Anyone have a learned opinion on what 1-2 months of 1800-2400 mg/day of ibuprofen may do to one's CAT3 cycling performance?
Speed
Endurance
Power
(I have been on this dosage and I feel my cycling performace has changed - cause, coincidence, or correlation?)
Health Nutrition and Supplements · Public discussion
ibuprofen & performance
This thread is locked and is currently read-only.
Thread navigation
Jump through the discussion
Go to the original post, the replies on this page, or the latest preserved contribution.
Thread details
What we know about this thread
- Original section
- Health Nutrition and Supplements
- Published
- 19 May 2006
- Last activity
- 27 May 2006
- Original author
- 9606
- Posts
- 14
- Discussion status
- Public discussion
- Total views
- 3,531
- Views / 30 days
- 0
The navigation and discussion metadata provide context. Posts remain in their original chronological order.
-
-
I have spent a significant amount of the past 10 or so years being fed Motrin, as a member of the USAF - it's a favorite cure all. I think the biggest concern should be your stomach lining. Ensure you have something in the tank when you are mucking those things, I haven't had any problems, but I know of several folks that their stomach had difficulty handling 2400mg per day.
Otherwise when I plan a long ride 4 hours+ I take a 200 prior to starting, and another when I get back.
HR
-
9606 said:
Anyone have a learned opinion on what 1-2 months of 1800-2400 mg/day of ibuprofen may do to one's CAT3 cycling performance?
Speed
Endurance
Power
(I have been on this dosage and I feel my cycling performace has changed - cause, coincidence, or correlation?)
Be careful! Besides your stomach, you run the risk of glomerulosclerosis, i.e. renal damage with constant use. Highly unrecommended. There have been a number of professional athletes in the U.S. who have had problems due to chronic NSAID use. -
9606 said:
Anyone have a learned opinion on what 1-2 months of 1800-2400 mg/day of ibuprofen may do to one's CAT3 cycling performance?
Speed
Endurance
Power
(I have been on this dosage and I feel my cycling performace has changed - cause, coincidence, or correlation?)I strongly agree with sportdoc.
NSAIDS interfere with prostaglandin synthesis; one of the prostaglandins-prostacyclin is thought to be responsible for maintaining the patency of certain types of blood vessels, such as those supplying blood to the glomerulus in the kidney or coronary arteries in the heart. Additional research is demonstrating that perhaps those patients who suffer from essential hypertension actually have a variety of prostaglandin deficiency. In other words, blood vessels probably shrink in diameter with NSAIDS "on board." This shrinkage can be made even worse by hypovolemia-dehydration. Of course dehydration NEVER occurs during a ride, right??
Take NSAIDS only when you need them; chronic exposure may be very bad.
-
What about the low-dosage aspirin regimin which is popular these days??
-
so that withered lump that feel into my sock the other day is my kidney?
HR
-
While I have no learned opinion on the subject, I do have another question. Namely, isn't it possible that riding while on pain-killers could have more detrimental effects to your body? That is, there is an old saw that when your body hurts it's for a reason. Thus, artificially blocking your body's pain signals and riding anyway is pretty much ignoring your body's signals to stop or pause the stresses your are placing on it. Now, I realize that endurance athletes are often gluttons for punishment who may view riding through pain/injury (w/ or w/o analgesics) as simply another achievment. However, from a different perspective, which sees training as a means to improve the health/efficiency of the body, I wonder if training with pain killers makes much sense. All that being said, I am a former (following surgery) sufferer of chronic pain (migraines) and have the deepest measure of sympathy for all those who find themselves in that situation. Furthermore, while I may question the benefits, I do have an enourmous amount of respect for people who are willing to endure that extra level of pain due to an injury/chronic pain source. At any rate, I'm mostly curious as to other's opinions on the subject.
-
In addition to the possiblity of ulcers and kidney damage that was already mentioned, I just read a study describing how Ibuprofen inhibited skeletal muscle hypertrophy in rats. It is rats, but still interesting.
-
I was taking the dosage for a situation unrelated to cycling.
While on the dosage my cycling performance seemed to degrade.
I am wondering if it is just a coincidence, or if there is a physiological cause? -
flapsupcleanup said:
What about the low-dosage aspirin regimin which is popular these days??
Low dose aspirin inhibits glycoprotein IIb/IIIa, which is what causes platelets to stick together. By preventing platelet adhesion, low dose aspirin reduces the risk of heart atack. According to Sir John Vane, the Nobel Lauriate who first described aspirin's effect on prostaglandins, the ideal dose of aspirin would be 62.5 mg every third day. That would be enough to block GP IIb/IIIa without blocking prostacyclin; however, no one would remember to take something once every third day.
While it is true that prostacyclin (PGI2) prevent platlets from aggregating, most prostaglandins cause platlets to aggregate. The COX2 specific antagonists and most NSAIDs reduce PGI2 to a greater extent than they reduce the agents that cause platelet aggregation; thus shifting the balance towards platelet aggregation. This increases the risk of heart attack and stroke.
Since the effect of aspirin is nonselective, the balance is shifted towards less platelet aggregation, and therefore reduces the risk of stroke and heart attack.
-
9606 said:
I was taking the dosage for a situation unrelated to cycling.
While on the dosage my cycling performance seemed to degrade.
I am wondering if it is just a coincidence, or if there is a physiological cause?Perhaps it was the condition for which you were taking ibuprofen, and not the ibuprofen, that reduced your performance ability. Phenylbutazone, one of the original NSAIDs, is often given to thoroughbred horses to improve their racing performance. Whether this practice is legal or not varies from state to state. In 1968, it was illegal in Kentucky, and Dancer's Image, who crossed the finish line first, was disqualified from the Kentucky Derby because phenylbutazone was found in his post-race urine sample. Since that time, the use of phenylbutazone has been legalized in Kentucky and in most other states. It is widely accepted, though, that NSAIDs do improve performance.
-
RickF said:
It is widely accepted, though, that NSAIDs do improve performance.
Interesting. Unless you are referring to the inhibition of endoperoxides and prostacyclin synthesis which would decrease the tissue response to bradykinins resulting in decreased pain and edema, then I can conceive no way that NSAIDs can improve performance.Additionally, a quick medline (admittedly not the best database for such searches) search has revealed absolutely no literature regarding performance enhancement and NSAIDs.
Furthermore, I can think of no physiological/pharmacological mechanism that NSAIDs could confer to enhance performance. Rather, NSAIDs should: 1.) increase SVR. 2.) increase PVR, which 3.) increases myocardial O2 consumption, which should result in 4.) decreased SvO2, which should result in 5.) decreased peripheral O2 delivery resulting in 6.) performance decrements.
Just my thoughts.
-
RickF said:
Low dose aspirin inhibits glycoprotein IIb/IIIa.
Is there some new literature?Everything that I have been taught or read suggests glycoprotein IIb/IIIa elaboration has nothing to do with COX1 or 2 inhibition. Classically, these are two completely unrelated pathways. As such, special IIb/IIIa inhibitors have been developed to bridge the platelet aggregation gaps that ASA does not fill and have subsequently been given to patients peri-ACS.
Again, just my thoughts.
-
SoDakker said:
Again, just my thoughts.
I believe you are spot on. GP IIb/IIIa inhibitors are a completely different class of drug. As mentioned ASA is a COX-1/2 inhibitor. It's effects are due to swinging the balance of Thromboxane and Prostacyclin more towards Prostacyclin (vasodilation and decreased platelet adhesion). I also don't feel there is support for NSAIDS providing performance enhancement. I had previously posted a new study showing how NSAIDS inhibited skeletal muscle hypertrophy in rats.
Active in the last 60 minutes
Active in this thread
0 users · 0 guests ·0 bots ·0 total
No signed-in users are active right now.
No known search crawlers active right now.