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What is the best anti-inflammatory?

heavydutyhit

New member
I am working on getting my right shoulder joint back to normal. It has been fatiguing early during some of my lifts and aching a bit. I saw a doc and he said to take ibuprofen 3 times daily for two weeks to see if it helped with the inflammation before going any further. I also threw in a decent amount of glucosamine, chondroitin, msm, and fish oil in addition to the ibuprofen. I ice it about twice a day and warm it up a bit with a heating pad prior to going to the gym. So far the progress is great. However I have read that somehow ibuprofen can hamper muscle growth by interfering with protein synthesis.
I am posting to get some feed back on A: your opinions of my "rehab" routine. B: any opinions/personal experience with the ibuprofen, muscle growth theory. And B: I want to get some alternative anti-inflammatory choices from you guys from personal experience, or from things you have read. Thanks in advance to those who offer assistance with this matter.
 
For those interested I thought I would post a study on this matter. For the full study, here is the link.

http://ajpendo.physiology.org/cgi/content/full/282/3/E551


Given the mechanisms of action and the widespread use of ibuprofen and acetaminophen, we believed it was necessary to better understand the potential metabolic implications of consuming these over-the-counter drugs after eccentric resistance exercise. The primary findings of this study were that ibuprofen blunted the protein synthesis response that is normally seen after the type of exercise used in this study; surprisingly, acetaminophen also had a similar effect on protein metabolism.

From our data, it appears that the mechanism of blunting protein metabolism in skeletal muscle by cyclooxygenase inhibition outlined by Rodemann and Goldberg (30) nearly 20 yr ago in rats may also be intact in humans. These authors showed an inhibition of protein synthesis in isolated rat skeletal muscle with three different cyclooxygenase inhibitors (aspirin, indomethacin, and meclofenamate). In the current study, we hypothesized that ibuprofen would also block cyclooxygenase and have a similar effect on muscle protein metabolism. However, it is difficult to determine how the amount of inhibitors (drugs) used in the previous studies that showed this effect in isolated muscles (24, 25, 30, 34) compare with the levels in human muscle after consumption of maximal over-the-counter doses of ibuprofen. Nonetheless, from our data, it is clear that the 1.2 g/day maximal over-the-counter dose of ibuprofen is potent enough to blunt the protein synthesis response to resistance exercise.

What is less clear is why acetaminophen also inhibited the increase in FSR after the resistance exercise bout. The most logical hypothesis is that acetaminophen also inhibits cyclooxygenase in skeletal muscle; however, to our knowledge, no other studies have examined the influence of acetaminophen on skeletal muscle metabolism. In addition, all of the previous data and the resultant nonperipheral effect of acetaminophen hypothesis are derived from studies of the central nervous system and other nonskeletal muscle organ studies (8, 11, 15, 32, 36).

The small sample size of the FSR values for the ACET group may appear to limit the interpretation of the findings. However, in an attempt to determine an underlying mechanism for the drug-induced blunting of the postexercise increase in FSR, we measured prostaglandin (PG)F2alpha in the same muscle samples analyzed for the measurement of FSR taken during the pre- and postexercise infusions (33). PGF2alpha is a product of the cyclooxygenase enzyme and has been shown to stimulate skeletal muscle protein synthesis (24, 30). Similar to the FSR results, PGF2alpha after exercise was significantly increased (77%) in the PLA group, whereas it was unchanged in the ACET and IBU groups (33). Thus it appears that both ACET and IBU attenuate the postresistance exercise increase in FSR by blocking the production of PGF2alpha via the cyclooxygenase enzyme. These results, coupled with the fact that the PGF2alpha measurements were completed on all eight subjects from each group, suggest that the effect of ACET on postexercise FSR is valid.

The implications of our data are important for those individuals that chronically consume either ibuprofen or acetaminophen during a period in which muscle hypertrophy is expected (i.e., resistance training). Although we did not measure the long-term effects of consumption of either of these drugs on muscle hypertrophy during resistance training, we speculate that the continued attenuation of the normal increase in protein synthesis after each resistance training bout would result in a blunting of the hypertrophic response. Our speculation assumes that the muscle protein breakdown response coincides with the protein synthesis response. This assumption seems appropriate, since the resting and postresistance exercise skeletal muscle FSR and fractional breakdown rate have been shown to be significantly correlated (26), suggesting that these two processes are linked.

Our resting (preexercise) protein synthesis (FSR) results are comparable to previous studies of young to middle-aged men in the postabsorptive state that have examined mixed muscle protein from the vastus lateralis (7, 29). The increase in FSR of the PLA group in the current study (76%) also compares favorably with previous studies when training status, dietary state, muscle studied, and the amount of exercise are considered (12, 26, 39).

In this study, we used the Ra of phenylalanine as a measure of whole body protein breakdown. Our data suggest, as others have found (26), that whole body protein breakdown is unchanged 24 h after resistance exercise. Our data also suggest that neither ibuprofen nor acetaminophen had any influence on protein breakdown at the whole body level. To this end, Gann et al. (16) have shown that chronic consumption of the NSAID indomethacin does not affect whole body protein synthesis or nitrogen retention in elderly subjects. This finding is consistent with the fact that the action of the drugs in the current study appears to be at the level of the skeletal muscle, and muscle protein metabolism constitutes only about one-third of whole body protein metabolism (21).

The exercise bout resulted in large increases in serum CK activity and ratings of perceived muscle soreness, which have been shown in previous studies (3, 13). The lack of effect of either drug on CK response to this type of exercise has also been reported (3, 9, 18), although higher prophylactic doses of ibuprofen (5 days before; 2.4 mg/day) have been shown to reduce circulating CK compared with placebo after eccentric muscular activity (28). The lack of effect of similar over-the-counter analgesic drugs on ratings of perceived muscle soreness has also been shown previously (3, 4, 9). However, Hasson et al. (18) reported that prophylactic and therapeutic doses of ibuprofen similar to those used in the current study do reduce levels of perceived muscle soreness 24 or 48 h after exercise with the use of a protocol that was less intense than the one used in the present study. It may appear somewhat surprising that neither of these drugs provided any level of analgesia compared with placebo, given the aforementioned study and the proven pain-reducing benefits of acetaminophen and ibuprofen for individuals with arthritis, headaches, and other symptoms (10, 11). However, the level of pain, soreness, and edema was high enough to severely inhibit the gait of the subjects in our study during the days after the exercise bout. It is quite possible that the level of soreness and pain was too severe for the dose of these drugs to be effective. It is also possible that the scale used for the measurement of perceived soreness among the groups was not able to discern small differences in soreness that were physiologically relevant.

We included only males in our study population, and it is unclear whether these same responses would hold in a similar group of females. However, there are no data to suggest that the metabolism of ibuprofen or acetaminophen or the mechanism of action of these two drugs is different between men and women. Furthermore, several studies of muscle protein metabolism at rest and after resistance exercise have not shown a difference between women and men (26, 27, 31, 38).

In conclusion, the increased rate of muscle protein synthesis normally seen 24 h after high-intensity eccentric resistance exercise was attenuated by consumption of ibuprofen and acetaminophen at over-the-counter levels. The long-term influence of this acute response after resistance exercise for individuals who chronically consume these (or similar) drugs cannot be determined from this study. However, long-term use of these drugs may inhibit the normal hypertrophic response to resistance training. Future studies on the impact of chronic consumption of over-the-counter doses of these drugs on skeletal muscle are warranted.
 
heavydutyhit said:
For those interested I thought I would post a study on this matter. For the full study, here is the link.

http://ajpendo.physiology.org/cgi/content/full/282/3/E551


Given the mechanisms of action and the widespread use of ibuprofen and acetaminophen, we believed it was necessary to better understand the potential metabolic implications of consuming these over-the-counter drugs after eccentric resistance exercise. The primary findings of this study were that ibuprofen blunted the protein synthesis response that is normally seen after the type of exercise used in this study; surprisingly, acetaminophen also had a similar effect on protein metabolism.

From our data, it appears that the mechanism of blunting protein metabolism in skeletal muscle by cyclooxygenase inhibition outlined by Rodemann and Goldberg (30) nearly 20 yr ago in rats may also be intact in humans. These authors showed an inhibition of protein synthesis in isolated rat skeletal muscle with three different cyclooxygenase inhibitors (aspirin, indomethacin, and meclofenamate). In the current study, we hypothesized that ibuprofen would also block cyclooxygenase and have a similar effect on muscle protein metabolism. However, it is difficult to determine how the amount of inhibitors (drugs) used in the previous studies that showed this effect in isolated muscles (24, 25, 30, 34) compare with the levels in human muscle after consumption of maximal over-the-counter doses of ibuprofen. Nonetheless, from our data, it is clear that the 1.2 g/day maximal over-the-counter dose of ibuprofen is potent enough to blunt the protein synthesis response to resistance exercise.

What is less clear is why acetaminophen also inhibited the increase in FSR after the resistance exercise bout. The most logical hypothesis is that acetaminophen also inhibits cyclooxygenase in skeletal muscle; however, to our knowledge, no other studies have examined the influence of acetaminophen on skeletal muscle metabolism. In addition, all of the previous data and the resultant nonperipheral effect of acetaminophen hypothesis are derived from studies of the central nervous system and other nonskeletal muscle organ studies (8, 11, 15, 32, 36).

The small sample size of the FSR values for the ACET group may appear to limit the interpretation of the findings. However, in an attempt to determine an underlying mechanism for the drug-induced blunting of the postexercise increase in FSR, we measured prostaglandin (PG)F2alpha in the same muscle samples analyzed for the measurement of FSR taken during the pre- and postexercise infusions (33). PGF2alpha is a product of the cyclooxygenase enzyme and has been shown to stimulate skeletal muscle protein synthesis (24, 30). Similar to the FSR results, PGF2alpha after exercise was significantly increased (77%) in the PLA group, whereas it was unchanged in the ACET and IBU groups (33). Thus it appears that both ACET and IBU attenuate the postresistance exercise increase in FSR by blocking the production of PGF2alpha via the cyclooxygenase enzyme. These results, coupled with the fact that the PGF2alpha measurements were completed on all eight subjects from each group, suggest that the effect of ACET on postexercise FSR is valid.

The implications of our data are important for those individuals that chronically consume either ibuprofen or acetaminophen during a period in which muscle hypertrophy is expected (i.e., resistance training). Although we did not measure the long-term effects of consumption of either of these drugs on muscle hypertrophy during resistance training, we speculate that the continued attenuation of the normal increase in protein synthesis after each resistance training bout would result in a blunting of the hypertrophic response. Our speculation assumes that the muscle protein breakdown response coincides with the protein synthesis response. This assumption seems appropriate, since the resting and postresistance exercise skeletal muscle FSR and fractional breakdown rate have been shown to be significantly correlated (26), suggesting that these two processes are linked.

Our resting (preexercise) protein synthesis (FSR) results are comparable to previous studies of young to middle-aged men in the postabsorptive state that have examined mixed muscle protein from the vastus lateralis (7, 29). The increase in FSR of the PLA group in the current study (76%) also compares favorably with previous studies when training status, dietary state, muscle studied, and the amount of exercise are considered (12, 26, 39).

In this study, we used the Ra of phenylalanine as a measure of whole body protein breakdown. Our data suggest, as others have found (26), that whole body protein breakdown is unchanged 24 h after resistance exercise. Our data also suggest that neither ibuprofen nor acetaminophen had any influence on protein breakdown at the whole body level. To this end, Gann et al. (16) have shown that chronic consumption of the NSAID indomethacin does not affect whole body protein synthesis or nitrogen retention in elderly subjects. This finding is consistent with the fact that the action of the drugs in the current study appears to be at the level of the skeletal muscle, and muscle protein metabolism constitutes only about one-third of whole body protein metabolism (21).

The exercise bout resulted in large increases in serum CK activity and ratings of perceived muscle soreness, which have been shown in previous studies (3, 13). The lack of effect of either drug on CK response to this type of exercise has also been reported (3, 9, 18), although higher prophylactic doses of ibuprofen (5 days before; 2.4 mg/day) have been shown to reduce circulating CK compared with placebo after eccentric muscular activity (28). The lack of effect of similar over-the-counter analgesic drugs on ratings of perceived muscle soreness has also been shown previously (3, 4, 9). However, Hasson et al. (18) reported that prophylactic and therapeutic doses of ibuprofen similar to those used in the current study do reduce levels of perceived muscle soreness 24 or 48 h after exercise with the use of a protocol that was less intense than the one used in the present study. It may appear somewhat surprising that neither of these drugs provided any level of analgesia compared with placebo, given the aforementioned study and the proven pain-reducing benefits of acetaminophen and ibuprofen for individuals with arthritis, headaches, and other symptoms (10, 11). However, the level of pain, soreness, and edema was high enough to severely inhibit the gait of the subjects in our study during the days after the exercise bout. It is quite possible that the level of soreness and pain was too severe for the dose of these drugs to be effective. It is also possible that the scale used for the measurement of perceived soreness among the groups was not able to discern small differences in soreness that were physiologically relevant.

We included only males in our study population, and it is unclear whether these same responses would hold in a similar group of females. However, there are no data to suggest that the metabolism of ibuprofen or acetaminophen or the mechanism of action of these two drugs is different between men and women. Furthermore, several studies of muscle protein metabolism at rest and after resistance exercise have not shown a difference between women and men (26, 27, 31, 38).

In conclusion, the increased rate of muscle protein synthesis normally seen 24 h after high-intensity eccentric resistance exercise was attenuated by consumption of ibuprofen and acetaminophen at over-the-counter levels. The long-term influence of this acute response after resistance exercise for individuals who chronically consume these (or similar) drugs cannot be determined from this study. However, long-term use of these drugs may inhibit the normal hypertrophic response to resistance training. Future studies on the impact of chronic consumption of over-the-counter doses of these drugs on skeletal muscle are warranted.
I have a chronic injury in my shoulder too, I stop training made some physical therapy and got better but not 100% , I use animal flex and cissus but do not expect miracles...
 
heavydutyhit said:
For those interested I thought I would post a study on this matter. For the full study, here is the link.

http://ajpendo.physiology.org/cgi/content/full/282/3/E551


Given the mechanisms of action and the widespread use of ibuprofen and acetaminophen, we believed it was necessary to better understand the potential metabolic implications of consuming these over-the-counter drugs after eccentric resistance exercise. The primary findings of this study were that ibuprofen blunted the protein synthesis response that is normally seen after the type of exercise used in this study; surprisingly, acetaminophen also had a similar effect on protein metabolism.

From our data, it appears that the mechanism of blunting protein metabolism in skeletal muscle by cyclooxygenase inhibition outlined by Rodemann and Goldberg (30) nearly 20 yr ago in rats may also be intact in humans. These authors showed an inhibition of protein synthesis in isolated rat skeletal muscle with three different cyclooxygenase inhibitors (aspirin, indomethacin, and meclofenamate). In the current study, we hypothesized that ibuprofen would also block cyclooxygenase and have a similar effect on muscle protein metabolism. However, it is difficult to determine how the amount of inhibitors (drugs) used in the previous studies that showed this effect in isolated muscles (24, 25, 30, 34) compare with the levels in human muscle after consumption of maximal over-the-counter doses of ibuprofen. Nonetheless, from our data, it is clear that the 1.2 g/day maximal over-the-counter dose of ibuprofen is potent enough to blunt the protein synthesis response to resistance exercise.

What is less clear is why acetaminophen also inhibited the increase in FSR after the resistance exercise bout. The most logical hypothesis is that acetaminophen also inhibits cyclooxygenase in skeletal muscle; however, to our knowledge, no other studies have examined the influence of acetaminophen on skeletal muscle metabolism. In addition, all of the previous data and the resultant nonperipheral effect of acetaminophen hypothesis are derived from studies of the central nervous system and other nonskeletal muscle organ studies (8, 11, 15, 32, 36).

The small sample size of the FSR values for the ACET group may appear to limit the interpretation of the findings. However, in an attempt to determine an underlying mechanism for the drug-induced blunting of the postexercise increase in FSR, we measured prostaglandin (PG)F2alpha in the same muscle samples analyzed for the measurement of FSR taken during the pre- and postexercise infusions (33). PGF2alpha is a product of the cyclooxygenase enzyme and has been shown to stimulate skeletal muscle protein synthesis (24, 30). Similar to the FSR results, PGF2alpha after exercise was significantly increased (77%) in the PLA group, whereas it was unchanged in the ACET and IBU groups (33). Thus it appears that both ACET and IBU attenuate the postresistance exercise increase in FSR by blocking the production of PGF2alpha via the cyclooxygenase enzyme. These results, coupled with the fact that the PGF2alpha measurements were completed on all eight subjects from each group, suggest that the effect of ACET on postexercise FSR is valid.

The implications of our data are important for those individuals that chronically consume either ibuprofen or acetaminophen during a period in which muscle hypertrophy is expected (i.e., resistance training). Although we did not measure the long-term effects of consumption of either of these drugs on muscle hypertrophy during resistance training, we speculate that the continued attenuation of the normal increase in protein synthesis after each resistance training bout would result in a blunting of the hypertrophic response. Our speculation assumes that the muscle protein breakdown response coincides with the protein synthesis response. This assumption seems appropriate, since the resting and postresistance exercise skeletal muscle FSR and fractional breakdown rate have been shown to be significantly correlated (26), suggesting that these two processes are linked.

Our resting (preexercise) protein synthesis (FSR) results are comparable to previous studies of young to middle-aged men in the postabsorptive state that have examined mixed muscle protein from the vastus lateralis (7, 29). The increase in FSR of the PLA group in the current study (76%) also compares favorably with previous studies when training status, dietary state, muscle studied, and the amount of exercise are considered (12, 26, 39).

In this study, we used the Ra of phenylalanine as a measure of whole body protein breakdown. Our data suggest, as others have found (26), that whole body protein breakdown is unchanged 24 h after resistance exercise. Our data also suggest that neither ibuprofen nor acetaminophen had any influence on protein breakdown at the whole body level. To this end, Gann et al. (16) have shown that chronic consumption of the NSAID indomethacin does not affect whole body protein synthesis or nitrogen retention in elderly subjects. This finding is consistent with the fact that the action of the drugs in the current study appears to be at the level of the skeletal muscle, and muscle protein metabolism constitutes only about one-third of whole body protein metabolism (21).

The exercise bout resulted in large increases in serum CK activity and ratings of perceived muscle soreness, which have been shown in previous studies (3, 13). The lack of effect of either drug on CK response to this type of exercise has also been reported (3, 9, 18), although higher prophylactic doses of ibuprofen (5 days before; 2.4 mg/day) have been shown to reduce circulating CK compared with placebo after eccentric muscular activity (28). The lack of effect of similar over-the-counter analgesic drugs on ratings of perceived muscle soreness has also been shown previously (3, 4, 9). However, Hasson et al. (18) reported that prophylactic and therapeutic doses of ibuprofen similar to those used in the current study do reduce levels of perceived muscle soreness 24 or 48 h after exercise with the use of a protocol that was less intense than the one used in the present study. It may appear somewhat surprising that neither of these drugs provided any level of analgesia compared with placebo, given the aforementioned study and the proven pain-reducing benefits of acetaminophen and ibuprofen for individuals with arthritis, headaches, and other symptoms (10, 11). However, the level of pain, soreness, and edema was high enough to severely inhibit the gait of the subjects in our study during the days after the exercise bout. It is quite possible that the level of soreness and pain was too severe for the dose of these drugs to be effective. It is also possible that the scale used for the measurement of perceived soreness among the groups was not able to discern small differences in soreness that were physiologically relevant.

We included only males in our study population, and it is unclear whether these same responses would hold in a similar group of females. However, there are no data to suggest that the metabolism of ibuprofen or acetaminophen or the mechanism of action of these two drugs is different between men and women. Furthermore, several studies of muscle protein metabolism at rest and after resistance exercise have not shown a difference between women and men (26, 27, 31, 38).

In conclusion, the increased rate of muscle protein synthesis normally seen 24 h after high-intensity eccentric resistance exercise was attenuated by consumption of ibuprofen and acetaminophen at over-the-counter levels. The long-term influence of this acute response after resistance exercise for individuals who chronically consume these (or similar) drugs cannot be determined from this study. However, long-term use of these drugs may inhibit the normal hypertrophic response to resistance training. Future studies on the impact of chronic consumption of over-the-counter doses of these drugs on skeletal muscle are warranted.
very interesting read..
 
3 times a day is LUDICCROUS

do NOT have advil near a workout as it will mask pain to a point where you may get MORE injured

if you have advil, have 200-300 mgs before bed
 
Evening Primrose
(GLA) Anti-inflammatory. Rich source of gamma linoleic acid, an essential fatty acid. May lower cholesterol and help prevent clots. May alleviate eczema and PMS.


FeverFew
Works as an Anti-inflammatory, reduces the frequency and severity of migraine headaches

Boswellia

Anti-inflammatory; joint health

Turmeric

The yellow-orange color of turmeric comes from yellow pigment found in the rhizomes called curcumin. Supplements standardized to curcumin are now found in the market. Specific complaints for which turmeric has been shown effective include peptic ulcers, artherosclerosis, and alcohol induced liver toxicity. In one clinical study of smokers, curcumin was found to reduce the incidence of cell mutation. The anti-inflammatory activity of turmeric has been compared to that of topical hydrocortisone


All of these can be found anywhere, even walmart
 
Anaprox (naproxen) is a great NSAID. Indomethacin is the most powerful, but it's probably a little too strong for a shoulder injury. It has a lot of side effects.

Fish oil supplements also have an anti-inflammatory effect as well. The two can be synergistic.
 
OMEGA said:
3 times a day is LUDICCROUS

do NOT have advil near a workout as it will mask pain to a point where you may get MORE injured

if you have advil, have 200-300 mgs before bed


+1
 
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