text:
Talk:Windermere

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Comments
The title of this article is incorrect as it is geographically inccurate and tautologous. The name Windermere incorporates the concept of lake as -mere means lake.Dabbler 16:49, 12 Dec 2004 (UTC)

 * You're right Dabbler! I would suggest the title of "Windermere (Lake)", the clarification in brackets to distinguish the article from Windermere (Town) and perhaps other places called Windermere - of which there must be at least one in the USA! So how do you change an article title - anyone? Arcturus 17:17, 12 Dec 2004 (UTC)

I note with some surprise the comment that the lake "is bordered on the south by ranges of hills that provide panoramic views and have long been popular with hikers". While there are some pleasant foothills to the south of the lake, surely north is meant, not south, though in any case can a lake which is so narrow be "bordered" north or south by "ranges of hills"? StephenDawson 16:36, 10 Feb 2005 (UTC)

 * There are hills to the south-west and south-east of the lake, and yes they do afford panoramic views of Furness and Morecambe Bay, not to mention the Lake District to the north. However, the statement seems out of place here. Certainly there are mountains to the north, but I would suggest perhaps removing this entire sentence. Incidentally, giving precedence to metric units also seems out of place. I know there's a sort of standard in Wikipedia, but in the UK it makes more sense to give precendence to the units that are actually used in society (similarly for US-related articles). I can just about live with depths in metres, but to say that Windermere town is 1 kilometre from the lake just sounds a bit daft. I suggest imperial units be used with their metric equivalents in brackets.Arcturus 17:33, 10 Feb 2005 (UTC)

 * I see there is lots of discussion about units of measurement at Measurements Debate, and no individual is going to resolve those different views in a hurry, and certainly not me, and not here. I have a lot of sympathy for your view, but on balance (narrowly) disagree as, although this is an article on a UK feature, it is in an international encyclopedia. I measured the distances on a metric map (all UK maps for many years have been produced in metric): to me giving that as an imperial measurement seems a bit odd altogether, but using both measurements is the best compromise. As it was measured in metric units, I've given those first, as the imperial values are conversions of the metric measurements. (The speed limit still has imperial first, as the metric value is a conversion of the imperial value in the byelaw.) UK society is increasingly using metric, and I am personally entirely comfortable with the town being 1km from the lake, but recognise that many in the UK (almost certainly the majority) are not; the global society, however, is metric to an even greater extent, though I would accept that whether this is true of users of the English-language Wikipedia is not clear. I would agree with your preference if I were writing a guide-book for the UK market, but not in this context. However, I don't feel that strongly about it – I would not revert the page if someone were to change it, for example. StephenDawson 22:02, 10 Feb 2005 (UTC)

 * At least UK folks are generally capable of translating from metric to "English units" ... we in the U.S. are flummoxed by the whole idea (except for two-litre bottles of Coke) and mildly indignant that there are people who think differently than we do. The nerve! - DavidWBrooks 15:39, 11 Feb 2005 (UTC)

An example of where we have proved incapable of translating to metric is in fact the Windermere speed limit which reads   "10miles per hour (16.093) Kilometres per hour)" the national parks insist that the 10 miles per hour means nautical miles but the metric equivalent would be 18.52kilometers per hour. and the bylaw would read 10 mph (8.68mph) this has led to confusion about what the speed limit actually is as can be seen in the main article where the writer has seen a totally different meaning to 10 miles per hour. Andy40329 22:27, 29 June 2007 (UTC)

Photos
Three pictures of the lake is, IMHO, pushing it. They're all very nice, but kind of repetitive. Anybody else think so? - DavidWBrooks 19:18, 24 May 2005 (UTC)

 * Yes, I would agree. With the traditonal skin one of the pictures overlaps the margin as well. Also, as I've commented before, the use of the metric unit kilometre does seem way out of place here. Anyone object to me changing distances to miles with km in brackets? Arcturus 19:49, 24 May 2005 (UTC)

 * I added the top picture because neither of the previous two really showed much of the lake layout. On reflection, I also think 3 is excessive, but decided to leave the decision of which to delete to someone who (a) feels more strongly about it, and (b) isn't one of the photographers (to dissuade photonepotism). Next time I will remember to post a note to that effect :) --Jmstylr 21:02, 24 May 2005 (UTC)

 * I think three images is not excessive. I've tried to fix the formatting issue. Lupin 21:34, 24 May 2005 (UTC)

 * I think the cloudy day photo needs to go, it may reflect our weather well, but it's so dreary. BigglesPiP

Lake monster?
I've lived out on Ferry Nab for almost 20 years now, and I aint never seen no monster in that there lake. Nor have I ever met anyone who claims to have seen one, just the odd person who wants a Nessie of their own. There are plenty of Frog men go diving here, but most of them are fairly human. If I don't see some citation of a proper legend style monster I'm deleting the section. PiP 00:15, 25 March 2007 (UTC)

I see it's become an eel like creature now (pike IMO), there must be two, something keeps leaving black greasy hand-prints under the waterline of boats. And on the deck in the case where a boat is sailing with quite a list. PiP (talk) 04:18, 13 April 2008 (UTC)

MV Swift
What happened to the MV Swift? Should this be referenced ? Obrienaj 08:57, 9 November 2007 (UTC)

 * It corroded, very similar to the Tern PiP (talk) 04:15, 13 April 2008 (UTC)

Requested move

 * The following discussion is an archived discussion of the . Please do not modify it. Subsequent comments should be made in a new section on the talk page. No further edits should be made to this section.

Move Duja ► 14:00, 24 September 2007 (UTC)

Windermere (lake) → Windermere — The lake is the original and most common use of the term —Reginmund 02:07, 16 September 2007 (UTC)

Survey

 * Feel free to state your position on the renaming proposal by beginning a new line in this section with  or  , then sign your comment with  . Since polling is not a substitute for discussion, please explain your reasons, taking into account Wikipedia's naming conventions.

 * Support - as nominator. Reginmund 02:07, 16 September 2007 (UTC)
 * Weak oppose - there are a chunk of other places at the Windermere page, including one Florida site that has gotten publicity in the US because of celebrities living there. I don't think there's any confusion in having it this way (instead of having a Windermere (disambiguation) page). - DavidWBrooks 13:05, 16 September 2007 (UTC)
 * Weird - I didn't know until making the above note that there *is* a Windermere (disambiguation)! Plain old Windermere forwards to it, which is an odd situation. - DavidWBrooks 14:55, 16 September 2007 (UTC)

 * Support - this is, after all, the name sake of all the others (including the neighbouring town). David Arthur 14:33, 16 September 2007 (UTC)
 * Oppose To avoid confusion with the town, Windermere, Cumbria, which comes to mind as well as the lake, and articles on the disambiguation page. Tbo 157   talk  16:08, 16 September 2007 (UTC)
 * Changing to Support based on the evidence provided in the discussion below.  Tbo 157   (talk)    (review)  23:59, 21 September 2007 (UTC)
 * Support per nom. Although, I thought Lake Windermere was the more common name for it. Epbr123 07:05, 17 September 2007 (UTC)
 * Weak support per nom. I am supportive of the 'primary usage' argument, but 'Lake Windermere' would surely do the trick just as well per Epbr123. Ben MacDui (Talk) 08:05, 17 September 2007 (UTC)
 * Very Weak Support for reasons as given by the nominator, but surely, as others have noted "Lake Windermere" is by far the most usual and common name by which it is known. I suggest the proposed name change by altered accordingly.  DDStretch    (talk)  09:50, 17 September 2007 (UTC)
 * Support and Comment (changed opinion): In line with revised comments in the discussion below: the lake should be renamed "Windermere" as this is the name given on the Ordnance Survey maps as well as various official local council websites (all verifiable and capable of being cited). It therefore constitutes the official name for the body of water. The name of the town should be "Windermere (Cumbria)" in line with other similar dab cases. Dab pages must be revised if necessary.  DDStretch    (talk)  14:26, 21 September 2007 (UTC)

 * Comment - "original" doesn't generally carry weight in page naming. Dekimasu よ! 15:49, 17 September 2007 (UTC)
 * Support as per discussion I added below - lake is most generally known as plain "Windermere". Follow pattern of Buttermere. PamD 14:20, 21 September 2007 (UTC)

Discussion

 * Any additional comments:

 * I would like anyone voting to please note that the town in Cumbria has 2,295 people, the town in Florida has 2,019, the place in Seattle is let alone a neighbourhood, all of the places have been named after the lake. Windermere is also a part of English heritage considering that it is the largest natural lake. it is also the primary (and only) usage on Britannica Reginmund 17:24, 16 September 2007 (UTC)
 * When I think of Windermere, I think of both the town and the lake. If I typed in Windermere, I would expect to see the disambiguation page.   Tbo 157   talk  17:51, 16 September 2007 (UTC)
 * I hardly think that the town should have a higher rank above the lake. After all, the town was named after the lake and not the other way around. Reginmund 22:14, 16 September 2007 (UTC)
 * I agree but don't you think calling the article Windermere (lake) would be easier for users to differentiate between the town and the lake. This wouldn't give either the town or the lake a higher status.  I think Windermere should simply direct to the disambiguation page, where the lake is at the top.  Not everyone searching for Windermere would be looking for the article about the lake.  Tbo 157   (talk)    (review)  22:36, 16 September 2007 (UTC)

 * But this is why we have primary uses. That is why such cities as Birmingham and Cambridge go directly to their primary uses and not Birmingham, Alabama or Cambridge, Massachusetts. Or how about this, since the town is so important considering that it is a destination for travellers to the lake. We could have Windermere go directly to the lake and have a link to the town above the link to the DAB page. It worked for Birmingham. Reginmund 23:06, 16 September 2007 (UTC)
 * I propose that the name should really be changed to "Lake Windermere" as that is the primary name by which is it known in the UK. The other issues about disambiguation pages then become moot. I suggest this alteration to the proposal would solve the problem as well as defuse any potential contentious issues about places having the same name.  DDStretch    (talk)  09:53, 17 September 2007 (UTC)
 * The problem with "Lake Windermere" is that it is tautologous and generally understood to be incorrect. It would also strike up some confusion as to what was named after what. Reginmund 14:09, 17 September 2007 (UTC)
 * Tautologous, such as, for example, Bredon Hill, and Pendle Hill, both of which are supposed to mean mean "hill hill hill"? In which case, I don't think something being tautologous should rule it out on a priori grounds. In terms of it "generally understood to be incorrect", I take your point, but there are, nevertheless, quite a few refences to it as "Lake Windermere" (sometimes alongside other variations) around: see, , , , , , to name but a few. If a more authoritative source can be found that states "Windermere" is the correct name, then so be it, and I would be happy if it were found. But on the basis of wikipedia having to reflect actual usage, rather than prescribing correct usage, it isn't as clear-cut as it could be at the moment, that "Lake Windermere" can be so lightly dismissed as an alternative.  DDStretch    (talk)  15:37, 17 September 2007 (UTC)
 * Unless the aformentioned hills have been accepted into the English lexicon as correct, there is no reason that they should not stay. However, I found an opinion on Windermere's nasty appendage. Reginmund 23:28, 17 September 2007 (UTC)
 * ...at an article titled "Journeying Through Time on Lake Windermere." —  AjaxSmack   07:49, 18 September 2007 (UTC)
 * Yes, but it points out that stricly speaking it is incorrect. Rather it be a correct title page than a colloquialism? Reginmund 21:41, 18 September 2007 (UTC)
 * "Incorrect" is a reach since mere is arguably only a regional term. Maybe etymologically redundant is better but it is something that sometimes occurs, notably with toponyms originally from other languages (e.g., River Avon, Caloosahatchee River, Mekong River, Tannu-Ola Mountains, and others mentioned above). —   AjaxSmack     01:47, 19 September 2007 (UTC)
 * Well, it says "incorrect" on the site. I don't know about the others. That is one of the reasons that Sahara is not a "Sahara Desert" Reginmund 06:28, 19 September 2007 (UTC)
 * I agree with you that "Lake Windermere" may be incorrect but I still think its worth keeping the article at its current location to avoid confusion with the town and numerous other cities. Tbo 157   (talk)    (review)  17:09, 19 September 2007 (UTC)
 * Then what would you say is the most common rendering of "Windermere"? For names such as Birmingham, it may be ambiguous with the city in Alabama, however it isn't disambiguated. Reginmund 22:29, 20 September 2007 (UTC)
 * Clearly, wikipedia is inconsistent on this issue, partly because it's not a clear-cut matter; we're not going to find an "objective", "correct" way to proceed. Here's a question that will help me decide: Is there an overwhelmingly common usage in towns around the lake itself: Is it regularly called Lake Windermere (or Windermere Lake) thereabouts, or just Windermere? - DavidWBrooks 22:34, 20 September 2007 (UTC)
 * I wouldn't know about the towns in Cumbria because I live in London but here, the lake is just refered to as "Windermere". In fact, I didn't know that there was a town next to it of the same name. Reginmund 22:50, 20 September 2007 (UTC)

 * Windermere is the name of the lake, and of the town. It is a "well known fact" that "there is only one lake in the Lake District" - Bassenthwaite Lake.  See  for the National Park Authority info about Windermere, named as such.  I'd support calling the lake's page "Windermere", with link to a dab page, and calling the town's page "Windermere, Cumbria". This is the pattern at Buttermere.    PamD 14:18, 21 September 2007 (UTC)

 * I checked the OS maps of the area, and, going by them, PamD is correct. Therefore, I withdraw my suggestion that Lake Windermere might be an alternative usefully considered (I've struck it out, above). It should be "Windermere" with suitable link to a dab page, and the town should read "Windermere, Cumbria", in line with other similar cases, and also as suggested by PamD.  DDStretch    (talk)  14:23, 21 September 2007 (UTC)

 * Windermere, Cumbria could refer to the lake or the town. Tbo 157   (talk)    (review)  16:18, 21 September 2007 (UTC)

 * Then one has suitable dab notices at the top of each page.  DDStretch    (talk)  16:24, 21 September 2007 (UTC)

 * I agree with PamD. Reginmund 23:20, 21 September 2007 (UTC)

 * Based on the evidence presented, I also agree with PamD. Tbo 157   (talk)    (review)  23:57, 21 September 2007 (UTC)
 * The above discussion is preserved as an archive of the . Please do not modify it. Subsequent comments should be made in a new section on this talk page. No further edits should be made to this section.

Are you sure about the whole of the lake being within Westmoreland?
All the old county maps I have seen show the lake being entirely within Lancashire - the northern half of the lake forming a border with Westmoreland on the eastern shore, and the south of the lake wholly within Lancashire by several miles. In 1842, 'Barclay's Complete & Universal Dictionary' described Lancashire as "...a county of England, lying on the Irish Sea, and bounded by Cumberland, Westmoreland, Yorkshire, and Cheshire. It is 75 miles in length, and 30 in breadth............... The principal rivers are the Mersey, Irwell, Ribble, Lune, Leven, Wyre, Hodder, Roche, Duddon, Winster, Kent, and Calder, and it has two considerable lakes, Windermere and Coniston Water. Lancaster is the county town. Population, 1,667,054. It returns 26 members to parliament. " Angelogravity (talk) 23:56, 23 July 2010 (UTC)

 * I'm no expert on this, but if you zoom in and look at the map in the article at full resolution, there seems to be a dotted line along the whole western shore and the southern half of the eastern shore, which I would assume to be the county boundary, as it then was. --  Dr Greg   talk  00:58, 24 July 2010 (UTC)

Largest natural lake in England?
I can easily believe that this is the largest natural lake in England, but I came to this article hoping to find an inline citation that said so. Is there such a citation, and I missed it? If not, can one be supplied? --DThomsen8 (talk) 17:05, 18 November 2012 (UTC)

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How many islands?
The article claims that Windemere has 18 islands. The citation is an archived National Park (Lake District) page. https://web.archive.org/web/20120624045128/http://www.lakedistrict.gov.uk/visiting/windermere/windermere_outonthelake/windermere-islands The page claims 18 islands, but at the bottom of the page has a list which shows 18 items. One of these is 'Lilies of the Valley East and West', which are two islands, not one. The article itself includes a list of 19 islands. Windermere 2A00:23C6:3B89:8A00:687F:363A:37F5:AFC2 (talk) 20:02, 31 May 2019 (UTC)

Ecology
https://www.independent.co.uk/climate-change/news/raw-sewage-windermere-water-algae-b2146970.html Xx236 (talk) 10:24, 25 August 2022 (UTC)
 * Cyanobacteria Xx236 (talk) 10:29, 25 August 2022 (UTC)

Long distance swimming
The section on Swimming implies that interest in long-distance swimming in Windermere began in 2008. Whilst researching the article on Jenny James (swimmer), first Welsh person to swim the English Channel, I came across a reference to her gaining the women's Windermere Record in 1958, and to other swimmers being listed as "Windermere Swimmers": https://bldsa.org.uk/wp-content/uploads/BLDSA1stLochLomondChampionshipprogramme-August1959.pdf. So long distance swimming of Windermere would appear to have been an established institution in the 1950s.Ntmr (talk) 11:24, 7 October 2023 (UTC)

Brendan Chase
Article should include if possible mention of the Brendan Chase in historic Windermere and David Maloney a.k.a. the Respected Gentleman, its former proprietor. Okay? 12.182.218.186 (talk) 11:05, 17 June 2024 (UTC)

title: Talk:Windermere


text:
Codlea

Codlea (Zeiden; Transylvanian Saxon dialect: Zäöeden; Feketehalom) is a city in Brașov County, Transylvania, Romania.

Name
The Romanian name "Codlea" could be a derivation from the Latin codella, a diminutive of Latin coda (edge, rearward); or it could be a derivation from the Slavic cotal ("kettle"), as the Măgura Codlei (in this reading: "Kettle Hill") looks like a kettle. In Romanian, măgură means "large hill, mound, forest located on a high place".

The hill also provides the Hungarian name of the city, Feketehegy, "Black Hill".

The German name's origin is unknown, but there is a theory that it was derived from Zeidler, an antiquated word for "beekeeper".

History
During the 13th century, the Teutonic Order built a fortress known as Schwarzburg ("black castle") near the "Măgura Codlei". The castle's name was first noted in 1265 and was rebuilt for the last time in 1432 by the craftsmen's guild that worked in the town. The city of Codlea is believed to have been also founded by Germans. The fortified church in the city is the largest in the Burzenland historic region. Codlea was well known for its flowers and was called the city of flowers.

Climate
Codlea has a warm-summer humid continental climate (Dfb in the Köppen climate classification).

Population

 * 1510: 670
 * 1814: 3,264
 * 1849: 3,764
 * 1890: 4,035
 * 2,680 Germans (67%)
 * 1,211 Romanians (30%)
 * 44 Hungarians (1%)
 * 100 Jews and others (2%)
 * 1930: 5,219
 * 3,111 Germans (60%)
 * 1,916 Romanians (36%)
 * 192 Hungarians (4%)
 * 1941: 6,214
 * 1966: 13,075
 * 1977: 22,744
 * 1982: 23,500
 * 1992: 24,620
 * 2002: 24,286
 * 2011: 21,708
 * 2021: 20,534

As of the 2011 census, 90.2% of inhabitants were Romanians, 5.6% Roma, 2.8% Hungarians, and 1% Germans. As of 2002, 86.8% were Romanian Orthodox, 3.7% Roman Catholic, 3.1% Pentecostal, 2.2% Christian Evangelical, 1% Evangelical Augustan Confession, and 0.8% Reformed.

Natives

 * Fritz Klein (1888–1945), Nazi SS doctor hanged for war crimes
 * Doina Popescu (1938–), volleyball player
 * Alexandru Zaharescu (1961–), mathematician

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Codlea


text:
Tamoxifen

Tamoxifen, sold under the brand name Nolvadex among others, is a selective estrogen receptor modulator used to prevent breast cancer in women and men. It is also being studied for other types of cancer. It has been used for Albright syndrome. Tamoxifen is typically taken daily by mouth for five years for breast cancer.

Serious side effects include a small increased risk of uterine cancer, stroke, vision problems, and pulmonary embolism. Common side effects include irregular periods, weight loss, and hot flashes. It may cause harm to the baby if taken during pregnancy or breastfeeding. It is a selective estrogen-receptor modulator (SERM) and works by decreasing the growth of breast cancer cells. It is a member of the triphenylethylene group of compounds.

Tamoxifen was initially made in 1962, by chemist Dora Richardson. It is on the World Health Organization's List of Essential Medicines. Tamoxifen is available as a generic medication. In 2020, it was the 317th most commonly prescribed medication in the United States, with more than 900thousand prescriptions.

Dysmenorrhea
Tamoxifen has been used effectively to improve blood flow, reduce uterine contractility and pain in dysmenorrhea patients.

Breast cancer
Tamoxifen is used for the treatment of both early and advanced estrogen receptor-positive (ER-positive or ER+) breast cancer in pre- and postmenopausal women. Tamoxifen increases the risk of postmenopausal bleeding, endometrial polyps, hyperplasia, and endometrial cancer; using tamoxifen with an intrauterine system releasing levonorgestrel might increase vaginal bleeding after 1 to 2 years, but reduces somewhat endometrial polyps and hyperplasia, but not necessarily endometrial cancer. Additionally, it is the most common hormone treatment for male breast cancer. It is also approved by the FDA for the prevention of breast cancer in women at high risk of developing the disease. It has been further approved for the reduction of contralateral (in the opposite breast) cancer. The use of tamoxifen is recommended for 10 years.

In 2006, the large STAR clinical study concluded that raloxifene is also effective in reducing the incidence of breast cancer. Updated results after an average of 6.75 years of follow up found that raloxifene retains 76% of tamoxifen's effectiveness in preventing invasive breast cancer, with 45% fewer uterine cancers and 25% fewer blood clots in women taking raloxifene than in women taking tamoxifen.

Infertility
Tamoxifen is used for ovulation induction to treat infertility in women with anovulatory disorders. It is given at days three to seven of a woman's cycle.

Tamoxifen improves fertility in males with infertility by disinhibiting the hypothalamic–pituitary–gonadal axis (HPG axis) via ER antagonism and thereby increasing the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and increasing testicular testosterone production.

Tamoxifen is widely used for the treatment of male factor and idiopathic infertility. It has been shown that tamoxifen induces sperm production and so improves male fertility. The results indicated that although the tamoxifen did not affect the sperm count,motility, and viability parameters, it could elevate the percentage of sperm cells with abnormal morphology and abnormal chromatin at both doses. In addition, in comparison with the control mice, a significant elevation was observed in spermatozoa with residual histones (assessed by AB staining) at high doses of tamoxifen. Our experimental data in mice suggested that the use of tamoxifen for treating male infertility might increase the rates of spermatozoa with abnormal chromatin in a dose-dependent manner.

Gynecomastia
Tamoxifen is used to prevent and treat gynecomastia. It is taken as a preventative measure in small doses, or used at the onset of any symptoms such as nipple soreness or sensitivity. Other medications are taken for similar purposes such as clomifene and the anti-aromatase drugs which are used in order to try to avoid the hormone-related adverse effects.

Early puberty
Tamoxifen is useful in the treatment of peripheral precocious puberty, for instance due to McCune–Albright syndrome, in both girls and boys. It has been found to decrease growth velocity and the rate of bone maturation in girls with precocious puberty, and hence to improve final height in these individuals.

Available forms

Tamoxifen is available as a tablet or oral solution.

Contraindications
Tamoxifen has a number of contraindications, including known hypersensitivity to tamoxifen or other ingredients, individuals taking concomitant coumarin-type anticoagulant therapy, and women with a history of venous thromboembolism (deep vein thrombosis or pulmonary embolism).

Side effects
A report in September 2009 from Health and Human Services' Agency for Healthcare Research and Quality suggests that tamoxifen, raloxifene, and tibolone used to treat breast cancer significantly reduce invasive breast cancer in midlife and older women, but also increase the risk of adverse side effects.

Endometrial cancer
Tamoxifen is a selective estrogen receptor modulator (SERM). Even though it is an antagonist in breast tissue it acts as partial agonist on the endometrium and has been linked to endometrial cancer in some women. Therefore, endometrial changes, including cancer, are among tamoxifen's side effects. With time, risk of endometrial cancer may be doubled to quadrupled, which is a reason tamoxifen is typically only used for five years.

The American Cancer Society lists tamoxifen as a known carcinogen, stating that it increases the risk of some types of uterine cancer while lowering the risk of breast cancer recurrence.

Cardiovascular and metabolic
Tamoxifen treatment of postmenopausal women is associated with beneficial effects on serum lipid profiles. However, long-term data from clinical trials have failed to demonstrate a cardioprotective effect. For some women, tamoxifen can cause a rapid increase in triglyceride concentration in the blood. In addition, there is an increased risk of thromboembolism especially during and immediately after major surgery or periods of immobility. Use of tamoxifen has been shown to slightly increase risk of deep vein thrombosis, pulmonary embolism, and stroke.

Liver toxicity
Tamoxifen has been associated with a number of cases of hepatotoxicity. Several different varieties of hepatotoxicity have been reported. Tamoxifen can also precipitate non-alcoholic fatty liver disease in obese and overweight women (not in normal weight women) at an average rate of 40% after a year use with 20 mg/day.

Overdose
Acute overdose of tamoxifen has not been reported in humans. In dose-ranging studies, tamoxifen was administered at very high doses in women (e.g., 300 mg/m2) and was found to produce acute neurotoxicity including tremor, hyperreflexia, unsteady gait, and dizziness. These symptoms occurred within three to five days of therapy and disappeared within two to five days of discontinuation of therapy. No indications of permanent neurotoxicity were observed. QT prolongation was also observed with very high doses of tamoxifen. There is no specific antidote for overdose of tamoxifen. Instead, treatment should be based on symptoms.

Interactions
Patients with variant forms of the gene CYP2D6 may not receive full benefit from tamoxifen because of too slow metabolism of the tamoxifen prodrug into its active metabolites. On 18 October 2006, the Subcommittee for Clinical Pharmacology recommended relabeling tamoxifen to include information about this gene in the package insert. Certain CYP2D6 variations in breast cancer patients lead to a worse clinical outcome for tamoxifen treatment. Genotyping therefore has the potential for identification of women who have these CYP2D6 phenotypes and for whom the use of tamoxifen is associated with poor outcomes. Recent research has shown that 7–10% of women with breast cancer may not receive the full medical benefit from taking tamoxifen due to their genetic make-up. DNA Drug Safety Testing can examine DNA variations in the CYP2D6 and other important drug processing pathways. More than 20% of all clinically used medications are metabolized by CYP2D6 and knowing the CYP2D6 status of a person can help the doctor with the future selection of medications. Other molecular biomarkers may also be used to select appropriate patients likely to benefit from tamoxifen.

Recent studies suggest that taking the selective serotonin reuptake inhibitors (SSRIs) antidepressants paroxetine (Paxil), fluoxetine (Prozac), and sertraline (Zoloft) can decrease the effectiveness of tamoxifen, as these drugs compete for the CYP2D6 enzyme which is needed to metabolize tamoxifen into its active forms. A U.S. study presented at the American Society of Clinical Oncology's annual meeting in 2009 found that after two years, 7.5% of women who took only tamoxifen had a recurrence, compared with 16% who took either paroxetine, fluoxetine or sertraline, drugs considered to be the most potent CYP2D6 inhibitors. That difference translates to a 120% increase in the risk of breast cancer recurrence. Patients taking the SSRIs Celexa (citalopram), Lexapro (escitalopram), and Luvox (fluvoxamine) did not have an increased risk of recurrence, due to their lack of competitive metabolism for the CYP2D6 enzyme. A newer study demonstrated a clearer and stronger effect from paroxetine in causing the worst outcomes. Patients treated with both paroxetine and tamoxifen have a 67% increased risk of death from breast cancer, from 24% to 91%, depending on the duration of coadministration.

Tamoxifen interacts with certain other antiestrogens. The aromatase inhibitor aminoglutethimide induces the metabolism of tamoxifen. Conversely, the aromatase inhibitor letrozole does not affect the metabolism of tamoxifen. However, tamoxifen induces the metabolism of letrozole and significantly reduces its concentrations.

Selective estrogen receptor modulator activity

Tamoxifen acts as a selective estrogen receptor modulator (SERM), or as a partial agonist of the estrogen receptors (ERs). It has mixed estrogenic and antiestrogenic activity, with its profile of effects differing by tissue. For instance, tamoxifen has predominantly antiestrogenic effects in the breasts but predominantly estrogenic effects in the uterus and liver. In breast tissue, tamoxifen acts as an ER antagonist so that transcription of estrogen-responsive genes is inhibited. A beneficial side effect of tamoxifen is that it prevents bone loss by acting as an ER agonist (i.e., mimicking the effects of estrogen) in this cell type. Therefore, by inhibiting osteoclasts, it prevents osteoporosis. When tamoxifen was launched as a drug, it was thought that tamoxifen would act as an ER antagonist in all tissues, including bone, and therefore it was feared that it would contribute to osteoporosis. It was therefore very surprising that the opposite effect was observed clinically. Hence tamoxifen's tissue selective action directly led to the formulation of the concept of SERMs.

Tamoxifen is a long-acting SERM, with a nuclear retention of the ER–tamoxifen (or metabolite) complex of greater than 48 hours. It has relatively little affinity for the ERs itself and instead acts as a prodrug of active metabolites such as endoxifen (4-hydroxy-N-desmethyltamoxifen) and afimoxifene (4-hydroxytamoxifen; 4-OHT). These metabolites have approximately 30 to 100 times greater affinity for the ERs than tamoxifen itself. Per one study, tamoxifen had 7% and 6% of the affinity of estradiol for the ERα and ERβ, respectively, whereas afimoxifene had 178% and 338% of the affinity of estradiol for the ERα and ERβ, respectively. Hence, afimoxifene showed 25-fold higher affinity for the ERα and 56-fold higher affinity for the ERβ than tamoxifen. The antiestrogenic potencies of endoxifen and afimoxifene are very similar. However, endoxifen occurs in much higher concentrations than afimoxifene and is now thought to be the major active form of tamoxifen in the body.

Tamoxifen binds to ER competitively (with respect to the endogenous agonist estrogen) in tumor cells and other tissue targets, producing a nuclear complex that decreases DNA synthesis and inhibits estrogen effects. It is a nonsteroidal agent with potent antiestrogenic properties which compete with estrogen for binding sites in breast and other tissues. Tamoxifen causes cells to remain in the G0 and G1 phases of the cell cycle. Because it prevents (pre)cancerous cells from dividing but does not cause cell death, tamoxifen is cytostatic rather than cytocidal. Tamoxifen binds to ER, the ER/tamoxifen complex recruits other proteins known as co-repressors, and the complex then binds to DNA to modulate gene expression. Some of these proteins include NCoR and SMRT. Tamoxifen function can be regulated by a number of different variables including growth factors. Tamoxifen needs to block growth factor proteins such as ErbB2/HER2 because high levels of ErbB2 have been shown to occur in tamoxifen resistant cancers. Tamoxifen seems to require a protein PAX2 for its full anticancer effect. In the presence of high PAX2 expression, the tamoxifen/ER complex is able to suppress the expression of the pro-proliferative ERBB2 protein. In contrast, when AIB-1 expression is higher than PAX2, tamoxifen/ER complex upregulates the expression of ERBB2 resulting in stimulation of breast cancer growth.

Tamoxifen is antigonadotropic in postmenopausal women and partially suppresses levels of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in such women. However, it has progonadotropic effects in premenopausal women and increases estrogen levels by 6-fold in them. Due to the nature of tamoxifen as a competitive ER ligand, this increase in estrogen levels is liable to interfere with the antiestrogenic efficacy of tamoxifen. The effects of tamoxifen on breast cancer Ki-67 expression, sex hormone-binding globulin (SHBG) levels, and IGF-1 levels are dose-dependent across a dosage range of 1 to 20 mg/day in women with breast cancer. Tamoxifen has been found to decrease insulin-like growth factor 1 (IGF-1) levels by 17 to 38% in women and men. Suppression of IGF-1 production in the liver is a well-known action of estrogens and SERMs. A 10 mg/day dosage of tamoxifen is nearly as effective as a 20 mg/day dosage in suppressing IGF-1 levels.

Other activities
Afimoxifene is an agonist of the G protein-coupled estrogen receptor (GPER) with relatively low affinity. Its affinity for the receptor is in the range of 100 to 1,000 nM, relative to 3 to 6 nM for estradiol.

In addition to its activity as a SERM, afimoxifene binds to both the estrogen-related receptor β and estrogen-related receptor γ and is an antagonist of the estrogen-related receptor γ (ERRγ).

Norendoxifen (4-hydroxy-N,N-didesmethyltamoxifen), another active metabolite of tamoxifen, has been found to act as a potent competitive aromatase inhibitor (IC50 = 90 nM), and may also be involved in the antiestrogenic activity of tamoxifen.

In addition to its activity as a SERM, tamoxifen is a potent and selective protein kinase C inhibitor, and is active in this regard at therapeutic concentrations. This action is thought to underlie the efficacy of tamoxifen in the treatment of bipolar disorder.

Tamoxifen is an inhibitor of P-glycoprotein.

Absorption
Tamoxifen is rapidly and extensively absorbed from the intestines with oral administration. The oral bioavailability of tamoxifen is approximately 100%, which is suggestive of minimal first-pass metabolism in the intestines and liver. Following intake, peak levels of tamoxifen occur after three to seven hours. Steady state levels of tamoxifen are reached typically after 3 to 4 weeks but possibly up to 16 weeks of daily administration. Steady state levels of afimoxifene are achieved after 8 weeks of daily tamoxifen administration. Peak levels of tamoxifen after a single 40 mg oral dose were 65 ng/mL and steady state levels at 20 mg/day were 310 ng/mL. Levels of tamoxifen show clear dose dependency across a dosage range of 1 to 20 mg/day. Endoxifen levels are approximately 5 to 10 times higher than afimoxifene levels, with large interindividual variability. Endoxifen levels have been reported as 10.8 to 15.9 ng/mL at steady state in CYP2D6 normal metabolizers during therapy with 20 mg/day tamoxifen. The most abundant metabolites of tamoxifen in terms of circulating concentrations are N-desmethyltamoxifen, N,N-didesmethyltamoxifen, (Z)-endoxifen, and tamoxifen N-oxide.

Distribution
The volume of distribution of tamoxifen is 50 to 60 L/kg and its clearance has been estimated as 1.2 to 5.1 L/hour. High concentrations of tamoxifen have been found in breast, uterus, liver, kidney, lung, pancreas, and ovary tissue in animals and humans. Levels of tamoxifen in the uterus have been found to be 2- to 3-fold higher than in the circulation and in the breasts 10-fold higher than in the circulation. The plasma protein binding of tamoxifen and afimoxifene is greater than 99%. A majority of tamoxifen is bound to albumin. Albumin alone binds 98.8% of tamoxifen while other plasma proteins are not greatly involved.

Metabolism
Tamoxifen is a prodrug and is metabolized in the liver by the cytochrome P450 isoforms CYP3A4, CYP2C9, and CYP2D6 into active metabolites such as endoxifen (4-hydroxy-N-desmethyltamoxifen) and afimoxifene (4-hydroxytamoxifen). Conversion of tamoxifen by N-demethylation into N-desmethyltamoxifen, which is catalyzed primarily by CYP3A4 and CYP3A5, is responsible for approximately 92% of tamoxifen metabolism. Conversely, 4-hydroxylation of tamoxifen into afimoxifene is responsible for only about 7% of tamoxifen metabolism. Following its formation, N-desmethyltamoxifen is oxidized into several other metabolites, the most notable of which is endoxifen. Another active metabolite, norendoxifen (4-hydroxy-N,N-didesmethyltamoxifen), is formed via N-demethylation of endoxifen or 4-hydroxylation of N,N-didesmethyltamoxifen. Tamoxifen and its metabolites undergo conjugation, including glucuronidation and sulfation. Tamoxifen may inhibit its own metabolism.

Elimination
Tamoxifen has a long elimination half-life of typically 5 to 7 days, with a range of 4 to 11 days. Similarly, the half-life of afimoxifene is 14 days. Conversely, the half-life of endoxifen is 50 to 70 hours (2–3 days). The long half-lives of tamoxifen and afimoxifene are attributed to their high plasma protein binding as well as to enterohepatic recirculation. Upon discontinuation of treatment, levels of tamoxifen and its metabolites persist in the circulation for at least 6 weeks. Tamoxifen is excreted in bile and is eliminated in feces, while small amounts are eliminated in urine.

Chemistry
Tamoxifen is a nonsteroidal SERM of the triphenylethylene family and was structurally derived from diethylstilbestrol-like estrogens and antiestrogens such as chlorotrianisene and ethamoxytriphetol. Initially, clomifene was synthesized, and tamoxifen was developed subsequently. Tamoxifen is closely related structurally to other triphenylethylenes, such as clomifene, nafoxidine, ospemifene, toremifene, and numerous others. Other SERMs, like raloxifene, are structurally distinct from tamoxifen and other triphenylethylenes.

History
In the late 1950s, pharmaceutical companies were actively researching a newly discovered class of anti-estrogen compounds in the hope of developing a morning-after contraceptive pill. Arthur L Walpole was a reproductive endocrinologist who led such a team at the Alderley Park research laboratories of ICI Pharmaceuticals. It was there in 1962 that chemist Dora Richardson first synthesized tamoxifen, back then known as ICI-46,474, when she was looking to create triphenylethylene derivatives for the contraceptive pill project that her team was researching.

This compound was originally created to work as an estrogen inhibitor, but instead was found to stimulate ovulation in participants of the drug testing trial. Walpole and his colleagues filed a UK patent covering this compound in 1962, but patent protection on this compound was repeatedly denied in the US until the 1980s. Tamoxifen did eventually receive marketing approval as a fertility treatment, but the class of compounds never proved useful in human contraception. A link between estrogen and breast cancer had been known for many years, but cancer treatments were not a corporate priority at the time, and Walpole's personal interests were important in keeping support for the compound alive in the face of this and the lack of patent protection. It was only when Walpole threatened to leave his position that corporate decided to allow trials and testing for tamoxifen as a drug that could be used to treat breast cancer. Without Walpole's effort towards defending the work that his team had done in discovering a possibly revolutionary source for breast cancer treatment, tamoxifen could have become a discarded or under-researched idea. Walpole's team consisted of Dora Richardson and G. A. Snow, who worked on the chemistry portion of the project, along with G. E. Paget and J. K. Walley, who focused primarily on the biological side.

Tamoxifen is one of three drugs in an anti-angiogenetic protocol developed by Dr. Judah Folkman, a researcher at Children's Hospital at Harvard Medical School in Boston. Folkman discovered in the 1970s that angiogenesis – the growth of new blood vessels – plays a significant role in the development of cancer. Since his discovery, an entirely new field of cancer research has developed. Clinical trials on angiogenesis inhibitors have been underway since 1992 using many different drugs. The Harvard researchers developed a specific protocol for a golden retriever named Navy who was cancer-free after receiving the prescribed cocktail of celecoxib, doxycycline, and tamoxifen – the treatment subsequently became known as the Navy Protocol. Furthermore, tamoxifen treatment alone has been shown to have anti-angiogenetic effects in animal models of cancer which appear to be, at least in part, independent of tamoxifen's ER antagonist properties.

Other antiestrogens, such as ethamoxytriphetol (MER-25) and clomifene (MRL-41), were assessed for treatment of breast cancer and found to be effective before tamoxifen, but were plagued with toxicity issues. The first clinical study of tamoxifen took place at the Christie Hospital in 1971, and showed a convincing effect in advanced breast cancer, but nevertheless ICI's development programme came close to termination when it was reviewed in 1972. In an unpublished article from the early days of the trial, Dora Richardson documented her team's excitement about tamoxifen's effects in counteracting infertility problems and the early positive effects found in breast cancer patients. Unfortunately, this work was not well received by everyone, as the team was supposed to be looking for a contraceptive pill. Tamoxifen's further development may have been bolstered by a second clinical study by Harold W.C. Ward at the Queen Elizabeth Hospital, Birmingham. Ward's study showed a more definitive response to the drug at a higher dosage. Walpole also may have helped to convince the company to market tamoxifen for late stage breast cancer in 1973. He was also instrumental in funding V. Craig Jordan to work on tamoxifen. In 1972, ICI Pharmaceuticals Division abandoned development of tamoxifen for financial reasons. The drug was subsequently reinvented from a failed contraceptive, to become tamoxifen, the gold standard for the adjuvant treatment of breast cancer and the pioneering medicine for chemprevention for high-risk women. Two books, Estrogen Action, Selective Estrogen Receptor Modulators and Women's Health (Imperial College Press 2013) and Tamoxifen: Pioneering Medicine in Breast Cancer (Springer 2013) tell this story.

1980 saw the publication of the first trial to show that tamoxifen given in addition to chemotherapy improved survival for patients with early breast cancer. In advanced disease, tamoxifen is now only recognized as effective in ER+ patients, but the early trials did not select ER+ patients, and by the mid-1980s the clinical trial picture was not showing a major advantage for tamoxifen. Nevertheless, tamoxifen had a relatively mild side-effect profile, and a number of large trials continued.

The pharmacology of SERMs was discovered, defined, and deciphered during the 1980s. A clinical strategy was described that led to the creation of SERMs as a group of multifunctional medicines aimed at the treatment or prevention of many conditions in postmenopausal women, e.g. osteoporosis and breast cancer. This story is told in: V. Craig Jordan, ed. 2013. "Estrogen Action, Selective Estrogen Receptor Modulators and Women's Health" Imperial College Press, Singapore.

The early sales of tamoxifen in both the UK and in the U.S. far exceeded ICI's original estimate, but despite this, at the annual portfolio review ICI's board members still asserted that "there was no market for cancer", leaving the drug's marketing success to rely on its clinical results and clinicians' and scientists' interests in it. Shortly after, Dora Richardson published a history of tamoxifen that, unusually for that type of paper, included personal accounts and letters from patients who attributed their healing to the drug. It is by giving voice to cancer patients using tamoxifen, and so helping to push it forward, by justifying it both morally and scientifically to corporations.

It was not until 1998 that the meta-analysis of the Oxford-based Early Breast Cancer Trialists' Collaborative Group showed definitively that tamoxifen was effective for early breast cancer.

Brand names
Tamoxifen is marketed under the brand names Nolvadex and Soltamox, and a variety of other brand names throughout the world.

Economics
Global sales of tamoxifen in 2001 were approximately $1.02 billion. Since the expiration of the patent in 2002, it is widely available as a generic drug around the world. , tamoxifen was the world's largest selling hormonal drug for the treatment of breast cancer.

Research
In McCune-Albright syndrome (MAS) tamoxifen has been used to treat premature puberty and the consequences of premature puberty. Tamoxifen has been seen to decrease rapid bone maturation which is the result of excessive estrogen and alter predicted adult height (PAH). The same effects have also been seen in short pubertal boys. However, one in vitro study in 2007 and later an in vivo study in 2008 have shown that tamoxifen induces apoptosis in growth plate chondrocytes, reduces serum insulin-like growth factor 1 (IGF-1) levels and causes persistent retardation of longitudinal and cortical radial bone growth in young male rats, leading the researchers to express concern giving tamoxifen to growing individuals.

Tamoxifen has been studied in the treatment of the rare conditions of retroperitoneal fibrosis and idiopathic sclerosing mesenteritis. It has also been proposed as part of a treatment plan for Riedel's thyroiditis.

Tamoxifen is used as a research tool to trigger tissue-specific gene expression in many conditional expression constructs in genetically modified animals including a version of the Cre-Lox recombination technique. While widely used in transgenic research, the strong anabolic effect of tamoxifen on bone might confound this approach, especially as it relates to bone-targeted constructs.

Tamoxifen may be effective in the treatment of mania in people with bipolar disorder. This is thought to be due to blockade of protein kinase C (PKC), an enzyme that regulates neuron activity in the brain. Researchers believe PKC is overactive during the mania in bipolar patients. , endoxifen, a major active metabolite of tamoxifen with a 4-fold more potent PKC inhibition, was in phase III clinical trials for bipolar disorder.

title: Tamoxifen


text:
1998–99 FA Premier League

The 1998–99 FA Premier League (known as the FA Carling Premiership for sponsorship reasons) was the seventh season of the Premier League, the top division of English football, since its establishment in 1992. Manchester United won a treble of the league title, the FA Cup and the UEFA Champions League. They secured their fifth league title in seven seasons after outlasting Arsenal and Chelsea in a closely fought title race, losing just three league games all season.

The season was also the 100th season of top flight football in England, not counting years lost to the two World Wars. Of the original clubs in the first Football League season, only Aston Villa, Blackburn Rovers, Derby County and Everton were present for this season.

Arsenal failed to retain their title, despite having the same points tally as last season 78 points, but had at one point looked as though they were on the brink of winning the title, after beating fellow rivals Tottenham Hotspur, while Manchester United had drawn against Liverpool, 2–2. However, Manchester United pushed on and took advantage of Arsenal's 1–0 defeat at Leeds United in the penultimate match of the season and despite going 1–0 down against Tottenham on the final day, came back to win 2–1 and clinch the title. Should they have failed to win, Arsenal would have been crowned champions once more.

Chelsea, looking to build on a fourth-placed finish the previous season, were flying for much of the season and were in a good position to claim a first league title in 44 years. The Blues were second at Christmas and went top on Boxing Day. A loss at Highbury at the start of February was just a second in the league all season, and kept Chelsea in second place, just a point off the summit. Eventually, three draws in April against winnable opposition (mid-table sides Middlesbrough and Leicester City, and relegation-threatened Sheffield Wednesday) is what cost Chelsea a first Premiership crown. Had they won these, the Blues would've been champions. Chelsea had to settle for third place, earning a maiden Champions League appearance.

To achieve their success, the Manchester United playing squad had been altered substantially during the close season. A total of more than £28 million had been spent on Dwight Yorke, Jaap Stam and Jesper Blomqvist, while several older players left the club; Gary Pallister returned to Middlesbrough after nine years for £2.5 million, while Brian McClair returned to Motherwell on a free transfer. In December, however, McClair was back in the Premier League as Brian Kidd's assistant at Blackburn Rovers.

Season summary
At the end of 1998–99, the Premiership would have three Champions League places. Manchester United as well as runners-up Arsenal and third placed Chelsea would be playing in the following season's Champions League. There would only be one automatic UEFA Cup place from the league – taken by fourth-placed Leeds United. Fifth-placed West Ham United qualified for the UEFA Cup via the Intertoto Cup after achieving their highest league finish since 1986 as they continued to make progress under Harry Redknapp, outperforming several "bigger" clubs with greater resources. Also qualifying were Newcastle United via the 1998–99 FA Cup final, and Tottenham Hotspur via the League Cup.

Manchester United regained the title from Arsenal on the final day of the season, and had faced competition from Chelsea until the final stages of the season, while Aston Villa had led the table for much of the first half of the season before finishing sixth.

Bottom of the Premiership in the final table came Nottingham Forest, who suffered their third relegation in seven seasons. One notable low for Forest this season was an 8–1 drubbing at home, by Manchester United. Second from bottom came Blackburn Rovers, who just four seasons earlier had been Premiership champions. The final relegation place went to Charlton Athletic, who went down at the end of their first spell in the top flight for nine seasons. The only newly promoted club to survive was Middlesbrough, who finished in ninth place - their highest final position for more than 20 years.

None of the teams relegated from the Premiership the previous season regained their top division status in 1999, although First Division champions Sunderland regained their Premiership place after a two-year exile. The other two relegation places went to long-term absentees from the top division. Playoff winners Watford regained their top division place after an absence of 11 years, but runners-up Bradford had been outside of the top division for 77 years. These two promotion winners surprised the observers more than any other Division One side during 1998–99, but were widely expected to struggle in the top flight.

Teams
Twenty teams competed in the league – the top seventeen teams from the previous season and the three teams promoted from the First Division. The promoted teams were Nottingham Forest, Middlesbrough (both teams sealing an immediate return to the top flight after a single season), and Charlton Athletic (playing in the top flight after an eight-year absence). This was also Charlton Athletic's first season in the Premier League. They replaced Bolton Wanderers, Barnsley and Crystal Palace, with all three relegated teams returning to the First Division after a single season in the top flight.

Personnel and kits
(as of 16 May 1999)

Hat-tricks

 * Note: 4 Player scored 4 goals; P Player scored a perfect hat-trick; † Player scored hat-trick as a substitute; (H) – Home; (A) – Away

title: 1998–99 FA Premier League


text:
Enskede-Årsta

Enskede-Årsta was a borough (stadsdelsområde) in the southern part of Stockholm, Sweden from 1998 to 1 January 2007. It was formed when the boroughs of Enskede and Årsta merged, and was primarily made up of Enskede (Gård, -fältet, Gamla-) and Årsta. The other districts that made up the borough were Johanneshov, Stureby and Östberga. The population as of 2004 was 46,072 on an area of 12.72 km2, giving it a density of 3,622/km2. In 2007, Enskede-Årsta merged with the borough of Vantör to form the Enskede-Årsta-Vantör borough.

title: Enskede-Årsta


text:
Ata-Malik Juvayni

Atâ-Malek Juvayni (1226–1283), in full, Ala al-Din Ata-ullah (علاءالدین عطاءالله), was a Persian historian and an official of the Mongol state who wrote an account of the Mongol Empire entitled Tarikh-i Jahangushay ("History of the World Conqueror").

Early life
Juvayni was born in Joveyn, a city in Khorasan in eastern Persia. Both his grandfather and his father, Baha al-Din, had held the post of sahib-divan or Minister of Finance for Muhammad Jalal al-Din and Ögedei Khan respectively. Baha al-Din also acted as deputy c. 1246 for his immediate superior, the emir Arghun Aqa, in which role he oversaw a large area, including the Kingdom of Georgia.

Career
Juvayni, just as his predecessors became an important state official. He visited the Mongol capital of Karakorum twice, beginning his history of the Mongols conquests on one such visit (c. 1252–53). He was with Ilkhan Hulagu in the 1256 campaign at the taking of Alamut, where he selected many 'choice books' from the famous Alamut library for his own purposes and burnt those books that he did not like. He was responsible for saving part of its celebrated library. He had also accompanied Hulagu during the sack of Baghdad in 1258, and the next year was appointed governor of Baghdad, Lower Mesopotamia, and Khuzistan. Around 1282, Juvayni attended a Mongol quriltai, or assembly, held in the Ala-Taq pastures northeast of Lake Van. He died the following year in Mughan.

Siege of Alamut
Juvayni's brother was the powerful Shams al-Din Mohammad Sahib-Divan, who had served as Minister of Finance under Hulagu and Abaqa Khan. A skillful leader in his own right, Shams al-Din also had influential in-laws: his wife Khoshak was the daughter of Avag Mkhargrdzeli, Lord High Constable of Georgia, and Gvantsa, a noblewoman who went on to become queen of Georgia.

Work and legacy
Juvayni's position at court and his family connections made him privy to information unavailable to other historians. For unknown reasons, Juvayni's Tarikh-i Jahangushay ends in 1260, more than twenty years before his death.

The standard edition of Juvayni's history is published under the title Tarikh-i Jahangushay, ed. Mirza Muhammad Qazwini, 3 vol, Gibb Memorial Series 16 (Leiden and London, 1912–37). An English translation by John Andrew Boyle The History of the World-Conqueror was republished in 1997.

title: Ata-Malik Juvayni


text:
Talk:Mozart's name

Deletion debate
For the May 2005 deletion debate on this article, see Votes for deletion/Mozart's name.

Who used multiple-language versions of their name?
I think it's probably better to keep the wording that says that multiple-language names were characteristic of composers, not emigrants. The reason is that Beethoven went by "Luigi" and "Louis" despite the fact that, to my knowledge, he never set foot in either Italy or France. The crucial bit seems to have been the need to publish in other countries, not necessarily to visit them. Also, a reader of Mozart's name is probably more interested in composers in general than in travellers in general. Opus33 16:57, 12 Dec 2004 (UTC)

 * I don't want to question that Mozart probably was exceptional in the degree to which he varied his name over his lifetime, but names in the 18th century weren't as fixed in one particular form as they mostly are today. The way the article is written now, it displays a somewhat naïve and anachronistic surprise at something that was quite common at the time for anyone using different languages in different contexts, including but not excusively composers and other musicians. It is also an anachronism to write that Mozart's name was "shortened" from Wolfgangus to Wolfgang. Use of Latin forms of personal names was common in contexts where Latin was otherwise used, for instance in baptismal records, in school, and at matriculation at university. / up+land 21:58, 12 Dec 2004 (UTC)

In a book "Allt som du trodde du visste men som faktiskt är alldeles fel" [Bokförlaget Semic 2000, Sweden] (meaning about "All that you knew is in fact wrong"), it is mentioned that Mozart himself dropped "Johannes" at the age of 14 because he didn't like it. Ok, not the most reliable source, but just wanted to mention this. SamuliK

 * For what it´s worth, I agree with up+land above AND deny he was exceptional among cosmopolitans of the time. --83.253.55.89 17:32, 22 October 2007 (UTC)

Well, I recently read that the name mozart has had multiple spellings. We can look at his name reengineer it to a more original form: It is actually Moss+Hart, the z usage is similar to Salzburg. Salſs or Salß+burg the z was used as a glottal stop. The h was optional like Ricardo. Double ss are often translated as t example wasser and water. Perhaps he did not want to be Mothart or Moathart. Maybe he did not like Moths. Mos'hart does sound funny for English speakers; the shart part of course. So what does the name Mosa Hart mean? Mosa and Mose are of Biblical etymology... von Mose(15th Century) or better known as Moses (from the Marsh). The e and the a disappear during word formation. Example- Judgment... Hart- I differ on the interpretation of Hart as Harsh. I think it is related to the words Court and Quarter (Square) instead... A Marsh is also a border- for example the Muse river. River-Border-Court. "A court that borders the river." Alright so maybe my explanation sucks. Maybe you can find someone to make this look presentable with the correct annotation.

Theophilus = Gottlieb
Hello, I think that it would be worth to mention the German version of the name Amadeus (Theophilus) - Gottlieb - since several sources (Google for "Gottlieb Mozart") pretend that this was the name that was actually used (until Amadeus or Amadé was preferred) and "Theophilus" was just a formal record in the register.

But I don't want to touch the article myself, I would leave this to someone with better knowledge of German language and Austria (if he can confirm the statement above). (And with better knowledge of English of course ;-)

 * err, forgot to sign --Kavol 10:32, 1 February 2006 (UTC)

Amadè error
The text uses Amadè, while I believe the correct accent is Amadé.

It could perhaps be mentioned that this is simply the French form.

I also echo the comments about Gottlieb

David Vaughn —The preceding unsigned comment was added by 82.224.103.123 (talk) 19:55, 8 January 2007 (UTC).

No, if one looks at the actual signatures, it is/was Amadè and NOT Amadé. QwertyUSA 13:50, 8 September 2007 (UTC)

Ditto. Deutsch (cited in article) gives the grave-accented form, and he was a careful scholar. Opus33 17:13, 8 September 2007 (UTC)

Just to note that the German usage is to use the acute accent (é), because German doesn't really use the grave accent, and I guess because it is to denote that the pronounciation should be something like "ah-ma-day", where the stress on the "e" is indicated by the acute accent (as opposed to French, which actually distinguishes between a "eh" (long e, acute accent) sound and a "e" (short e, grave accent) sound). mdl27 23:24, 25 May 2011 (UTC)

So what does the above mean -- was it written with a grave accent, but pronounced as modern-day é would be? If so, wouldn't it be more appropriate to make modern readers pronounce it properly by writing it with an acute accent?--Geke (talk) 20:35, 20 December 2011 (UTC)

It's really pretty simple: Mozart himself spelled it with a grave accent, so we have to spell it with a grave accent. Opus33 (talk) 22:17, 20 December 2011 (UTC)

 * Oops, sorry. As I've since learned, Mozart freely used either accent (or indeed, no accent).  The choice of Amadè in the article text follows Deutsch, but in fact I can't find out which spelling Mozart used most often.  See new text in article for details and source. Opus33 (talk) 17:23, 13 July 2014 (UTC)

Chrystostom
"Chrystostom" must be a misspelling, as the correct spelling is Chrysostom, from Greek Chrysostomos (golden mouth), latin Chrysostomus. It has nothing to do with Christ (Christos). —Preceding unsigned comment added by 193.212.171.26 (talk) 08:12, 27 June 2008 (UTC)

I've changed it, in two places.--Geke (talk) 20:31, 20 December 2011 (UTC)

Intro
I think it would be better to leave the baptismal names out of the intro. They played a very minor role in Mozart's life, and because they are in Latinized form, they aren't even really all that "official". Let's let the main text of the article explain all the angles here, and then the reader can decide for herself what to call Mozart. Opus33 (talk) 18:01, 21 December 2008 (UTC)

Who knows the whereabouts of Mozart's two sons? —Preceding unsigned comment added by 71.172.80.88 (talk) 20:32, 16 February 2010 (UTC)

I presume they are dead. 159.50.249.150 (talk) 09:57, 5 September 2011 (UTC)

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Amadé
"Amadé" looks obviously as a short for "Amadeus", but I don't know if he tried to write in French, like when he wrote "Cher papa", when he wrote "Amadé", as the French would have been "Amédée", maybe there's some other old French form that looks like "Amédé", I don't know. — Preceding unsigned comment added by 87.91.51.235 (talk) 17:55, 6 February 2020 (UTC)

 * @87.91.51.235 No, this is a mistake. Mozart called himself "Amadé", refined from German. From Germany with love. Stephphie (talk) 16:05, 28 November 2022 (UTC)

Did Mozart sign Amade on his marriage contract?
The article states that Mozart signed his 'middle name' as Amade on his marriage contract and that's what Deutsch seems to say as well (on p.204, see here). However looking at a scan of the contract from the British Library, I am having a real hard time convincing myself that Mozart signs his middle name as Amade. Am I just reading things incorrectly? Tripler06 (talk) 16:34, 19 August 2023 (UTC)

title: Talk:Mozart's name


text: User talk:68.14.159.9

title: User talk:68.14.159.9


text:
Ally MacLeod

Alistair Reid MacLeod (26 February 1931 – 1 February 2004) was a Scottish professional football player and manager. He is perhaps best known for his time as the Scotland national football team manager, including their appearance at the 1978 FIFA World Cup. MacLeod played as a left winger for Third Lanark (two spells), St Mirren, Blackburn Rovers, Hibernian and Ayr United. He then managed Ayr United (three spells), Aberdeen, Scotland, Motherwell, Airdrieonians and Queen of the South.

Early years
Alistair Reid MacLeod was born in the south side of Glasgow on 26 February 1931. His family lived in Clydebank for a while but the house was bombed during the Second World War. At length they settled in Mount Florida, near to Hampden Park and Cathkin Park. MacLeod signed provisionally for Third Lanark when he was still a schoolboy. He made swift dashes up the left wing. His distinctive running action earned him the nickname "Noddy".

Playing career
MacLeod started his playing career at Third Lanark as a provisional signing as a schoolboy in 1947. He made his first-team debut against Stirling Albion at Cathkin Park on 6 November 1949.

In 1953, MacLeod was in the Thirds side that trounced Alloa Athletic in the League Cup opener, 10–0. Sitting 8–0 up, MacLeod's teammates' main objective was to get him on the scoresheet. He had set up five goals but had missed several sitters himself. A left-foot rocket shot, and a simple tap in took Thirds' tally to 10. He joined the Royal Scots for National Service but was still able to turn out for the Thirds.

MacLeod was reluctant to move to St Mirren in 1956, but having secured a guarantee that the reported £8,000 fee would tremendously help Third Lanark's survival, he moved on. He spent only six weeks at St Mirren before moving to English team Blackburn Rovers. Managed by fellow Scot Dally Duncan, MacLeod was man of the match in the 1960 FA Cup Final, but the game was lost 3–0 to Wolves. While at Blackburn he made strenuous efforts along with the PFA steward Jimmy Hill to help abolish the maximum wage, but when subsequently his promised wage increase was not forthcoming, while other players in the team were raised from £20 to £25 per week, he entered into discussions with Hibernian. When Blackburn realised that they were going to lose him to Hibs they matched their offer with an increase from £20 to £25. MacLeod, having already accepted Hibs' offer, felt he could not go back on his word, so left Blackburn to go back to Scotland.

He played with Hibs until 1963, when he returned to Third Lanark. In 1964 he signed for Ayr United, where he finished his playing career, with no major honours won.

Ayr United
He started his managerial career in 1966 when he took charge of Ayr United. He took Ayr back to Scotland's top division and turned them into a well respected side. He took them to a Scottish and a League Cup semi-final and also set their attendance record with 25,225 watching a 2–1 success over Rangers F.C. In 1973, MacLeod was named Ayr's "Citizen of the Year".

Aberdeen
In November 1975, after nine years at Ayr, he moved to Aberdeen where he guided them to a League Cup final success over Celtic.

1978 World Cup qualification and preparation
After success with Ayr and Aberdeen, in May 1977 the Scottish Football Association appointed him manager of the Scotland national team. He introduced himself to the squad with the blunt statement: "My name is Ally MacLeod and I am a winner." In his first months in charge, Scotland beat England at Wembley and qualified for the 1978 World Cup from a group containing Czechoslovakia, who had won the 1976 European Championship, and Wales. Scotland's World Cup expectations gathered momentum with MacLeod happy with the wave of massive optimism, saying to the press his team would return with "at least a medal". Scottish comedian Andy Cameron recorded a version of "Ally's Tartan Army", which reached number 6 in the UK charts just before the World Cup.

Qualification was particularly sweet for Scotland since, for the second World Cup in succession, Scotland had achieved what their traditional rivals England had not. Defeat against England in the 1977–78 British Home Championship was taken to mean little. Spirits remained sky-high as 25,000 people came to Hampden Park to watch the squad circle the ground in an open-top bus prior to their departure for Argentina. Prestwick Airport was packed with supporters seeing the team off. When a journalist asked him "What do you plan to do after the World Cup?" MacLeod replied: "Retain it." This anecdote, though, is denied in some accounts of the Scottish saga at the 1978 World Cup and has been cited as one of the most popular hoaxes in British football.

1978 World Cup finals
Some observers were worried by the absence through injury of full-back Danny McGrain. Opponents Peru's impressive credentials went overlooked and were not expected to provide many problems in the first match. Peru, however, won the game 3–1. Scotland took the lead but Don Masson missed a penalty and in general failed to play to their potential. Before the match journalist James McKillop had written in The Glasgow Herald that "The suggestion that we might not win is unthinkable and can be dismissed out of hand." As MacLeod himself put it, the performance against Peru was "rank bad". Plentiful excuses emerged: there had been a dispute concerning bonuses, the hotel swimming pool had no water in it, there was nothing for the players to do. It was then revealed that the winger Willie Johnston had taken a cold tablet which contained a banned stimulant fencamfamine (Reactivan). He was sent home. MacLeod, at a press conference, saw a mongrel dog approach: "I think he is the only friend I have got left", he said, stretching out a hand.

The game with Iran finished a 1–1 draw, after a poor display by the Scots. They then needed to beat the Netherlands, one of the tournament favourites, by three clear goals, to qualify. The next day's The Glasgow Herald ran the result of the Iran game as their main story under the headline "Ally's night of shame". Herald reporter James McKillop described the match as "Ally's Alamo" and said Scotland had "turned disgrace into humiliation". Adding that at full-time the Scotland players "were lucky not to be lynched", he said he had "never seen Scotland supporters more angry". McKillop's report also stated that in response to the result MacLeod offered "excuses, if not reasons", with MacLeod stated that "the team had been under tremendous pressure in Argentina".

For the Netherlands match MacLeod gave Graeme Souness his first game of the World Cup and was rewarded with a much-improved team performance. When Archie Gemmill scored what is widely thought to be one of the greatest World Cup goals ever (it was officially ranked seventh best by FIFA), to make the score 3–1 to Scotland, qualification to the next phase looked possible. Three minutes later, though, the Dutch pulled a goal back; the game ended 3–2 and Scotland were eliminated on goal difference. The Netherlands proceeded to the final, where they lost to Argentina.

Aftermath and resignation
Following the squads return to Scotland, Macleod's future was discussed by the SFA's International Committee at a meeting in July to consider the team's failure in Argentina. Macleod was present at this four and half hour meeting where a motion to remove him was proposed. The six-man committee agreed to keep Macleod in place as the motion was defeated, but The Glasgow Herald reported that it was understood that the motion for dismissal had only been defeated on the casting vote of the Committee's chairman, Tom Laughlan of Kilmarnock F.C. An editorial in the same newspaper noted that "the football public expected more from Mr MacLeod in the Scotland job than he was able to deliver. He emerges from a chastening experience a wiser man."

Although MacLeod had survived this immediate inquest by the sport's authorities, he resigned after one more game in charge, only 17 matches and about 500 days after his appointment. His old club Ayr United had been given permission by the Scottish Football Association to talk to MacLeod about him returning as Ayr manager. MacLeod accepted the offer although Ayr were in the second tier and the job was thought to pay around £12,000 per year, £3,000 less than he received as Scotland manager. MacLeod admitted that the World Cup failure, and the fallout which followed it, "had taken a lot out of him", but said he was now relaxed and wanted "to prove myself again." His decision to resign and return to club management echoed that of his predecessor in the Scotland job, Willie Ormond. MacLeod's departure left Scotland needing to quickly appoint a manager ahead of their next UEFA Euro 1980 qualifying match against Norway. The Glasgow Herald sports reporter Jim Reynolds dismissed the idea that MacLeod might be asked to stay on in a part-time basis until after this match, saying that "Too many people inside Park Gardens", which was the SFA's headquarters, would "breath a sigh of relief" at MacLeod's departure.

The Scottish Football Association's annual report, issued in May 1979, stated that, "regardless of the depressing aspects of Mr MacLeod's latter days in the Association's employ, it would be quite unfair not to comment that he was largely responsible for kindling an enthusiasm for the Scottish team that far exceeded anything which had gone before. The Association benefited considerably from that enthusiasm and should not forget it".

In his autobiography, The Ally MacLeod Story (1979), he wondered whether he had "generated just too much excitement. Had I raised the level of national optimism just too high?" But he was able to console himself: "Would the Scottish fans have tolerated anything less from me than whole-hearted conviction?" MacLeod also reassured the reader that he, for one, never thought that Scotland were invincible, and claimed to be perfectly at peace with himself. "I am a very good manager who just happened to have a few disastrous days, once upon a time, in Argentina."

Later career
His subsequent managerial career included spells at Motherwell (1979–1981), Airdrie (1984–1985) and a third spell at Ayr (1986–1989) when he won a Second Division (third tier) title in 1988. His last job in football was with Dumfries club Queen of the South. In 1992, he played in a game for Queens' reserve team, scoring a goal from a penalty at the age of 61.

Death and tributes
Increasingly again treated with affection by the Scottish footballing public, in July 2003, at Hampden Park, he was presented with a crystal decanter in appreciation of his services to the national team and to Scottish football.

He died in 2004, aged 72, after a long battle with Alzheimer's disease. MacLeod was posthumously inducted to the Scottish Football Hall of Fame in 2015.

Honours
Third Lanark
 * Glasgow Charity Cup: 1955–56

Hibernian
 * East of Scotland Shield: 1960–61

Blackburn Rovers
 * Football League Second Division promotion: 1957–58
 * FA Cup runner-up: 1959–60

Manager
Ayr United
 * Scottish Division Two: 1965–66
 * Scottish Division Two promotion: 1968–69
 * Scottish Second Division: 1987–88
 * Ayrshire Cup: 1969; 1970; 1971; 1975; 1988

Aberdeen
 * Scottish League Cup: 1976–77

Scotland
 * British Home Championship: 1976–77

Motherwell
 * Lanarkshire Cup: 1981

Airdrieonians
 * Lanarkshire Cup winners: 1984

title: Ally MacLeod


text: Category:Driving techniques

title: Category:Driving techniques


text:
Altitude training

Altitude training is the practice by some endurance athletes of training for several weeks at high altitude, preferably over 8000 ft above sea level, though more commonly at intermediate altitudes due to the shortage of suitable high-altitude locations. At intermediate altitudes, the air still contains approximately 20.9% oxygen, but the barometric pressure and thus the partial pressure of oxygen is reduced.

Depending on the protocols used, the body may acclimate to the relative lack of oxygen in one or more ways such as increasing the mass of red blood cells and hemoglobin, or altering muscle metabolism. Proponents claim that when such athletes travel to competitions at lower altitudes they will still have a higher concentration of red blood cells for 10–14 days, and this gives them a competitive advantage. Some athletes live permanently at high altitude, only returning to sea level to compete, but their training may suffer due to less available oxygen for workouts.

Altitude training can be simulated through use of an altitude simulation tent, altitude simulation room, or mask-based hypoxicator system where the barometric pressure is kept the same, but the oxygen content is reduced which also reduces the partial pressure of oxygen. Hypoventilation training, which consists of reducing the breathing frequency while exercising, can also mimic altitude training by significantly decreasing blood and muscle oxygenation.

Background history
The study of altitude training was heavily delved into during and after the 1968 Olympics, which took place in Mexico City, Mexico: elevation 7349 ft. It was during these Olympic Games that endurance events saw significant below-record finishes while anaerobic, sprint events broke all types of records. It was speculated prior to these events how the altitude might affect performances of these elite, world-class athletes and most of the conclusions drawn were equivalent to those hypothesized: that endurance events would suffer and that short events would not see significant negative changes. This was attributed not only to less resistance during movement—due to the less dense air —but also to the anaerobic nature of the sprint events. Ultimately, these games inspired investigations into altitude training from which unique training principles were developed with the aim of avoiding underperformance.

Training regimens
Athletes or individuals who wish to gain a competitive edge for endurance events can take advantage of exercising at high altitude. High altitude is typically defined as any elevation above 5000 ft.

Live-high, train-low
One suggestion for optimizing adaptations and maintaining performance is the live-high, train-low principle. This training idea involves living at higher altitudes in order to experience the physiological adaptations that occur, such as increased erythropoietin (EPO) levels, increased red blood cell levels, and higher VO2 max, while maintaining the same exercise intensity during training at sea level. Due to the environmental differences at high altitude, it may be necessary to decrease the intensity of workouts. Studies examining the live-high, train-low theory have produced varied results, which may be dependent on a variety of factors such as individual variability, time spent at high altitude, and the type of training program. For example, it has been shown that athletes performing primarily anaerobic activity do not necessarily benefit from altitude training as they do not rely on oxygen to fuel their performances.

A non-training elevation of 2100 - 2500 m and training at 1250 m or less has shown to be the optimal approach for altitude training. Good venues for live-high train-low include Mammoth Lakes, California; Flagstaff, Arizona; and the Sierra Nevada, near Granada in Spain.

Altitude training can produce increases in speed, strength, endurance, and recovery by maintaining altitude exposure for a significant period of time. A study using simulated altitude exposure for 18 days, yet training closer to sea-level, showed performance gains were still evident 15 days later.

Opponents of altitude training argue that an athlete's red blood cell concentration returns to normal levels within days of returning to sea level and that it is impossible to train at the same intensity that one could at sea level, reducing the training effect and wasting training time due to altitude sickness. Altitude training can produce slow recovery due to the stress of hypoxia. Exposure to extreme hypoxia at altitudes above 5000 m can lead to considerable deterioration of skeletal muscle tissue. Five weeks at this altitude leads to a loss of muscle volume of the order of 10–15%.

Live-high, train-high
In the live-high, train-high regime, an athlete lives and trains at a desired altitude. The stimulus on the body is constant because the athlete is continuously in a hypoxic environment. Initially VO2 max drops considerably: by around 7% for every 1000 m above sea level. Athletes will no longer be able to metabolize as much oxygen as they would at sea level. Any given velocity must be performed at a higher relative intensity at altitude.

Repeated sprints in hypoxia
In repeated sprints in hypoxia (RSH), athletes run short sprints under 30 seconds as fast as they can. They experience incomplete recoveries in hypoxic conditions. The exercise to rest time ratio is less than 1:4, which means for every 30 second all out sprint, there is less than 120 seconds of rest.

When comparing RSH and repeated sprints in normoxia (RSN), studies show that RSH improved time to fatigue and power output. RSH and RSN groups were tested before and after a 4-week training period. Both groups initially completed 9–10 all-out sprints before total exhaustion. After the 4 week training period, the RSH group was able to complete 13 all out sprints before exhaustion and the RSN group only completed 9.

Possible physiological advantages from RSH include compensatory vasodilation and regeneration of phosphocreatine (PCr). The body's tissues have the ability to sense hypoxia and induce vasodilation. The higher blood flow helps the skeletal muscles maximize oxygen delivery. A greater level of PCr resynthesis augments the muscles power production during the initial stages of high-intensity exercise.

RSH is still a relatively new training method and is not fully understood.

Artificial altitude
Altitude simulation systems have enabled protocols that do not suffer from the tension between better altitude physiology and more intense workouts. Such simulated altitude systems can be utilized closer to competition if necessary.

In Finland, a scientist named Heikki Rusko has designed a "high-altitude house." The air inside the house, which is situated at sea level, is at normal pressure but modified to have a low concentration of oxygen, about 15.3% (below the 20.9% at sea level), which is roughly equivalent to the amount of oxygen available at the high altitudes often used for altitude training due to the reduced partial pressure of oxygen at altitude. Athletes live and sleep inside the house, but perform their training outside (at normal oxygen concentrations at 20.9%). Rusko's results show improvements of EPO and red-cell levels.

Artificial altitude can also be used for hypoxic exercise, where athletes train in an altitude simulator which mimics the conditions a high altitude environment. Athletes are able to perform high intensity training at lower velocities and thus produce less stress on the musculoskeletal system. This is beneficial to an athlete who had a musculoskeletal injury and is unable to apply large amounts of stress during exercise which would normally be needed to generate high intensity cardiovascular training. Hypoxia exposure for the time of exercise alone is not sufficient to induce changes in hematologic parameters. Hematocrit and hemoglobin concentrations remain in general unchanged. There are a number of companies who provide altitude training systems, most notably Hypoxico, Inc. who pioneered the artificial altitude training systems in the mid-1990s.

A South African scientist named Neil Stacey has proposed the opposite approach, using oxygen enrichment to provide a training environment with an oxygen partial pressure even higher than at sea level. This method is intended to increase training intensity.

Principles and mechanisms
Altitude training works because of the difference in atmospheric pressure between sea level and high altitude. At sea level, air is denser and there are more molecules of gas per litre of air. Regardless of altitude, air is composed of 21% oxygen and 78% nitrogen. As the altitude increases, the pressure exerted by these gases decreases. Therefore, there are fewer molecules per unit volume: this causes a decrease in partial pressures of gases in the body, which elicits a variety of physiological changes in the body that occur at high altitude.

The physiological adaptation that is mainly responsible for the performance gains achieved from altitude training, is a subject of discussion among researchers. Some, including American researchers Ben Levine and Jim Stray-Gundersen, claim it is primarily the increased red blood cell volume.

Others, including Australian researcher Chris Gore, and New Zealand researcher Will Hopkins, dispute this and instead claim the gains are primarily a result of other adaptions such as a switch to a more economic mode of oxygen utilization.

Increased red blood cell volume
At high altitudes, there is a decrease in oxygen hemoglobin saturation. This hypoxic condition causes hypoxia-inducible factor 1 (HIF1) to become stable and stimulates the production of erythropoietin (EPO), a hormone secreted by the kidneys, EPO stimulates red blood cell production from bone marrow in order to increase hemoglobin saturation and oxygen delivery. Some athletes demonstrate a strong red blood cell response to altitude while others see little or no gain in red cell mass with chronic exposure. It is uncertain how long this adaptation takes because various studies have found different conclusions based on the amount of time spent at high altitudes.

While EPO occurs naturally in the body, it is also made synthetically to help treat patients with kidney failure and to treat patients during chemotherapy. Over the past thirty years, EPO has become frequently abused by competitive athletes through blood doping and injections in order to gain advantages in endurance events. Abuse of EPO, however, increases RBC counts beyond normal levels (polycythemia) and increases the viscosity of blood, possibly leading to hypertension and increasing the likelihood of a blood clot, heart attack or stroke. The natural secretion of EPO by the human kidneys can be increased by altitude training, but the body has limits on the amount of natural EPO that it will secrete, thus avoiding the harmful side effects of the illegal doping procedures.

Other mechanisms
Other mechanisms have been proposed to explain the utility of altitude training. Not all studies show a statistically significant increase in red blood cells from altitude training. One study explained the success by increasing the intensity of the training (due to increased heart and respiration rate). This improved training resulted in effects that lasted more than 15 days after return to sea level.

Another set of researchers claim that altitude training stimulates a more efficient use of oxygen by the muscles. This efficiency can arise from numerous other responses to altitude training, including angiogenesis, glucose transport, glycolysis, and pH regulation, each of which may partially explain improved endurance performance independent of a greater number of red blood cells. Furthermore, exercising at high altitude has been shown to cause muscular adjustments of selected gene transcripts, and improvement of mitochondrial properties in skeletal muscle.

In a study comparing rats active at high altitude versus rats active at sea level, with two sedentary control groups, it was observed that muscle fiber types changed according to homeostatic challenges which led to an increased metabolic efficiency during the beta oxidative cycle and citric acid cycle, showing an increased utilization of ATP for aerobic performance.

Due to the lower atmospheric pressure at high altitudes, the air pressure within the breathing system must be lower than it would be at low altitudes in order for inhalation to occur. Therefore, inhalation at high altitudes typically involves a relatively greater lowering of the thoracic diaphragm than at low altitudes.

title: Altitude training