1) Official Race Results
NAME:
Dxxxx Sxxx
EVENT:
Full Marathon
DATE:
Sunday, December 2nd, 2007
BIB/DIV:
6xx / M3539
TIME:
4h:22m:51s (gun) / 4h:21m:57s (net)
Splits (acc to timing chip)
Time Start: 5:31:06
7k700m: 12:46:35
21k: 2:01:08
26k750m: 2:29:46
Gun time: 4:22:51
Chip Finish: 4:21:57
Average Splits: 6m12s/km
Rank: 1002 (FM-Males), 1127 Overall
Link here --> http://www.runpix.biz/sin07/42/finord.php?LastName=632&lan=&aset=0
Splits (acc to Polar)
10k: 00:57:22
21.1k: 2:00:23
28k: 2:40:26
42.2k: 4:21:59
2) Visit to Atlas Chiropractic
I went to see my chiro on Tuesday evening after the race. By then still had soreness mainly over the quads, and a little tightness of the hams. Left knee pain had almost totally gone, phew! Didn't want a repeat of the ITB problem I had last time out.
Had me up on the table and gave me the once over. Hip was out of alignment he said, contributing to a limb length discrepancy (L>R). Did the usual side-pulling with all the crackling coming from the nether regions of the back and hips. Don't ask me how it works, but it works! The hip and quad pain significantly reduced with a 5-minute procedure. Next, worked on my ankles, again the twisting and crackling. Last, worked his way up to my shoulders. Now, I hadn't mentioned my shoulder and upper back cramps during the race, but Terence picked up on it straight away. More pulling and crackling.
All in all, felt looser and less achy after the session. Terence asks for some advice on training, wants to do the full next Dec! Gotta to remember to send him some stuff.
Wednesday, December 5, 2007
Monday, December 3, 2007
SCSM 2007
Race Report
My Race:
Felt quite undertrained for this event. Compared to previous 2, total mileage is probably down by about 20%, longest LSD short by 3k. Only saving grace is some speed work done. Also, tried a late taper as suggested by RW. My thoughts on this are a little mixed. I think my last LSD, a week later than I would usually run it, was probably about 3-4 days too close to the event. On the other hand, I think it did provide me with a much needed training boost. It may mean I will need to split the difference and run it mid-week in future.On the morning itself, still feeling a little leg heavy from fairly hard training 2 weeks prior, plus chasing the kids whole of Sat.
Got on the bus, and was at the esplanade shortly thereafter. True to my usual routine, queued for the esplanade toilets, thankfully still empty at around 4.50am. Nothing to pass out though, despite sitting on the bowl for a good 10 minutes.Had my last drink of 100plus, took half a banana and went to pee one more time at a porta-loo. Time was 5.15 and I made may way to the start line. Saw Sealboon on the side of the sub-4 pen, seemed very focussed so I did not trouble him. Didn't recognise anybody else.
Horn blows, away we go. First couple of clicks going as it typically does, some speedsters streaking away, some slowbies who have decided that they need to start in front, but the wide open avenue makes it less painful for everone. Stop at the telok ayer market toilet for a pee, good to get this out of the way early! Once the adrenaline kicks in, urine output will be minimal and I don't expect to need to use the loo anymore for the rest of the race. For the first 10k, fairly uneventful, was walk-breaking more frequently than expected as I couldn't properly identify stations with isotonic, so pretty much every water point I slowed downed to take a swig. Unfortunately, that meant each walk break was shorter than usual. Did this contribute to the crash? Maybe. Out of marina south and past the esplanade again. Huge crowds, which was nice and a good boost at this part of the race. Going better than expected at this point, clocking 5:30-5:40 pace and at the halfway point time was 2:01, just a little off my AHM 2007 timing. HR still under 162 average.
Now fully into the East Coast Park. Support was tremendous! Thank you volunteers. Was tracking an older gentleman who was running bow-legged. He was fast enough but I wonder what sort of impact this type of running biomechanic would hold for his knees in the future. At the 23km point, I see Freddy coming back own the other direction. Holy cow! What a smoking quick run he was doing! I am beginning to feel it. Pace average dropping off, now around 5:40-5:50 per km. Made the u-turn, back towards the city. The sun is now high enough to make a difference. I stretch my arms a little, and BANG, my whole upper back and shoulders cramp up. It was excruciating in the extreme and I almost stop running. I hang my arms down and push on. Pace is now 6+min/km. Legs are getting noticeably heavier, at 28km, its 2:41, still on target for a sub-4. A short while later, twing, and my left calf seizes momentarily. Oh no, the dreaded cramps. I've blown it, it was going to be a real struggle from here. And indeed, when I hit this wall, the fall was precipitous. In a matter of 1km, left calf, left thigh, right thigh, left hamstring, all started to threaten to cramp. I slow to a walk-run. For the first time, I gratefully accept deep heat, I have never ever used that stuff before. It seemed to work and the worst of the cramps were staved off. I mentally prepare myself to struggle for another 12km.
The rest of the way was pure agony, basically completely played by ear, shuffled when I could, walked when my legs refused to respond, stopped at almost every drink station. My lack of training and over-ambitious start had caught up with me. No chance of my heart giving out, now ticking along at 145/min, not even 85% max! Definitely the legs are rate limiting. Amazingly, still averaging around 7:30/km. I was going to come in PB! The last 500m, picked up to a decent trot so that I don't look too bad in the pictures :p.
Completed in 4:22.A PB by 6 minutes, despite being undertrained, hotter weather, less rest and being 3kg heavier. I think with a more discliplined and smarter program, better taper and race strategy, a sub-4 will be achievable by next year end. 2008 will be the year to try. Perversely, I felt as good about myself for having struggled through the last 12km and having run a good pace for the first 30!
Organisation:
Overall, a 9/10 for the organisers. Bag check was smooth and painless. Porta-loos seemed a plenty. Start point management was also pretty smooth with a nice clear avenue for folk to get to their starting pens. A 5.30 start is good, gives us a chance to get the miles in before the full brunt of the morning heat. Have not actually run the full in SG before, but apart from the first 10k in the quiet of Marina South, the rest of the way was quite well supported. Drink stations were plentiful, although it wasn't clear which had isotonic and which did not. Made my drink stop strategy a little messy. At the end, bag collection was a cinch. Well done organisers! Some feedback for improvement below.
Feedback to organisers
a. Get pacers positioning right
b. Get isotonic on all stations, or at least post in advance which stations will have them
My Race:
Felt quite undertrained for this event. Compared to previous 2, total mileage is probably down by about 20%, longest LSD short by 3k. Only saving grace is some speed work done. Also, tried a late taper as suggested by RW. My thoughts on this are a little mixed. I think my last LSD, a week later than I would usually run it, was probably about 3-4 days too close to the event. On the other hand, I think it did provide me with a much needed training boost. It may mean I will need to split the difference and run it mid-week in future.On the morning itself, still feeling a little leg heavy from fairly hard training 2 weeks prior, plus chasing the kids whole of Sat.
Got on the bus, and was at the esplanade shortly thereafter. True to my usual routine, queued for the esplanade toilets, thankfully still empty at around 4.50am. Nothing to pass out though, despite sitting on the bowl for a good 10 minutes.Had my last drink of 100plus, took half a banana and went to pee one more time at a porta-loo. Time was 5.15 and I made may way to the start line. Saw Sealboon on the side of the sub-4 pen, seemed very focussed so I did not trouble him. Didn't recognise anybody else.
Horn blows, away we go. First couple of clicks going as it typically does, some speedsters streaking away, some slowbies who have decided that they need to start in front, but the wide open avenue makes it less painful for everone. Stop at the telok ayer market toilet for a pee, good to get this out of the way early! Once the adrenaline kicks in, urine output will be minimal and I don't expect to need to use the loo anymore for the rest of the race. For the first 10k, fairly uneventful, was walk-breaking more frequently than expected as I couldn't properly identify stations with isotonic, so pretty much every water point I slowed downed to take a swig. Unfortunately, that meant each walk break was shorter than usual. Did this contribute to the crash? Maybe. Out of marina south and past the esplanade again. Huge crowds, which was nice and a good boost at this part of the race. Going better than expected at this point, clocking 5:30-5:40 pace and at the halfway point time was 2:01, just a little off my AHM 2007 timing. HR still under 162 average.
Now fully into the East Coast Park. Support was tremendous! Thank you volunteers. Was tracking an older gentleman who was running bow-legged. He was fast enough but I wonder what sort of impact this type of running biomechanic would hold for his knees in the future. At the 23km point, I see Freddy coming back own the other direction. Holy cow! What a smoking quick run he was doing! I am beginning to feel it. Pace average dropping off, now around 5:40-5:50 per km. Made the u-turn, back towards the city. The sun is now high enough to make a difference. I stretch my arms a little, and BANG, my whole upper back and shoulders cramp up. It was excruciating in the extreme and I almost stop running. I hang my arms down and push on. Pace is now 6+min/km. Legs are getting noticeably heavier, at 28km, its 2:41, still on target for a sub-4. A short while later, twing, and my left calf seizes momentarily. Oh no, the dreaded cramps. I've blown it, it was going to be a real struggle from here. And indeed, when I hit this wall, the fall was precipitous. In a matter of 1km, left calf, left thigh, right thigh, left hamstring, all started to threaten to cramp. I slow to a walk-run. For the first time, I gratefully accept deep heat, I have never ever used that stuff before. It seemed to work and the worst of the cramps were staved off. I mentally prepare myself to struggle for another 12km.
The rest of the way was pure agony, basically completely played by ear, shuffled when I could, walked when my legs refused to respond, stopped at almost every drink station. My lack of training and over-ambitious start had caught up with me. No chance of my heart giving out, now ticking along at 145/min, not even 85% max! Definitely the legs are rate limiting. Amazingly, still averaging around 7:30/km. I was going to come in PB! The last 500m, picked up to a decent trot so that I don't look too bad in the pictures :p.
Completed in 4:22.A PB by 6 minutes, despite being undertrained, hotter weather, less rest and being 3kg heavier. I think with a more discliplined and smarter program, better taper and race strategy, a sub-4 will be achievable by next year end. 2008 will be the year to try. Perversely, I felt as good about myself for having struggled through the last 12km and having run a good pace for the first 30!
Organisation:
Overall, a 9/10 for the organisers. Bag check was smooth and painless. Porta-loos seemed a plenty. Start point management was also pretty smooth with a nice clear avenue for folk to get to their starting pens. A 5.30 start is good, gives us a chance to get the miles in before the full brunt of the morning heat. Have not actually run the full in SG before, but apart from the first 10k in the quiet of Marina South, the rest of the way was quite well supported. Drink stations were plentiful, although it wasn't clear which had isotonic and which did not. Made my drink stop strategy a little messy. At the end, bag collection was a cinch. Well done organisers! Some feedback for improvement below.
Feedback to organisers
a. Get pacers positioning right
b. Get isotonic on all stations, or at least post in advance which stations will have them
Sunday, December 2, 2007
Personal Journal (SCSM2007)
This will be a long entry to reflect the prep I had for this race and also my observations of race-day events and my own performance.
1) Prep
I hadn't expected to do the SCSM this early in my running 'career'. Both of my marathons to date had been in the US in freezing temperatures. I had wanted to 'save' the SCSM to a later time I had started to run out of events to take part in. Ah well, events conspired to render my participation in US races difficult. Hadn't been travelling as much and had lingering ITB problems from the previous event in Chicago from Oct 2006, and therefore had pathetic mileage in training. So in July of this year, signed up for the local marathon. About this time, was when I became more active in SGRunners forum. So set up a 5 month programme, entered the AHM and NB realrun for prep, and determined to do a good one. No preset idea of what time to complete in, just needed to make sure I give a good account of myself.
2) Training
See above
6) Learning points
a. Get technical running socks
b. Use a cap/visor
c. Start taper 16-19 days before, last LSD no closer than 19 days to event.
d. Arm pouch is a no-go
e. Don't compromise on walk-breaks early on
f. Fibre diet is ok pre-race
g. Does deep heat help?
1) Prep
I hadn't expected to do the SCSM this early in my running 'career'. Both of my marathons to date had been in the US in freezing temperatures. I had wanted to 'save' the SCSM to a later time I had started to run out of events to take part in. Ah well, events conspired to render my participation in US races difficult. Hadn't been travelling as much and had lingering ITB problems from the previous event in Chicago from Oct 2006, and therefore had pathetic mileage in training. So in July of this year, signed up for the local marathon. About this time, was when I became more active in SGRunners forum. So set up a 5 month programme, entered the AHM and NB realrun for prep, and determined to do a good one. No preset idea of what time to complete in, just needed to make sure I give a good account of myself.
2) Training
What would I do different this time? I thought speed work was the key. Previously, being a marathon newbie, was pretty nervous about completing the event even, without looking like a complete idiot. Naturally the focus was on getting in those long miles to build up an aerobic and endurance base. The consensus from many different books and websites was that in order to run fast, you really had to train fast. How fast? I thought a 4:00-4:10 finish was a reasonable target, given my previous PB of 4:28. This time round, made sure I had at least 1 speed session per week, which usually ended up being hill repeats. Also, wanted to continue to build up an even better aerobic base. Alas, reality collides with theory, at the end of the day, only managed one LSD > 30km and 2 runs > 25km. All in all, would have considered myself significantly undertrained for the event.
Also, tried a shorter taper with my last LSD coming only 2 weekends before the event. It was probably a little too close for me.
Also, for the first time, used a camelbak for a few of my runs. I must say, it is a nifty invention. Will definitely make more use in the future. Mine is a small 1.5L version, but in truth could probably take 1.2L at most if it was to be used comfortably. When filled fully was pressing into my spine and felt better only after I swigged a few mouthfuls.
How did I set my target? I used the MacMillan race predictor which gives a comprehensive race time prediction based on real previous performances. With that, I had a target and training pace to use.
3) Equipment
My trusty arm pouch is turning out to be much more of a pain than I anticipated. I'd say it was a minor contributor to my near crash of this event. Whilst the previous Nike ones were good by not giving abrasions, this current black kit repeatedly caused armpits abrasions. Need to seriously rethink how to carry gear/food on runs.
Bought a pair of technical running socks for the first time the week before the race. Ran a 6k in it and it felt really really good. Only problem, with it being so thin, there was too much room inside of my shoe. Too risky to do something new at this stage. So reverted to my trusty cotton socks. At about the 35k mark, the socks bunched up and caused a horrid foot pain, to add to everything else going on.
Had an interesting exchange with a fellow forumer on the use of cap/visor in this race. My conclusion? It is invaluable! Just as a comparison, I took off the cap for a short bit on the return leg and I thought the glare and heat was intolerable. Next stop, a proper running visor.
4) Nutrition
So fibre or no fibre the days before a run? I must vote to go with your normal diet, no matter what it is. I switched to low fibre and although there weren't major issues, I just never felt entirely comfortable with it. No bulk for stools on race morning, but had a sense of constipation. Not really troubling but I think I'd stick with usual fruit and veggies.
On race, I knew they had bananas at 35k, so I could afford to eat stuff at 15k and 25k. As it turned out, ended up taking an extra mini-Mars bars with me so downed a Mars bar at 8k as well. A little sticky but as the drink stations are well posted, strategy was to slow down a short distance from station, chomp down the bar and then wash down with fluids. This works for me and somehow seems more pleasurable than gulping gel.
5) Race ReportSee above
6) Learning points
a. Get technical running socks
b. Use a cap/visor
c. Start taper 16-19 days before, last LSD no closer than 19 days to event.
d. Arm pouch is a no-go
e. Don't compromise on walk-breaks early on
f. Fibre diet is ok pre-race
g. Does deep heat help?
Friday, November 9, 2007
NUS Hill Run
After a couple of half-starts, finally managed to complete a proper NUS Hill run this week. What a turn out it was, 11 runners in total. Finally go to put some faces to nicks. Was undertaking this with a no small amount of trepidation, as had crashed and burned the first time I took on the hills. Once again started out at a pace somewhat faster than I am comfortable with (thanks to xdd!). 5:20min/km, HR up to 160 already and barely 1km into the run. Chatted with DO at the beginning and soon came up to HPV. Really cool to get into the park, probably not been there in over 25years. No time for sightseeing though, hit the top of the hill and waited for the rest to catch up. Nice to have an early break, and mindful of Vigilante Drive to come. Down the back lane and out to Zehnder Road, everyone still going strong. Soon hit the foot of Vigi Drive, don't care how slow I look, I am JOGGING up this slope. Sure enough, soon left behind as everybody else charged up. Took my time to get to the top, but as I got there, felt relieved as I had got to the top in good shape and now I knew I was going to finish the run at least! Down the slope, into SP1 and water break. All the breaks are making this a very manageable run. Retrospectively this was really good interval training, sweat it up the slopes, then take ample rest, then repeat.
Ok, onwards. Up science park, chatted with Freddy. First time he was doing this route and he was enjoying it tremendously. Gave him some tips on the area and soon we were turning back down South Buona Vista road. Cutting across SBV back down to SP2 is a really hazardous exercise, can't see round the bend and who knows what crazies may be driving.
Cut a long story short, the group hung tight till we hit the base of PGP (near guild house) again. wend88 calls it a day on her first NUS Hill Run. She's done fantastically well keeping up with the pace up till now. I remember my first Hill Run when I walked the last 6km after trying to keep up with Ronnie and tktan inthe first 3. Last 5 km around NUS. Freddy, DR, Ronnie decide to attack the PGP hill with gusto. I am hanging back a little. Finally, into NUS, around UCC and the last 1km. Everybody SPEEDS up! Finally, guild house comes into sight. I've officially COMPLETED a NUS Hill Run. xdd, I want my cert.
Post run refreshments were great. Drinks and fruit, thanks tktan and BR.
As usual, scoot off for my meetings. Heard the guys enjoyed dinner. Hopefully I'll get a chance next time.
Some pics here --> tktan's, BR's
Till next week (or this week, actually)
Ok, onwards. Up science park, chatted with Freddy. First time he was doing this route and he was enjoying it tremendously. Gave him some tips on the area and soon we were turning back down South Buona Vista road. Cutting across SBV back down to SP2 is a really hazardous exercise, can't see round the bend and who knows what crazies may be driving.
Cut a long story short, the group hung tight till we hit the base of PGP (near guild house) again. wend88 calls it a day on her first NUS Hill Run. She's done fantastically well keeping up with the pace up till now. I remember my first Hill Run when I walked the last 6km after trying to keep up with Ronnie and tktan inthe first 3. Last 5 km around NUS. Freddy, DR, Ronnie decide to attack the PGP hill with gusto. I am hanging back a little. Finally, into NUS, around UCC and the last 1km. Everybody SPEEDS up! Finally, guild house comes into sight. I've officially COMPLETED a NUS Hill Run. xdd, I want my cert.
Post run refreshments were great. Drinks and fruit, thanks tktan and BR.
As usual, scoot off for my meetings. Heard the guys enjoyed dinner. Hopefully I'll get a chance next time.
Some pics here --> tktan's, BR's
Till next week (or this week, actually)
Wednesday, November 7, 2007
Salt Supplementation for Exercise and Training?
For some reason, exercise and training seem to attract a fair amount of myth and magic. Is salt supplemenation really needed for aerobic training? Lets find some evidence.
http://www.ajcn.org/cgi/reprint/72/2/564S
http://www.ultrunr.com/noakes.html
I quote;
Other electrolytes and minerals
Potassium is the major intracellular ion and is lost from the body in sweat and urine during exercise. However these losses are small (<1 gm even during very prolonged exercise) and are replaced by the normal daily dietary intake of 2-4 g. There is no evidence that potassium supplementation is required by the physically active.
Magnesium is another intracellular ion that, like potassium, is lost in sweat and urine during exercise. But the losses are trivial. There is no published evidence showing that magnesium deficiency is either common amongst the physically active, or that magnesium supplementation can either increase the intracellular magnesium stores, or enhance performance (15). The balance of evidence indicates that although body iron stores may be marginally reduced in some athletes, especially long distance runners, the incidence of true iron deficiency requiring treatment is no higher in the physically-active than in the sedentary population (16,17). Furthermore, the causes of iron deficiency anaemia in the physically active are not different from the causes of the condition present in sedentary persons. There is no indication for the indiscriminate use of iron supplementation by the physically active.
The intake of calcium especially by adolescent females, whether or not they are physically active, is usually less than the Recommended Daily Allowance (RDA). Hence adolescent female athletes come from a population that is already predisposed to an inadequate calcium intake. Female athletes in activities that favour thinness such as gymnastics, ballet dancing and running, are especially likely to eat kilojoule-restricted and therefore calcium-deficient diets. The chronic ingestion of a low calcium diet is associated with a reduced adult bone mass (18) and greater risk for the development of osteoporosis including the complications of fractures of the hip (19) or, in athletes, stress fractures (20). Hence there is a need to insure that females especially, ingest sufficient calcium throughout life.
There is no published evidence that the dietary requirements for chromium, copper, zinc or phosphate are increased in the physically active or that supplementation with any of these nutrients will improve athletic performance.
http://www.ajcn.org/cgi/reprint/72/2/564S
http://www.ultrunr.com/noakes.html
I quote;
Other electrolytes and minerals
Potassium is the major intracellular ion and is lost from the body in sweat and urine during exercise. However these losses are small (<1 gm even during very prolonged exercise) and are replaced by the normal daily dietary intake of 2-4 g. There is no evidence that potassium supplementation is required by the physically active.
Magnesium is another intracellular ion that, like potassium, is lost in sweat and urine during exercise. But the losses are trivial. There is no published evidence showing that magnesium deficiency is either common amongst the physically active, or that magnesium supplementation can either increase the intracellular magnesium stores, or enhance performance (15). The balance of evidence indicates that although body iron stores may be marginally reduced in some athletes, especially long distance runners, the incidence of true iron deficiency requiring treatment is no higher in the physically-active than in the sedentary population (16,17). Furthermore, the causes of iron deficiency anaemia in the physically active are not different from the causes of the condition present in sedentary persons. There is no indication for the indiscriminate use of iron supplementation by the physically active.
The intake of calcium especially by adolescent females, whether or not they are physically active, is usually less than the Recommended Daily Allowance (RDA). Hence adolescent female athletes come from a population that is already predisposed to an inadequate calcium intake. Female athletes in activities that favour thinness such as gymnastics, ballet dancing and running, are especially likely to eat kilojoule-restricted and therefore calcium-deficient diets. The chronic ingestion of a low calcium diet is associated with a reduced adult bone mass (18) and greater risk for the development of osteoporosis including the complications of fractures of the hip (19) or, in athletes, stress fractures (20). Hence there is a need to insure that females especially, ingest sufficient calcium throughout life.
There is no published evidence that the dietary requirements for chromium, copper, zinc or phosphate are increased in the physically active or that supplementation with any of these nutrients will improve athletic performance.
Thursday, November 1, 2007
Sub-2hr Marathon?
In the wake of HG's phenomenal run in Berlin, there was an interesting discussion in SG Runners on the possibility of a sub-2hr marathon in the future. I beleive that the time will be soon, due to the greater opportunities and technologies that now exist.
http://sgrunners.com/forum/index.php?showtopic=5858&st=30&p=194107&#entry194107
http://sgrunners.com/forum/index.php?showtopic=5858&st=30&p=194107&#entry194107
Glycerol Hyperhydration?
An interesting discussion on glycerol hyperhydration. Does it work?
-->http://www.ultrunr.com/glycerin.html
An excerpt;
I have read the postings on the glycerol issue with interest, and need to inform you of several facts.
I am one of the University of New Mexico scientists who first researched glycerol hyper hydration for improved exercise performance. Based on our and Bud Riedesel's findings (1987), the university invested in patent protection for using glycerol as a hyper hydration agent suitable for use during exercise. In 1996, the patent was purchased by InterNutria, a nutritional supplements company within the larger InterNueron Pharmaceutical Company. Thus, InterNutria has patent protection for using glycerol hyper hydration for enhancing exercise performance.
I am currently contracted by InterNutria to provide scientific advice and commentary on their glycerol product - "ProHydrator". ProHydrator was scheduled to be released to market this June, but the USOC ban on glycerol 'came out of the blue' and has delayed the product release. Such a delay was decided by the company due to the sponsorship of USA Triathlon, as well as several professional triathletes.
From my understanding, the USOC ban is based on glycerol being classified as a tissue dehydrator. Other tissue dehydrators are mannitol, sorbitol, and urea. Such substances are routinely used in clinical practice to dehydrate the brain and eye as a treatment for edemas resulting from a variety of clinical disorders. It just so happens that mannitol, sorbitol, and urea are also potent osmotic diuretics. Glycerol seems to have been included in the banned list of mannitol and sorbitol due to the potential for glycerol-induced diuresis.
I have recently written a major review of the clinical and applied uses of glycerol ingestion. It is currently in review. Within this manuscript is a section that pertains to glycerol-induced diuresis. It is important to remember that glycerol ingestion is not the same as glycerol hyper hydration. The latter involves the additional ingestion of 1-2 L of water. Simply ingesting a concentrated solution of glycerol will not hyper hydrate the body, but dramatically increase glycerol concentrations in the blood, interstitial fluid, and kidney filtrate. Increased urinary glycerol has the potential to increase urine flow due to retarding water reabsorption in the kidney. This is the mechanism of the diuresis from mannitol and sorbitol.
Glycerol does not cause a marked diuresis, however, because glycerol is still rapidly reabsorbed in the proximal and distal tubules. Mannitol and sorbitol are not. There is no evidence in the medical literature for a glycerol-induced diuresis. Nevertheless, anecdotal expressions of glycerol-induced diuresis occur in many manuscripts.
I have written a scientific reply to InterNutria for use in the company petitioning the USOC to remove the ban on glycerol.
It is ironic that glycerol has been used by the world's elite athletes for many years. Although it is easy to assay for urinary glycerol, and interpret data, I do not think the testing lab has or is currently performing the assay. It would be easy to detect exaggerated use of glycerol as the kidney can reabsorb almost all glycerol up to blood glycerol concentrations approximating 1.2 mmol/L. As resting blood glycerol approximates 0.05 mmol/L and may increase to 0.5 mmol/L during extreme prolonged exercise and carbohydrate depletion, the only way to cause glycerol to appear in the urine is to ingest large quantities. Thus, if the USOC wanted to, they could easily determine a urinary concentration indicating large amounts of glycerol ingestion. For your information, urinary glycerol can increase to above 20 mmol/L within 30 min after ingesting 1.2 g glycerol/kg body wt.
The USOC is not justified in the ban on glycerol for hyper hydration or proposed metabolic advantages to athletes. Hyper hydration is no worse than ingesting liquid carbohydrate or water during exercise. In addition, glycerol turnover data indicate that 60% of glycerol is converted to glucose in the liver and kidney, 30% is incorporated into glycolysis for oxidation, and the remainder is presumably involved in triacylglycerol metabolism.
It appears that the ban on glycerol is a mistake and should be reversed in the near future. Failure to reverse the ban will not only expose to elite athletes to continued high risks of heat injury, but potentially result in a series of law suits from athletes and nutritional companies against the USOC.
I hope these facts help you understand the glycerol saga !
Rob Robergs, Ph.D. Director: The Center For Exercise and Applied Human Physiology The University of New Mexico
-->http://www.ultrunr.com/glycerin.html
An excerpt;
I have read the postings on the glycerol issue with interest, and need to inform you of several facts.
I am one of the University of New Mexico scientists who first researched glycerol hyper hydration for improved exercise performance. Based on our and Bud Riedesel's findings (1987), the university invested in patent protection for using glycerol as a hyper hydration agent suitable for use during exercise. In 1996, the patent was purchased by InterNutria, a nutritional supplements company within the larger InterNueron Pharmaceutical Company. Thus, InterNutria has patent protection for using glycerol hyper hydration for enhancing exercise performance.
I am currently contracted by InterNutria to provide scientific advice and commentary on their glycerol product - "ProHydrator". ProHydrator was scheduled to be released to market this June, but the USOC ban on glycerol 'came out of the blue' and has delayed the product release. Such a delay was decided by the company due to the sponsorship of USA Triathlon, as well as several professional triathletes.
From my understanding, the USOC ban is based on glycerol being classified as a tissue dehydrator. Other tissue dehydrators are mannitol, sorbitol, and urea. Such substances are routinely used in clinical practice to dehydrate the brain and eye as a treatment for edemas resulting from a variety of clinical disorders. It just so happens that mannitol, sorbitol, and urea are also potent osmotic diuretics. Glycerol seems to have been included in the banned list of mannitol and sorbitol due to the potential for glycerol-induced diuresis.
I have recently written a major review of the clinical and applied uses of glycerol ingestion. It is currently in review. Within this manuscript is a section that pertains to glycerol-induced diuresis. It is important to remember that glycerol ingestion is not the same as glycerol hyper hydration. The latter involves the additional ingestion of 1-2 L of water. Simply ingesting a concentrated solution of glycerol will not hyper hydrate the body, but dramatically increase glycerol concentrations in the blood, interstitial fluid, and kidney filtrate. Increased urinary glycerol has the potential to increase urine flow due to retarding water reabsorption in the kidney. This is the mechanism of the diuresis from mannitol and sorbitol.
Glycerol does not cause a marked diuresis, however, because glycerol is still rapidly reabsorbed in the proximal and distal tubules. Mannitol and sorbitol are not. There is no evidence in the medical literature for a glycerol-induced diuresis. Nevertheless, anecdotal expressions of glycerol-induced diuresis occur in many manuscripts.
I have written a scientific reply to InterNutria for use in the company petitioning the USOC to remove the ban on glycerol.
It is ironic that glycerol has been used by the world's elite athletes for many years. Although it is easy to assay for urinary glycerol, and interpret data, I do not think the testing lab has or is currently performing the assay. It would be easy to detect exaggerated use of glycerol as the kidney can reabsorb almost all glycerol up to blood glycerol concentrations approximating 1.2 mmol/L. As resting blood glycerol approximates 0.05 mmol/L and may increase to 0.5 mmol/L during extreme prolonged exercise and carbohydrate depletion, the only way to cause glycerol to appear in the urine is to ingest large quantities. Thus, if the USOC wanted to, they could easily determine a urinary concentration indicating large amounts of glycerol ingestion. For your information, urinary glycerol can increase to above 20 mmol/L within 30 min after ingesting 1.2 g glycerol/kg body wt.
The USOC is not justified in the ban on glycerol for hyper hydration or proposed metabolic advantages to athletes. Hyper hydration is no worse than ingesting liquid carbohydrate or water during exercise. In addition, glycerol turnover data indicate that 60% of glycerol is converted to glucose in the liver and kidney, 30% is incorporated into glycolysis for oxidation, and the remainder is presumably involved in triacylglycerol metabolism.
It appears that the ban on glycerol is a mistake and should be reversed in the near future. Failure to reverse the ban will not only expose to elite athletes to continued high risks of heat injury, but potentially result in a series of law suits from athletes and nutritional companies against the USOC.
I hope these facts help you understand the glycerol saga !
Rob Robergs, Ph.D. Director: The Center For Exercise and Applied Human Physiology The University of New Mexico
Tuesday, August 28, 2007
SBR and AHM, 26th August 2007
Army Half Marathon 2007
Have had a long lay off from racing after Chicago last October, due to BAD ITB problems. Thankfully, have had a few things occur that have made it right recently. 1) Saw my chiro, which isolated the problem, 2) Saw a sports medicine specialist, who got my foot type checked correctly and recommended the right shoes, and 3) Attended a sports injury talk at CGH, which finally gave me an insight to what the whole issue was.
Suitably prepared, I targeted the AHM as my first competitive run for the year, despite a less than good impression of the route and organisation last time out. Also this time, no pussyfooting and making this merely an LSD training session. If I were going to pay money and get up at 4 in the morning, it had better be worth it!
The difference in my training this time was a more focussed attitude on quality of training as opposed to quantity. As long as I got 1 LSD and 1 tempo/hill, and one or two "fitness maintainers" in a week, I was going to be happy. I believe this was very effective for me.
Week before the race, struck down with flu. Had one 12 clicker in at the start of the week before the flu got bad, and was simply laid up for the rest of the week till Friday. Snuck out for a light 4 clicker on Friday evening. Total mileage for the week....16km! Yuks!
Race Day. Flu lifted, legs feeling bouncy. This was going to be a great day! Indeed, it started well. Timed the toilet visits well, got myself to really near the front. Horn blows, away we go. Running by myself (which I prefer), I am doing 5:05 pace for the first 2km, it is too fast and I deliberately slow it down. No choke point going into ECP this year, which was a real morale buster last time. Hit the upslope, then saw the 2:30 pacer, running at close to sub-2 pace! Poor fellow, must have kenna arrowed by his CO or something. Distance reading on Polar is underestimating a little, its ok, this round foot pod calibration is a little off, as long as its by fixed factor, I can recalculate mentally. Down the bridge and I arrive at the 7km water point, my first stop. Typically, I would stop every 4-5km during training. This time out, with cool weather and good prior hydration, I was going to try a 2-stop strategy. So far so good, looking at a sub-2hr finish.
Turn into Fort road, heading into the parkway. Are those runners coming back down the other way ALREADY??!! Oh my Goodness!! Humbling to say the least. Nevertheless, in the zone now and chugging along. At around 10km, toilet stop at one of those park toilets. Now if you ever have to stop in the middle of run to urinate, BE CAREFUL! Being the highly trained athlete you are, your vagal tone is mighty high. Stopping suddenly to urinate may drop your heart rate and BP drastically.
Ok, more than halfway, still on course and feeling good. At 15 km, 2nd and final water stop. Sun up for a bit already and the air is warming up. A little later, foot pod goes wonky. Grrrrr........not the first time it has happened during a race! Garmin, here I come. Anyhow, pace info not really important anymore, run according to heart rate. Had been chugging along at 5:40 pace, HRM now going at 160. Told myself I will not allow it to get higher than 170, no matter what. Too much risk for an old ticker to bear. Little did I realise the poignancy of that thought at that time. Push for the last 2 km, finished at 1:59 according to stop watch. PB for the half, and plenty happy for it. It was a nice run. Route was good, no choke points, no traffic interruptions, plenty of water/isotonic stops. Well down Army.
Took a couple of bananas, had my drink, and headed straight for the train station. EZ-link card and cash is in my arm pouch, hate the idea of bag check (good decision, as it turned out). Home by 8.30, gave my medal to the elder boy (he's 4), and still got to church only a little late.
Had a late breakfast with church friends later. "How was your morning?", they asked........
"It was GREEEAAATTT!"
Have had a long lay off from racing after Chicago last October, due to BAD ITB problems. Thankfully, have had a few things occur that have made it right recently. 1) Saw my chiro, which isolated the problem, 2) Saw a sports medicine specialist, who got my foot type checked correctly and recommended the right shoes, and 3) Attended a sports injury talk at CGH, which finally gave me an insight to what the whole issue was.
Suitably prepared, I targeted the AHM as my first competitive run for the year, despite a less than good impression of the route and organisation last time out. Also this time, no pussyfooting and making this merely an LSD training session. If I were going to pay money and get up at 4 in the morning, it had better be worth it!
The difference in my training this time was a more focussed attitude on quality of training as opposed to quantity. As long as I got 1 LSD and 1 tempo/hill, and one or two "fitness maintainers" in a week, I was going to be happy. I believe this was very effective for me.
Week before the race, struck down with flu. Had one 12 clicker in at the start of the week before the flu got bad, and was simply laid up for the rest of the week till Friday. Snuck out for a light 4 clicker on Friday evening. Total mileage for the week....16km! Yuks!
Race Day. Flu lifted, legs feeling bouncy. This was going to be a great day! Indeed, it started well. Timed the toilet visits well, got myself to really near the front. Horn blows, away we go. Running by myself (which I prefer), I am doing 5:05 pace for the first 2km, it is too fast and I deliberately slow it down. No choke point going into ECP this year, which was a real morale buster last time. Hit the upslope, then saw the 2:30 pacer, running at close to sub-2 pace! Poor fellow, must have kenna arrowed by his CO or something. Distance reading on Polar is underestimating a little, its ok, this round foot pod calibration is a little off, as long as its by fixed factor, I can recalculate mentally. Down the bridge and I arrive at the 7km water point, my first stop. Typically, I would stop every 4-5km during training. This time out, with cool weather and good prior hydration, I was going to try a 2-stop strategy. So far so good, looking at a sub-2hr finish.
Turn into Fort road, heading into the parkway. Are those runners coming back down the other way ALREADY??!! Oh my Goodness!! Humbling to say the least. Nevertheless, in the zone now and chugging along. At around 10km, toilet stop at one of those park toilets. Now if you ever have to stop in the middle of run to urinate, BE CAREFUL! Being the highly trained athlete you are, your vagal tone is mighty high. Stopping suddenly to urinate may drop your heart rate and BP drastically.
Ok, more than halfway, still on course and feeling good. At 15 km, 2nd and final water stop. Sun up for a bit already and the air is warming up. A little later, foot pod goes wonky. Grrrrr........not the first time it has happened during a race! Garmin, here I come. Anyhow, pace info not really important anymore, run according to heart rate. Had been chugging along at 5:40 pace, HRM now going at 160. Told myself I will not allow it to get higher than 170, no matter what. Too much risk for an old ticker to bear. Little did I realise the poignancy of that thought at that time. Push for the last 2 km, finished at 1:59 according to stop watch. PB for the half, and plenty happy for it. It was a nice run. Route was good, no choke points, no traffic interruptions, plenty of water/isotonic stops. Well down Army.
Took a couple of bananas, had my drink, and headed straight for the train station. EZ-link card and cash is in my arm pouch, hate the idea of bag check (good decision, as it turned out). Home by 8.30, gave my medal to the elder boy (he's 4), and still got to church only a little late.
Had a late breakfast with church friends later. "How was your morning?", they asked........
"It was GREEEAAATTT!"
Monday, August 27, 2007
Aetiology of Muscular Cramps in Marathon Runners
Review of article outlining Current State of Knowledge for Muscle Cramps after Long Distance Running
Martin P. Schwellnus; Sports Med 2007; 37 (4-5): 364-367
This is not a novel article as such, but more a review of other articles, and therefore is short on data. So, take it for what it is.
EAMC is the commonly used term, or, "exercise associated muscular contraction", which the author expands and adds qualifications to become "a painful spasmodic involuntary contraction of skeletal muscle that occurs during or after exercise."
Two of the more commonly hypothesised aetiological causes of "muscle cramps" have been "electrolyte imbalance" and "dehydration". He explains why electrolyte imbalance, although implicated in severe enough cases, with generalised muscle spasm, is unlikely to be the cause in localised muscle cramps of the type seen in sports or distance running. Likewise, he describes a
number of studies that seemingly disprove dehydration as a causative agent.
The rest of the article puts forth the position that "muscle fatigue" is the chief cause of EAMC. It is quite technical so I will spare the details. Suffice to say, lack of details notwithstanding, I find this hypothesis more credible than others, and bears out my own personal experience.
My editorial;
I have had my share of muscle cramps in my younger days from other sports like soccer and tennis. Invariably, they occurred after prolonged sessions in either sport. When you are young you think you are invincible and will push well past your limit. To date, have not had any cramps while training or racing long distance running. This of course is occurring only recently for me, in my more prudent, middle aged state, when I rarely push so hard outside my envelope. I did, during my very first marathon, feel a cramp coming on in my right quad at about 35km, a distance I have not reached before in training. Having been the "beneficiary" of previous cramps, I backed off the speed and ended up run-walk the rest of the way.
I believe, hydration, electrolyte top-up and so forth as useful insofar as they put off the point when fatigue sets in. But at the end of the day, it would appear that your exertions on the day, in relation to your training levels, will determine how quickly and badly you fatigue, and hence how prone you will be to cramping.
Martin P. Schwellnus; Sports Med 2007; 37 (4-5): 364-367
This is not a novel article as such, but more a review of other articles, and therefore is short on data. So, take it for what it is.
EAMC is the commonly used term, or, "exercise associated muscular contraction", which the author expands and adds qualifications to become "a painful spasmodic involuntary contraction of skeletal muscle that occurs during or after exercise."
Two of the more commonly hypothesised aetiological causes of "muscle cramps" have been "electrolyte imbalance" and "dehydration". He explains why electrolyte imbalance, although implicated in severe enough cases, with generalised muscle spasm, is unlikely to be the cause in localised muscle cramps of the type seen in sports or distance running. Likewise, he describes a
number of studies that seemingly disprove dehydration as a causative agent.
The rest of the article puts forth the position that "muscle fatigue" is the chief cause of EAMC. It is quite technical so I will spare the details. Suffice to say, lack of details notwithstanding, I find this hypothesis more credible than others, and bears out my own personal experience.
My editorial;
I have had my share of muscle cramps in my younger days from other sports like soccer and tennis. Invariably, they occurred after prolonged sessions in either sport. When you are young you think you are invincible and will push well past your limit. To date, have not had any cramps while training or racing long distance running. This of course is occurring only recently for me, in my more prudent, middle aged state, when I rarely push so hard outside my envelope. I did, during my very first marathon, feel a cramp coming on in my right quad at about 35km, a distance I have not reached before in training. Having been the "beneficiary" of previous cramps, I backed off the speed and ended up run-walk the rest of the way.
I believe, hydration, electrolyte top-up and so forth as useful insofar as they put off the point when fatigue sets in. But at the end of the day, it would appear that your exertions on the day, in relation to your training levels, will determine how quickly and badly you fatigue, and hence how prone you will be to cramping.
Tuesday, August 14, 2007
ACL Reconstruction Experience
Posted as a contribution to sgrunners forum:
I had a complete tear of my right ACL in 1999, confirmed on MRI and clinical examination. Injury incurred during a soccer game. Reconstruction done 8 months later, and during arthroscope, was confirmed that ligament was completely torn
A few points;
1) Knee stability with ACL tear.
The ACL is one of the ligaments of the knee that stabilises the joint. Specifically, it restrains the femur (thigh bone) from sliding backwards on top of the tibia (shin bone), and vice-versa. It is [u]actually POSSIBLE to continue running safely [/u]with a completely torn ACL. My ortho surgeon suggested as much, and 2 weeks after the injury, I was back to normal running >5K with little problem. The point is that if you have decent muscle strength, sub-sprint running on an even surface does not stress knee stability that much. If you do want to play sports, however, it is a different story. For games like soccer, tennis, and the like, changes in direction are the norm. If your ACL is torn, the instability could lead to further knee injury.
2) Further and associated injuries with ACL tear.
Very often, the force required to cause an ACL to rupture is huge, and other knee structures get injured as well, most commonly, the meniscus. Do check out if you have associate meniscal injuries, the MRI should help. Fortunately, I did not. With increased instability, the risk of incurring a meniscal injury, even if you did not originally have one, is now quite great. This was the main reason I decided to go for a recon, because I had wished to continue with other sports. If all the exercise you did were swimming, biking and running on a flat surface, I'd say you could get away WITHOUT doing a recon, provided you had good muscles already providing ancillary stability.
3) Cause of the tear.
Fatigue Fatigue Fatigue. As you get tired, your start losing attention and your muscles are less able to cope with stress and loads. The injury occurred during a competition and I was playing my 3rd game of the morning, about 100 minutes of game time. As I leapt to evade a tackle, when I landed standing there was a loud crack and my knee gave way. Basically the hamstrings were just too tired to help take the force of the landing and the entire weight bore down on the ACL, causing the rupture. Take care of the body and don't overexercise!
4) Consequences of an ACL recon.
Not nice! You could be walking in about 3-4 days, but muscles withered away and fully took me 6 months to get the bulk up. But there would always be a deficit compared to the normal side, up to 10% less strength or more. Definitely lost explosive strength on that leg. However, got good stability and now back to racquet sports, but no serious soccer, just kick-about with kids.
I had a complete tear of my right ACL in 1999, confirmed on MRI and clinical examination. Injury incurred during a soccer game. Reconstruction done 8 months later, and during arthroscope, was confirmed that ligament was completely torn
A few points;
1) Knee stability with ACL tear.
The ACL is one of the ligaments of the knee that stabilises the joint. Specifically, it restrains the femur (thigh bone) from sliding backwards on top of the tibia (shin bone), and vice-versa. It is [u]actually POSSIBLE to continue running safely [/u]with a completely torn ACL. My ortho surgeon suggested as much, and 2 weeks after the injury, I was back to normal running >5K with little problem. The point is that if you have decent muscle strength, sub-sprint running on an even surface does not stress knee stability that much. If you do want to play sports, however, it is a different story. For games like soccer, tennis, and the like, changes in direction are the norm. If your ACL is torn, the instability could lead to further knee injury.
2) Further and associated injuries with ACL tear.
Very often, the force required to cause an ACL to rupture is huge, and other knee structures get injured as well, most commonly, the meniscus. Do check out if you have associate meniscal injuries, the MRI should help. Fortunately, I did not. With increased instability, the risk of incurring a meniscal injury, even if you did not originally have one, is now quite great. This was the main reason I decided to go for a recon, because I had wished to continue with other sports. If all the exercise you did were swimming, biking and running on a flat surface, I'd say you could get away WITHOUT doing a recon, provided you had good muscles already providing ancillary stability.
3) Cause of the tear.
Fatigue Fatigue Fatigue. As you get tired, your start losing attention and your muscles are less able to cope with stress and loads. The injury occurred during a competition and I was playing my 3rd game of the morning, about 100 minutes of game time. As I leapt to evade a tackle, when I landed standing there was a loud crack and my knee gave way. Basically the hamstrings were just too tired to help take the force of the landing and the entire weight bore down on the ACL, causing the rupture. Take care of the body and don't overexercise!
4) Consequences of an ACL recon.
Not nice! You could be walking in about 3-4 days, but muscles withered away and fully took me 6 months to get the bulk up. But there would always be a deficit compared to the normal side, up to 10% less strength or more. Definitely lost explosive strength on that leg. However, got good stability and now back to racquet sports, but no serious soccer, just kick-about with kids.
Thursday, August 9, 2007
New Route from near home to Singapore Botanical Gardens
Tried a new route this morning. Mostly pavement and cool in the morning.
Wednesday, August 8, 2007
To Run or Not to Run. The Contradiction of Cardiac Risk in Exercise
My contribution to a discussion in the SGRunners forum on the dilemma facing wannabe runners with risk factors for cardiac disease.
Given the dramatic nature of a young and apparently fit sportsperson collapsing after a race, it is understandable that the lay public may draw the wrong conclusions and become leery of exercise. Isn't exercise supposed to be good for your heart? Why are all these "fit" men running marathons and racing triathlons keeling over then? How to reconcile the apparent contradiction?
It is probably best described in the sentence below, excerpted from the article cited in the next paragraph.
"Physical exercise reduces the incidence of atherosclerotic heart disease by managing atherosclerotic risk factors such as a high heart rate and hypertension(1). Vigorous physical activity such as endurance exercise increases the risk for myocardial infarction and sudden cardiac death in patients with diagnosed and latent heart disease(2)."
Am J Cardiol. 2007 Mar 15;99(6):849-51. Epub 2007 Jan 26
Major adverse cardiac events during endurance sports. Belonje A, Nangrahary M, de Swart H, Umans V. Department of Cardiology, Medical Center Alkmaar, Alkmaar, The Netherlands.
In other words, it would appear that in the long term, exercise is a useful, and indeed, essential strategy for folk who are at risk for cardiac events to control their risk factors. A proper exercise regime has been shown to lower lipids, blood pressure, and allow the heart muscle to withstand a heart attack better. This is not to say the risk is completely eliminated. As has been amply demonstrated, extraordinarily fit folk can also be struck down. Sometimes you just can't escape genetics. It is noteworthy that the article ends with the following paragraph;
"The incidence of MACEs in well-trained marathon athletes is very low. In our series, it occurred in only 4 of 62,862 participants, and none of these participants died. All events occurred shortly after or just before the completion of the races. A rapidly available manual defibrillator is among the lifesaving medical equipment that should be on site at all major sporting events."
In the 2 references quoted above, the first describes the health benefits of long term exercise;
(1) Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease. Thompson PD. Arterioscler Thromb Vasc Biol. 2003 Aug 1;23(8):1319-21.
Exerpts describe reduced blood pressure;
"A meta-analysis of 44 randomized controlled trials including 2674 participants6 demonstrated average reductions in systolic and diastolic blood pressure of 2.6 and 1.8 mm Hg in normotensive subjects and 7.4 and 5.8 mm Hg in hypertensive subjects, respectively."
delayed/reduced onset of type2 diabetes;
"In the DPP, an average 4-kg decrease in body weight and a 593-kcal increase in weekly energy expenditure (approximately 6 miles of walking) reduced the onset of type II diabetes in individuals at high risk for this disease by 58% compared with usual care. The lifestyle intervention was also significantly more powerful than the 31% reduction in the onset of diabetes produced by metformin 850 mg taken twice daily."
amongst other benefits. If you have already had a cardiac event, exercise plays a critical role in rehab;
""Total mortality decreased 27% (P[1]0.05) with the exercise only intervention, but only 13% (P NS) with the more comprehensive rehabilitation programs suggesting that the exercise training is critically important for the beneficial effect. Cardiac mortality was reduced 31% (P[1]0.05) and 26% (P[1]0.05) for the exercise only and comprehensive programs, respectively."
So, lots of pluses. What are the downsides.
Thompson PD. The cardiovascular complications of vigorous physical activity. Arch Intern Med 1996;156:2297–2302.
"The predominant causes of exercise-related cardiovascular complications are congenital abnormalities in young subjects and atherosclerotic coronary disease in adults. The absolute incidence of exercise deaths is low. Only approximately 0.75 and 0.13 per 100,000 young male and female athletes and 6 per 100,000 middle-aged men die during exertion per year. Nevertheless, exercise does acutely and transiently increase the risk of cardiac events. CONCLUSIONS: Routine cardiovascular testing to prevent exercise events (echocardiography in the young and exercise testing in adults) has limited usefulness because of the rarity of such events, the cost of screening, and poor predictive accuracy of exercise testing for exercise events. Physicians should (1) perform routine screening and cardiac auscultation in young athletes; (2) carefully evaluate exercise-induced symptoms; and (3) ensure that adults know the symptoms of cardiac ischemia."
In a nutshell, exercise is good for you, just be careful when doing it!
Cheers.
Given the dramatic nature of a young and apparently fit sportsperson collapsing after a race, it is understandable that the lay public may draw the wrong conclusions and become leery of exercise. Isn't exercise supposed to be good for your heart? Why are all these "fit" men running marathons and racing triathlons keeling over then? How to reconcile the apparent contradiction?
It is probably best described in the sentence below, excerpted from the article cited in the next paragraph.
"Physical exercise reduces the incidence of atherosclerotic heart disease by managing atherosclerotic risk factors such as a high heart rate and hypertension(1). Vigorous physical activity such as endurance exercise increases the risk for myocardial infarction and sudden cardiac death in patients with diagnosed and latent heart disease(2)."
Am J Cardiol. 2007 Mar 15;99(6):849-51. Epub 2007 Jan 26
Major adverse cardiac events during endurance sports. Belonje A, Nangrahary M, de Swart H, Umans V. Department of Cardiology, Medical Center Alkmaar, Alkmaar, The Netherlands.
In other words, it would appear that in the long term, exercise is a useful, and indeed, essential strategy for folk who are at risk for cardiac events to control their risk factors. A proper exercise regime has been shown to lower lipids, blood pressure, and allow the heart muscle to withstand a heart attack better. This is not to say the risk is completely eliminated. As has been amply demonstrated, extraordinarily fit folk can also be struck down. Sometimes you just can't escape genetics. It is noteworthy that the article ends with the following paragraph;
"The incidence of MACEs in well-trained marathon athletes is very low. In our series, it occurred in only 4 of 62,862 participants, and none of these participants died. All events occurred shortly after or just before the completion of the races. A rapidly available manual defibrillator is among the lifesaving medical equipment that should be on site at all major sporting events."
In the 2 references quoted above, the first describes the health benefits of long term exercise;
(1) Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease. Thompson PD. Arterioscler Thromb Vasc Biol. 2003 Aug 1;23(8):1319-21.
Exerpts describe reduced blood pressure;
"A meta-analysis of 44 randomized controlled trials including 2674 participants6 demonstrated average reductions in systolic and diastolic blood pressure of 2.6 and 1.8 mm Hg in normotensive subjects and 7.4 and 5.8 mm Hg in hypertensive subjects, respectively."
delayed/reduced onset of type2 diabetes;
"In the DPP, an average 4-kg decrease in body weight and a 593-kcal increase in weekly energy expenditure (approximately 6 miles of walking) reduced the onset of type II diabetes in individuals at high risk for this disease by 58% compared with usual care. The lifestyle intervention was also significantly more powerful than the 31% reduction in the onset of diabetes produced by metformin 850 mg taken twice daily."
amongst other benefits. If you have already had a cardiac event, exercise plays a critical role in rehab;
""Total mortality decreased 27% (P[1]0.05) with the exercise only intervention, but only 13% (P NS) with the more comprehensive rehabilitation programs suggesting that the exercise training is critically important for the beneficial effect. Cardiac mortality was reduced 31% (P[1]0.05) and 26% (P[1]0.05) for the exercise only and comprehensive programs, respectively."
So, lots of pluses. What are the downsides.
Thompson PD. The cardiovascular complications of vigorous physical activity. Arch Intern Med 1996;156:2297–2302.
"The predominant causes of exercise-related cardiovascular complications are congenital abnormalities in young subjects and atherosclerotic coronary disease in adults. The absolute incidence of exercise deaths is low. Only approximately 0.75 and 0.13 per 100,000 young male and female athletes and 6 per 100,000 middle-aged men die during exertion per year. Nevertheless, exercise does acutely and transiently increase the risk of cardiac events. CONCLUSIONS: Routine cardiovascular testing to prevent exercise events (echocardiography in the young and exercise testing in adults) has limited usefulness because of the rarity of such events, the cost of screening, and poor predictive accuracy of exercise testing for exercise events. Physicians should (1) perform routine screening and cardiac auscultation in young athletes; (2) carefully evaluate exercise-induced symptoms; and (3) ensure that adults know the symptoms of cardiac ischemia."
In a nutshell, exercise is good for you, just be careful when doing it!
Cheers.
Monday, August 6, 2007
7 Reasons Why a Low Carb Diet is Wrong!
Reproduced from Sports Performance Bulletin (6 Aug 07):
Sports Performance Bulletin nutritional expert, Charles Remington, explains the health problems you may experience with a low carbohydrate diet.
Obesity is now the second leading cause of preventable deaths in America. The medical community used to see it as simply the result of poor eating habits or a lack of will power but now they are beginning to define obesity as a disease that poses a dire threat to our public health. Low carbohydrate diets have become popular as the solution in our battle to lose weight. Unfortunately the human body is equipped to use carbohydrate as its primary source of fuel.
Sadly the latest low carbohydrate fad diets are not the fuel the human body was designed to run on. Low carbohydrate diets can cause several health concerns over time. Here are my top seven.
1. Poor exercise performance and recovery
Carbohydrates are the primary fuel for your muscles and brain. Eating a low carbohydrate diet prevents proper maintenance of muscle and liver glycogen (storage form of carbohydrate and water), thus decreasing muscle performance and increasing muscle fatigue. ATP is the main source of energy for all muscle contraction.When a muscle is used, a chemical reaction breaks down ATP to produce energy. There is only enough ATP stored in the muscle for a few contractions. More ATP is needed. There are three enzyme systems that can create more ATP. The three sources of ATP for muscle contraction are carbohydrates, fatty acids and amino acid proteins. Carbohydrates metabolise efficiently and are therefore used first. If carbohydrates are not available, your muscles metabolise fatty acids and amino acids as secondary sources of ATP. These secondary sources are not efficient, which consequently cause your strength and endurance to drop drastically. It needs to be customised to your amount of muscle and exercise schedule. High-fibre, low-glycaemic (turn into blood sugar slowly) carbohydrates can provide up to 50% of your calories, which will lead to increases in strength and muscle endurance.
2. Gout
Gout is a form of arthritis that occurs when excessive uric acid levels start to crystallise in joints, leading to pain and inflammation. Uric acid is a waste product in the liver's metabolism of protein. Excessive amounts of protein may lead to an inability to eliminate uric acid. I would recommend you should not exceed 1 to 1.25 grams of protein per lean pound of body weight.
3. Kidney stones
Kidney stones are hard masses that form in the kidneys when uric acid or calcium oxalate crystallise and over time form stones. Insoluble fibre found only in carbohydrates reduces the absorption of calcium, which cause urinary calcium levels to drop thereby preventing the formation of kidney stone. I would recommend the consumption of 30 or more grams of fibre daily. This is not attainable on low carbohydrate diets.
4. Constipation and poor intestinal health
To maintain good intestinal health our bodies require 30 or more grams of fibre daily. Fibre is divided into two types, soluble and insoluble. Insoluble fibre is vital in formation of stools and decreases the time process of waste elimination. Low carbohydrate diets are too low in insoluble fibre and increase risk of constipation. Poor transit time of waste material increases risk of certain colon cancers. Insoluble fibres prevent the build-up of mucus on intestinal walls which lead to poorabsorption of nutrients into the body. Low carbohydrate diets are inadequate to maintain good intestinal wall health. I would recommend you use whole grains, oats, beans, fruits and vegetable which are rich in soluble and insoluble fibre. This lowers the risk for constipation, haemorrhoids, irritable bowel, diverticulitis, Crohn's disease, and colon cancers.
5. Rise in cholesterol levels and an increased risk of heart disease
The risk of heart disease increases on low carbohydrate, low fibre diets. These diets promote excessive amounts of animal protein, cholesterol and saturated fat. Exuberant amounts of protein increase homocysteine, which is a by-product of the amino acid methionine. Many experts believe that high homocysteine levels have many toxic effects which lead to increase risk of heart disease and hardening of arteries. Low carbohydrate, low fibre diets reduce the absorption and eliminationof digestive bile in the intestines. Digestive bile is produced in the liver from cholesterol. A decrease in digestive bile production raises blood serum cholesterol levels which increases the risk of heart disease. Unlike low carbohydrate diets I would promote a nutritional balance providing 30% protein, 50% high fibre carbohydrates and 20% fat.
6. Osteoporosis
Osteoporosis is the reduction of bone density, due to the loss of calcium over long periods of time. Several dietary factors increase the risk of osteoporosis. When dietary protein reaches excessive levels, so does the loss of calcium in the urine. Most studies show that a life-long high protein diet results in an increase of obsteoporosis. Poor intestinal health due to low fibre diets cause inadequate absorption of calcium in intestines contributing to poor bone formation. This would suggest that no low carbohydrate diets can become a life long lifestyle of eating. This is only one of many reasons why low carbohydrate diets provide poor long term weight control. Interestingly, a diet too low in protein can also increase risk of osteoporosis. There is no one size fits all when managing our weight so it has to be customised to the individual, providing the right balance of protein, carbohydrate and fat.
7. Loss of muscle and reduction of metabolism
Any diet that applies the restriction of calories less than the body's daily requirements over long periods of time will result in the loss of lean muscle tissue and a decrease in the metabolism. All low carbohydrate diets are focused solely on weight loss. The loss of fat comes at a high cost, which is the loss of lean muscle. The loss of muscle reduces the resting metabolic rate, which is the major cause for rebound weight gain. Research shows 95% of all dieters will regain that weight . We do not fail at diets - diets fail us! The secret is not to try to lose fat every day as this will result in losing muscle and reducing metabolism.
Final thoughtsLong-term success in managing weight starts with the right approach. If you are overweight, the real problem is that you have too much body fat for how much muscle you possess. A body composition solution is needed, not just a weight loss diet. Your goal should be to lose fat without losing muscle or sacrificing your health in the process. To maintain your results your eating habits must develop life-long character. Low carbohydrate diets provide initial weight loss, but at the high cost of losing muscle and reducing metabolism. They are inadequate sources of fuel to support exercise activity, which is vital in maintaining good health. The risks to your health long term make low carbohydrate diets poor solutions for life-long weight management.
Sports Performance Bulletin nutritional expert, Charles Remington, explains the health problems you may experience with a low carbohydrate diet.
Obesity is now the second leading cause of preventable deaths in America. The medical community used to see it as simply the result of poor eating habits or a lack of will power but now they are beginning to define obesity as a disease that poses a dire threat to our public health. Low carbohydrate diets have become popular as the solution in our battle to lose weight. Unfortunately the human body is equipped to use carbohydrate as its primary source of fuel.
Sadly the latest low carbohydrate fad diets are not the fuel the human body was designed to run on. Low carbohydrate diets can cause several health concerns over time. Here are my top seven.
1. Poor exercise performance and recovery
Carbohydrates are the primary fuel for your muscles and brain. Eating a low carbohydrate diet prevents proper maintenance of muscle and liver glycogen (storage form of carbohydrate and water), thus decreasing muscle performance and increasing muscle fatigue. ATP is the main source of energy for all muscle contraction.When a muscle is used, a chemical reaction breaks down ATP to produce energy. There is only enough ATP stored in the muscle for a few contractions. More ATP is needed. There are three enzyme systems that can create more ATP. The three sources of ATP for muscle contraction are carbohydrates, fatty acids and amino acid proteins. Carbohydrates metabolise efficiently and are therefore used first. If carbohydrates are not available, your muscles metabolise fatty acids and amino acids as secondary sources of ATP. These secondary sources are not efficient, which consequently cause your strength and endurance to drop drastically. It needs to be customised to your amount of muscle and exercise schedule. High-fibre, low-glycaemic (turn into blood sugar slowly) carbohydrates can provide up to 50% of your calories, which will lead to increases in strength and muscle endurance.
2. Gout
Gout is a form of arthritis that occurs when excessive uric acid levels start to crystallise in joints, leading to pain and inflammation. Uric acid is a waste product in the liver's metabolism of protein. Excessive amounts of protein may lead to an inability to eliminate uric acid. I would recommend you should not exceed 1 to 1.25 grams of protein per lean pound of body weight.
3. Kidney stones
Kidney stones are hard masses that form in the kidneys when uric acid or calcium oxalate crystallise and over time form stones. Insoluble fibre found only in carbohydrates reduces the absorption of calcium, which cause urinary calcium levels to drop thereby preventing the formation of kidney stone. I would recommend the consumption of 30 or more grams of fibre daily. This is not attainable on low carbohydrate diets.
4. Constipation and poor intestinal health
To maintain good intestinal health our bodies require 30 or more grams of fibre daily. Fibre is divided into two types, soluble and insoluble. Insoluble fibre is vital in formation of stools and decreases the time process of waste elimination. Low carbohydrate diets are too low in insoluble fibre and increase risk of constipation. Poor transit time of waste material increases risk of certain colon cancers. Insoluble fibres prevent the build-up of mucus on intestinal walls which lead to poorabsorption of nutrients into the body. Low carbohydrate diets are inadequate to maintain good intestinal wall health. I would recommend you use whole grains, oats, beans, fruits and vegetable which are rich in soluble and insoluble fibre. This lowers the risk for constipation, haemorrhoids, irritable bowel, diverticulitis, Crohn's disease, and colon cancers.
5. Rise in cholesterol levels and an increased risk of heart disease
The risk of heart disease increases on low carbohydrate, low fibre diets. These diets promote excessive amounts of animal protein, cholesterol and saturated fat. Exuberant amounts of protein increase homocysteine, which is a by-product of the amino acid methionine. Many experts believe that high homocysteine levels have many toxic effects which lead to increase risk of heart disease and hardening of arteries. Low carbohydrate, low fibre diets reduce the absorption and eliminationof digestive bile in the intestines. Digestive bile is produced in the liver from cholesterol. A decrease in digestive bile production raises blood serum cholesterol levels which increases the risk of heart disease. Unlike low carbohydrate diets I would promote a nutritional balance providing 30% protein, 50% high fibre carbohydrates and 20% fat.
6. Osteoporosis
Osteoporosis is the reduction of bone density, due to the loss of calcium over long periods of time. Several dietary factors increase the risk of osteoporosis. When dietary protein reaches excessive levels, so does the loss of calcium in the urine. Most studies show that a life-long high protein diet results in an increase of obsteoporosis. Poor intestinal health due to low fibre diets cause inadequate absorption of calcium in intestines contributing to poor bone formation. This would suggest that no low carbohydrate diets can become a life long lifestyle of eating. This is only one of many reasons why low carbohydrate diets provide poor long term weight control. Interestingly, a diet too low in protein can also increase risk of osteoporosis. There is no one size fits all when managing our weight so it has to be customised to the individual, providing the right balance of protein, carbohydrate and fat.
7. Loss of muscle and reduction of metabolism
Any diet that applies the restriction of calories less than the body's daily requirements over long periods of time will result in the loss of lean muscle tissue and a decrease in the metabolism. All low carbohydrate diets are focused solely on weight loss. The loss of fat comes at a high cost, which is the loss of lean muscle. The loss of muscle reduces the resting metabolic rate, which is the major cause for rebound weight gain. Research shows 95% of all dieters will regain that weight . We do not fail at diets - diets fail us! The secret is not to try to lose fat every day as this will result in losing muscle and reducing metabolism.
Final thoughtsLong-term success in managing weight starts with the right approach. If you are overweight, the real problem is that you have too much body fat for how much muscle you possess. A body composition solution is needed, not just a weight loss diet. Your goal should be to lose fat without losing muscle or sacrificing your health in the process. To maintain your results your eating habits must develop life-long character. Low carbohydrate diets provide initial weight loss, but at the high cost of losing muscle and reducing metabolism. They are inadequate sources of fuel to support exercise activity, which is vital in maintaining good health. The risks to your health long term make low carbohydrate diets poor solutions for life-long weight management.
Running for My Life
Greetings,
its been an amazing 2 years for me as of today (Aug 6th 2007). Got kickstarted on running again, got my Polar HRM, and actually hit the road with some seriousness. On National Day 2005, actually got up in the morning, something I had not done since NS, and did 6 km, the longest distance I have run in years and years.
Over the ensuing months, lost 12 kg, completed my first 10km (SCSM 2005), and signed up for the 2006 Virginia Beach Marathon. To my knowledge, I was the only Singaporean at the race, which I completed in 4:32. Next stop, Chicago, done and dusted at 4:28. My wife had her own marathon up and down the Magnificent Mile.
Running has been an incredible change agent for me. If you are a doubter and reading this for the first time, don't wait anymore. Buy a pair of shoes and JUST DO IT!
its been an amazing 2 years for me as of today (Aug 6th 2007). Got kickstarted on running again, got my Polar HRM, and actually hit the road with some seriousness. On National Day 2005, actually got up in the morning, something I had not done since NS, and did 6 km, the longest distance I have run in years and years.
Over the ensuing months, lost 12 kg, completed my first 10km (SCSM 2005), and signed up for the 2006 Virginia Beach Marathon. To my knowledge, I was the only Singaporean at the race, which I completed in 4:32. Next stop, Chicago, done and dusted at 4:28. My wife had her own marathon up and down the Magnificent Mile.
Running has been an incredible change agent for me. If you are a doubter and reading this for the first time, don't wait anymore. Buy a pair of shoes and JUST DO IT!
Bruce! Bruce! Thy protocol does hurt!
With all the publicity around young fit guys keeling over, I really thought it would be a good idea to get myself checked out as I ramped up my mileage. The ECG stress test was an optional part to my biennial company health screen anyhow, which was due.
On the day, had checked in at the medical centre, had blood drawn, then waited at the cardiology centre. Shortly after, into the test room. There was a basic looking treadmill in a corner, hooked up to a computer, and an ECG machine with attendant wires. Shirt off, shoes on, wires stuck on, and off we went.......
.....and I thought I was in pretty good shape, Good Grief! Let me warn you, if you ain't trained in running, this is NOT an easy test.
Started off easy enough, but once I got to stage 3, I knew I was in trouble. By stage 4, I could barely keep on the treadmill. Don't let the slow speed fool ya, the 16% gradient by that stage is a killer. I stopped after a minute and a half at stage 4. I was near maximum predicted HR, sweating like a pig, and glutes and calves burning. Anyhow, as far as I could make out, seemed not to have any significant findings on the ECG tracing, and no symptoms to boot.
So all set! AHM in a 3 weeks and SCSM on the horizon. God keep me safe in my training.
For those interested in what the Bruce Protocol Stress Test is, here is one link -->
http://www.topendsports.com/testing/tests/bruce.htm
On the day, had checked in at the medical centre, had blood drawn, then waited at the cardiology centre. Shortly after, into the test room. There was a basic looking treadmill in a corner, hooked up to a computer, and an ECG machine with attendant wires. Shirt off, shoes on, wires stuck on, and off we went.......
.....and I thought I was in pretty good shape, Good Grief! Let me warn you, if you ain't trained in running, this is NOT an easy test.
Started off easy enough, but once I got to stage 3, I knew I was in trouble. By stage 4, I could barely keep on the treadmill. Don't let the slow speed fool ya, the 16% gradient by that stage is a killer. I stopped after a minute and a half at stage 4. I was near maximum predicted HR, sweating like a pig, and glutes and calves burning. Anyhow, as far as I could make out, seemed not to have any significant findings on the ECG tracing, and no symptoms to boot.
So all set! AHM in a 3 weeks and SCSM on the horizon. God keep me safe in my training.
For those interested in what the Bruce Protocol Stress Test is, here is one link -->
http://www.topendsports.com/testing/tests/bruce.htm
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