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[nowayout]

The issue of exercise and antioxidant supplementation has been discussed before in these forums. I have collected a number of studies and thought it might be useful to list them together.

The overall lesson seems to be not to mix exercise with too much antioxidant supplementation. Furthermore, it seems if you have to choose between exercise and megadosing antioxidant supplements, choose exercise. Of course it makes sense to avoid deficiencies (but maybe not even - see one of the studies below suggesting exercise can compensate even for dietary deficiencies).


Exercise is an antioxidant, but this effect can be blocked by supplementation with oral antioxidants:

Moderate exercise is an antioxidant: upregulation of antioxidant genes by training.
Gomez-Cabrera MC, Domenech E, Viña J. Department of Physiology, Faculty of Medicine, University of Valencia, Blasco Ibañez, 15, 46010 Valencia, Spain.

Exercise causes oxidative stress only when exhaustive. Strenuous exercise causes oxidation of glutathione, release of cytosolic enzymes, and other signs of cell damage. However, there is increasing evidence that reactive oxygen species (ROS) not only are toxic but also play an important role in cell signaling and in the regulation of gene expression. Xanthine oxidase is involved in the generation of superoxide associated with exhaustive exercise. Allopurinol (an inhibitor of this enzyme) prevents muscle damage after exhaustive exercise, but also modifies cell signaling pathways associated with both moderate and exhaustive exercise in rats and humans. In gastrocnemius muscle from rats, exercise caused an activation of MAP kinases. This in turn activated the NF-kappaB pathway and consequently the expression of important enzymes associated with defense against ROS (superoxide dismutase) and adaptation to exercise (eNOS and iNOS). All these changes were abolished when ROS production was prevented by allopurinol. Thus ROS act as signals in exercise because decreasing their formation prevents activation of important signaling pathways that cause useful adaptations in cells. Because these signals result in an upregulation of powerful antioxidant enzymes, exercise itself can be considered an antioxidant. We have found that interfering with free radical metabolism with antioxidants may hamper useful adaptations to training.

Here is an interesting article showing that endogenous antioxidant defenses in response to exercise training can compensate for deficiencies in dietary antioxidants. In other words, exercise is an antioxidant:

Beneficial effects of gradual intense exercise in tissues of rats fed with a diet deficient in vitamins and minerals: A pilot study. PMID: 19131214
Teixeira A, Müller L, Santos AA, Reckziegel P, Emanuelli T, Rocha JB, Bürger ME. Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria, Santa Maria, Rio Grande do Sul, Brazil.

OBJECTIVE: This study evaluated the preliminary effects of intense physical training (swimming) on oxidative stress in rats with nutritional deficiencies. METHODS: Rats were fed with a standard diet or a diet deficient in vitamins and minerals for 4 months. The deficient diet contained one-fourth of the recommended vitamin and mineral levels for rats. From the second month, half of the animals were subjected to a swimming exercise in a plastic container with water maintained at 34 +/- 1 degrees C for 1 h/d, five times per week, for 11 wk. The rats were subjected to swimming exercise with loads attached to the dorsal region, which were progressively increased according to their body weight (1% to 7%). Sedentary rats were transported to the experimental room and handled as often in a similar way as the exercise group, except that they were not put in water. RESULTS: In the exercised group, blood lactate levels were significantly lower and the heart weight/body weight ratio was significantly higher than in the sedentary group (P < 0.05). Increased lipid peroxidation was observed in the liver, heart, and skeletal muscle of rats fed with the deficient diet, but it was completely reversed by exercise. Exercise also decreased lipid peroxidation levels in the heart and skeletal muscle of rats fed with the standard diet (P < 0.05). CONCLUSION: This pilot study leads to the continuity of the studies, because the partial results observed suggest that inadequate nutrition may enhance oxidative stress, and that intense chronic physical training may activate antioxidant defenses, possibly by hormesis.

Oral antioxidants can block beneficial adaptations from exercise (lowering of blood pressure in this case):

Oral antioxidants and cardiovascular health in the exercise trained and untrained elderly: a radically different outcome.
Wray DW, Uberoi A, Lawrenson L, Bailey DM, Richardson RS. Both antioxidant supplementation and exercise training have been identified as interventions which may reduce oxidative stress and thus improve cardiovascular health, but the interaction of these interventions on arterial blood pressure and vascular function has not been studied in older humans. Thus, in six older (71 +/- 2 yrs) mildly hypertensive men, arterial blood pressure was evaluated non-invasively at rest and during small muscle mass (knee-extensor) exercise with and without a pharmacologic dose of oral antioxidants (Vitamins C, E, and alpha-lipoic acid). The efficacy of the antioxidant intervention to decrease plasma free radical concentration was verified via electron paramagnetic resonance (EPR) spectroscopy, while changes in endothelial function in response to exercise training and antioxidant administration were evaluated via flow-mediated vasodilation (FMD). Subjects were re-evaluated after a six-week aerobic exercise training program. Prior to training, acute antioxidant administration did not change resting arterial blood pressure or FMD. Six weeks of knee-extensor exercise training reduced systolic (from 150 +/- 8 to 138 +/- 3 mmHg, pre- vs. post-training) and diastolic (from 91 +/- 5 to 79 +/- 3 mmHg, pre- vs. post-training) blood pressure, and improved FMD (1.5 +/- 1% to 4.9 +/- 1%, pre- vs. post-training). However, antioxidant administration after exercise training negated these improvements, returning subjects to a hypertensive state and blunting training-induced improvements in FMD. The paradoxical effects of these interventions suggest a need for caution when exercise and acute antioxidant supplementation are combined in elderly, mildly hypertensive individuals.

The following study shows that reactive oxygen species play an important and positive role in vasodilation during exercise, and that oral antioxidants can block this response:

Exercise-induced brachial artery vasodilation: role of free radicals.
Richardson RS, Donato AJ, Uberoi A, Wray DW, Lawrenson L, Nishiyama S, Bailey DM. Dept of Medicine, Physiology Division, Univ of California San Diego, La Jolla, CA 92093-0623, USA. rrichardson@ucsd.edu

Originally thought of as simply damaging or toxic "accidents" of in vivo chemistry, free radicals are becoming increasingly recognized as redox signaling molecules implicit in cellular homeostasis. Indeed, at the vascular level, it is plausible that oxidative stress plays a regulatory role in normal vascular function. Using electron paramagnetic resonance (EPR) spectroscopy, we sought to document the ability of an oral antioxidant cocktail (vitamins C, E, and alpha-lipoic acid) to reduce circulating free radicals, and we employed Doppler ultrasound to examine the consequence of an antioxidant-mediated reduction in oxidative stress on exercise-induced vasodilation. A total of 25 young (18-31 yr) healthy male subjects partook in these studies. EPR spectroscopy revealed a reduction in circulating free radicals following antioxidant administration at rest ( approximately 98%) and as a consequence of exercise ( approximately 85%). Plasma total antioxidant capacity and vitamin C both increased following the ingestion of the antioxidant cocktail, whereas vitamin E levels were not influenced by the ingestion of the antioxidants. Brachial artery vasodilation during submaximal forearm handgrip exercise was greater with the placebo (7.4 +/- 1.8%) than with the antioxidant cocktail (2.3 +/- 0.7%). These data document the efficacy of an oral antioxidant cocktail in reducing free radicals and suggest that, in a healthy state, the aggressive disruption of the delicate balance between pro- and antioxidant forces can negatively impact vascular function. These findings implicate an exercise-induced reliance upon pro-oxidant-stimulated vasodilation, thereby revealing an important and positive vascular role for free radicals.

This article shows that exercise can pretty much completely prevent age-dependent loss of endogenous plasma antioxidant capacity. This is quite dramatic, and I am not aware of any supplement that can achieve this.

Physical activity, plasma antioxidant capacity, and endothelium-dependent vasodilation in young and older men.
Franzoni F, Ghiadoni L, Galetta F, Plantinga Y, Lubrano V, Huang Y, Salvetti G, Regoli F, Taddei S, Santoro G, Salvetti A. Department of Internal Medicine, University of Pisa, Pisa, Italy. f.franzoni@int.med.unipi.it

BACKGROUND: Sedentary aging is associated with oxidative stress and endothelial dysfunction. The aim of this study was to evaluate the relationship between long-term physical activity, plasma antioxidant status, and conduit artery endothelial function in young and older healthy men. METHODS: In young (n = 16) and older athletes (n = 16) and in matched healthy sedentary subjects, endothelium-dependent flow-mediated dilation (FMD) and endothelium-independent response to glyceryl trinitrate (GTN), 400 microg, were measured in the brachial artery from high-resolution ultrasonography. Plasma malondialdehyde (MDA) and antioxidant capacity as total oxyradical scavenging capacity (TOSC) were also evaluated. RESULTS: We found that FMD was lower (< or =0.01) in sedentary older subjects (2.3% +/- 1.0%) as compared with older athletes (5.3% +/- 3.2%) and both sedentary (5.4% +/- 2.0%) and athletically trained (6.1% +/- 3.2%) young subjects. Sedentary older subjects showed higher (P < or = .05) MDA levels and lower (P < .0001) plasma antioxidant capacity as compared with the other subgroups, whereas in older athletes MDA levels and antioxidant capacity were similar to those observed in the young subgroups. In the whole group, FMD, but not GTN, was negatively related to age (r = -0.31, P < .05) and directly related (P < or = .01) to VO2max (r = 0.49) and TOSC against peroxyl (r = 0.69) and hydroxyl radicals (r = 0.53). In the multivariate analysis, TOSC against peroxyl radicals resulted as the most significant predictor of FMD (R2 = 0.60; P = .003). CONCLUSIONS: These results suggest that regular physical activity is associated with preserved antioxidant defenses and endothelial function in older individuals.

Another article showing that exercise not only upregulates endogenous antioxidants and repair enzymes but also attenuates ROS production.

Hormetic effects of regular exercise in aging: correlation with oxidative stress.
Goto S, Naito H, Kaneko T, Chung HY, Radák Z. Tokyo Metropolitan Institute of Gerontology, Sakae-cho, Itabashi, Tokyo 173-0015, Japan. goto@tmig.or.jp

To explore mechanisms of the beneficial consequences of regular exercise, we studied the effects of regular swimming and treadmill exercise on oxidative stress in the brain and liver of rats. Protein carbonyl was significantly reduced and the activity of proteasome was upregulated in the brain extracts of young and middle-aged animals after 9 weeks of swimming training. Furthermore, their cognitive functions were significantly improved. In separate experiments, the activation of transcription nuclear factor kappaB was attenuated in the liver of old rats after 8 weeks of regular treadmill exercise and the DNA binding activity of glucocorticoid receptor reduced with age was restored, suggesting that inflammatory reactions are alleviated by the regimen. This was accompanied by upregulation of the glutathione level and reduced reactive oxygen species generation. Similar training reduced the 8-oxodeoxyguanosine content in the nuclear and mitochondrial DNA of the liver of old rats. Thus, these findings, together with reports of other investigators, suggest that moderate regular exercise attenuates oxidative stress. The mild oxidative stress possibly elicited by regular exercise appears to manifest a hormesis-like effect in nonmuscular tissues, constituting beneficial mechanisms of exercise by adaptively upregulating various antioxidant mechanisms, including antioxidative and repair-degradation enzymes for damaged molecules. Importantly, the adaptation induced by regular exercise was effective even if initiated late in life.

Free radicals may also be important regulator signals in muscular function:

Free radicals generated by contracting muscle: by-products of metabolism or key regulators of muscle function?
Jackson MJ. Division of Metabolic and Cellular Medicine, School of Clinical Sciences, University of Liverpool, Liverpool L69 3GA, UK. m.j.jackson@liverpool.ac.uk

Skeletal muscle fibers generate reactive oxygen species (ROS) at a number of subcellular sites and this generation is increased by contractile activity. Early studies suggested that generation of superoxide as a by-product of mitochondrial oxygen consumption was the major source of muscle ROS generation and that the species produced were inevitably damaging to muscle, but recent data argue against both of these possibilities. Developments in analytical approaches have shown that specific ROS are generated in a controlled manner by skeletal muscle fibers in response to physiological stimuli and play important roles in the physiological adaptations of muscle to contractions. These include optimization of contractile performance and initiation of key adaptive changes in gene expression to the stresses of contractions. These positive benefits of the ROS that are induced by contractile activity contrast starkly with the increasing evidence that ROS-induced degenerative pathways are fundamental to aging processes in skeletal muscle. A fuller understanding of these contrasting roles is recognized to be important in the design of strategies to maintain and optimize skeletal muscle function during exercise and to help prevent the devastating effects of sarcopenia and other muscle-wasting conditions.

A study showing that too much gamma-tocopherol may completely blunt a beneficial exercise-induced protective adaptation (HSP-72 plays a protective role in protecting against cell damage under stress):

Vitamin E isoform-specific inhibition of the exercise-induced heat shock protein 72 expression in humans
Christian P. Fischer,¹ Natalie J. Hiscock,² Samar Basu,³ Bengt Vessby,³ Anders Kallner,⁴ Lars-Börje Sjöberg,⁵ Mark A. Febbraio,² and Bente K. Pedersen¹

ABSTRACT

Increased levels of reactive oxygen and nitrogen species, as seen in response to exercise, challenge the cellular integrity. Important protective adaptive changes include induction of heat shock proteins (HSPs). We hypothesized that supplementation with antioxidant vitamins C (ascorbic acid) and E (tocopherol) would attenuate the exercise-induced increase of HSP72 in the skeletal muscle and in the circulation. Using randomization, we allocated 21 young men into three groups receiving one of the following oral supplementations: RRR--tocopherol 400 IU/day + ascorbic acid (AA) 500 mg/day (CE), RRR--tocopherol 290 IU/day + RRR--tocopherol 130 IU/day + AA 500 mg/day (CE), or placebo (Control). After 28 days of supplementation, the subjects performed 3 h of knee extensor exercise at 50% of the maximal power output. HSP72 mRNA and protein content was determined in muscle biopsies obtained from vastus lateralis at rest (0 h), postexercise (3 h), and after a 3-h recovery (6 h). In addition, blood was sampled for measurements of HSP72, -tocopherol, -tocopherol, AA, and 8-iso-prostaglandin-F₂ (8-PGF₂). Postsupplementation, the groups differed with respect to plasma vitamin levels. The marker of lipid peroxidation, 8-iso-PGF₂, increased from 0 h to 3 h in all groups, however, markedly less (P < 0.05) in CE. In Control, skeletal muscle HSP72 mRNA content increased 2.5-fold (P < 0.05) and serum HSP72 protein increased 4-fold (P < 0.05) in response to exercise, whereas a significant increase of skeletal muscle HSP72 protein content was not observed (P = 0.07). In CE, skeletal muscle HSP72 mRNA, HSP72 protein, and serum HSP72 were not different from Control in response to exercise. In contrast, the effect of exercise on skeletal muscle HSP72 mRNA and protein, as well as circulating HSP72, was completely blunted in CE. The results indicate that -tocopherol comprises a potent inhibitor of the exercise-induced increase of HSP72 in skeletal muscle as well as in the circulation.

Oral antioxidants can worsen muscle injury due to exercise:

Supplementation with vitamin C and N-acetyl-cysteine increases oxidative stress in humans after an acute muscle injury induced by eccentric exercise.

Childs A, Jacobs C, Kaminski T, Halliwell B, Leeuwenburgh C.

Biochemistry of Aging Laboratory, Center for Exercice Science, College of Human Performance, University of Florida, Gainesville, FL 32611, USA.

There has been no investigation to determine if the widely used over-the-counter, water-soluble antioxidants vitamin C and N-acetyl-cysteine (NAC) could act as pro-oxidants in humans during inflammatory conditions. We induced an acute-phase inflammatory response by an eccentric arm muscle injury. The inflammation was characterized by edema, swelling, pain, and increases in plasma inflammatory indicators, myeloperoxidase and interleukin-6. Immediately following the injury, subjects consumed a placebo or vitamin C (12.5 mg/kg body weight) and NAC (10 mg/kg body weight) for 7 d. The resulting muscle injury caused increased levels of serum bleomycin-detectable iron and the amount of iron was higher in the vitamin C and NAC group. The concentrations of lactate dehydrogenase (LDH), creatine kinase (CK), and myoglobin were significantly elevated 2, 3, and 4 d postinjury and returned to baseline levels by day 7. In addition, LDH and CK activities were elevated to a greater extent in the vitamin C and NAC group. Levels of markers for oxidative stress (lipid hydroperoxides and 8-iso prostaglandin F2alpha; 8-Iso-PGF2alpha) and antioxidant enzyme activities were also elevated post-injury. The subjects receiving vitamin C and NAC had higher levels of lipid hydroperoxides and 8-Iso-PGF2alpha 2 d after the exercise. This acute human inflammatory model strongly suggests that vitamin C and NAC supplementation immediately post-injury, transiently increases tissue damage and oxidative stress.

Somewhat off topic and perhaps a little out there, but an interesting article showing that at least in C. elegans, ROS may play a role in increasing lifespan.

Glucose Restriction Extends Caenorhabditis elegans Life Span by Inducing Mitochondrial Respiration and Increasing Oxidative Stress
Tim J. Schulz^1,2,Kim Zarse¹,Anja Voigt^1,2,Nadine Urban¹,Marc Birringer¹andMichael Ristow<sup>1,2,

1</sup> Department of Human Nutrition, Institute of Nutrition, University of Jena, D-07743 Jena, Germany
² German Institute of Human Nutrition Potsdam-Rehbrücke, D-14558 Nuthetal, Germany



Summary
Increasing cellular glucose uptake is a fundamental concept in treatment of type 2 diabetes, whereas nutritive calorie restriction increases life expectancy. We show here that increased glucose availability decreases Caenorhabditis elegans life span, while impaired glucose metabolism extends life expectancy by inducing mitochondrial respiration. The histone deacetylase Sir2.1 is found here to be dispensable for this phenotype, whereas disruption of aak-2, a homolog of AMP-dependent kinase (AMPK), abolishes extension of life span due to impaired glycolysis. Reduced glucose availability promotes formation of reactive oxygen species (ROS), induces catalase activity, and increases oxidative stress resistance and survival rates, altogether providing direct evidence for a hitherto hypothetical concept named mitochondrial hormesis or mitohormesis. Accordingly, treatment of nematodes with different antioxidants and vitamins prevents extension of life span. In summary, these data indicate that glucose restriction promotes mitochondrial metabolism, causing increased ROS formation and cumulating in hormetic extension of life span, questioning current treatments of type 2 diabetes as well as the widespread use of antioxidant supplements.

Slightly off-topic, but exercise may preserve your telomeres:

The Association Between Physical Activity in Leisure Time and Leukocyte Telomere Length Lynn F. Cherkas, PhD; Janice L. Hunkin, BSc; Bernet S. Kato, PhD; J. Brent Richards, MD; Jeffrey P. Gardner, PhD; Gabriela L. Surdulescu, MSc; Masayuki Kimura, MD, PhD; Xiaobin Lu, MD; Tim D. Spector, MD, FRCP; Abraham Aviv, MD


Arch Intern Med. 2008;168(2):154-158.

Background Physical inactivity is an important risk factor for many aging-related diseases. Leukocyte telomere dynamics (telomere length and age-dependent attrition rate) are ostensibly a biological indicator of human aging. We therefore tested the hypothesis that physical activity level in leisure time (over the past 12 months) is associated with leukocyte telomere length (LTL) in normal healthy volunteers.

Methods We studied 2401 white twin volunteers, comprising 2152 women and 249 men, with questionnaires on physical activity level, smoking status, and socioeconomic status. Leukocyte telomere length was derived from the mean terminal restriction fragment length and adjusted for age and other potential confounders.

Results Leukocyte telomere length was positively associated with increasing physical activity level in leisure time (P < .001); this association remained significant after adjustment for age, sex, body mass index, smoking, socioeconomic status, and physical activity at work. The LTLs of the most active subjects were 200 nucleotides longer than those of the least active subjects (7.1 and 6.9 kilobases, respectively; P = .006). This finding was confirmed in a small group of twin pairs discordant for physical activity level (on average, the LTL of more active twins was 88 nucleotides longer than that of less active twins; P = .03).

Conclusions A sedentary lifestyle (in addition to smoking, high body mass index, and low socioeconomic status) has an effect on LTL and may accelerate the aging process. This provides a powerful message that could be used by clinicians to promote the potentially antiaging effect of regular exercise.

[ajnast4r]

excellent post. this has been discussed a few times i believe, zoolander specifically has mentioned sporadic periods of antioxidant deprivation to induced increased exercise adaptation.

i make sure not to have anything too high in antioxidants immediately after, or in the meal following my workout.

Edited by ajnast4r, 29 January 2009 - 05:43 PM.

[dupez]

i run 2.5 Miles / 330 cals 8 am every other day, havnt watched my antioxidants before. I know i'm intaking quite a bit. Havnt had a problem..

[Sillewater]

excellent post. this has been discussed a few times i believe, zoolander specifically has mentioned sporadic periods of antioxidant deprivation to induced increased exercise adaptation.

i make sure not to have anything too high in antioxidants immediately after, or in the meal following my workout.

Did zoolander discuss that on this forum? I never take antioxidants on days I exercise, but since Vitamin E is fat soluble, and Vitamin C could be stored after a certain serum level has been reached, I'm wondering if I should re-think my anti-oxidant intake.

[niner]

Here's my anecdotal experience with antioxidants and exercise. For years I have been taking some form of antioxidants, and exercising. I have been on a strength and endurance plateau for some while. Things bumped up a couple years ago when I started taking ALCAR, but have been pretty steady since then. A couple months ago, I began skipping antioxidants on days that I exercise. Shortly after starting this, my endurance and strength shot up a lot. So much so that I thought the exercise bike I was using was broken, and I switched to another one. The only change I can pin this on is dropping the antioxidants around exercising. Now I'm wondering how much of an antioxidant I can get away with. I figure that things like C, E, and lipoic acid are out, but what about GTE and Pomegranate extract? Resveratrol?

[JLL]

I'd leave green tea extract out as well.

[mitkat]

I've fully cut out all antioxidants for at least a few hours around workouts, foods and supplements with a high or exclusively antioxidant activity have been gone for a while, I can't say I've noticed too much of a change. Good thread

[nowayout]

Here's my anecdotal experience with antioxidants and exercise. For years I have been taking some form of antioxidants, and exercising. I have been on a strength and endurance plateau for some while. Things bumped up a couple years ago when I started taking ALCAR, but have been pretty steady since then. A couple months ago, I began skipping antioxidants on days that I exercise. Shortly after starting this, my endurance and strength shot up a lot. So much so that I thought the exercise bike I was using was broken, and I switched to another one. The only change I can pin this on is dropping the antioxidants around exercising.

Very interesting. By the way, what have your experiences been with ALCAR? I also take ALCAR, although probably at too low a dose to make much difference to exercise. There seems to be quite a bit of anecdotal evidence for ALCAR, LCT and PLCAR (sometimes at rather high doses, though) on bodybuilding boards, but I am wondering if these might not also blunt endogenous adaptations to training by analogous mechanisms as those proposed for antioxidants (by making things too easy on the body), even though these are not antioxidants (or are they? - I can't find a straight answer). It also worries me a little that there are claims that at least some of the carnitines may affect testosterone metabolism in some way - if true, one might imagine worrying about withdrawal effects upon cessation (like for steroids).

Edited by andre, 18 February 2009 - 01:15 PM.

[quarter]

Here's my anecdotal experience with antioxidants and exercise. For years I have been taking some form of antioxidants, and exercising. I have been on a strength and endurance plateau for some while. Things bumped up a couple years ago when I started taking ALCAR, but have been pretty steady since then. A couple months ago, I began skipping antioxidants on days that I exercise. Shortly after starting this, my endurance and strength shot up a lot. So much so that I thought the exercise bike I was using was broken, and I switched to another one. The only change I can pin this on is dropping the antioxidants around exercising. Now I'm wondering how much of an antioxidant I can get away with. I figure that things like C, E, and lipoic acid are out, but what about GTE and Pomegranate extract? Resveratrol?

This seems placebo like to me:

1. You mention twice in the one post about the addition/subtraction of a supplement(s) significantly impacting your endurance performance, suggesting you may have had a pre-conceived notion that the act of doing so would affect such.

2. I'll freely admit before making this point that I haven't delved into the literature on this, I haven't even read all the abstracts at the top of this thread (a paradoxical combination of busyness and laziness) , but is it not the case that oral anti-oxidant supplementation is supposed to alleviate some of the stresses of the exercise hence limiting the body's adaption response? If my understanding is correct then oral anti-oxidant supplementation should positively affect any individual exercise performance but negatively affect long term training adaptions, therefore an acute improvement in endurance performance would seem unlikely to be due to the dropping of the anti-oxidants. (I could have misunderstood the anti-oxidant exercise relationship though).

3. Your marker for the improvement in endurance seems to be your own perception of the level of difficulty of an exercise bike session - perceived endurance improvement without quantitative values would seem to be particularity susceptible to the placebo effect.

[zorba990]

Here's my anecdotal experience with antioxidants and exercise. For years I have been taking some form of antioxidants, and exercising. I have been on a strength and endurance plateau for some while. Things bumped up a couple years ago when I started taking ALCAR, but have been pretty steady since then. A couple months ago, I began skipping antioxidants on days that I exercise. Shortly after starting this, my endurance and strength shot up a lot. So much so that I thought the exercise bike I was using was broken, and I switched to another one. The only change I can pin this on is dropping the antioxidants around exercising. Now I'm wondering how much of an antioxidant I can get away with. I figure that things like C, E, and lipoic acid are out, but what about GTE and Pomegranate extract? Resveratrol?

I'd have to say the opposite is true for me where NAC, Vitamin E and especially Vitamin C is concerned.
I take extra Vitamin C on workout days, up to 5-6 grams (as opposed to 2 grams on rest days), and extra vitamin E (1200iU alpha plus two LEF Gamma- Es)
I try to follow Colgan's Optimum Sports Nutrition recommendations.

But everyone has to find out what works for them.

[ksbalaji]

Thanks for the excellent discussion.

I read that new research by universities of Queensland and Melbourne shows that half-an-hour in the gym will not make up for the waist-expanding damage caused by spending the rest of the day sitting. The study measured the intensity of physical activity in 168 subjects over seven days. It found that, regardless of how much moderate-to-vigorous exercise they did or their total sedentary time, those who took more breaks from sitting had lower waist circumferences, lower body mass indexes and lower levels of triglycerides and glucose in blood. The study joins the growing body of evidence suggesting too much sitting might undo the benefits of exercise. But the good news in the report is that pottering about the house or gently walking around the office while on the phone might be enough to keep one fit.

This information is gathered at:
http://www.hinduonne...00902241731.htm

Now I have an important (or may be silly?)question. With all this information and motivation, why do people skip regular exercise? Why do we just lean on lame excuses like "no time available, busy schedule, forgot the appoinment, etc.,?"

I confess. I am sedentary. And still trying to join the regularly exercising lot. I also wonder how many imminsts are sedentary and trying to come out of it.

[tunt01]

I confess. I am sedentary. And still trying to join the regularly exercising lot. I also wonder how many imminsts are sedentary and trying to come out of it.

I'm working to overcome my rather sedentary past lifestyle. Although your msg is a few weeks old now, I thought I would let you know a lot of us are trying to improve total and health and just drop you a few of my own thoughts.

I think the biggest issue is to constantly keep moving. Hence my daily goal right now is:

1. 45 mins - 1 hr of cardiovascular upon wake
2. 20 mins walk after lunch
3. 30 mins - 1 hr of cardio after work before dinner.

i work at a desk job as a researcher and unless i buy one of these:

http://www.treadmill-desk.com/
http://store.steelca...;utm_medium=cpc

then i have to try to keep my metabolic up rate throughout the day through other methods. getting up to walk around and move every hour or so is a good idea.

[czGLoRy]

Maybe taking oxidants before exercise would be beneficial ?
this is quite interesting, I wonder how long exactly one would need to stop taking antioxidant supplements before exercising (or after?) from negating the benefits of exercise.

standing while using your computer (great for when simply reading forums, not doing anything too interactive and the such) burns roughly 70 calories an hour and your body reacts drastically to the simple change. I can't find the article related to this, but will post it here if I find it, its pretty interesting. A WOW player lost a huge amount of weight using a bicycle pedal device that fits under the computer. The treadmill is also a good idea.

[Nate-2004]

So I've noticed a negative change over the last week or so after including more antioxidants in my supplements.

 

In the mornings I take anywhere from 250 to 500mg of NR and on Wednesdays I take 1g. In the afternoons I take 250. With this I take Pterostilbene/Resveratrol 50/200mg, honokiol 200mg, C60OO up to 20ml (14mg) in the morning for 5-7 days every couple of weeks.

 

At first my workouts were great, but now my workouts are feeling really sluggish. Prior to taking these I sometimes had sluggish days, but they were 1 in 9 work outs, now it's every day. It's really tough for me to get my heart rate up to the target (161) and I feel like I'm working a whole lot harder to do that. Someone said that antioxidants are bad for workouts. Is it possible that I need to do my workout in the mornings before taking any of this stuff, or take a couple weeks off to recycle? 

 

What's the best strategy for balancing exercise with antioxidants given all of the original poster's references?  He concludes that it's a choice of either or and to side with exercise. I have my doubts about that because while exercise may be hugely beneficial and will slow aging, it was certainly not helping in the same way nor to the degree that the above cocktail I mention is helping me in many other areas outside of exercise.

 

Edited by Nate-2004, 06 June 2016 - 02:16 AM.

[normalizing]

green tea was claimed to help with excercise, dear lord did that crap never help at all. i know i know its only one case, but hell, did this shit was too obvious not to mention! it will turn you into some type of a zombie, it just completely inhibited all that felt good about sweating.

[shifter]

I thought that exercising increased the need for antioxidants

 

In exercise, my metabolism is working a lot faster, my breathing more heavy and more often. Now, if I were running on a beautiful alpine mountain with no pollution around, great. But if I were running or cycling next to a road with endless petrol and diesel fumes from traffic around me, perhaps the added antioxidants coupled with my increased rate of breathing and metabolism working harder and faster is a good idea.

 

You can of course live without antioxidant supplementation. You cant really 'live' without exercise. But for the best of good health I think both are crucial.

[Nate-2004]

It might increase the need for them but at the same time it appears to be negatively affected by them because exercise involves oxidation that's quite necessary during strenuous activity.

[nowayout]

I thought that exercising increased the need for antioxidants

 

In exercise, my metabolism is working a lot faster, my breathing more heavy and more often. Now, if I were running on a beautiful alpine mountain with no pollution around, great. But if I were running or cycling next to a road with endless petrol and diesel fumes from traffic around me, perhaps the added antioxidants coupled with my increased rate of breathing and metabolism working harder and faster is a good idea.

 

You can of course live without antioxidant supplementation. You cant really 'live' without exercise. But for the best of good health I think both are crucial.

 

Exercising in traffic fumes might be worse than not exercising. Taking antioxidants is unlikely to protect you much from diesel pollution. If you don't have access to clean outside air I'd rather join a gym with good air conditioning. 

[Nate-2004]

Today I experimented with not taking antioxidants till after my workout. It's an n=1 and one data point experiment so far but I didn't feel nearly as sluggish and most of the latter half of the workout was quite easy by comparison to identical workouts the days before. So I think my plan is to do my workouts first part of the day and save the stack I have for the latter half of the day.

[shifter]

I always figured their would be no positive gain cycling to work if it meant inhaling traffic fumes (in a deeper and more rapid way) for an hour each way. Someone should tell the lycra brigade to get off the bike and into the car for the sake of their own health.

Edited by shifter, 07 June 2016 - 11:25 PM.

[nowayout]

I always figured their would be no positive gain cycling to work if it meant inhaling traffic fumes (in a deeper and more rapid way) for an hour each way. Someone should tell the lycra brigade to get off the bike and into the car for the sake of their own health.

 

Or better, tell all the drivers to get on bikes or public transport for everyone's health, including their own.

[Nate-2004]

Second day of refraining from antioxidants until after I've worked out was even better than the day before. My workouts are no longer feeling sluggish and like I'm low on energy or oxygen or something. I was able to hit my target heart rate pretty easily and stay there sailing through the end. I'm not counting this just yet but it looks like this is how it's done. I want to try one more day on Friday because I didn't take the C60OO yesterday. 

Edited by Nate-2004, 08 June 2016 - 06:46 PM.

[normalizing]

you should try green tea prior and after workout to compare results. i believe green tea really fucks with you when you excercise on it

[aconita]

The issues with antioxidants and exercise are about disrupting the process of super compensation, not about performance in the immediate.

 

Disrupting the process of super compensation means you don't get better, you stale, you don't improve over your actual levels.

 

For whom trains just for health reasons that might be irrelevant (likely just a waste of money) but for whom seeks improvements in performance (and/or possibly in hypertrophy) it might be something to keep in consideration.

 

The appropriate antioxidants might very likely enhance performances in the immediate.

 

 

 

 

[douglis]

So what kind of exercise has the greatest effect at the endogenous antioxidant status? Isometric training seems to be promising...

 

Short-term isometric exercise reduces systolic blood pressure in hypertensive adults: possible role of reactive oxygen species.

Peters PG1, Alessio HM, Hagerman AE, Ashton T, Nagy S, Wiley RL.

Abstract

OBJECTIVE:

A short-term isometric exercise protocol was tested in ten hypertensive individuals to determine its efficacy as a high blood pressure-reducing intervention.

DESIGN:

The study was a prospective case study of 10 hypertensive individuals (8 men, 2 woman, mean age = 52 + 5 years) who underwent six weeks of isometric exercise training (three sessions/week).

METHODS:

Blood pressure, blood lipids and markers of oxidative stress were monitored before, during and following the isometric intervention. Electron spin resonance spectroscopy was used to directly measure radicals in the blood samples.

RESULTS:

After six weeks, systolic blood pressure decreased an average 13 mm Hg (p < 0.05) from a mean blood pressure of 146 to 133 mm Hg, a level that is below the usual 140 mm Hg hypertension threshold. Blood lipids were unchanged, but markers of oxidative stress were affected, with a dramatic decrease in exercise-induced oxygen centered radicals (-266%), (p < 0.05) and an increased resting whole blood glutathione:oxidized glutathione (+61%) in hypertensive adults following six weeks of isometric exercise.

CONCLUSION:

Six weeks of isometric exercise training was effective in lowering systolic but not diastolic blood pressure in pre-hypertensive and hypertensive individuals, and enhanced antioxidant protection is a likely underlying mechanism.

 

[Nate-2004]

Months later and I'm still confused about all this.

 

There obviously needs to be more study in this area. I switched to drinking green tea in the morning because black coffee sucks with intermittent fasting. I also take GTE (EGCG) in the mornings to help with appetite. I don't know if any of this affects my workouts that occur later in the day (around 2 or 3pm on most days).

 

While I usually wait to take any supplements till after my work out, with a meal, I am still wondering about green tea in the mornings before afternoon workouts.

[Jiminy Glick]

 

So I've noticed a negative change over the last week or so after including more antioxidants in my supplements.

 

In the mornings I take anywhere from 250 to 500mg of NR and on Wednesdays I take 1g. In the afternoons I take 250. With this I take Pterostilbene/Resveratrol 50/200mg, honokiol 200mg, C60OO up to 20ml (14mg) in the morning for 5-7 days every couple of weeks.

 

At first my workouts were great, but now my workouts are feeling really sluggish. Prior to taking these I sometimes had sluggish days, but they were 1 in 9 work outs, now it's every day. It's really tough for me to get my heart rate up to the target (161) and I feel like I'm working a whole lot harder to do that. Someone said that antioxidants are bad for workouts. Is it possible that I need to do my workout in the mornings before taking any of this stuff, or take a couple weeks off to recycle? 

 

What's the best strategy for balancing exercise with antioxidants given all of the original poster's references?  He concludes that it's a choice of either or and to side with exercise. I have my doubts about that because while exercise may be hugely beneficial and will slow aging, it was certainly not helping in the same way nor to the degree that the above cocktail I mention is helping me in many other areas outside of exercise.

 

 

Where do you get your Honokiol?

[Nate-2004]

Liftmode but I cycle it and really only take it at night sometimes.

 

My stack has been refined quite a bit though and I've begun cycling a lot of things in and out with the stack because of the exercise/antioxidant issue among other reasons.

 

NR

Curcumin (cycled)

EGCG (maybe cycle this in on days w/o exercise I dunno)

D3

K

L-theanine

Taurine

Inositol

Magnesium

Ginger (cycled)

Fish oil & Krill oil

Tbsp EV olive oil (cycled)

Grape Seed Extract (cycled)

Rosmarinic Acid (cycled)

Honokiol (cycled)

 

[Nate-2004]

What I really came here for was to see what effect green tea has on both the benefits of exercise and the benefits of fasting related to autophagy. Seems most studies posted by the OP are unrelated to green tea and mostly related to C, E and NAC. Those are a different kind of antioxidants so not sure if it's the same or what.