text:
Derek Holland was more satisfied with how he finished than his perfect start against the Seattle Mariners.
Holland, the Texas Rangers 25-year-old left-hander, was perfect for the first five innings and finished with a five-hitter as the Rangers rolled to a 5-0 decision for their eighth straight victory.
It was Holland's fourth career complete game -- all shutouts -- his third this season and second straight. He went the route in his previous outing July 7 against Oakland, a 6-0 decision.
He is the first Ranger to throw back-to-back shutouts since Charlie Hough had three straight Aug. 28-Sept. 7, 1983, two years before Holland was born. The last Ranger lefty to have successive shutouts was Jim Umbarger (May 23 and 28, 1976).
Holland (8-4), who matched his career high for wins, retired the first 15 batters until walking Franklin Gutierrez on a 3-2 pitch to open the sixth. He then lost his no-hitter when the next batter, Chone Figgins slashed a single to right.
"I just got caught looking at the scoreboard at the wrong time," Holland said. "I got a reminder when I walked that guy and the crowd started cheering. I knew I needed to bear down. I gave up the perfect game but had to keep going from there."
He retired the next three batters to end the threat. He gave up a pair of singles in both the seventh and ninth but also settled down and kept the Mariners off the board.
"That's huge for me, part of the maturing process," Holland said. "It was starting to build right there but I made my pitches where I needed to do and the defense was making the plays. I'm sure everyone else saw it (coming), but I got out of it. Seventh and ninth, too."
Mike Napoli, Josh Hamilton and Nelson Cruz each homered for Texas.
Jason Vargas (6-7) went six innings for Seattle, allowing five runs, a season-high 12 hits.
"Really the story was their guy (Holland) and the way he pitched," Mariners manager Eric Wedge said, "and what we did not do against him."
Holland threw just 54 pitches in the first five innings and the closest the Mariners came to a hit was Ichiro Suzuki's slow-hit bouncer to second baseman Ian Kinsler in the fourth. Kinsler raced to his left and had time only to slap the ball with his glove to first baseman Mike Napoli to beat Suzuki by a half step.
Miguel Olivo had two of the Mariners four hits.
The Mariners have lost six straight to fall 8½ games behind the AL West-leading Rangers.
"That's two in a row throwing the ball the way we know he's capable of throwing," Rangers Manager Ron Washington said. "He had his breaking ball, he moved it around, he elevated, he threw down, he moved their feet. He pitched very well tonight.
"He was in attack mode. That's where he has to be. He has to attack with quality strikes, not just throwing the ball over the plate."
Hamilton got it started in the first, hitting a 2-2 pitch into the right-field seats for his 12th home run. Since May 23 when he came off the disabled list, Hamilton has a major league-leading 43 RBI.
Cruz hit a 1-0 pitch over the right-field wall in the second for his 21st home run. Right fielder Suzuki appeared to have a chance of catching it, but hit his back on the wall to curtail his jump.
Cruz also came off the DL May 23 and has the second-most RBI (38) in the majors since then.
"We finished first half strong. It's good to start second half the way we started today," Cruz said. "The way Holland threw is amazing. It look like he doesn't need that many runs for support."
Michael Young knocked in his 60th run in the third, a two-out single to right scoring Elvis Andrus from second.
Napoli connected on his 13th home run, hitting a 1-0 pitch into the right-center bleachers in the fifth. Napoli has nine hits in his 23 at-bats (.391) since coming off the DL July 4.
Andrus added an RBI single later in the inning.
NOTES: The Rangers relievers struggled for much of the first half but Manager Ron Washington believes the bullpen is turning the corner. "The way they are pitching right now, it definitely can be an asset," he said. "Mark Lowe caused that. Tommy Hunter caused that." ... Mariners manager Eric Wedge addressed the players before the game, telling them, "expect a lot of yourselves, expect good things to happen." He said the primary goal in the second half "is a more consistent ballclub. It's a process. It takes time."


text: On Wed, Jun 27, 2012 at 12:02:28AM +0200, Vincent Danjean wrote: > ocl-icd is small and the core code should not change a lot until > OpenCL 1.3 or more appears. The core code of the version already in > testing is very similar to the one waiting in NEW. > In that case, hopefully it will be processed before we freeze, or the diff will be small enough that we can review it. > Considering the young of the package (upstream and in Debian), > the fact that this is a free replacement of non-free packages, the > fact that we are at the beginning of the freeze, the fact that there > is no reverse dependencies, I would like to ask you for a freeze > exception of ocl-icd 1.3-2. > Having ocl-icd 1.3-2 in wheezy would improve the quality of > wheezy without any risk of problems for the distribution. > This could be phrased another way: The package is not shown to be mature enough, is introducing a new package that hasn't been in the main release of debian before, and has missed the freeze date. Not having ocl-icd in wheezy would remove the risk of another package that could go wrong during the release. :) I would suggest we wait and see as per the above. Neil

subset: commoncrawl


text:
OMAHA, Neb. - As Georgia collected more and more victories this season, the congratulatory texts and e-mails David Perno received from his childhood friend, Robbie Kamerschen, began to pile up.
Perno and Kamerschen played little league baseball together in Athens and later won an American Legion baseball state title and Clarke Central's last football state title in 1985. Perno eventually played baseball at Georgia. Kamerschen played at Stanford.
The two have kept in touch throughout the years, mostly with updates by e-mail.
"All of a sudden, it looks like we're dead on course for Stanford," Perno said of Georgia's College World Series bracket. "I stopped getting (the e-mails). I know he's a little torn, but I know where his heart is deep down. It will be a win-win situation for him watching that game."
So who will Kamerschen be pulling for today when Georgia and Stanford play for the second time this week?
"In any other context, I would always pull for Stanford because I have such strong feelings about the program and about the school and the opportunities it gave me," he said.
PHOTOS: View a gallery of Georgia's Friday practice for its game Saturday against Stanford in the 2008 CWS:
View gallery
"The way the group of guys in Athens were reared - they are my extended family. Even though it is very hard and I would pull for Stanford against anyone else in the country, at the end of the day, I've found myself pulling for Georgia - mainly because I'm pulling for Perno."
Kamerschen was a pitcher on Stanford's 1987 and 1988 national championship teams.
He experienced what it was like to be the best in country a few years before Perno did in 1990 with Georgia's national title.
"It's the pinnacle," Kamerschen said. "It's what these guys at Georgia want to experience. It's a dog pile on the pitcher's mound. You work all year for that. ... It really was special. Twenty years later, the perspective makes it even more special. You see how rare that is. You see that it's what put Stanford in the upper echelon of college baseball."
Kamerschen and Perno faced each other when Georgia won its national title in 1990. The Bulldogs defeated the Cardinal 16-2, then Stanford beat Georgia 4-2 and Georgia ended Stanford's season with a 5-1 win.
"By 1990, which most people thought was our best team at Stanford, we caught a very, very hot Georgia team," Kamerschen said.
DOGWIRED: Listen as baseball writer Jennifer Iannone talks with sports editor John Kaltefleiter about the game delay and what to expect in today's matchup against Stanford:
"They beat Mike Mussina twice in the span of a week to knock us out of the tournament and then win the whole thing."
A few years later, Perno was just starting out as a coach and picked Kamerschen's brain about Stanford coach Mark Marquess.
"David was a sponge," Kamerschen said. "He had such a great respect for coach Marquess and still does. We would sit for an hour and talk about how coach Marquess ran a practice. ... He knew he wanted to make a career of coaching. An opportunity to have a look inside in one of the best program's in America was just something that he relished. He wanted to get every bit of it."
Nearly 15 years later, Perno still has that same respect for Marquess.
"He's as good as there is when it comes to coaching college baseball," Perno said. "He won back-to-back national championships. When we played them in '90, I already had an iconic view of coach Marquess. He's just a class act and does an unbelievable job with his program."
On Monday, Perno faced Marquess for the first time as a coach. The Bulldogs rallied to a 4-3 victory to get out to their best start at the CWS since 1990.
AUDIO: Listen as Georgia third baseman Ryan Peisel talks about the frustration of waiting four days to play:
"It's unfortunate that we have to go through Stanford again," Perno said. "Hopefully, it will turn out the same way it did 1990."
Game 1 rewind
Georgia (43-23-1)
What went right: The Bulldogs outhit the Cardinal 9-6 and the bullpen allowed one hit in six scoreless innings.
What went wrong: Ryan Peisel and David Thoms were caught stealing. Starter Nick Montgomery gave up three runs, including a two-run homer to Jason Castro.
Stanford (41-23-2)
What went right: Starter Jeffrey Inman went 51/3 innings. He gave up two earned runs on seven hits and threw 101 pitches. Zach Jones scored the first run after a triple. Jason Castro hit a two-run homer and went 2-for-3. Joey August was 2-for-4.
What went wrong: After Bryce Massanari's ball to right field was ruled a foul, reliever Austin Young pegged Massanari and gave up Cerione's hit. Colin Walsh grounded into an game-ending double play.
LIVE BLOG: Be part of the action by visiting OnlineAthens.com today at 2 p.m., and follow the Dogs in our live blogs and share your own comments throughout the game.
Join our Live Blog
Series glance
North Carolina 7, LSU 3; LSU eliminated
Georgia (43-23-1) vs. Stanford (41-23-2), 2 p.m.
Fresno State (44-29) vs. North Carolina (53-13), 7 p.m.
Stanford vs. Georgia, if necessary, 2 p.m.
Fresno State vs. North Carolina if necessary, 7 p.m.
Note: If there is one game, it will be played at 7 p.m.
Championship series
Best-of-three format
Monday, 7 p.m.
Tuesday, 7 p.m.
Wednesday, 7 p.m. (if necess.)
North Carolina (52-13), late
Georgia (43-23-1) vs.
Stanford (41-23-2) 2 p.m.
at Rosenblatt Stadium
Radio: WRFC 960-AM; TV: ESPN2
© 2017. All Rights Reserved. | Contact Us


text:
QUAKER-ROOTS-L ArchivesArchiver > QUAKER-ROOTS > 1998-09 > 0904925596
From: "Melvin L. Woodard" <>
Subject: Re: hinshaw cd query
Date: Fri, 04 Sep 1998 12:13:16 -0400
J. Smith wrote:
> I must have missed something. Where can I find information about the
> Hinshaw book on CD? I scoured the Broderbund website but found no
> mention of Hinshaw. Thanks.
> - Joyce Smith
> Newark, NJ
Pull up the following site:
Scroll down and on the right side you will see a listing of "The Latest
Family Archive CDs, and click on the very first one listed;
*Genealogical Records: The Encyclopedia of Quaker Genealogy,
1740-1930 (#192)
This thread:
|Re: hinshaw cd query by "Melvin L. Woodard" <>


text:
Many of us are convinced our computers have minds of their own. In this bizarre case of iTunes moving music files around, there may well be a ghost in the machine:
Ok. I got one for you that has stumped EVERYONE that I have proposed this problem to, including Mac Geniuses and numerous techie friends.
iTunes keeps all music organized inside the Music folder in the Home folder. For the last several months, periodically when I add a new song, or change something regarding songs already in the library (add artwork, adjust genre, etc) SOME songs will relocate themselves to Macintosh HD >Music >iTunes >iTunes Music [outside the Home folder].
I tend to see the same few artists move, but then it moves not only the song that may or may not have been adjusted, but it'll move all/part of that subsequent album. For example, if I add artwork to the Beatles 1 album, the entire artist folder for Beatles will relocate itself. Or perhaps a second Beatles folder will relocate itself into the Macintosh HD level, but only bring along 5 of the 6 possible albums that I have.
iTunes updates the location information in its database file, so there is no difference seen when playing music through iTunes. The Apple Store's opinion was that it's "not a big deal since the music plays anyway, why do you care?" It just tends to drive me nuts and I'd like an explanation rather than just a blow off.
Let's hope I don't stump you too.
Hi Julie,
Yes that is an odd problem. I'm not surprised that the Genius Bar was uninterested in in-depth sleuthing, but clearly something is going on. Is there any consistency to which files get moved? Are they always items you purchased from the iTunes Store?
A couple things to check:
-do you have your iTunes Media folder location set to /Users/homefolder/Music/iTunes/iTunes Music?
-in iTunes Preferences –> Advanced tab, do you have "Copy files to iTunes Media folder when adding to library" checked?
If yes to both, try this: go to File –> Library –> Organize Library, and choose Consolidate files. This will put everything into the library inside the Music Folder. Then quit iTunes, rename the top level Music folder (outside your home folder) to something other than "Music", then relaunch iTunes. See if things then behave normally or the problem recurs.
Adam, thanks for trying to help
I do not purchase many files from the iTunes store, so I cannot verify if those are the files that move frequently. However, it does seem as if the same artists consistently move, and I do not know if this is because I listen to them the most, or what.
Yes, to both of your questions about where my iTunes library is located. And I often consolidate files when I consolidate files, they either do not actually copy (the scroll bar does come up) or they readjust permissions back to the Macintosh HD level quickly. Now, if I quit iTunes, and rename the folder to something different, when I open iTunes the next time, it adjusts the name to now meet the new name.
It is interesting to note that this does not ALWAYS happen, but it happens frequently enough that I know to check for it. Sometimes it moves one artist, tonight when I was checking what you suggested, it moved almost 2GB of music. I tend to just go and correct it the fix myself since it will update as I move files, but it is getting annoying.
In the last week, I have also tried reinstalling iTunes to no avail.
I would try reinstalling Mac OS X next, and keep the existing user account. Worth a shot.
Readers, have any other ideas for Julie?


text:
Hotels in Cortez, Colorado
Search & Compare Cortez Hotels
Get Secret Prices on select hotels
These prices aren't available to everyone.
Best hotels in Cortez
Cortez overviewCortez is a budget-friendly place known for its archaeology and museums, and surrounded by picturesque views of mountains and parks. You'll find extensive café and dining options. Spend a relaxing day at Park Point and Yucca House National Monument when the weather is nice. Don't miss your chance to see attractions like Cortez Cultural Center and Colorado Welcome Center at Cortez. Cortez is a family-friendly destination while offering something for everyone.
Where to stay in CortezWhether you're planning to stay for a night or for the week, the area around Cortez has accommodations to fit every need. Search for hotels in Cortez with Hotels.com by checking our online map. Our maps display the areas and neighborhoods around all Cortez hotels so you can see how close you are from landmarks and attractions, and then refine your search within the larger area. The best Cortez hotel deals are here with our lowest price guarantee.
How to get to CortezFly in to Cortez, CO (CEZ-Montezuma County), 4 mi (6.4 km) from downtown Cortez.
What to see around CortezFun outings can include a visit to:
- • Guy Drew Winery
- • Sutcliffe Vineyards
- • Cortez Cultural Center
- • Colorado Welcome Center at Cortez
- • Crow Canyon Archaeological Center
- • Anasazi Heritage Center
- • Rio Grande Southern Railroad Museum
- • Long House
- • Step House Trail
- • Spruce Tree House
- • Cliff Palace
- • Balcony House
- • Park Point
- • Yucca House National Monument
- • Knife Edge Trail
- • Mesa Verde National Park Entrance
- • Point Lookout Trail
- • Guy Drew Winery
- • Wetherill Mesa
- • Mesa Verde Visitor and Research Center
- • Dolores River Brewery
- • Prater Ridge Trail
When to visit CortezIf you're still deciding when to visit, here are the seasonal norms to help you plan:
Seasonal temperature averages
- January-March: 58°F day, 15°F night
- April-June: 88°F day, 29°F night
- July-September: 89°F day, 41°F night
- October-December: 72°F day, 16°F night
- January-March: 2.87 inches
- April-June: 2.17 inches
- July-September: 4.33 inches
- October-December: 3.23 inches


text:
Today is an important day for Americans, as we go to the polls and decide the direction of our nation for the next two years. Sorry, the next round of elections is in 2014, no two ways around it. That said, when you go to the polls, you should go to the polls informed.
Settle It does just that.
Built by Web site PolitiFact, the app is essentially a more streamlined version of their website's B.S. detecting blog entries. For those unfamiliar, Politifact rates politician's claims on a scale ranging from True to Pants On Fire, and despite what those on both sides of the aisle like to claim, the site doesn't have a political bias: Obama and Romney get it stuck to them with equal measure.
Settle It is pretty simple. Search a politician, topic, or keyword, and get a load of what's been said about it and how true it is.
Mostly it's a useful education in how both sides can take away two very different and equally wrong interpretations of the facts. But at least now if there's BS, you have a way to sniff it out.
Settle It! [iTunes Store, also available on Android]


text:
There was good and bad news over the summer in the A-level and GCSE results for the Telegraph's Make Britain Count campaign, which returns today as the new term gathers pace. Among 18 year-olds, numbers opting to take mathematics increased for the fifth year in succession, now accounting for almost 10 per cent of all A-level entries. And further maths has seen a bigger rise – up by 7.6 per cent compared with last year, the largest climb in any subject. However, performance levels in maths did not show any corresponding upturn, and it remains predominantly a subject taken by boys rather than girls.
At GCSE, the picture is more troubling. There was a drop of 0.4 per cent in pupils attaining an A* to C grade – in line with overall performance across the range of subjects, but hardly an encouraging sign given how much effort has been targeted on maths in recent times. Worse, numbers achieving A* and A grades – those most likely to go forward to maths at A-level and university fell more steeply, by 1.1 per cent since 2011 to 15.4 per cent of those sitting the exam.
There was an alarming 12.6 per cent decrease in those taking GCSE maths in the summer of 2012 compared to the previous year, but it was offset by a steep rise of 17.6 per cent in those sitting the paper at the additional date in March. This could mean that some pupils are being entered early, or that there have been a large number of resits from the previous year.
Neither is a happy scenario. Experts have long decried the growing habit of schools entering pupils early "to get maths out of the way". It is often aimed at achieving the minimum C grade rather than stretching to get it up to B or A. And high numbers of resits mean that pupils are grinding through the maths GCSE paper in the hope of a decent grade: hardly a process likely to develop confidence in the subject.
Reversing the trend towards taking maths early at GCSE was one of eight manifesto aims that Make Britain Count published in July in an open letter to Michael Gove, Secretary of State for Education. That has now been overtaken by his decision to include maths as one of the core subjects in his planned English baccalaureate. And, for all the progress that Mr Gove rightly highlights elsewhere in improving performance at maths in order to make Britain a more numerate society and workforce, boosting our economic performance, there is clearly a great deal more to do.
The causes of the decline in maths standards are deep-rooted. To change them needs persistence, determination and courage. And that is why Make Britain Count, with the backing of Telegraph readers, and of the public support of the teaching profession and employer bodies, will continue this autumn to make the case for reform.


text:
Kimberly Bryant
Show: The Real Housewives of Orange County
Appearances: Season 1
Reason for Leaving: The stay-at-home mom and her family moved to Chicago after her son discovered a benign, but still pre-cancerous, mole. Bryant herself was diagnosed with skin cancer at age 27.
Post-Housewives Career: Still living in the Chicagoland area, Bryant stays out of the spotlight. She did, however, make cameo appearances on The Real Housewives of Orange County in seasons 3 and 4.Back to top


text:
I'M so worried about my ex-partner.
Of course you worry about him as a friend but your relationship is over. You've moved on and you both have someone new
Even though we split in 2010, I still have feelings for him because he's basically a decent person. But his lover is a monster.
I'm aware she constantly demands money from him in return for kinky sex. He denies she's a ruthless prostitute but I don't know what else to call her.
I've met her three times now at the house we used to share. Each time she was dressed for a nightclub in a short dress and high boots.
The last time she was rude to me. She complained that my ex was selfish and mean and owed her cash. She actually seemed to be suggesting that I should give her money.
I told her to show me some respect and she became verbally abusive and quite threatening. She spat that she could fully understand why we split up in the first place because I was "dried up and frigid". My ex ended up bundling me out.
He is a very intelligent, sensitive man. I don't understand how he's allowed himself to be sucked in by this monster.
Friends tell me it's all about the sex and booze. Apparently she'll do anything for the right price but he has to get drunk to get over his natural inhibitions. I'm with someone new now. I live in my current partner's house and, thankfully, I don't have money worries.
But I'm just worried my ex is going to lose his home to this bloodsucker. What can I do to save him?
JANE SAYS: DOES your ex actually wish to be saved? Has he asked you to intervene on his behalf and rescue him from his demanding lover?
If the answer is "no" then I suggest you walk away and accept your ex is his own man. He's not your responsibility.
Of course you worry about him as a friend but your relationship is over. You've moved on and you both have someone new.
You may not approve of his choice. You may call her all sorts of unpleasant names but if he chooses to throw his time and his money in her direction then that's not your business.
I know it's hard to step back because you care for the bloke but he's not the guy you fell in love with any more.
If he's drinking heavily, indulging in kinky sex and paying for the privilege, then that's up to him.
Surely your new partner deserves all your time and attention now. Don't be sidetracked.


text:
Tina Fey
Tina Fey is an award winning comedic actress. She is well-known for her work on Saturday Night Live, during which she won AP Entertainer of the Year for her satirical impersonation of Sarah Palin. Fey also starred in the movie Mean Girls, for which she wrote the screenplay, and the TV show 30 Rock, which she created.


text:
I never did get to that second WFC blog post, did I? Well, life rolls on. And I just returned from Barnes & Noble, in Bayside, where I was picking up some gifts and a few things for myself, of course.
That, and a few books that have come in the mail, and once again, I'm way behind on my reading. Here is what's on the immediate agenda for this reader.
First off I should mention that I'm reading, at the recommendation of my sister, who has taken on a role of a fantasy reader (a new love in addition to her thriller and horror roots), the Jim Butcher Codex Alera series. I purchased on my android phone using the B&N Nook app, and am almost done with book one, The Furies of Calderon. Good pacing, interesting magic system, and a world that is just starting to take shape for me.
And today's B&N purchase included British fantasy author, Joe Abercrombie, and his novel, The Blade Itself, which I've been meaning to pick up since I met the guy at NY Comic Con back in October. Well, I finally have copy in hand and am ready to take plunge. Additional details to come. There are only so many times you can hear from your friends, "Oh, Jay, you'd really like this guy, his stuff is right up your alley."
Next is an interesting near-future, sf thriller I was sent by UK author, John Trevillian, The A-Men. John had sent me a nice email as he saw my blog, and I mentioned I'd check out the book -- and at least mention it here -- so more on this is to come. This series by Trevillian looks promising and I look forward to digging in.
In my attempts to keep literary, I've read so much about Roberto Bolano's 2666, that I finally had to pick up the trade paperback so that I can read and share reading with my wife. When Mediabistro.com's ebooknewster blog put it up as their "free book of the day" and then immediately took it down, I had read a sample then felt obligated to purchase a copy out of respect for the deceased author (currently no digital version of the book is available). Also I was hooked once I started this mammoth and beautifully written novel. I will continue in print and report back much later when I finish it.
Alright, I've sort of updated you all on what I'm reading, and in addition to that I'm editing a wonderful World War II narrative non-fiction book, which I think is going to be really terrific, but that's all I can say about that right now. Stay tuned.
3 comments:
- redhead said...
The Blade Itself is SO good! Be warned, it's gonna spoil you! Such a good book!
- November 14, 2010 at 7:58 PM
- Jayf said...
Hi Red! Thanks for your note. I just checked out your blog, I like it, I'll be sure to add it to my blog roll. Thanks for stopping by!
- November 14, 2010 at 8:21 PM
- Francis said...
Bolano's best, all you need to read, ignore the rash of post death book hype, 2666 is real deal.
Lunch soon...getting a new phone soon.
- November 15, 2010 at 10:38 AM
Subscribe to: Post Comments (Atom)


text:
Aging is associated with progressive loss of neuromuscular function that often leads to progressive disability and loss of independence. The term sarcopenia is now commonly used to describe the loss of skeletal muscle mass and strength that occurs in concert with biological aging. By the seventh and eighth decade of life, maximal voluntary contractile strength is decreased, on average, by 20-40% for both men and women in proximal and distal muscles. Although age-associated decreases in strength per unit muscle mass, or muscle quality, may play a role, the majority of strength loss can be accounted for by decreased muscle mass. Multiple factors lead to the development of sarcopenia and the associated impact on function. Loss of skeletal muscle fibers secondary to decreased numbers of motoneurons appears to be a major contributing influence, but other factors, including decreased physical activity, altered hormonal status, decreased total caloric and protein intake, inflammatory mediators, and factors leading to altered protein synthesis, must also be considered. The prevalence of sarcopenia, which may be as high as 30% for those ≥60 yr, will increase as the percentage of the very old continues to grow in our populations. The link between sarcopenia and disability among elderly men and women highlights the need for continued research into the development of the most effective interventions to prevent or at least partially reverse sarcopenia, including the role of resistance exercise and other novel pharmacological and nutritional interventions.
- skeletal muscle
- muscular strength
- muscle quality
- motoneuron
- countermeasures
- muscle protein
it is well established that the human aging process, from maturity to senescence, is associated with a significant decline in neuromuscular function and performance (34, 51, 109, 128). Characteristic of this decline is the inevitable reduction in skeletal muscle mass and associated loss of strength that occurs even in the healthy elderly. Rosenberg (110) first coined the term Sarcopenia, from the Greek, which literally means poverty of flesh, to describe age-associated loss of skeletal muscle mass. Sarcopenia is now generally used to describe age-related changes that occur within skeletal muscle and thus encompasses the effects of altered central and peripheral nervous system innervation, altered hormonal status, inflammatory effects, and altered caloric and protein intake. These multiple factors all contribute to sarcopenia and to the characteristic skeletal muscle atrophy and weakness, both of which are considered major contributing factors to the loss of functional mobility, independence, and frailty present in many older adults (111, 113). As our population ages, it is clear that we require greater understanding of the underlying mechanisms leading to sarcopenia. Only then can we begin to develop effective targeted interventions to prevent disability and optimize independence in older men and women. This review will examine sarcopenia from the context of age-related losses of muscle mass and strength, potential etiological factors, and its epidemiology. In particular, the role of motoneuron loss and its impact on muscle fiber numbers and muscle mass will be examined. Interventions to reverse or counter sarcopenia, including resistance training, are briefly examined.
Loss of skeletal muscle strength is a commonly recognized consequence of aging. Age-related decline in strength has been well established with multiple cross-sectional studies of limb muscles tested under isometric and dynamic conditions, most often comparing groups of healthy young, middle-aged, and older men and women (34, 103, 128). The knee extensors, because of their functional importance, ease of testing, and presence of comparative histological data, have been the most frequently examined.
As outlined in Table 1, multiple studies have compared knee extensor strength in groups of young and healthy older subjects in their seventh and eighth decades. The average reported age-related decreases in strength are on the order of 20-40% (71, 93, 94, 140, 141). Even greater losses (50% or more) have been reported for those in their ninth decade and beyond (93, 94). In general, similar declines in strength have been reported for proximal and distal limb muscles, including the ankle plantar and dorsiflexors, elbow flexors and extensors, and hand grip (6, 25, 26, 35, 43, 62, 84, 131). Relative losses appear similar for men and women; however, because men typically start from higher baseline values, their absolute losses of strength are greater. In concert with age-related slowing of electrically evoked muscle contractile properties (18, 26, 32, 35, 69, 95, 129), some reports have shown more significant losses of strength with isokinetic testing at higher angular velocities (25, 71, 97). One important exception to these observations is the consistent finding of relative preservation of strength under eccentric testing conditions (104, 130). It has been postulated that this may be related to slower contractile properties and increased or altered connective tissue content and muscle stiffness in older adults.
Although it has been well established that resistance training interventions can partially reverse losses of strength in even the very old (42, 46, 103, 128), the extent to which lifelong activity patterns and training can prevent age-related declines in strength has not been prospectively examined. However, Klitgaard and coworkers (70), in a cross-sectional study, compared elderly men (mean age 69 yr) who had either trained with running, swimming, or strength training regularly for between 12 and 17 yr with young and elderly sedentary controls. Compared with the young controls, they reported that strength declines in the sedentary elderly group for maximal isometric torque for the knee extensors (44%) and elbow flexors (32%). However, although the older swimmers and runners exhibited similar declines in strength as the sedentary elderly, the strength-trained elderly men had maximal isometric strength and muscle cross-sectional areas (CSAs) similar to the young controls. These results are clearly limited by the cross-sectional study design but do provide evidence that, at least in a selected population, strength losses with aging may be attenuated by resistance exercise.
The rate of strength decline with aging remains largely unknown. Vandervoort and McComas (131) used a cross-sectional design whereby they examined young, middle-aged, and elderly men and women. Maximal voluntary and electrically evoked maximal twitch forces were determined for the ankle plantar flexor and dorsiflexor muscles. Men were stronger than women at all ages, and aging was associated with substantial declines in force for both muscle groups. Strength losses were relatively similar for men and women, and these declines were similar for both evoked and voluntary contractions. In an attempt to determine the extent to which reduced central drive may contribute to decreased volitional strength, the twitch interpolation technique was used (9). An important finding of this study, in keeping with the observations for other muscle groups (35, 101), was that most older men and women were able to maximally activate the lower motoneuron pool for maximal force production. Thus the reduced volitional strength with aging was predominately attributed to decreased muscle mass as opposed to the inability to adequately recruit the available contractile tissue. From these data, it was established that ankle strength did not begin to decline until the sixth decade of life and then proceeded at a rate of ∼1.3% per year thereafter.
Longitudinal studies have provided important insights into the rate of strength decline with aging. For example, Bassey and Harries (6) reported a 3% loss of grip strength per year for men and 5% for women over 4 yr. These losses were greater than those reflected in their initial cross-sectional analysis. Alternatively, Kallman et al. (62), from cross-sectional analysis of 847 subjects from 20 to 100 yr, reported that grip strength peaked in the fourth decade and then declined in a curvilinear fashion thereafter, such that by the ninth decade strength had declined by 37%. Their longitudinal analysis, however, showed that 15% of the subjects aged 60 yr and over exhibited no strength decline during an average 9-yr follow-up, suggesting significant interindividual variability. Similarly, Rantanen et al. (106) reported declines in grip strength of ∼1%/yr in a large cohort (3,680) of Japanese-American men with a 27-yr average follow-up. A more significant rate of decline was present in those older at baseline or with chronic diseases such as diabetes and arthritis.
A number of studies have longitudinally examined age-related strength decline in the knee extensors. Aniansson et al. (2) reported a decline of 3.2%/yr in a 7-yr follow-up of 23 men aged 73-86 yr, whereas Greig et al. (49) found that strength was essentially unchanged over 8 yr in a group of men and women aged 79-89 yr. Frontera et al. (44) reexamined the strength of 9 of 12 men who had taken part in a training study 12 yr earlier. Isokinetic strength losses for the knee and elbow flexors and extensors ranged from 9% for elbow extension at 180°/s to 30% for knee extension at 240°/s. These changes were accompanied by significant reductions in muscle CSA as shown by computerized tomography scanning. Winegard et al. (136) longitudinally examined 22 men and women from the 69 initially studied by Vandervoort and McComas (131). Over the 12-yr follow-up period, significant decreases of 30% for men and 25% for women were noted for ankle plantar flexors, whereas less dramatic losses of 9.5 and 3.3% were reported for dorsiflexors. Hughes and coworkers (56) longitudinally studied a large cohort of men and women initially examined cross-sectionally ∼10 yr earlier. They obtained a 64% response rate and reexamined the knee flexors and extensors and elbow dorsiflexors and plantar flexors in 68 women and 52 men. Rates of decline were similar for men and women for knee flexors and extensors (11.8-17.6% per decade). Women, however, demonstrated substantially lower rates of decline for elbow flexors and extensors (2% per decade) than men (12% per decade). Although knee extensor strength was related to total muscle mass (estimated from 24 urine creatinine collections), this accounted for only 5% of the observed variance in strength. This observation is limited by the comparison of strength in a specific muscle group with an estimate of total body muscle mass; however, it does point out the importance of other factors, including neural, metabolic, and cellular changes, that may have an impact on strength decline with aging. In particular, this study also highlights that there may be differential effects in men and women with regard to age-related changes in upper and lower body strength.
Thus it appears that healthy men and women in their seventh and eighth decades exhibit, on average, 20-40% less strength compared with their younger counterparts. These losses are even greater (50% or more) for the very old. In general, similar losses are present for proximal and distal muscles in the upper and lower extremities, and men and women experience similar losses on a relative basis. Longitudinal studies, with some exceptions, have reported somewhat greater losses of strength over time (1-3%/year) compared with cross-sectional studies. The majority of these studies, however, have examined older populations over a limited duration of follow-up and thus may not predict the rate of decline in young or middle-aged populations.
Age-related declines in strength are directly impacted by, and correlated with, losses of skeletal muscle mass. It has been demonstrated that total muscle CSA decreases by ∼40% between the ages of 20 and 60 yr (34, 103, 128). CSAs have been determined for various limb muscle groups with ultrasound, computed tomographic scanning, magnetic resonance imaging (MRI), and direct measurement of whole muscle cross sections from cadaveric specimens. For example, Young et al. (140, 141), using ultrasonographic imaging, reported 25-35% reductions in the CSAs of the quadriceps muscles in older men and women compared with young controls. Computed tomographic scanning has shown similar results for the quadriceps muscle (70, 98), the biceps brachii (70, 108), and triceps brachii (108) in men. Additionally, highlighting the inaccuracy of simple anthropometric measures of limb circumference, Rice et al. (108) found 27, 45, and 81% more nonmuscle tissue (fat and connective tissue) for the arm flexors, arm extensors, and plantar flexors, respectively. Similarly, Overend et al. (98) reported increases in nonmuscle tissue of 59% for the quadriceps and 127% for the hamstrings. CSA measurements taken directly from whole muscle obtained postmortem showed similar average reductions of 40% for subjects between 20 and 80 yr old (76). The average reduction was 10% at 50 yr and accelerated thereafter.
The above studies used small sample sizes, measured the CSA of only one to three muscles, and comprised only male subjects. Two recent studies, however, have overcome many of these limitations. Gallagher et al. (48) measured arm skeletal muscle mass, leg skeletal muscle mass, and total appendicular skeletal muscle mass (TASM) using dual-energy X-ray absorptiometry (DEXA) in a sample of 148 women and 136 men between 20 and 90 yr of age. After adjustments for height, body weight, and age were made, men were shown to have larger TASM than women. Moreover, men exhibited larger age-related decreases in TASM compared with women (14.8 vs. 10.8%). Similarly, Janssen et al. (61) used whole body magnetic resonance imaging to determine skeletal muscle mass in a sample of 268 men and 200 women between 18 and 88 yr of age. Again, men had significantly greater skeletal muscle mass than women with greater losses of skeletal muscle mass with aging. The mechanisms leading to greater losses of muscle mass with aging in men compared with women are unknown but have been postulated to relate to hormonal factors, including growth hormone, insulin-like growth factor, and testosterone (61). Although greater losses of muscle mass occur with aging in men, it has been suggested that sarcopenia may be a greater public health concern for women since they live longer and generally exhibit higher rates of disability (113).
The term muscle quality (MQ) refers to strength per unit CSA or strength per unit muscle mass and is considered a more meaningful indicator of muscle function than strength alone (113).
There are significant challenges in setting out to determine MQ in vivo in humans. There is the obvious assumption that both the measurements of force and muscle mass or CSA are valid and accurate. Measurements of maximal voluntary strength, especially of large proximal or intermediate muscles (e.g., knee flexors and extensors, biceps and triceps, and ankle dorsiand plantar flexors) are dependent on multiple factors, including the need for full central activation, difficulties in ensuring that only the muscles of interest participated in force or torque production, and the effects of pain and other neural inhibitory factors limiting or modifying central drive. Additionally, there are potential limitations and errors related to the method used for determination of muscle mass or CSA. Given these potential limitations, early studies provided variable results. For example, Young et al. (140) found no difference in force/CSA in the knee extensors of older women in the eighth decade vs. young controls. Alternatively, losses in MQ were reported for older men by a number of investigators (45, 62, 97, 107, 141). The differing methods for determining muscle mass or CSA and force measurement may be largely responsible for the variability in these earlier studies. More recently, Kent-Braun and Ng (67) reported no age-related impairment in force/CSA for the ankle dorsiflexors. They had carefully controlled for central activation and used MRI scanning to accurately quantify the CSA for the anterior compartment of the leg. Alternatively, Klein et al. (69) reported that, although the physiological CSA of the elbow flexors and extensors significantly declined with age in older men, the force/CSA was decreased for the flexors, but not extensors. Proposed mechanisms for this finding included changes in the architecture of the triceps brachii, increased coactivation of the biceps, and reduced muscle fiber-specific tension. The observations of Macaluso et al. (78) have further supported potential reductions in force/CSA in older women. They reported decreased force/CSA in both the knee flexors and extensors of elderly women in their seventh decade. The decreased force/CSA in the knee extensors was accompanied by increased coactivation of the antagonist knee flexors, again suggesting a potential neural mechanism for the decreased force/CSA.
Some potential sex differences in MQ with aging have been demonstrated. For example, in a recent comprehensive study, Lynch et al. (77) set out to determine differences in MQ between arm and leg muscles across the life span. Reliable measures were used for both concentric and eccentric strength, and muscle mass was determined from whole body DEXA scanning with estimation of arm and leg muscle mass. They reported that the age-associated losses in arm MQ were greater for men than for women, whereas leg MQ declined similarly. Second, arm MQ was higher than leg MQ across all age groups for men and women; however, although arm MQ declined at the same rate as leg MQ for men, the decline in leg MQ was greater than arm MQ for women. These age-related losses in MQ are potentially related, among other factors, to changes in neural drive, altered muscle pennation, and increases in connective tissue. With regard to this latter point, Kent-Braun et al. (68) recently reported a two- to threefold increase in intramuscular noncontractile tissue in the anterolateral compartment muscles. Although similar increases were noted for men and women, an inverse relationship was found between physical activity and the extent of noncontractile tissue in women.
Finally, gender differences in MQ with aging may be related to altered contractile properties of the muscle fibers themselves. Frontera et al. (47) examined whole muscle strength and whole muscle cross-sectional area (WMCSA) as well as the contractile properties of chemically skinned segments from single fibers of the vastus lateralis in young men and older men and women. Strength and WMCSA of the knee extensors were significantly higher in younger men compared with older subjects and in older men compared with older women. The age-related but not the gender-related differences were eliminated after controlling for WMCSA. Moreover, muscle fibers expressing the same myosin heavy chain isoform from young men were stronger than fibers from older men, and type I and IIA fibers from older men were stronger than similar fibers from older women, even after adjustments for size. These important findings provide direct evidence for differences in MQ in older men and women. The mechanisms underlying such gender-related differences with aging remain in question. However, hormonal factors may play a role, as it has been demonstrated that specific force is similar in men and premenopausal women, whereas there was a dramatic decline in specific force around the time of menopause; the latter, however, was diminished in women who used hormone replacement therapy (HRT) (102).
Age-associated loss of muscle mass appears inevitable and is likely the most significant contributing factor to the decline in muscle strength (109, 111, 113, 128). Although all men and women experience some degree of sarcopenia, this is variable and on a continuum. However, in a similar fashion to bone mineral density scores for osteoporosis, it is possible to dichotomize this continuous process by establishing a lower limit of normal such as 2 SD below the mean appendicular muscle mass for healthy young adults. For example, Baumgartner et al. (7), in the New Mexico Elder Survey, measured appendicular muscle mass by DEXA in 883 randomly selected elderly Hispanic and white men and women. Sarcopenia was defined as losses greater than 2 SD below the mean for young healthy controls. The prevalence of sarcopenia ranged from 13 to 24% in persons aged 65 to 70 yr and was over 50% for those older than 80 yr. In this study, the prevalence was higher for men over age 75 yr (58%) than for women (45%). In a similar study, the prevalence based on total skeletal mass determined by DEXA was 10% for men and 8% for women between 60 and 69 yr and 40 and 18%, respectively, for men and women over 80 yr (85). Because these prevalence rates are relative to gender-specific younger control populations, they suggest greater declines in muscle mass for men than women. Iannuzzi-Sucich et al. (58) used DEXA to quantify appendicular skeletal muscle mass in 195 women aged 64-93 yr and 142 men aged 64-92 yr. They defined sarcopenia as 2 SD below the muscle mass/height (m)2 for young controls. The overall prevalence of sarcopenia so defined was 22.6% in women and 26.8% in men. These values climbed to 31 and 45%, respectively, for women and men over 80 yr. Similarly, Janssen et al. (61) used whole body MRI to examine skeletal muscle mass and distribution in a large cohort of 468 men and women from 18 to 88 yr of age. They observed a decline in body in skeletal muscle mass beginning in the third decade; however, this did not become substantial until the end of the fifth decade. An important finding of this study was that the loss of muscle mass with aging was greater in the lower body in men and women. This finding may reflect decreased activity or altered patterns of activity of the lower extremity muscles with aging and has important implications for functional mobility and disability.
Although sarcopenia most specifically refers to loss of skeletal muscle mass, clearly, functional ability is of the utmost importance to elderly men and women. It would seem intuitive that a relationship should exist between muscle mass, strength, and the ability to carry out functional tasks. This was evident in the New Mexico study in which sarcopenic women had 3.6 times higher rates of disability and men had 4.1-fold higher rates compared with those with greater muscle mass (7). The use of assistive walking aids and the number of falls were also higher in these subjects. More recently, Janssen et al. (60) reported a higher prevalence of more severe sarcopenia in women compared with men over 60 yr. These researchers found that functional impairment and disability were two times greater in older men and three times greater in older women.
Multiple, interrelated factors contribute to the development and progression of sarcopenia (Fig. 1). These factors, no doubt, contribute in varying degrees to the age-related losses of muscle mass, strength, MQ, and the degree of functional impairment and reserve present in older men and women. It is also probable that certain underlying mechanisms are of greater influence than others when considering any specific age group, gender, or association with comorbid states.
Regardless of any potential age-related impairment in MQ, loss of muscle mass is the largest contributing factor to strength decline and associated disability in older men and women. Histological data, predominately from needle biopsy sampling, has provided some insight into the cause of the age-related atrophy. The majority of these studies have been undertaken on the vastus lateralis muscle, and the overall findings are reasonably consistent. That is, the average type II fiber size is diminished with age, whereas the size of type I fibers is much less affected (34, 51, 72-74, 76, 109, 128). Although reductions in type II area range from 20 to 50%, type I fiber area losses range from 1 to 25%. The variability noted in these studies relates to sampling variability, potential sampling bias with muscle biopsy, and the undoubted inherent variability in both the older and younger control populations.
The above reductions in fiber size, however, are moderate compared with the reductions in muscle mass; therefore, reductions in muscle fiber number have been proposed. Lexell et al. (76), using whole muscle cross-sections from the vastus lateralis muscle obtained postmortem, reported that, by the ninth decade, ∼50% fewer type I and type II fibers were present compared with muscles from those 20 yr old. The fact that similar losses of muscle fibers were present for type I and II fibers stood in contrast to earlier work from samples obtained with muscle biopsy (71, 72). Further analysis determined that the CSA of the vastus lateralis, at least, is mainly determined by the total number of fibers and, to a lesser extent, by the size or number of type II fibers (73, 74, 76).
Further to this, in concert with type II atrophy, there is histochemical evidence of fiber type grouping, fiber atrophy, and increased coexpression of myosin heavy chain isoforms in the same fiber, thought consistent with a progressive denervation and reinnervation process secondary to a chronic neuropathic process (1, 36, 96). Given these findings and the previously noted losses of muscle fibers, it has been suggested that α-motoneuron loss may be largely responsible for age-related loss of muscle mass (15, 31-33, 36, 109).
Is there any support for such a hypothesis? Electrophysiological studies that used either macro electromyographic techniques (118) or motor unit number estimation techniques (30, 33) have demonstrated substantive losses of whole functioning motor units in proximal and distal muscles in the upper and lower extremities (28, 33, 119). These reported losses are on the order of 50% for the thenar, hypothenar, and biceps/brachialis muscle groups (15, 16, 31, 35, 115) and are consistent with anatomic data that has demonstrated losses of anterior horn cells and ventral root fibers with aging (31, 35, 64, 65, 86, 125). These findings, taken together with muscle morphological changes consistent with a chronic neuropathic process, point toward age-associated losses of motoneurons as an important contributing factor to reduced muscle fiber number and muscle mass (3, 17, 34, 35). No longitudinal studies have examined this process, but cross-sectional studies would suggest that motoneuron or motor unit numbers are well maintained until the seventh decade and then begin to decline precipitously thereafter (18, 81, 82). Whether the progressive loss of motor units continues to occur to the same extent into the eighth and ninth decade has not yet been examined, especially for larger proximal muscles. If so, as occurs in the postpolio syndrome, this may be an important factor leading to progressive atrophy in the very old as losses of muscle mass become exponential as progressively larger motor units drop out (33, 83). It is unknown whether physical activity or hormonal or genetic factors potentially influence the extent or rate of motor unit loss.
Loss of muscle mass secondary to muscle fiber loss and secondarily fiber atrophy appear largely responsible for sarcopenia. However, other hormonal, metabolic, nutritional, immunologic, and molecular factors also contribute to sarcopenia. (see Refs. 113 and 132 for recent reviews). In general, it has been postulated that with aging there is a withdrawal of, or resistance to, anabolic factors and potential development of catabolic influences on skeletal muscle.
The relationship between hormonal mediators and sarcopenia has been the topic of a number of recent reviews (11, 63, 88, 91, 114). Serum levels of both testosterone and the adrenal androgens decline with age (120-122), and there are epidemiological data supporting the relationship between the fall in testosterone and the decline in muscle mass (8), strength (8, 100), and functional status (100). The decline in estrogen in women associated with menopause is well recognized; estrogen may also have anabolic effects on muscle, possibly as a result of its conversion to testosterone (113). Estrogen and testosterone may also inhibit the production of IL-1 and IL-6, suggesting that decreased levels of these hormones may have an indirect catabolic effect on muscle (113).
Testosterone replacement has resulted in increased muscle mass (92) and strength in hypogonadal populations (10) and elderly men (116, 127) and increased strength in elderly women (27). A recent randomized, placebo-controlled trial reported increased total and leg lean body mass and leg and arm strength resulting from 6 mo of testosterone treatment designed to maintain serum testosterone within the physiological range for younger men (40). These changes were accompanied by increased expression of insulin-like growth factor I (IGF-I), which may point toward it as an important mechanism for muscle anabolism in older men. Although these data are promising, further work is required to determine the ideal dosing regimen, potential risks with long-term use, and perhaps, most importantly, the impact on functional outcomes.
Menopause is associated with decreased levels of circulating 17β-estradiol concentrations in middle-aged and older women (29). Impaired muscle performance has been observed during perimenopause in concert with rapid and dramatic decreases in ovarian hormone production (117). This observation suggests that female sex steroids may play an important role in regulating muscle performance in middle-aged and older women. It has been demonstrated that HRT attenuates the loss of muscle mass that occurs in the perimenopausal period (29, 102), whereas a recent study reported that the rate of sarcopenia was as common in nonobese long-term HRT users as those not using HRT (66). HRT did not augment the increases in fat-free mass or leg strength in postmenopausal women aged 60-72 yr after 11 mo of high-impact weight-bearing exercise (14), whereas another recent study reported improvements in lower extremity power and muscle CSA in response to resistance training and HRT in a group of younger postmenopausal women (117). These limited data suggest that HRT, possibly in concert with resistance exercise, may be most beneficial in the early postmenopausal period; however, more studies are required to further elucidate the role of HRT in relation to improving or maintaining muscle mass, strength, and function.
Levels of both growth hormone and IGF-I decline with age, and, based on their known anabolic effects, there has been interest in their potential therapeutic benefit to counter sarcopenia (87) (91). In general, however, studies have shown that growth hormone administration in pharmacological doses increases muscle mass but not strength (142). For example, 1 mo of growth hormone or IGF-I in older women increased nitrogen balance, protein turnover, and muscle protein synthesis; however, in response to a 16-wk resistance training program, growth hormone conferred no greater gains in strength or protein synthesis (139). It is believed, given the side effects, cost, and equivocal results in the literature, that growth hormone cannot be recommended now as an efficacious intervention for sarcopenia (139, 142).
It is well recognized that aging is associated with a decline in food intake; this so-called anorexia of aging is considered an important factor in the development and progression of sarcopenia (89-91). Anorexia increases the risk of developing severe muscle wasting, such as occurs during illness or other potential catabolic states such as after hip fracture. This wasting, if severe, can lead to cachexia and progressive functional decline (89, 90).
The multiple complex mechanisms and interactions leading to decreased food intake with aging have recently been reviewed (91). They include early satiety secondary to decreased relaxation of the fundus, increased release of cholecystokinin in response to fat intake, increased leptin levels, which may in part be due to increase in fat mass with aging, and the effects of neurotransmitters such as opioids and neuropeptides (91). It remains unclear whether this physiological anorexia contributes to sarcopenia because the intake of protein is below the levels necessary to maintain muscle mass or because the intake of essential dietary nutrients, including creatine (91), is decreased.
Reversal or treatment of age-related anorexia and associated protein malnutrition is challenging and often focused on the treatment of coexisting disorders such as depression, the effects of polypharmacy, and other potentially reversible causes (91). Oral liquid caloric and protein supplements have been demonstrated to be effective in randomized trials in patients with hip fracture (5, 91). The roles of enteral feeding and pharmacological agents to reverse anorexia, including anabolic steroids, megestrol acetate, growth hormone, and cannabis derivatives, remain in question (5, 91).
Eating one-half the recommended dietary allowance (RDA) of protein of 0.8 g·kg-1·day-1 has been shown to lead to significant declines in strength, body cell mass, and IGF-I in postmenopausal women (23). The extent to which less substantial reductions in dietary protein intake contributes to sarcopenia is unknown. This is an important consideration, however, as it has been shown that 15% of those over 60 yr eat less than 75% of the RDA (113). Furthermore, the extent to which the RDA for protein is adequate for elderly men and women remains in question. Several studies have suggested that the dietary protein requirements for older adults are greater than the currently recommended 0.8 g·kg-1·day-1 (19-22). For example, reduced thigh muscle CSA was associated with a diet containing 0.8 g·kg-1·day-1 in men and women aged 55-77 yr (22), and gains in fat-free mass with resistance training were greater in men aged 51-69 yr who consumed a meat-containing diet compared with an isonitrogenous lacto-ovo vegetarian diet (19). These differences were unlikely because of increased myofibrillar protein synthetic rate, as this was unchanged in response to progressively higher protein intakes in older men and women (135).
In addition to declines in anabolic stimuli with advanced age, there is evidence for an increase in catabolic stimuli. For example, Roubenoff et al. (112) have reported increased production of IL-6 and IL-1 receptor antagonist (IL-1ra) by peripheral blood mononuclear cells in elderly subjects. IL-6 is mildly catabolic, whereas IL-Ira is a pure cytokine antagonist without direct catabolic effects (123). In this same study, however, there was no increase in production of the more catabolic cytokines TNF-α or IL-1β (112). It has not been established whether aging is associated with directly increased cytokine production within muscle; thus their direct role in sarcopenia remains in question (113). Again, this may be an important consideration in the setting of illness or injury superimposed on aging.
The role of altered protein turnover and protein metabolism in the development of sarcopenia has been the topic of a number of excellent reviews (99, 105, 124). In general, regardless of the mechanisms, muscle atrophy occurs when protein breakdown exceeds synthesis. To this end, there is evidence that aging is associated with a lower fractional synthetic rate of mixed muscle protein (54, 138), myofibrillar protein (actin/myosin) (4, 134, 138), and mitochondrial proteins. The reduced basal muscle synthetic rate is associated with a reduction in mRNA responsible for myofibrillar protein gene expression (133).
Given these findings and the relationship between muscle mass and function, there has been obvious interest in examining the capacity for increased anabolic activity in older adults in association with resistance exercise. For example, Yaresheski et al. (139) reported increased mixed muscle protein synthesis (∼50%) accompanied by strength gains after 16 wk of progressive resistance training in older men (65-75 yr). Additionally, a subsequent study reported that 3 mo of resistance training increased the mixed protein synthetic rate in the vastus lateralis muscles of men and women between 72 and 92 yr (137). Thus, in concert with other studies (see below) that have reported increased strength and muscle mass with resistance training, even the very old retain the ability to upregulate protein synthesis in response to progressive overload.
Finally, physical inactivity is a significant contributing factor to age-related sarcopenia. It is well established that older men and women who are less physically active have less skeletal muscle mass and increased prevalence of disability (37-39, 103, 113, 128). Clearly, it is difficult from cross-sectional studies to draw inferences regarding causation. However, the results of numerous studies that have documented that resistance exercise can reverse sarcopenia provide sound evidence for the relationship between activity and skeletal muscle mass and strength (38, 103, 128). As summarized in Table 2, short-term training studies, typically of 10- to 12-wk duration, with training two or three times per week have consistently resulted in significant strength gains in elderly men and women (13, 24, 42, 46, 79, 80, 103, 128). Increased strength and muscle mass with resistance exercise has been achieved even for the frail elderly ≥90 yr old (42). Strength gains were variable across studies, which reflects multiple factors, including the study population, intensity, and duration of the training and the outcome measured. Typically, increases in muscle CSA were on the order of 5-10%, suggesting a significant neural adaptation associated with the reported strength gains. Nevertheless, increases in muscle fiber CSA ranging from 5% to over 40% have also been reported, confirming that strength gains likely result from a combination of both central (neural) and peripheral (muscle mass) factors. Further in depth discussion of resistance training for sarcopenia is beyond the scope of this review; however, it should be noted that, so far, no other intervention has proven to be as efficacious as resistance exercise in reversing sarcopenia. The optimal exercise modality, duration, and intensity for healthy older men and women to maintain muscle mass remain in question; moreover, the benefits of resistance or other forms of exercise for specific targeted populations of at-risk elderly patients have not been adequately addressed.
The extent to which countermeasures, including exercise and nutritional and pharmacological interventions, are able to not only reverse or partially reverse sarcopenia but improve function and decrease disability in the elderly remains to be established. To this point, although numerous resistance training studies, for example, have successfully shown gains in muscle mass and strength, these studies have typically either not included or were underpowered from the standpoint of establishing the relationship between such gains and functional outcomes. Well-designed intervention trials, including meaningful functional outcome measures, directed toward well-defined populations, are required to begin to answer these important questions.
- Copyright © 2003 the American Physiological Society


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Tuesday, April 08, 2008
French Toast and Bacon
We had some ripe bananas so I sliced one to go on top of the bready goodness. SP asked for some bacon to go alongside as well. I'm starting to get the whole salty/sweet thing after some of the syrup got onto the bacon.
3 comments:
I've been quietly drooling over most of your recent meals, but this looks absolutely amazing! I would so love to eat this!!!! As you know, I love the bacon and maple syrup combo - love banana and love french toast. This is my idea of a perfect meal.ReplyDelete
tfp - I KNEW you would be a fan of this meal. I was actually going to link to your post where you talk about French toast and bacon. :) I never liked the mix of the salty bacon and sweet syrup but it's growing on me.ReplyDelete
That looks amazing! I'm drooling on the keyboard. I only recently discovered your blog and I'm glad I did, it's great.ReplyDelete
I've been told there are issues with comments going through. After you comment, you should see the following message: "Your comment has been saved and will be visible after blog owner approval." If you don't see a message it means the comment didn't go through. Please try commenting again! I'm sorry!


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Next up is Brandon & Savannah, a brother and sister pair who are part of a band.
They are in.
Next up is Brandon & Savannah, a brother and sister pair who are part of a band.
They are in.
Comedian Taylor Williamson moves on.
Next up is magician Jacob Calle.
He swallows some string, pulls it out through his stomach, he puts a scorpion in his mouth and tries to blow bubbles while it's still in there. He gets three X's and is rejected.
Some other magicians also get rejected.
Next up is escape artist Naathan Phan who's gonna try to get out of a straitjacket while singing "I Want to Break Free".
He gets buzzed by two judges.
But, he's been given another chance to perform another trick.
Nathan then does a card trick and gets a ticket to Vegas.
The last act is three guys who just met a few days ago. They're called Forte and they're singing an opera piece. They do a great job and are put through.
They were being pimped all week though so I knew they were gonna make it.
I loved Forte! I don't watch commercials so I had not seen them before their performance. Pie Jesu is such a beautiful song when sung well.
Whenever you see darkness, there is extraordinary opportunity for the light to burn brighter.
I don't know who my favorites were this week. I liked Forte and Hammerstep. I honestly didn't care for the comedian.
Did they ever show the dancer Sophia Lucia? I saw her in a brief clip during one of the kid segments, she was getting direction backstage on how to use the mic. She's a very gifted dancer.
I'm going to watch later on the app, too many recording conflicts to be able to record it and I watch SYTYCD while this is on.
Thanks for giving me hints on who to watch out for and....yay a Virginia act!
Avatar: Eastern Amberwing dragonfly photo by me.
Sophia was shown, and I read that she performed on DWTS once.
I wonder who I'll be hating on this year. Last year it was Turf, the year before it was Silhouettes, and the year before it was Christina and Ali. It would be nice not to hate on anybody, for once.


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I wanted to look through the yearbook before I decided whether or not I would purchase one to commemorate Andrew's fourth grade year at his school.
In the end, it wasn't what I saw that made my decision for me — it was what I didn't see.
Other than their classroom photos, I couldn't find one single picture of the special needs students on campus engaged in an activity, watching an assembly, playing with a friend on the playground, or participating in a lesson. Not one.
It was like they didn't even exist.
And that, my friends, is a problem.
There was a time I would've allowed feelings of anger and frustatration to consume me and spent the better part of the school year fuming about the unfairness of it all.
But that, my friends, is not a solution.
They're tucked towards the back of the modest-sized campus; four portable classrooms in the left corner, dedicated to the special education students that comprise a healthy chunk of the overall student population at the school.
At any given time you can see these kindergarten through 6th graders walking around campus, assisted by an aide or teacher, making their way to the playground or the lunch tables or speech therapy.
At any given time you can sneak a peak at their sweet, determined faces as they work so very hard to master new skills and practice old ones.
They are every bit as worthy and valuable as the other students, and yet they're the last ones to get picked during games and the first ones to get picked on at recess.
I'm not telling you this to garner pity or sympathy.
I'm telling you this because it's TRUE.
A few months ago my best friend's son informed me of the way things play out at his school:
"You know Auntie Jo, not everyone at my school is very nice."
"Why not honey?"
"Well, a lot of the kids say things about the special needs kids like, 'Those handicappers are aliens,' then laugh at them."
"How old are these kids?"
"Second grade."
I had a hard time sleeping that night. Between the yearbook situation and hearing firsthand from a young child what's being said about the special needs kids on his school campus, my heart was heavy.
And it's under this enormous weight that I know what I must do next.
I'm pouring snacks into cupcake liners, 134 of them to be exact. Another mom pours the juice.
And then, with my heart gently thumping out of my chest, I wait.
Minutes later, they begin to line up. They grab a drink and I hand them a snack, making eye contact with as many of them as possible.
I want to know them.
I want them to know me.
I want them to know my son, to see him on the playground and say, "Hey! There's Andrew Ashline! Let's go say hi!"
He will rely on them someday, these children. They are his age. They will grow old with him. It's important that they see him as a valuable member of society so that they will unflinchingly honor him as a fellow human being, vote for causes that will assist him in his life, protect him from the people who will choose to point and laugh and disregard him.
It's important now to teach them to open doors for him instead of shut them in his face.
To pick him, instead of pick on him.
To trailblaze on his behalf.
I hand them their snacks and I think, "Yes, you will know me, and I will know you, and I will help you know my son and together we can change the world because a world where second graders think that people with special needs are aliens is a world that is not good enough for any of us."
My knees are wobbly, my hands shake slightly but it's not the crowd that has me feeling nervous — it's the importance of what I'm about to say to them.
I clear my throat, and introduce myself.
"My name is Jo Ashline, and I'm the newly-appointed Special Needs Coordinator on the PTA Board."
I scan their faces and see some confusion among fellow moms and dads, but I continue, despite the lump in my throat.
"My son Andrew is a student here and he is in the special education program on campus. He and his friends are amazing children and I want to help you and your kids get to know them better."
"It's my belief that our kids have so much to offer one another, but they need guidance from the adults in their lives. While it's true we currently share the same campus, we don't share a sense of community, and it's my hope that I can help change that this year. We have an opportunity to teach the kids at this school the true meaning of friendship and diversity, but first we must work together to bring about awareness and acceptance. And that's where I come in. I promise to make it my mission to eradicate the fear of the unknown while educating and empowering our youth to acknowledge and appreciate our special needs students."
And then, a light. And another one. The confused stares from before were now a sea of clarity. A nod. A clap. More clapping.
I sit down, my hands still shaky, my knees still wobbly, but this time from a surge of pure joy.
I leave campus later that morning careful not to let Andrew see me because if he catches a glimpse of his mama, he'll never want to let me out of his sight.
Somehow the school looks a little different then it did when I first arrived. Less daunting; more friendly.
I get in my car and reach down to remove the badge the PTA President gave me when I first arrived on campus. I trace my name with my finger, let my eyes linger on the black font for a few seconds, and let the importance of this badge and what it represents sink in for a moment.
And I decide to wear it for just a little while longer.
If I can prevent just one child, just one parent, from thinking less of my child, if I can help lift the veil of ignorance just a tiny bit and replace it with understanding and support, then I will be the best darn volunteer anyone has ever seen.
And that is why I finally joined the PTA.
* * *
This Modified Life is a column by Jo Ashline for and about the families in Orange County living with special needs. Jo is a married mother of two who writes regularly for OC Moms, the Orange County Register's parenting section.


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Unlike the Iraqi army they did not flee as ISIS gunmen rampaged their way through this part of northern Iraq, previously considered a stronghold of Baghdad's army.
Hundreds of Peshmerga soldiers man a mud berm. The ISIS fighters are a short distance away on the other side and there is regular contact between the two sides.
Bullets whistle overhead as Kurd fighters look for targets and any sign of movement by the Islamists.
The soldiers say that ISIS are holed up in Sunni villages about 800m away and for the past few days have attacked the Kurdish positions, sometimes from trucks mounted with heavy weapons and sometimes with mortars.
The Kurds just want to contain ISIS and keep them from entering Kirkuk once again.
ISIS are now heavily armed after looting the Iraqi army stores and here, as with much of Iraq, they are digging in and consolidating their positions.
Getting them out is going to prove very difficult.
The Kurdish commanders are staggered at the collapse of the Iraqi army but doubt that ISIS can get into Baghdad.
Sheltering from the blistering sun, Brigadier Sideeq Heerani told me he believes that someone gave the orders for the Iraqi Army to withdraw rather than defend their positions.
"There is a hand behind this. Someone is responsible and should be brought to justice, it makes no sense," he says wiping sweat from his eyes.
On the questions of Baghdad falling to ISIS he shakes his head and smiles.
"You think America would let this happen, Iran would let this happen?" he says.
He is probably correct in his analysis, but the microcosm of the Kurdish containment of ISIS in specific northern areas is not a working plan for huge swathes of the rest of Iraq.
Kirkuk was briefly terrorised by ISIS, but is now under the control of the Kurds and life has returned to normal.
In his heavily guarded offices, city governor Dr Najmaddin Karim is warning that ISIS will consolidate, introduce Sharia law and fundamentally change the lives of all citizens living in the areas they now control.
He believes that there needs to be an international response and it has to move quickly.
"ISIS are joining forces with former Baath party members and are growing," he says.
"There needs to be a response and it needs to be in Iraq and in Syria where these people have come from. Tony Blair is right this needs to be coordinated action," he says, promising Kurdish support.
While the government in Baghdad, the United States, Iran and a host of other countries consider how to respond to a problem that flowed here from Syria, but was exacerbated by internal rivalries and politics, the fact is that the Kurds are now the only northern resistance to ISIS and its brutal take over.


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Chest pains and anxiety worsen before and during period?
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chest pain and headackes and tightness, ...
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November 28th, 2011
Hi every one. Just recently... I've noticed that my chest pains and other anxiety symptoms gets worse before and during my menstrual cycle. Does this happen for you ladies? I've had numerous ekgs- blood work-and chest xrays. All came back normal. Should I be worried... Or is it just my anxiety? I dont want to go to the doctor to hear its just my anxiety and to spend more money. I hope I hear from someone soon. Thank you.
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Hi there!
I know this an old post of yours but I was doing research on the internet and came across your question/comment regarding chest pains. I have been feeling the SAME thing and now I have figured out the pattern that it's before my period. I am soo glad to know there are other people feeling the same thing. Not that I want others to be in pain but at least I know it's not in my head. From what I've read it could be hormone related (perhaps you are too young for that!) I was also researching and came across something called PRINZMETAL ANGINA. Gotta read some more. But yes, I have chest pains that feel like serious heart bur, almost like I pulled a muscle in my sternum area or something. I am curious, have you had a resolution to this problem or seen any doctors. Hope you feel better. Thanks
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The subject of intentional breeding or meat rabbits is prohibited. The answers provided on this board are for general guideline purposes only. The information is not intended to diagnose or treat your pet. It is your responsibility to assess the information being given and seek professional advice/second opinion from your veterinarian and/or qualified behaviorist.
LEADERS: Azerane Bam BinkyBunny JerseyGirl LBJ10 LittlePuffyTail LongEaredLions RabbitPam
For the first time since this site was created we are finally going to get our video gallery fixed and updated to something MUCH nicer. The current one is terrible...... so we never did much with it.
We hope to have several sections including:
There will be other sections too, but those are the top 4 to start off with, and of course if you have any ideas, please share.
The gallery won't be up and running fully for a few days, but now is the time to send in your videos and I will add them in to the new gallery when we gets it going.
Here's how:


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Creator Ben Nyberg tells the Daily Dot about his new bookmarklet, based on the eccentric and spammy musings of Twitter's @Horse_ebooks.
If you're craving more of the eccentric and quixotic musings from @Horse_ebooks, there's an antidote.
A new bookmarklet for Web browsers released Thursday transforms boring websites into dazzling @Horse_ebooks shrines with a click of a button.
After dragging the bookmarklet to your toolbar, subsequently clicking it changes pictures on any website to the synonymous @Horse_ebooks Twitter icon and words into tweets from the Twitter feed. That's it! Even the directions call it "absolutely useless."
It's based off the cult favorite Twitter account, @Horse_ebooks, which no one knows the origin or impetus of. It spews random phrases and occasionally tweets links to a shady spam website selling ebooks.
The bookmarklet was created by Ben Nyberg, a Brooklyn-based interactive designer and @Horse_ebooks fan. He was inspired by similar applications, such as bacolicio.us, that alters websites appearances, but he wanted to expand the Twitter feed's humor.
"What I wanted was to be able to take @Horse_ebooks's non sequiturs and put them in a different context to (hopefully) amplify the comedic absurdity of the whole thing," Nyberg wrote to the Daily Dot, adding that he loves seeing the bookmarklet used on Facebook pages.
Nyberg explained how the bookmarklet works. It scans the site's code for images then replaces them with the horse picture. The text is switched out with 200 of the most recent tweets from @Horse_ebooks. He said it took him two days to build the bookmarklet.
Twitter users thanked Nyberg for doing the Internet a "mitvah," while another user called Nyberg his "favorite person right now."
This isn't the only way @Horse_ebooks fans have been memorializing the feed. There's a comic strip dedicated to it, a locket necklace with tweets from the account engraved into it, and even a fan fiction Tumblr.
Here's how the new and improved CNN.com looks like.
Pure, uncut internet. Straight to your inbox.


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Analysis After Years of Neglect, Israel Forced to Address Tunnel Issue
Israel should grant a generous civilian concession to Hamas for a cease-fire, finish destroying the tunnels and get out of Gaza.
During one of the hardest moments of the Yom Kippur War, on a front in the Golan Heights, a senior officer and a soldier from the...
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WASHINGTON – The Obama administration's tightening of pollution regulations for new coal-fired power plants Tuesday is a step in the right direction, Maryland politicians and environmentalists said, but some said it doesn't go far enough.
The Environmental Protection Agency's pollution standards would require new coal-fired plants to install additional pollution controls such as carbon-capture technology. The standards do not apply to existing power plants or those that will start construction within the next 12 months.
Maryland Democratic Sen. Ben Cardin said the new rules should help improve the health of the imperiled Chesapeake Bay.
"I applaud the years of thoughtful work and rigorous scientific study" that went into the EPA's creation of the regulations, Cardin said. "The scientific evidence of the threat that increased greenhouse gas emissions pose to Maryland and the health of Chesapeake Bay, to our nation's farmers and natural ecosystems, and most importantly to the world our children will inherit, is irrefutable."
Others questioned the administration's reliance on carbon-capture technology — a way of trapping carbon emissions and storing them underground — as a tool for reducing pollution.
"There's nobody in the world that does that today. It's very expensive," said former Bush administration EPA Air Administrator Jeff Holmstead. In a recent report, the Department of Energy said that the carbon-capture technology won't be commercially available until 2020, according to Holmstead.
The ruling, Holmstead said, effectively bans new coal energy plants.
Tommy Landers, the director of the advocacy group Environment Maryland, also believes carbon capture is a questionable idea.
"I don't think (carbon capture) is a long-term solution. We need to reduce pollution at its source," he said.
The exemption of existing power plants affects Maryland because the state is at the end of a "tailpipe" of pollution from other states, Landers said.
In addition, there are nine coal-fired power plants in Maryland, and none of them use carbon-capture technology.
Pollutants released from coal-fired power plants include nitrous oxide, methane and sulfur dioxide. The gases are implicated in global warming as well as acid rain.
The new regulations are a result of a 2007 Supreme Court ruling which determined that greenhouse gas emissions are pollutants that are subject to the Clean Air Act.
Environment Maryland estimates that coal-fired power plant pollution is responsible for at least 100 premature deaths and 4,000 asthma attacks an year, according to a 2007 report.
In 2010, the coal-fired Morgantown Generating Station in Newburg was the state's dirtiest power plant. It emitted almost 7.3 million metric tons of carbon dioxide, 18,000 metric tons of methane and 38,000 metric tons nitrous oxide, according to the EPA.
Landers said that he is looking forward to working with EPA Administrator Lisa Jackson to regulate existing power plants as well.
"We certainly need to be doing more to clean up every power plant, but this (proposal) is a step in the right direction," he said.
The Chesapeake Bay Foundation declined to comment on the proposal.
There are no planned coal-fired plants in Maryland that will be affected by the new regulations, Holmstead said.
"That doesn't mean that Maryland won't be affected because it does import coal power from Pennsylvania," Holmstead said.
He described the regulation as a "political statement," and said that it may have little practical effect because low-priced natural gas is beginning to replace coal as a source of energy.
But he warned that "the rule can't stay in place if natural gas prices start to rise."


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Results 1 to 5 of 5
Thread: Can't settle on a name..
December 4th, 2013 07:32 AM #1Junior Member
- Join Date
- Dec 2013
- Posts
- 2
Can't settle on a name..
I have 4 boys all with unusual names always like to keep it unique, my baby girl is due in feb I just can't find a name to tie in with the boys names.. Which are
Jaiden Kyai
Shai Raine
Cruz Leon
Raylee Jak
I really like the name Amelia but it's very common what do u all think may go with my other children's names I want something really pretty and girlie which isn't common
December 4th, 2013 07:39 AM #3Senior Member
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- Nov 2013
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I notice you like the letters Y , I, and Z. So... I'll try...
Zoey (Might be too close to Raylee)
and I don't know why I'm saying this one... just a shot in the dark....
Veronica (I actually like Veronica Claire quite a bit though some might say it's dated)
December 4th, 2013 08:14 AM #5Cynthia/Luna
twenty-something name nerd. infj
Seraphina Juliette Audrey. Evangeline Laetitia Odette. Catalina Ariadne Helen. Valentina Bellatrix Yvaine
Violetta Catherine Lenore. Isabelle Faustina Clare. Rosalind Anna Belphoebe. Guinevere Cassia Ottilie
Vanessa Rose Aphrodite. Helena Edelweiss. Talitha Caroline. Aurelia Madelief
Peregrine Lysander James. Gavriel Alexander Callum. James Luca Auberon. Edmund Frederic Altair
Perseus Arthur Flynn. Cassius Jason Alaric. Damien Alexei Orion
December 4th, 2013 08:28 AM #7Senior Member
1 amazing son: Theodore IsaacWhy yes, I probably should be working!
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- Sep 2013
- Location
- Midwest
- Posts
- 771
Benjamin * Sebastian * Ezra * Edmund * Henry * Hugo * Cormac * Andrew * Winston * Levi * Zev
Arabella * Aviva * Ariella * Maeve * Matilda * Eleanor * Catherine * Charlotte * Beatrice
December 4th, 2013 09:03 AM #9Junior Member
- Join Date
- Dec 2013
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From the archives of The Daily News for June 21:
- In 1914, Swedish residents of Galveston celebrated midsummer day in Dickinson.
- In 1914, 35 tank workers went on strike for higher pay in Texas City.
- In 1964, immediate plans for expansion and remodeling of Nathan's, 2216 Postoffice, at a cost of approximately $550,000, were revealed by Neil Nathan, merchandise manager. This marked the store's third major remodeling project since 1947.
- In 1964, a monument to Norris Wright Cuney, an early leader in Galveston and Texas affairs, was dedicated.
- In 1989, members of the La Marque Police Association initiated a petition drive to call for an election that would give the police department collective bargaining power.
- In 1989, pretrial publicity concerning the murder trial of Allen Bethany resulted in 13 potential jurors being barred from the trial. Bethany was charged with committing a murder at the Tri-City Cafe in Texas City.
From Staff Reports