I’m trying to get my head around whether my daily antioxidant supplements are likely to interfere with muscle building. (Yes, I know that stimulating MTOR is counterindicated for longevity, but I’d like healthspan as well.)
Right now I am daily taking GlyNAC (6g glycine and 100g NACET which supposedly is 1-2g NAC equivalent) and starting this summer 12mg astraxanthin (for the sun protection but not sure if it does anything there, plus it is touted for many longevity and protective effects). Both are strong antioxidants, and I’m not sure either are doing anything. But when I lift weights, isn’t the signalling that my body should make more muscle a Reactive Oxidative Species (ROS)? So won’t having ample antioxidants flowing through by blood blunt these potentially positive impacts (including mitochondrial biosynthesis)? (I was ignorant to the fact that many weightlifters take vitamin C to aid their recovery.)
So what do you think? Should I drop astraxanthin on heavy lifting days? Should I drop GlyNAC on heavy lifting days? Should I drop either/both altogether? Should I stay the course? My gut is to drop astraxanthin (as the original intent was sun protection and it seems to be nil) and keep GlyNAC.
I must say if I am blunting mitochondrial biosynthesis with use of antioxidants, this could be a highly negative outcome: isn’t mitochondrial health a key marker for longevity (and healthspan)? That seems counterproductive for me.
There is building evidence that antioxidant supplementation can attenuate endurance training‐induced and ROS/RNS‐mediated enhancements in antioxidant capacity, mitochondrial biogenesis, cellular defence mechanisms and insulin sensitivity. However, this is not a universal finding, potentially indicating that there is redundancy in the mechanisms controlling skeletal muscle adaptation to exercise, meaning that in some circumstances the negative impact of antioxidants on acute exercise response can be overcome by training. Antioxidant supplementation has been more consistently reported to have deleterious effects on the response to overload stress and high‐intensity training, suggesting that remodelling of skeletal muscle following resistance and high‐intensity exercise is more dependent on ROS/RNS signalling. Importantly there is no convincing evidence to suggest that antioxidant supplementation enhances exercise‐training adaptions. Overall, ROS/RNS are likely to exhibit a non‐linear (hormetic) pattern on exercise adaptations, where physiological doses are beneficial and high exposure (which would seldom be achieved during normal exercise training) may be detrimental.
Experimental evidence does not support the “common knowledge” that antioxidant treatment greatly improves exercise performance and recovery. On the contrary, studies with antioxidant supplementations generally show no effect on muscle function during and after exercise. The exception is NAC treatment, which has been found to improve performance during submaximal exercise. The limited effects of ROS/RNS and antioxidants during exercise are unexpected in that increases in ROS/RNS are likely to occur and these are potentially harmful. It appears that muscle fibers are in some way protected against deleterious effects of oxidants during exercise and fibers are generally much more sensitive to exposure to oxidants in the rested state than during fatigue. For instance, experiments on single mouse muscle fibers have shown that application of 10 μM hydrogen peroxide did not affect fatigue development (Place et al., 2009), whereas concentrations as low as 100 pM hydrogen peroxide affected contraction and Ca2+ handling in rested fibers (Andrade et al., 2001). Thus, numerous questions remain to be answered in relation to the effects of oxidants during and after exercise.