Antioxidants... Do they hinder our gains or not?

[NO HYPE]

I personally feel the issue is less about anti oxidants and more about controlling inflammation.

It's great to see you have altered your diet to diminish the degree of inflammation however, supplementing particular herbal constituents which display antioxidant activity will elicit an even greater impact. The key to attenuating inflammation is diminishing the presence of excessive NF-kB transcription. Curcumin, resveratrol, and xanthohumol are potent NF-kB inhibitors. Additionally, the plumbagin content from Plumbago zeylanica appears to be eaqually as potent.

[Guardian]

It's great to see you have altered your diet to diminish the degree of inflammation however, supplementing particular herbal constituents which display antioxidant activity will elicit an even greater impact. The key to attenuating inflammation is diminishing the presence of excessive NF-kB transcription. Curcumin, resveratrol, and xanthohumol are potent NF-kB inhibitors. Additionally, the plumbagin content from Plumbago zeylanica appears to be eaqually as potent.

Not sure if any of my supps are in particular making the diff cause I started most of them same time but I feel better then ever in terms of less inflammation

I use
Controlled Labs Orange Triad and Greens and Fish Oil
Cinnamon
Ginger
Cayenne Pepper
Rhodiola Rosea
Aswhaghanda
Triphalia
Vit D-10iu a day
Maca

[Guardian]

Our research didn't focus on muscle bulk, but mTOR is activated by insulin signalling pathway, which is what made the results of my study indirectly applicable to this thread.

mTOR can be activated with Leucine independent of insulin.

This is significant in that insulin can lead to increased oxidative stress. One can use cinnamon and Leucine to decrease this without hampering mTOR.

[HealthyAt4n]

@topic

There some says (but no hard proof claim) that antioxidant supplementation can impede muscle growth.

Here’s a fact: Doing vigorous exercise, strengthening of the body's antioxidant defenses, particularly the glutathione system, to regulate the increased oxidative stress that can protect the cells in your body from oxidative damage.

That’s the reason why I not let my body lack in Antioxidants, I got nice from pureandhealthy.com.

[Guardian]

From my research compounds that are the strongest anti oxidants include cinnamon, cocoa, chocolate unsweetened, oregano, and cloves.

http://www.ars.usda.gov/sp2userfiles...rac/orac07.pdf

[NO HYPE]

From my research compounds that are the strongest anti oxidants include cinnamon, cocoa, chocolate unsweetened, oregano, and cloves.

Nutrients with high ORAC values mean little in terms of their strength as nutraceuticals or the pharmacodynamic impact in which they elicit. For example, none of the aforementioned antioxidants would have much of an impact of excessive NF-kB transcription --> which is exactly what is required to lessen the pressence of excessive inflammation and/or carcinogenic potential.

[NO HYPE]

The key to attenuating inflammation is diminishing the presence of excessive NF-kB transcription. Curcumin, resveratrol, and xanthohumol are potent NF-kB inhibitors. Additionally, the plumbagin content from Plumbago zeylanica appears to be eaqually as potent.

Food Chem Toxicol. 2010 May 14. Jeong JB, Jeong HJ. [Epub ahead of print]
Rheosmin, a naturally occurring phenolic compound inhibits LPS-induced iNOS and COX-2 expression in RAW264.7 cells by blocking NF-kB activation pathway.

Inflammation is part of the host defense mechanism against harmful matters and injury; however, aberrant inflammation is associated to the development of chronic disease such as cancer. Raspberry ketone is a natural phenolic compound. It is used in perfumery, in cosmetics, and as a food additive to impart a fruity odor. In this study, we evaluated whether rheosmin, a phenolic compound isolated from pine needles regulates the expression of iNOS and COX-2 protein in LPS-stimulated RAW264.7 cells. Rheosmin dose-dependently inhibited NO and PGE(2) production and also blocked LPS-induced iNOS and COX-2 expression. Rheosmin potently inhibited the translocation of NF-kB p65 into the nucleus by IkB degradation following IkB-alpha phosphorylation. This result shows that rheosmin inhibits NF-kB activation. In conclusion, our results suggest that rheosmin inhibits LPS-induced iNOS and COX-2 expression in RAW264.7 cells by blocking NF-kB activation pathway.

[JornT]

Scand J Med Sci Sports. 2010 Feb;20(1):e195-207. Epub 2009 Jun 3.
A COX-2 inhibitor reduces muscle soreness, but does not influence recovery and adaptation after eccentric exercise.

The aim of this study was to investigate the effect of a cyclooxygenase (COX)-2 inhibitor on the recovery of muscle function, inflammation, regeneration after, and adaptation to, unaccustomed eccentric exercise. Thirty-three young males and females participated in a double-blind, placebo-controlled experiment. Seventy unilateral, voluntary, maximal eccentric actions with the elbow flexors were performed twice (bouts 1 and 2) with the same arm, separated by 3 weeks. The test group participants were administered 400 mg/day of celecoxib for 9 days after bout 1. After both bouts 1 and 2, concentric and isometric force-generating capacity was immediately reduced (approximately 40-50%), followed by the later appearance of muscle soreness and increased serum creatine kinase levels. Radiolabelled autologous leukocytes (detected by scintigraphy) and monocytes/macro****es (histology) accumulated in the exercised muscles, simultaneously with increased satellite cell activity. These responses were reduced and recovery was faster after bout 2 than 1, demonstrating a repeated-bout effect. No differences between the celecoxib and placebo groups were detected, except for muscle soreness, which was attenuated by celecoxib. In summary, celecoxib, a COX-2 inhibitor, did not detectably affect recovery of muscle function or markers of inflammation and regeneration after unaccustomed eccentric exercise, nor did the drug influence the repeated-bout effect. However, it alleviated muscle soreness.

PMID: 19522751

[NO HYPE]

Scand J Med Sci Sports. 2010 Feb;20(1):e195-207. Epub 2009 Jun 3.
A COX-2 inhibitor reduces muscle soreness, but does not influence recovery and adaptation after eccentric exercise.

The aim of this study was to investigate the effect of a cyclooxygenase (COX)-2 inhibitor on the recovery of muscle function, inflammation, regeneration after, and adaptation to, unaccustomed eccentric exercise. Thirty-three young males and females participated in a double-blind, placebo-controlled experiment. Seventy unilateral, voluntary, maximal eccentric actions with the elbow flexors were performed twice (bouts 1 and 2) with the same arm, separated by 3 weeks. The test group participants were administered 400 mg/day of celecoxib for 9 days after bout 1. After both bouts 1 and 2, concentric and isometric force-generating capacity was immediately reduced (approximately 40-50%), followed by the later appearance of muscle soreness and increased serum creatine kinase levels. Radiolabelled autologous leukocytes (detected by scintigraphy) and monocytes/macro****es (histology) accumulated in the exercised muscles, simultaneously with increased satellite cell activity. These responses were reduced and recovery was faster after bout 2 than 1, demonstrating a repeated-bout effect. No differences between the celecoxib and placebo groups were detected, except for muscle soreness, which was attenuated by celecoxib. In summary, celecoxib, a COX-2 inhibitor, did not detectably affect recovery of muscle function or markers of inflammation and regeneration after unaccustomed eccentric exercise, nor did the drug influence the repeated-bout effect. However, it alleviated muscle soreness.

In relation to cyclooxygenase-inhibition & exercise....

In terms proinflammatory mediators, even though Cissus has been found to decrease xanthine oxidase-induced ROS, TNF-a, & cyclooxygenase activity, the majority of exercise induces anti-inflammatory effects to begin with [as evidenced via the induction of IL-6, IL-10, IL-1RA, and/or the reduction of TNF-a & C-reactive protein levels within the literature]. Either way, I would not be overly concerned about Cissus negatively impacting gains by any significant degree.

[DR_P]

J Physiol. 2005 Aug 15;567(Pt 1):113-20. Epub 2005 Jun 2.

Decreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise in rats.
Gomez-Cabrera MC, Borrás C, Pallardó FV, Sastre J, Ji LL, Viña J.

Catholic University of Valencia, Spain.

Abstract
Reactive oxygen or nitrogen species (RONS) are produced during exercise due, at least in part, to the activation of xanthine oxidase. When exercise is exhaustive they cause tissue damage; however, they may also act as signals inducing specific cellular adaptations to exercise. We have tested this hypothesis by studying the effects of allopurinol-induced inhibition of RONS production on cell signalling pathways in rats submitted to exhaustive exercise. Exercise caused an activation of mitogen-activated protein kinases (MAPKs: p38, ERK 1 and ERK 2), which in turn activated nuclear factor kappaB (NF-kappaB) in rat gastrocnemius muscle. This up-regulated the expression of important enzymes associated with cell defence (superoxide dismutase) and adaptation to exercise (eNOS and iNOS). All these changes were abolished when RONS production was prevented by allopurinol. Thus we report, for the first time, evidence that decreasing RONS formation prevents activation of important signalling pathways, predominantly the MAPK-NF-kappaB pathway; consequently the practice of taking antioxidants before exercise may have to be re-evaluated.

[Peter LeDrew]

J Physiol. 2005 Aug 15;567(Pt 1):113-20. Epub 2005 Jun 2.

Decreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise in rats.
Gomez-Cabrera MC, Borrás C, Pallardó FV, Sastre J, Ji LL, Viña J.

Catholic University of Valencia, Spain.

Abstract
Reactive oxygen or nitrogen species (RONS) are produced during exercise due, at least in part, to the activation of xanthine oxidase. When exercise is exhaustive they cause tissue damage; however, they may also act as signals inducing specific cellular adaptations to exercise. We have tested this hypothesis by studying the effects of allopurinol-induced inhibition of RONS production on cell signalling pathways in rats submitted to exhaustive exercise. Exercise caused an activation of mitogen-activated protein kinases (MAPKs: p38, ERK 1 and ERK 2), which in turn activated nuclear factor kappaB (NF-kappaB) in rat gastrocnemius muscle. This up-regulated the expression of important enzymes associated with cell defence (superoxide dismutase) and adaptation to exercise (eNOS and iNOS). All these changes were abolished when RONS production was prevented by allopurinol. Thus we report, for the first time, evidence that decreasing RONS formation prevents activation of important signalling pathways, predominantly the MAPK-NF-kappaB pathway; consequently the practice of taking antioxidants before exercise may have to be re-evaluated.

I always have issue when all antioxidants get classified into the same category.... antioxidants are either good or bad it seems in studies and in the media, depending on the study.

I doubt it is a bad idea to ingest antioxidant nutrients in sensible doses in a balanced and comprehensive blend... esp. from food. I also like supplemental things such as Powergrape, greens n' berries for various fruit and veggie extracts, NAC, creatine and many other nutrients that can also act as antioxidants. I am sure some antioxidants esp. high doses and solo, might be detrimental for cellular adaptations to exercise, but there seems to be many upsides to the right ones.


I also don't think allopurinol is a good example of the antioxidants I would look into using. It is actually a drug and seems fairly more risky than most nutrient antioxidants one would use before workouts.


http://en.wikipedia.org/wiki/Allopurinol

Side effects
Side effects of allopurinol are rare, though significant when they occur. A small percentage of people develop a rash and must discontinue this drug. The most serious adverse effect is a hypersensitivity syndrome consisting of fever, skin rash, eosinophilia, hepatitis, worsened renal function and, in some cases, allopurinol hypersensitivity syndrome. Allopurinol is one of the drugs commonly known to cause Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TENS), two life-threatening dermatological conditions.

Allopurinol can cause severe pancytopenia if given with azathioprine or mercaptopurine, due to inhibition of xanthine oxidase which metabolizes these drugs. It can also cause breast enlargement in both males and females.

[NO HYPE]

J Physiol. 2005 Aug 15;567(Pt 1):113-20. Epub 2005 Jun 2.

Decreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise in rats.
Gomez-Cabrera MC, Borrás C, Pallardó FV, Sastre J, Ji LL, Viña J.

Catholic University of Valencia, Spain.

Abstract
Reactive oxygen or nitrogen species (RONS) are produced during exercise due, at least in part, to the activation of xanthine oxidase. When exercise is exhaustive they cause tissue damage; however, they may also act as signals inducing specific cellular adaptations to exercise. We have tested this hypothesis by studying the effects of allopurinol-induced inhibition of RONS production on cell signalling pathways in rats submitted to exhaustive exercise. Exercise caused an activation of mitogen-activated protein kinases (MAPKs: p38, ERK 1 and ERK 2), which in turn activated nuclear factor kappaB (NF-kappaB) in rat gastrocnemius muscle. This up-regulated the expression of important enzymes associated with cell defence (superoxide dismutase) and adaptation to exercise (eNOS and iNOS). All these changes were abolished when RONS production was prevented by allopurinol. Thus we report, for the first time, evidence that decreasing RONS formation prevents activation of important signalling pathways, predominantly the MAPK-NF-kappaB pathway; consequently the practice of taking antioxidants before exercise may have to be re-evaluated.

M.A. Nicolas, G.K. McConell and G.D. Wadley
Exercise-training increases skeletal muscle mitochondrial biogenesis despite inhibition of xanthine oxidase

Reactive oxygen species (ROS) increase in skeletal muscle during exercise and there is some evidence that such small, physiological increases in ROS are required for normal increases in mitochondrial biogenesis following exercise (Gomez-Cabrera et al., 2008). Indeed, vitamin C, a non-specific antioxidant, prevents increases in mitochondrial biogenesis markers during exercise-training in rats (Gomez-Cabrera et al., 2008). Although several ROS producing sites have been identified in skeletal muscle during contraction, there is a lack of knowledge regarding the source(s) of ROS responsible for initiating pathways culminating in mitochondrial biogenesis in skeletal muscle during exercise. A recent study has identified the enzyme xanthine oxidase (XO) as a potential source of ROS responsible for initiating skeletal muscle mitochondrial biogenesis during exercise (Gomez-Cabrera et al., 2005). p38 MAPK is a putative mitochondrial biogenesis signalling molecule (Akimoto et al., 2005) and the inhibition of the XO-mediated ROS production during acute exercise in vivo with the XO inhibitor, allopurinol, prevented increases in gastrocnemius p38 MAPK phosphorylation immediately after exercise (Gomez-Cabrera et al., 2005). However, key mitochondrial biogenesis proteins were not analysed and the effect of allopurinol during exercise-training has not been examined. Therefore the aim of this investigation was to determine whether inhibiting XO-induced increases in ROS with allopurinol during exercise training attenuates key proteins involved in mitochondrial biogenesis.

Male Sprague-Dawley rats aged 5 weeks were randomly assigned into four groups: [1] Sedentary (SedWater) (n=6); [2] Exercise-trained (ExWater) (n=6); [3] Sedentary and treated with 0.25 mg/mL of allopurinol in drinking water (SedAllo) (n=6); and [4] Exercise-trained and treated with 0.25 mg/mL of allopurinol in drinking water (ExAllo) (n=6). Pilot testing revealed this treatment to inhibit phosphorylation of p38 MAPK during acute exercise. Trained rats were exercised 5 days/week on a treadmill at a 5% incline for 6 weeks. By the end of the sixth week trained rats were required to run for 90 minutes at a treadmill speed of 30 m/min. Sedentary rats were placed on a stationary treadmill for an identical period of time as the trained rats throughout the investigation. Rats were killed via an intraperitoneal injection of pentobarbital sodium (180 mg/kg) 48 hours after the last training bout. Gastrocnemius muscles were rapidly dissected and frozen in liquid nitrogen. Mitochondrial biogenesis markers were examined using commercially available antibodies for PPAR-g co-activator-1a (PGC-1a), mitochondrial transcription factor A (Tfam) and cytochrome c.

Exercise-training for 6 weeks significantly increased PGC-1a, Tfam and cytochrome c protein levels in gastrocnemius muscle of ExWater and ExAllo rats (p < 0.05). Interestingly, allopurinol did not alter the exercise-induced increases in these key mitochondrial biogenesis markers. No difference was observed in PGC-1a, Tfam and cytochrome c protein levels in SedAllo animals when compared to the SedWater controls. The fact that inhibition of XO-induced production of ROS with allopurinol failed to attenuate the increase in mitochondrial biogenesis markers with exercise-training suggests that XO may not be an essential source of ROS responsible for the stimulation of skeletal muscle mitochondrial biogenesis with exercise-training. Given that vitamin C has been shown to attenuate the increase in mitochondrial biogenesis with exercise-training (Gomez-Cabrera et al., 2008), further studies examining other ROS producing sites within skeletal muscle are required to determine which sources of ROS are involved with regulating skeletal muscle mitochondrial
biogenesis during exercise-training.

[De__eB]

Some nice information from a BJSM series on nutritional supplements

Antioxidants
S K Powers4, A N Kavazis4, W B Nelson44Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA
It is well established that physical exercise results in increased free-radical production in active skeletal muscles. Importantly, numerous reports indicate that exercise-induced free-radical production is responsible for oxidative damage to cells and contributes to muscular fatigue during prolonged exercise.5 The fact that working skeletal muscles produce radicals has motivated many athletes to begin using antioxidant supplements in hopes of preventing exercise-induced free-radical damage and/or muscular fatigue. However, whether or not antioxidant supplements are helpful or harmful to the athlete remains a highly debated topic. The purpose of this brief review is to summarise the arguments for and against antioxidant supplementation in athletes and other physically active individuals. The review begins with an overview of key terms related to free-radical biology and antioxidants.

Free-radical biology and antioxidants: key terms
Free radicals (hereafter referred to as radicals) are molecules or any chemical species that contain one or more unpaired electrons in their outer orbital.3 In cells, radicals can be formed by either losing a single electron or gaining an electron.3 An unpaired electron results in molecular instability, and therefore radicals are highly reactive molecules that can promote oxidative damage to proteins, lipids and DNA. This radical-mediated damage is referred to as “oxidative damage,” and oxidation of cellular constituents can lead to cellular dysfunction and, in extreme cases, cell death. Also, note that reactive oxygen species (ROS) is a general term that not only refers to oxygen-centred radicals but also includes non-radical but reactive derivatives of oxygen (eg, hydrogen peroxide).3

The term “oxidative stress” was introduced in 1985 and is commonly defined as a disturbance in the pro-oxidant–antioxidant balance in favour of oxidants with the imbalance leading to oxidative damage.3 Indeed, one of the hallmarks of oxidative stress in cells is the appearance of biomarkers of oxidative damage (eg, oxidised proteins and/or lipids).

Note, however, that exercise-induced oxidative stress is a transient occurrence. Indeed, the exercise-induced spike in radical production is short lived, and growing evidence suggests that this spike in oxidants after exercise is a required signalling pathway for training adaptations to occur. This brief rise in oxidants should not be confused with prolonged oxidative stress found in some pathological conditions.5

In the context of this review, antioxidants will be defined as any substance that significantly delays or prevents oxidative damage of a target molecule.3 Given that all cells produce radicals, it is not surprising that cells contain an endogenous antioxidant system composed of both enzymatic and non-enzymatic antioxidants. Moreover, dietary antioxidants (eg, vitamin C and vitamin E) cooperate with the endogenous antioxidant defence systems to form a united antioxidant network in muscle fibres. This cooperative interaction between endogenous antioxidants and dietary antioxidants has fuelled the argument that antioxidant supplementation will boost the muscle fibre’s ability to scavenge ROS and protect against exercise-induced oxidative damage and fatigue.

Can antioxidants protect against exercise-induced oxidative damage in muscle and improve performance?
Muscle fatigue is commonly defined as a reduction in the ability of a muscle to generate force. Exercise-induced muscle fatigue is a multifactorial process, and the specific causes of fatigue can vary widely. Nonetheless, growing evidence indicates that radical production in skeletal muscles contributes to fatigue during prolonged submaximal exercise (ie, events lasting >30 min). As mentioned previously, ROS production increases in contracting skeletal muscles, and low levels of ROS play an essential role in the regulation of muscle force production. Indeed, low levels of ROS in contracting skeletal muscles are required to achieve optimum force production. However, high levels of ROS can induce oxidative damage to muscle proteins and lipids, and diminish muscle force production. Indeed, well-controlled animal studies indicate that scavenging radicals via antioxidants can protect skeletal muscle against oxidative damage and also delay fatigue during prolonged submaximal exercise.5 In contrast, antioxidant scavengers are not effective in delaying muscle fatigue in animals performing high intensity exercise.5

Do radicals contribute to exercise-induced muscular fatigue in humans? The answer to this question remains under debate, but a growing number of studies suggest that acute administration of the antioxidant N-acetylcysteine (NAC) delays human muscle fatigue during prolonged submaximal exercise. Specifically, NAC administration has been shown to delay muscular fatigue in humans during submaximal exercise tasks (eg, electrically stimulated limb muscle, voluntary cycling exercise and repetitive handgrip exercise).5 Similar to the aforementioned animal studies, NAC does not retard human muscle fatigue during exercise close to VO2max. In contrast to the findings that acute NAC administration can delay muscle fatigue during prolonged submaximal exercise, there is little evidence that other more commonly used antioxidant supplements (eg, beta carotene, vitamin E and/or vitamin C) can improve human exercise performance.4 Based upon current evidence, we conclude that NAC may be able to increase performance during prolonged exercise in humans, but there is limited evidence to indicate that vitamin C, vitamin E or beta carotene can improve performance.

Does exercise increase the need for dietary antioxidants?
Regardless of whether antioxidants can delay muscular fatigue, advocates supporting antioxidant supplementation for athletes argue that rigorous exercise training results in increased ROS production in skeletal muscles. Therefore, they suggest that antioxidant supplements are required to protect skeletal muscle fibres against oxidative damage. Although this suggestion appears reasonable, there are numerous arguments against antioxidant supplementation for athletes. First, there is no evidence that exercise-induced radical production in skeletal muscle is detrimental to human health. Secondly, regular exercise training promotes increased enzymatic and non-enzymatic antioxidants in muscle fibres resulting in improved endogenous protection against exercise-mediated oxidative damage. Therefore, this increase in endogenous antioxidants may be sufficient to protect against exercise-induced oxidative damage. Moreover, if an athlete maintains an isocaloric diet that is nutritionally well balanced, it is feasible that the athlete may not require supplementary antioxidants above those contained in the diet.

There is one circumstance that may justify the use of antioxidant supplements in athletes. Specifically, some athletes may not consume well-balanced diets, and therefore these individuals could be deficient in antioxidant intake (eg, below the recommended daily allowance (RDA) for selected antioxidant vitamins). This is a reasonable point that is supported by studies investigating the nutritional habits of athletes.

Perhaps the two strongest arguments against antioxidant supplementation for athletes and other active individuals are the following. First, emerging evidence indicates that antioxidant supplementation prevents important exercise-induced adaptations in skeletal muscle. Indeed, compelling evidence indicates that exercise-induced ROS production serves as a required signal to promote the expression of numerous skeletal muscle proteins including antioxidant enzymes, mitochondrial proteins and heat-shock proteins.5 Secondly, two recent reports indicate that antioxidant supplementation with high levels of vitamins E and C (ie, ~16 times higher than RDA for adults) can blunt the training adaptation to exercise.2 6 Another key argument against antioxidant supplementation in athletes is that current research does not support the notion that antioxidant supplementation is beneficial to human health. Specifically, a meta-analysis of 68 randomised antioxidant supplement trials (total of 232 606 human participants) concluded that dietary supplementation above the RDA with beta carotene, vitamin A and vitamin E does not improve health outcomes and may increase mortality.1 These authors also concluded that the roles of vitamin C and selenium on human mortality are unclear and require further study before a recommendation can be rendered.

Summary
The problem of whether or not athletes should use antioxidant supplements remains an important and highly debated topic. Arguments for and against antioxidant supplementation exist, and additional research will be required to establish firmly whether antioxidant supplementation is beneficial or harmful to athletes. However, at present, there is limited scientific evidence to recommend antioxidant supplements to athletes or other physically active individuals. In fact, the current evidence suggests that athletes should use caution when considering supplementation with high doses of antioxidants.

[Harpagan]

Pretty interesting...

Vitamin C negates effects of endurance training
If you want to improve your condition, you’re better off not taking high-dose vitamin C pills. In fact, you may be best off not taking any supplements that neutralise the effects of free radicals at all. In 2008, physiologists at the University of Valencia published the results of a study in which a daily dose of 1 g vitamin C undermined the effect of 8 weeks of running training.

It’s the same story with free radicals as what we now know about cholesterol. At first researchers lumped them all into one category: ‘bad’. After all, free radicals damage cells and speed up the aging process. Anti-oxidants, such as vitamin C and E, which neutralise free radicals, were ‘good’. [...]

http://www.ergo-log.com/vitamincendurancetraining.html

[Barn01]

OK now I'm confused again.

Vitamins are good for your health but hinder muscle gains? Is this what I'm reading?

[BringnIt]

Pretty interesting...



http://www.ergo-log.com/vitamincendurancetraining.html

Also states that longer periods of time have shown no difference. Most likely due to a short-term decrease in the body's natural production of antioxidant enzymes.

That said, I remember at least one study showing androgens also decrease production of antioxidant enzymes like glutathione, and that is a big factor in the cardiovascular and hepatic issues associated with use. Antioxidant protocols would be vastly different in that group, seemingly. Also in the elderly.

Haven't read any of this thread yet, hopefully I'm not reposting excessively.

[Peter LeDrew]

Pretty interesting...



http://www.ergo-log.com/vitamincendurancetraining.html

Boo... I don't believe it... at least not when one is doing a more comprehensive supplementation program that incorporates network antioxidants and boosters to support each other... high doses of any 1 antioxidant or nutrient is likely not a good idea and that is old news to me.

[7percent]

How is this 13 pages long? Nobody is honestly going to stop taking vitamins because they may or many not hinder gains. What a joke, lift heavy, take a multi and stop obsessing over the little things that don't even matter.

[BringnIt]

How is this 13 pages long? Nobody is honestly going to stop taking vitamins because they may or many not hinder gains. What a joke, lift heavy, take a multi and stop obsessing over the little things that don't even matter.

No one has suggested not taking a multi or eliminating antioxidants? It's trying to establish the ideal timing, dosage and type of antioxidants. It's important not just from a lifting standpoint, but a health one?

Seriously cannot figure out what the point of your post is.

[Barn01]

No one has suggested not taking a multi or eliminating antioxidants? It's trying to establish the ideal timing, dosage and type of antioxidants. It's important not just from a lifting standpoint, but a health one?

Seriously cannot figure out what the point of your post is.

So after 13 pages ... is there any consensus yet on what/when/how much?

[BringnIt]

So after 13 pages ... is there any consensus yet on what/when/how much?

Consensus? No. Too complicated an issue with too many variables. For instance, the issue will likely be different in trained vs. untrained individuals, and age will play a role as well (when your body becomes less efficient at manufacturing glutathione/SOD).

As well as there being different types of antioxidants.

[7percent]

No one has suggested not taking a multi or eliminating antioxidants? It's trying to establish the ideal timing, dosage and type of antioxidants. It's important not just from a lifting standpoint, but a health one?

Seriously cannot figure out what the point of your post is.

You are once again, overthinking everything.

[Peter LeDrew]

You are once again, overthinking everything.

Kinda agree... there is also the whole newer scientific discussion of how antioxidants are actually working and providing benefits in the body.

How's this for food for thought!
http://www.nutraingredients.com/Rese...r-antioxidants

Here’s a radical thought for the marketers - the benefits of antioxidants may not be related to antioxidant activity.

[NO HYPE]

How is this 13 pages long?

Maybe it has something to do with the fact that 13,000+ people are interested in the subject. Go dig a hole or something.

[7percent]

Maybe it has something to do with the fact that 13,000+ people are interested in the subject. Go dig a hole or something.

13,000 people are interested in this thread? How did you get that number?

You are just mad that this thread is irrelevant.

[NO HYPE]

13,000 people are interested in this thread? How did you get that number?

Oh my mistake. I must have been looking at the "best of threads" just above it. Good thing you're around to correct me though.

You are just mad that this thread is irrelevant.

Are you still digging?

[NO HYPE]

stop obsessing over the little things that don't even matter.

That's going to be my new year's resolution pertaining to your posts.

[De__eB]

Oh my mistake. I must have been looking at the "best of threads" just above it. Good thing you're around to correct me though.

yeah, damn, its only 25,000 people. ****s irrelevant son.

[BringnIt]

Oh my mistake. I must have been looking at the "best of threads" just above it. Good thing you're around to correct me though.

Yeah, noob, this thread has 25,000 views, not 13,000.

[7percent]

Views = / = people.

Back to pubmed NO HYPE.