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
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.
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