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)
Friday, November 9, 2007
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
Subscribe to:
Posts (Atom)