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Thanks Sibiriak, I really missed that I don't know why. I'm going to resume in the other more IT thread.

Edited by mccoy

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On the issue of antioxidants and exercise raised by Clinton  above (https://www.crsociety.org/topic/16873-clintons-stack/?page=2&tab=comments#comment-30806):

The Ability of Exercise-Associated Oxidative Stress to Trigger Redox-Sensitive Signalling Responses


Antioxidants (Basel). 2017 Sep; 6(3): 63.
Published online 2017 Aug 10. doi: 10.3390/antiox6030063
PMCID: PMC5618091 PMID: 28796154




* * * * * * * *

A consequence of applying the concept of “hormesis” to exercise-associated redox-sensitive signalling may be that removal of the original exercise-associated oxidative stress could prevent the subsequent beneficial response. Activation of redox-sensitive signalling, and achievement of training adaptations or improvements in health, have been reported as being evident in cohorts undergoing exercise, but absent or blunted in matched cohorts who underwent both exercise and concurrent dietary antioxidant supplementation [25,30,31,50,86,87,88,89]. Thus, antioxidant supplementation reduced or abolished exercise-associated skeletal muscle mitochondrial biogenesis [89]; improvements in insulin sensitivity [50]; activation of PGC-1α signalling in skeletal muscle [87]; PPARγ and LXRα target-gene upregulation in monocytes [31]; and training-induced adaptations in VO2max [25]. These findings have been obtained using a range of different antioxidants, both commercial pharmacological supplements and dietary regimes involving “natural” antioxidant-rich foodstuffs; for example, Ristow et al.’s original study [50] reported that oral administration of pharmacological antioxidant preparations (1000 mg/day Vitamin C (ascorbic acid, Jenapharm) and 400 IU/day Vitamin E (RRR-/D-α-tocopherol, Jenapharm)) blunted generation of oxidised lipids in exercising participants [50], while it has recently been reported that oxysterol generation in rat liver tissue following exercise was prevented by co-administration of an antioxidant-containing broccoli extract-enriched diet [90].

However, there is a lack of consensus in the literature in this regard. As shown in Table 1, a review of selected studies that have investigated co-administration of exercise and dietary antioxidant supplementation reveals studies in which antioxidant supplementation blunts exercise-associated effects [25,30,31,50,87,89], studies in which antioxidant supplementation enhances exercise-associated effects [91,92,93], and studies in which antioxidant supplementation appears to have no impact on exercise-associated effects [94,95,96,97,98]. Nikolaidis [99] has suggested the following as potential explanations for this lack of accord: variability in training regimens and/or in antioxidant supplementation protocols, the inherent complexity of redox biochemistry at an organismal level, and the diversity of the cohorts participating in the different studies. Scrutiny of Table 1 is in accord with these suggestions; for example, Ryan et al. reported different effects of antioxidant supplementation with regard to improved capacity for positive work in the muscles of young versus aged rats following a programme of maximal muscular contractions [91]. The complexity and variety of methodologies by which redox biochemistry is assessed, and the numerous different biomarker approaches used to evaluate health (see columns 5 and 6 of Table 1), should also be mentioned in this context. In a commentary article [100], Gomez-Cabrera et al. have highlighted differences in methodological approach (and in identification of which outcomes should best be focused on) between studies reporting antioxidant-induced blunting effects [25,50,89] and those reporting an absence of such effects [94,96,98]. It is to be hoped that future research will ultimately establish a stronger consensus as to the best approach to use in any given context, and so avoid such methodological conflicts in future. But at present, it must be acknowledged that these methodological heterogeneities hinder clear evaluation of the available data.

Additionally, inter-species differences (given that animal models are frequently used), and differences within exercising human cohorts concerning traits such as genetic predispositions and acquired characteristics, should also be considered. For example, elite athletes’ endogenous antioxidant defence systems may be so highly developed that they leave little scope for “improvement” by dietary antioxidant supplementation, whereas this may not be the case for non-elite participants [99]. Given that a significant number of athletes consume vitamin supplements seeking beneficial effects on sporting performance [101], such findings need to be accounted for when designing exercise programmes, particularly with regard to considering the dietary Vitamin C/Vitamin E intake of exercising participants. A sensible recommendation would be to evaluate individuals’ basal oxidative status (and dietary antioxidant intake) before making decisions as to whether antioxidant supplementation is appropriate.

A major source of the lack of consensus in the literature appears to be the multifactorial nature of exercise’s impact on human physiology, and the diversity of the contexts in which exercise may exert effects on participants’ physiologies. Table 1 shows that in the majority of cases, non-exhaustive exercise-triggered increases in mitochondrial biogenesis, redox-signaling pathways such as those involving PPARγ/PGC-1α, and endurance time are blunted by antioxidant supplementation [25,31,50,87,89].

However, studies which used very intense exercise regimens and/or investigated different parameters such as VO2max, cytokine release, blood cell counts, tissue damage, and performance in non-endurance exercise tended to report an absence of antioxidant-associated blunting of exercise adaptations [94,95,96,97,98], or even antioxidant-associated enhancements of adaptations [91,92,93].

On balance, the literature appears to justify the view that redox-sensitive signalling effects (which are blockable by dietary antioxidants) are linked to moderate exercise’s ability to increase mitochondrial biogenesis and improve anti-oxidant and anti-inflammatory status, which points to their value in enhancing endurance performance, and management of chronic inflammatory conditions. As stated above, such effects are clinically important, as they can be used in settings such as community-based exercise [47] and exercise-referral [56] to bring benefits to patients with overt chronic inflammatory diseases [56,61].

However, where studies involve very intense/exhaustive exercise, or focus on outcomes such as muscle damage or power generation in resistance training, it appears that mechanisms distinct from redox-sensitive signalling may be predominant, and hence that these effects are not as susceptible to blunting by dietary antioxidants

* * * * *

[...] A further complication is the contrast between exogenous antioxidants such as Vitamins C and E and endogenous antioxidant systems. Use of supplementation which boosts the latter has recently been proposed as a potentially more effective strategy [2]. Specifically, supplementation with thiol-donors such as N-acetyl cysteine (NAC), whose ability to attenuate reduction of glutathione may prevent systemic oxidative stress and hence increase performance-related parameters such as power output and time-to-exhaustion in athletes [92,93], but possibly without preventing the original local stimulus which initiates redox-sensitive cell signalling responses. Accordingly, given that in some individuals oral or systemic administration of NAC can be poorly tolerated [2], alternative dietary sources of thiols such as taurine and hydrolysed keratin have been recommended [2,112]. However, it should be noted that in another study, NAC supplementation did conform to the hormesis principle by attenuating early adaptive responses to exercise in human skeletal muscle [88].

Edited by Sibiriak

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Update as of July 12, 2019:

I use the cronometer app to inform me which micronutrients I require to be topped-up to at least RDA levels using supplements.  Based on this and having reviewed several others' stacks I take the following supplements:

(The intent of this stack/regimen is to maximize healthspan & lifespan)


8 am AND 3pm (I take each item listed below 2x per day)

AOR Multi-Basics3  1 capsule (serving size is 3 per day)

45mcg of vitamin K2-MK7 1 capsule (Doctor's Best)

ZMA 1 capsule (NOW brand) (this is 5mg of B6 pyridoxine, 150mg Magnesium Aspartate and 10mg Zinc)

720mg Fish Oil 1 capsule (440 EPA 280 DHA) yeah it's Kirkland (kept in the freezer)

420mg of Phosphatidylcholine 1 capsule (provides 57mg choline)

750mg Glucosamine Sulfate 1 capsule (Kirkland)

Additional vitamin D3 to bring the total to approx. 2000IU per day - fwiw I live in Canada and don't get allot of sun.

I drink 2-3 cups of black coffee per day

ALL of my vitamins & mineral intake are at or above RDA levels


In my 8am AND 3pm smoothie I add the following (I consume the following 2x per day):

1/4 cup of total nuts about 50/50 mix of almonds & walnuts

1/4 cup of plain rolled oats

1 tbsp of ground flaxseeds (Webber from Costco - kept in the freezer)

1/4 cup frozen blueberries, 1/4 cup frozen raspberries

1/4 tsp Ceylon cinnamon, 1/4 tsp Creapure creatine (approx. 1g), 1/4 tsp beta-alanine (approx. 1g)

1/4 tsp taurine (approx. 750mg), lithium orotate approx. 0.5mg

½ cup plain kefir and ½ cup water

I eat all meals prior to 3pm and thus within about 7 hours per day; thus practicing 'Time Restricted Feeding' something like 17-7 daily


Maintain BMI of 22.5 with almost zero visceral fat – but aiming for a lower BMI; doing resistance training a few days per week and decent level of strength.  Sleep well each night often using a sleep mask & ear plugs ...


My meals between those smoothies are lots of beans & greens; chickpeas, black beans, green peas, broccoli, carrots, kale, spinach, onions, avocado, sweet potato, low-sodium V8 juice ... and typically a banana and an apple or other fruit.  I end up eating eggs and sardines for protein daily. 

I never eat less than 40g per day of fiber according to the Cronometer app; typically 50g per day; My Omega 6:3 intake ratio is approx. 2:1, Cu:Zn intake ratio approx. 1:10



After several years of staying lean, ensuring optimal nutrition and heavy resistance training, I am FINALLY adjusting to trying to actually adopt CRON in conjunction with 17-7 time-restricted feeding.

Also have completely re-evaluated my protein intake and am reducing protein to below 20% of total caloric intake.


I am interested to see with fewer calories and protein the effect on muscle size & strength.

Edited by Clinton

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