lunesta), although it doesn't work if I use it every night. Diphenhydramine or doxylamine help sometimes, but if I take enough to sleep through the night there's usually a hangover effect. Melatonin helps, just a little, although if I take more than 1 mg I'm usually sleepy the next day. Cannabis (consumed orally, not smoked) helps tremendously, but I can only do that on the weekends if I want to stay sharp on the job. High dose taurine or high dose GABA can help too, although I wake up after 3 hours and need a second dose to get back to sleep. Valerian helps just a tad, but not much. Same goes for ZMA or magnesium citrate. I'm planning on trying trazodone in the near future. In recent years, I'm finding that I'm taking something or other for sleep just about every night. I haven't found a single thing that works consistently every night over time.
What seems to work most of all is sex. After I fuck some hottie 2 or 3 times within a few hours, I sleep like a baby. If I get involved with bullshit relationship drama and stress, though, I'm pretty much guaranteed to have sleepless nights. I'll be set for life if I ever meet the drama-free nymphomaniac hottie I'm looking for.
It goes away after a while. You get used to it and sleep goes back to normal.
I workout at 8 to 8:30 at night...go to bed at 11 and up by 6.
But yeah, from what I understand..it's a CNS thing
I workout at 8 to 8:30 at night...go to bed at 11 and up by 6.
But yeah, from what I understand..it's a CNS thing
QUOTE(Proton Soup @ Dec 20 2007, 08:55 PM) [snapback]443890[/snapback]
try some ZMA
I shall.
It actually says disturbed sheep in the subtitle. Which is kind of amusing as the title was heavy lifting.
Benson did you realise this?
Anyway, I think the problem with anti-histamines, like diphen is simply that they last too long. Their action is quite ideal, according to our current understanding, in that the histamine signal controls circadian rhythm and the actions of other messengers so it is integrative in its actions. It is a primary switch if you like for controlling sleep with a natural diurnal rhythm in the release of histamine in the brain. histamine neurons are juxtaposed with other neurons that have a see-saw like relationship with each other, one set controls sleep, the other wakefulness. http://www.ninds.nih.gov/news_and_events/n...y_histamine.htm
IIRC certain cholinergic neurons (particularly from basal forebrain) induce sleep, histamine neurons induce wakefulness, and they have a direct antagonism of each other.
http://www.acnp.org/g4/GN401000037/Default.htm
But because diphen and other antihistamines act too long, it would be a disaster for phase delay sleeping problems.
What is needed is a sleep 'on' agent, that acts no longer than about 6-7 hours. Zolpidem is the closest thing. Regarding a general reduction of REM, in the early part of night this is good, and increased SWS is good as well.
Stress would be a good explanation for dissordered sleep with regular waking. . SWS is naturally induced by quality of day time experiences, which impact on BDNF.
The BDNF has been found to induce more SWS.
That would be expected to increase length of time asleep as regular waking suggests REM intrusion and outer cortical over-activity, which stress quite literally induces - the waking stages are stress-induced using the same hormones and rigourous nutrient uptake, in activity in the outer layer of the brain.
This might not be the case, but I think that you may not be getting off deeply enough. Your day activity may be masking a state of being that is under some level of duress and is less settled than you may think.
Benson did you realise this?
Anyway, I think the problem with anti-histamines, like diphen is simply that they last too long. Their action is quite ideal, according to our current understanding, in that the histamine signal controls circadian rhythm and the actions of other messengers so it is integrative in its actions. It is a primary switch if you like for controlling sleep with a natural diurnal rhythm in the release of histamine in the brain. histamine neurons are juxtaposed with other neurons that have a see-saw like relationship with each other, one set controls sleep, the other wakefulness. http://www.ninds.nih.gov/news_and_events/n...y_histamine.htm
IIRC certain cholinergic neurons (particularly from basal forebrain) induce sleep, histamine neurons induce wakefulness, and they have a direct antagonism of each other.
http://www.acnp.org/g4/GN401000037/Default.htm
But because diphen and other antihistamines act too long, it would be a disaster for phase delay sleeping problems.
What is needed is a sleep 'on' agent, that acts no longer than about 6-7 hours. Zolpidem is the closest thing. Regarding a general reduction of REM, in the early part of night this is good, and increased SWS is good as well.
Stress would be a good explanation for dissordered sleep with regular waking. . SWS is naturally induced by quality of day time experiences, which impact on BDNF.
The BDNF has been found to induce more SWS.
That would be expected to increase length of time asleep as regular waking suggests REM intrusion and outer cortical over-activity, which stress quite literally induces - the waking stages are stress-induced using the same hormones and rigourous nutrient uptake, in activity in the outer layer of the brain.
This might not be the case, but I think that you may not be getting off deeply enough. Your day activity may be masking a state of being that is under some level of duress and is less settled than you may think.
Oh boy, I couldn't have missed that. I think this title has been changed.
I didn't know that Benson had New Zealander roots?
I didn't know that Benson had New Zealander roots?
The play on words was intentional...
@methodice, if I did not live here, I would likely live there...although Iceland is also a distinct possibility...
@methodice, if I did not live here, I would likely live there...although Iceland is also a distinct possibility...
Maybe I'm missing the point here, but I get the same thing when I switch up lifting to something more heavy/damaging. This may be stupid, but I think its just my body telling me that it is hungry. I wake up and feel sore all over, in areas that weren't even necessarily worked out. I guess body is breaking down other tissues to repair those that were damaged due to lifting. Sometimes I couldnt even go back to sleep it was so bad, eventually though, in my non-sombulence I would venture into the kitchen, have a banana and some cottage cheese and a half an hour later I would be out like a lightbulb for the next 3 hours. I've just started having midnight snacks on heavy days, and I don't wake up as often anymore. Maybe I just conditioned my mind to say "snack time" though to wake me up.
I'd try high doses of evening relora. I know this is in a product you tried but I wonder at the dose. Elevated afternoon cortisol = generally fucked up rhythms? Phosphatidylserine might be useful too. I don't know if people suggested this shit, I didn't read the whole thread.
EDIT: That's a real nice post by ATB, I'm going to bookmark this now. Depth of daytime experiences ---> bdnf ---> SWS is critical.
EDIT: That's a real nice post by ATB, I'm going to bookmark this now. Depth of daytime experiences ---> bdnf ---> SWS is critical.
ZMA by itself did not seem to provide any improvement but ZMA plus 12.5mg of doxylamine was money...sleep soundly with no morning grogginess...
QUOTE(ATB @ Dec 22 2007, 04:05 AM) [snapback]444114[/snapback]
...
What is needed is a sleep 'on' agent, that acts no longer than about 6-7 hours. Zolpidem is the closest thing. Regarding a general reduction of REM, in the early part of night this is good, and increased SWS is good as well.
Stress would be a good explanation for dissordered sleep with regular waking. . SWS is naturally induced by quality of day time experiences, which impact on BDNF.
The BDNF has been found to induce more SWS.
What is needed is a sleep 'on' agent, that acts no longer than about 6-7 hours. Zolpidem is the closest thing. Regarding a general reduction of REM, in the early part of night this is good, and increased SWS is good as well.
Stress would be a good explanation for dissordered sleep with regular waking. . SWS is naturally induced by quality of day time experiences, which impact on BDNF.
The BDNF has been found to induce more SWS.
funny you should mention that. something i found recently.
QUOTE
free full text
Pharmacol Rep. 2005 Nov-Dec;57(6):713-8.Click here to read Links
Zinc and depression. An update.
Nowak G, Szewczyk B, Pilc A.
Department of Cytobiology and Histochemistry, Collegium Medicum, Jagiellonian University, Medyczna 9, PL 30-688 Kraków, Poland. nowak@if-pan.krakow.pl
Unsatisfactory clinical efficacy and a variety of adverse effects of current antidepressant drugs have incited search for better therapy. Zinc, an antagonist of the glutamate/N-methyl-D-aspartate (NMDA) receptor, exhibits antidepressant-like activity in rodent tests/models of depression. Similarly to antidepressants, zinc induces brain derived neurotrophic factor (BDNF) gene expression and increases level of synaptic pool of zinc in the hippocampus. Clinical observations demonstrated serum hypozincemia in depression, which was normalized by effective antidepressant treatment. Moreover, our preliminary clinical study demonstrated the benefit of zinc supplementation in antidepressant therapy. All the data indicate the important role of zinc homeostasis in psychopathology and therapy of depression and potential clinical antidepressant activity of this ion.
PMID: 16382189 [PubMed - indexed for MEDLINE]
Pharmacol Rep. 2005 Nov-Dec;57(6):713-8.Click here to read Links
Zinc and depression. An update.
Nowak G, Szewczyk B, Pilc A.
Department of Cytobiology and Histochemistry, Collegium Medicum, Jagiellonian University, Medyczna 9, PL 30-688 Kraków, Poland. nowak@if-pan.krakow.pl
Unsatisfactory clinical efficacy and a variety of adverse effects of current antidepressant drugs have incited search for better therapy. Zinc, an antagonist of the glutamate/N-methyl-D-aspartate (NMDA) receptor, exhibits antidepressant-like activity in rodent tests/models of depression. Similarly to antidepressants, zinc induces brain derived neurotrophic factor (BDNF) gene expression and increases level of synaptic pool of zinc in the hippocampus. Clinical observations demonstrated serum hypozincemia in depression, which was normalized by effective antidepressant treatment. Moreover, our preliminary clinical study demonstrated the benefit of zinc supplementation in antidepressant therapy. All the data indicate the important role of zinc homeostasis in psychopathology and therapy of depression and potential clinical antidepressant activity of this ion.
PMID: 16382189 [PubMed - indexed for MEDLINE]
QUOTE(Benson @ Dec 26 2007, 03:01 PM) [snapback]444711[/snapback]
ZMA by itself did not seem to provide any improvement but ZMA plus 12.5mg of doxylamine was money...sleep soundly with no morning grogginess...
i think some of the positive effects of zinc may not be immediate.
You could try raising the calories in your post-workout and pre-bed meals, high dose fish oils, I second the Zinc and magnesium (at least 50mg/1000mg), and if you're achy try some NSAIDs. 5-HTP sometimes helped me too.
QUOTE(Archaic @ Dec 27 2007, 02:41 PM) [snapback]444814[/snapback]
You could try raising the calories in your post-workout and pre-bed meals, high dose fish oils, I second the Zinc and magnesium (at least 50mg/1000mg), and if you're achy try some NSAIDs. 5-HTP sometimes helped me too.
Never achey, just wake up every hour or so, fall back to sleep, rinse, repeat. I'll run the ZMA for a while and see if that helps.
QUOTE
Zinc and depression. An update.
A study even showed it to be helpful for ADD/ADHD, improving the efficacy of medication. Besides mild NMDA antagonism it's essentially dopaminergic, as it combats prolactin.
QUOTE
50mg zinc
I can't seem to find it right now, but I read a very good article suggesting that 50mg of even a shitty chelate is too high and can impair immune function/testosterone/antioxidant status, the opposite of what you would achieve with more reasonable doses.
Not achy after starting a heavy lifting routine?? Please tell me your secret!
QUOTE(Archaic @ Dec 28 2007, 03:12 PM) [snapback]444981[/snapback]
Not achy after starting a heavy lifting routine?? Please tell me your secret!
I get some DOMS about 18-24 hours after heavy lifting but not the same day, the sleeping problems are 6-8hrs after lifting.
I don't know if this will help but some of my personal observations from my experience.
If I workout too late into the evening, say past 4PM... I am usually wide awake up until bed time even if I'm exhausted, but sleep is generally not disturbed. However if my workout is in any way intense and lasting longer than usual my sleep is entirely fucked. I'll have a sound sleep so to speak, but its light, very light, not deep not restful and I'll wake up feeling like shit. This happens especially when its intense and I've been training or pushing myself day after day. My heart usually beats consistently faster throughout the night and I feel warmer and less relaxed. I have heard exercise inhibits melatonin production, I don't know how long the effect lasts. I, like another poster, suspect its CNS/hormonal related and involves abnormal or "unnatural" activation of the SNS in relation to your circadian rhythm.
edit:
last but not least sodium and potassium intake do play really important roles in your circadium rhythm.. i suggest getting as much potassium as possible in your diet and keep the sodium below 1g
If I workout too late into the evening, say past 4PM... I am usually wide awake up until bed time even if I'm exhausted, but sleep is generally not disturbed. However if my workout is in any way intense and lasting longer than usual my sleep is entirely fucked. I'll have a sound sleep so to speak, but its light, very light, not deep not restful and I'll wake up feeling like shit. This happens especially when its intense and I've been training or pushing myself day after day. My heart usually beats consistently faster throughout the night and I feel warmer and less relaxed. I have heard exercise inhibits melatonin production, I don't know how long the effect lasts. I, like another poster, suspect its CNS/hormonal related and involves abnormal or "unnatural" activation of the SNS in relation to your circadian rhythm.
edit:
last but not least sodium and potassium intake do play really important roles in your circadium rhythm.. i suggest getting as much potassium as possible in your diet and keep the sodium below 1g
What about Lyrica? It seems to increase SWS at the expense of Stages 1 and 2, with REM unaffected.
I tried it for two weeks an found I would sleep soundly although I would wake up semi-groggy the next day. I also found its ability to diminish my nocturnal anxiety was decreased after a week of use, so I would stay awake with 600mgs of the stuff. I would get myoclonic jerks and feel strange overall until I would pass out one hour before waking up.
My intention was to use it as an anti-anxiety aid prior to sleep. I am giving it another go next week after two weeks of abstinence.
I tried it for two weeks an found I would sleep soundly although I would wake up semi-groggy the next day. I also found its ability to diminish my nocturnal anxiety was decreased after a week of use, so I would stay awake with 600mgs of the stuff. I would get myoclonic jerks and feel strange overall until I would pass out one hour before waking up.
My intention was to use it as an anti-anxiety aid prior to sleep. I am giving it another go next week after two weeks of abstinence.
QUOTE(Benson @ Dec 28 2007, 03:21 PM) [snapback]444982[/snapback]
I get some DOMS about 18-24 hours after heavy lifting but not the same day, the sleeping problems are 6-8hrs after lifting.
I've never had significant DOMS from heavy lifting per se. I always experience it when I use higher volume and/or slower negatives.
I was thinking about this, and this made actually a lot of sense.
Say for instance it really is an abnormal event or activation or something we'll say of your CNS in relation to your circadium rhythm. In this case its a direct SNS response that jolts you with adrenaline and catabolic hormones. So we'll say your NS is overactivated, overresponding, in a higher-level adaptation response. Melatonin production is overriden, thyroid levels are increased to increase energy production, catabolic hormones rise to break down materials for energy, and depending on your overall health your body is desperately trying to adapt to the stress at its overall particular best at that moment. You are definitely not in any in way shape or form to sleep.
We think we are supposed to go to bed at that particular time though because it coincides with the rest of our life but it does not actually coincide with the particular nervous state we are in. Any intense work requires an equal amount of your own energy to bring back equilibrium in your body. Its your body's actual adaptation process that is in question now. How efficient are you now? Are you providing the right nutrients to support anabolism? Did you not warm-up properly? We're you out of the gym too long? Are you mentally able to deal with the physical stress?
With that logic you can now create more factors from which you can potentially find answers from. It would make sense if you were to perhaps shorten your work-outs. Maybe you are mentally able to handle the stress which is why you are able to work-out so intensely, but physically speaking you are not and you are pushing yourself too hard and thus your nervous system reacts this way. Maybe you need to decrease the weight and maintain the same intensity. Maybe you're not eatting enough? Only you know...
Say for instance it really is an abnormal event or activation or something we'll say of your CNS in relation to your circadium rhythm. In this case its a direct SNS response that jolts you with adrenaline and catabolic hormones. So we'll say your NS is overactivated, overresponding, in a higher-level adaptation response. Melatonin production is overriden, thyroid levels are increased to increase energy production, catabolic hormones rise to break down materials for energy, and depending on your overall health your body is desperately trying to adapt to the stress at its overall particular best at that moment. You are definitely not in any in way shape or form to sleep.
We think we are supposed to go to bed at that particular time though because it coincides with the rest of our life but it does not actually coincide with the particular nervous state we are in. Any intense work requires an equal amount of your own energy to bring back equilibrium in your body. Its your body's actual adaptation process that is in question now. How efficient are you now? Are you providing the right nutrients to support anabolism? Did you not warm-up properly? We're you out of the gym too long? Are you mentally able to deal with the physical stress?
With that logic you can now create more factors from which you can potentially find answers from. It would make sense if you were to perhaps shorten your work-outs. Maybe you are mentally able to handle the stress which is why you are able to work-out so intensely, but physically speaking you are not and you are pushing yourself too hard and thus your nervous system reacts this way. Maybe you need to decrease the weight and maintain the same intensity. Maybe you're not eatting enough? Only you know...
UPDATE
Came across this study http://www.sciencedaily.com/releases/2008/...80301214734.htm which is interesting but not directly related because I don't have ADHD or take ritalin.
Came across this study http://www.sciencedaily.com/releases/2008/...80301214734.htm which is interesting but not directly related because I don't have ADHD or take ritalin.
I'm back to thinking this is the result of high cortisol. In doing some more reading I came across something that indicated that Pantothenic Acid was a good modulator of cortisol so I bought some 1000mg time-release tablets and have been taking one before bed....so far, it has resolved the sleep issues, even on nights after very heavy lifting.
The only trouble is I can only find references to B5's anti-cortisol effect in secondary sources...
The only trouble is I can only find references to B5's anti-cortisol effect in secondary sources...
Not sure if you can get access to this one, but it might be helpful:
Therapeutic action of pantothenic acid.
Fidanza A.
PMID: 6414981 [PubMed - indexed for MEDLINE]
Therapeutic action of pantothenic acid.
Fidanza A.
PMID: 6414981 [PubMed - indexed for MEDLINE]
QUOTE
The adrenal cholesterol
was markedly lowered on both pantothenic acid-deficient diets but was not
affected by the choline deficiency alone. The stress of partial inanition
may account for the increased size of the glands and the unusually large
concentration of cholesterol in the normal and choline-deficient animals.
About one-third of the rats on the pantothenic acid-deficient diets had
hemorrhagic adrenals, but all adrenals were normal in the other two groups.
was markedly lowered on both pantothenic acid-deficient diets but was not
affected by the choline deficiency alone. The stress of partial inanition
may account for the increased size of the glands and the unusually large
concentration of cholesterol in the normal and choline-deficient animals.
About one-third of the rats on the pantothenic acid-deficient diets had
hemorrhagic adrenals, but all adrenals were normal in the other two groups.
http://www.jbc.org/cgi/reprint/200/2/839
Comparative nutrition of pantothenic acid
Colleen M. Smithb, a and Won O. Song*Corresponding Author Contact Information, a, b, Corresponding Author Contact Information
a Department of Biochemistry, Temple University School of Medicine, Philadelphia, PA, USA
b Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI, USA
Received 14 March 1996; accepted 26 February 1997. Available online 10 May 1999.
Abstract
Pantothenic acid, a B-vitamin, is essential for all mammalian species that have been studied: humans, calves, pigs, dogs, rodents, and cats, as well as for poultry and fish. The different species develop various deficiency signs such as growth retardation; anorexia; changes in hair, feather, or skin; locomotor abnormalities; gastrointestinal problems; compromised immunofunctions; impaired adrenal functions; altered lipid and carbohydrate metabolism; and adverse breeding outcome. Because there are no reliable and sensitive criteria for assessing pantothenate status, the dietary requirements of different species are most frequently set at the level that results in maximum growth. The pantothenate requirement varies widely among different species and strains, and depends on the age, growth rate, and breeding stages of the animals. This review summarizes the deficiency signs and the requirements for pantothenate of different species, and discusses various factors that affect pantothenate requirements of the animals.
I don't have time to look up these references, but perhaps a clue:
http://www.lef.org/protocols/prtcl-002a.shtml
Pantothenic Acid
Pantothenic acid (vitamin B5) activates the adrenal glands. It is a precursor of acetyl CoA (a part of the Krebs's cycle which produces cellular energy) and acetylcholine (a primary neurotransmitter). Pantothenic acid deficiency results in adrenal insufficiency, which is characterized by fatigue, headache, sleep disturbances, nausea, and abdominal discomfort (Tarasov et al. 1985; Smith et al. 1996; Murray et al. 1997).
http://www.lef.org/protocols/prtcl-002a.shtml
Pantothenic Acid
Pantothenic acid (vitamin B5) activates the adrenal glands. It is a precursor of acetyl CoA (a part of the Krebs's cycle which produces cellular energy) and acetylcholine (a primary neurotransmitter). Pantothenic acid deficiency results in adrenal insufficiency, which is characterized by fatigue, headache, sleep disturbances, nausea, and abdominal discomfort (Tarasov et al. 1985; Smith et al. 1996; Murray et al. 1997).
I remember B-5 being a magical solution for acne a few years back...could there probably be a link?
QUOTE (dashforce @ Apr 8 2008, 11:04 AM) 
Pantothenic Acid
Pantothenic acid (vitamin B5) activates the adrenal glands. It is a precursor of acetyl CoA (a part of the Krebs's cycle which produces cellular energy) and acetylcholine (a primary neurotransmitter). Pantothenic acid deficiency results in adrenal insufficiency, which is characterized by fatigue, headache, sleep disturbances, nausea, and abdominal discomfort (Tarasov et al. 1985; Smith et al. 1996; Murray et al. 1997).
Pantothenic acid (vitamin B5) activates the adrenal glands. It is a precursor of acetyl CoA (a part of the Krebs's cycle which produces cellular energy) and acetylcholine (a primary neurotransmitter). Pantothenic acid deficiency results in adrenal insufficiency, which is characterized by fatigue, headache, sleep disturbances, nausea, and abdominal discomfort (Tarasov et al. 1985; Smith et al. 1996; Murray et al. 1997).
I've seen this...would seem to indicate that it allows for more cortisol formation not less...and besides, a dietary deficiency is almost unheard of...they don't call it pantothenic for nothing...
QUOTE (Bachovas @ Apr 8 2008, 11:10 AM)
I remember B-5 being a magical solution for acne a few years back...could there probably be a link?
Expand on this?
QUOTE (Benson @ Apr 8 2008, 11:33 AM)
Expand on this?
A few years back there was talk on the net about people using Panthotenic Acid to clear and prevent acne, particularly during cycles. IIRC, it worked great and many people (forums teenagers) started taking it and getting results. I believe Mike was the first to start selling it in bulk for this purpose.
Perhaps this high cortisol theory that you present also applies to the acne issues? Stress seems to 'breakout' people, so it would actually make sense....
"B-5 for cortisol control." Pretty sure that's way cheaper than most supplements.
Yes I am always surprised its not first line treatment for acne given its demonstrated efficacy and complete lack of toxicity. I have never connected acne breakouts with cortisol before but its possible there is a connection.
No, he's not kidding, I ran across this earlier today when looking for cortisol stuff.:
Pantothenic acid deficiency as the pathogenesis of acne vulgaris.
Leung LH.
Department of General Surgery, Hong Kong Central Hospital, Hong Kong.
For years, the pathogenesis of acne vulgaris has been known to be strongly influenced by hormonal factors. However, the exact role of and the interrelationship among the various hormones in question have not been well elucidated. Here, I wish to suggest a radically different theory for its pathogenesis and relate its basic pathology to a deficiency in pantothenic acid, a vitamin hitherto not known to cause any deficiency syndrome in humans. Hence, the effect of hormonal factors in this disease entity becomes secondary to that of the availability of pantothenic acid. A complete cure of this condition is effected by a very liberal replacement therapy with the vitamin.
PMID: 7476595 [PubMed - indexed for MEDLINE]
The basic idea (theoretically) is that insufficient CoA due to deficiency in the pantothenic acid moiety shunts acetate (well acetyl CoA) -> acetoacetate -> steroid biosynthesis. This should only be an issue during puberty with crazy hormones. And I think this doc that was the main proponent gave patients like 80,000 X RDI and claimed to see improvement/resolution in 1 week - 1 month of treatment.
AFA cortisol issues, I assume that normalizing adrenal function would help sleep overall. Something I've always wondered -- would cortisol insufficiency cause the body/adrenals to compensate with extra epinephrine output?
Pantothenic acid deficiency as the pathogenesis of acne vulgaris.
Leung LH.
Department of General Surgery, Hong Kong Central Hospital, Hong Kong.
For years, the pathogenesis of acne vulgaris has been known to be strongly influenced by hormonal factors. However, the exact role of and the interrelationship among the various hormones in question have not been well elucidated. Here, I wish to suggest a radically different theory for its pathogenesis and relate its basic pathology to a deficiency in pantothenic acid, a vitamin hitherto not known to cause any deficiency syndrome in humans. Hence, the effect of hormonal factors in this disease entity becomes secondary to that of the availability of pantothenic acid. A complete cure of this condition is effected by a very liberal replacement therapy with the vitamin.
PMID: 7476595 [PubMed - indexed for MEDLINE]
The basic idea (theoretically) is that insufficient CoA due to deficiency in the pantothenic acid moiety shunts acetate (well acetyl CoA) -> acetoacetate -> steroid biosynthesis. This should only be an issue during puberty with crazy hormones. And I think this doc that was the main proponent gave patients like 80,000 X RDI and claimed to see improvement/resolution in 1 week - 1 month of treatment.
AFA cortisol issues, I assume that normalizing adrenal function would help sleep overall. Something I've always wondered -- would cortisol insufficiency cause the body/adrenals to compensate with extra epinephrine output?
QUOTE (Benson @ Apr 8 2008, 04:46 AM)
I'm back to thinking this is the result of high cortisol. In doing some more reading I came across something that indicated that Pantothenic Acid was a good modulator of cortisol so I bought some 1000mg time-release tablets and have been taking one before bed....so far, it has resolved the sleep issues, even on nights after very heavy lifting.
The only trouble is I can only find references to B5's anti-cortisol effect in secondary sources...
The only trouble is I can only find references to B5's anti-cortisol effect in secondary sources...
Thanks to a drawer full of powders that I have yet to finish or throw away I now magically have 500mg capsules of B5. How have you been going about dosage? Label recommendations?
I am taking 1g before bed.
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