/fit/ - Fitness, Health, and Feels

>>132140

>Is it better…

Better for what? What are you talking about, give some context you retard.

>>132142

For gains you blithering moron, what do you think?!

Bump

>>132146

gainz is gainz dude

>>132222

But which method will make faster gains?

>>132225

I heard lifting weights and supplementing testosterone, usually helps creating new muscle mass.

>>132225

Testosterone is gay, and fuck you if you take it.

Fastest gains are made by eating as much protein rich foods as you can, 2g of protein per pound of bodyweight, and lifting heavy shit and avoiding too much cardio. Some cardio is okay for healthy cardiovascular health though.

Get a pedometer so you can measure how much you've burned form walking, estimate how much you've lost from standing, jacking off, everything. Time it all up and look it up. You want to make sure you're eating more than 2k calories a day. A lot more. Fuck the fat:carb:protein ratio. GOTTA GET THAT PROTEIN!

Gongrats. Fuck you.

>>132228

not sure if serious or trolling

>>132229

Dead.

>>132140

gonna ignore the blatant stupidposting on the rest of the thread for a moment for an honest answer

I was talking to the trainer in gym the other day and he explained that for optimal muscle growth (aka gainz), you need to pile up cell damage right after the tissue recovered

that is, for regular average workout, not light but not too hard either, you will need at least a whole 2 day recover time, if you train earlier than that you can risk over training, if go later you lose effectiveness

the more you pile up without resting the better overall gain you will have, for muscle growth, but you can even lose some strength in the process, have to tone down weight a bit to be able to keep it up, and after a period of 2~ months, have a de-load week and rest up to avoid injury

I was checking this and trying to gather from several sources and it appears to be the common practice indeed for natural people

so you have 2 or 3 training schedules and alternate between them each day during the week, I assure you it gets tiresome, but the best gainz I've seen were like that

the alternative would be to train a group only once a week, but pile up volume to really make it worth, but to be worth it really has to be a lot

which usually only works well for really heavy weight builders, or people that juice up, most of the time both

>>132234

>I gotta stop coming here tbqhwyf. It's killing my gains. And it's not just here, /ck/, /k/, /v/, porn, whatever

I had the same feeling too, more like killing mah life

but at least I'm spending way less time shitposting, I rarely visit this hellhole of a board

>>132140

1-2 days seems to be the agreed upon optimum so if you want to focus on a particular area and you lift 3 times a week theres no reason not to do it every workout. While I wouldn't recommend say squating 7 days a week it also probably won't be detrimental just not a great use of your time and energy.

>>132234

>browses leftypol

>>132140

There is no hard answer to this question, but if one looks for it, many varied dogmas and doctrines can be found anyways. My reasoning is simple: in life you find both slow people and fast people, and sometimes the difference in speed between the two is not just significant—but several orders of magnitude. These differences at the macro level of whole organisms also occur at the levels of cells and tissues, so the rate of recovery of one person's muscles, tendons, and bones does not necessarily inform the rate of recovery of another person's. Asking about the experiences and strategies of others can inform on the average and the paths already taken, but it cannot inform on what one will make of his own path except for those who have decided to abandon individuality and to only emulate or at least fixate on what others are doing. Buying into X number of days for a recovery period clouds the mind from recognizing both potential ways to recover faster and hindered progress from recovering too slowly.

>>132257

Mitochondrial uncoupling and lifespan

>the ideal balance between nutrient uptake, its transduction into usable energy, and the mitigation of damaging byproducts can be regulated by mitochondrial respiration and output (ATP, reactive oxygen species (ROS), and heat). Mitochondrial inefficiency through proton leak, which uncouples substrate oxidation from ADP phosphorylation, can comprise as much as 30% of the basal metabolic rate. This uncoupling is hypothesized to protect cells from conditions that favor ROS production. Uncoupling can also occur through pharmacological induction of proton leak and activity of the uncoupling proteins. Mitochondrial uncoupling is implicated in lifespan extension through its effects on metabolic rate and ROS production.

…

>This “rate of living” hypothesis predicts that increased metabolic rate per gram tissue correlates with shorter lifespan and vice versa. However, multiple examples of size-matched and metabolic rate-matched animals with significantly different lifespans, both ectothermic and endothermic, have contradicted rate-of-living as the sole determinant of aging (e.g., rats/pigeons (Barja, 1998), snakes (Robert et al., 2007), bats/mice (Jürgens and Prothero, 1987), deer mice/lab mice (Ungvari et al., 2008), naked mole rats (O'Connor et al., 2002).

…

>In a different study, a tightly-coupled muscle group showed greater deterioration with age than a relatively uncoupled one (Amara et al., 2007).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2924931/

Effects of acute and chronic endurance exercise on mitochondrial uncoupling in human skeletal muscle

>When expressed per unit of CS (a marker of mitochondrial volume) UCP3 and UCR decreased by 54% and 18%(P < 0.05). CS increased by 43% after acute exercise and remained elevated after 3 h of recovery (P < 0.05), whereas the other muscle parameters remained unchanged.

…

>Previous studies in humans have shown that UCP3 mRNA expression is increased after acute exercise (Pilegaard et al. 2000) but unchanged after endurance training (Tonkonogi et al. 2000a).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664806/

Reduced mitochondrial coupling in vivo alters cellular energetics in aged mouse skeletal muscle

>The mitochondrial theory of ageing proposes that the accumulation of oxidative damage to mitochondria leads to mitochondrial dysfunction and tissue degeneration with age. However, no consensus has emerged regarding the effects of ageing on mitochondrial function, particularly for mitochondrial coupling (P/O).

…

>These results indicate a nearly 50% reduction in the mitochondrial P/O in the aged animals (2.05 ± 0.07 versus 1.05 ± 0.36, P= 0.02). The higher resting ADP (30.8 ± 6.8 versus 58.0 ± 9.5 μmol g−1, P= 0.05) and decreased energy charge (ATP/ADP) (274 ± 70 versus 84 ± 16, P= 0.03) in the aged mice is consistent with an impairment of oxidative ATP synthesis. Despite the reduced P/O, uncoupling protein 3 protein levels were not different in the muscles of the two groups. These results demonstrate reduced mitochondrial coupling in aged skeletal muscle that alters cellular metabolism and energetics.

Effect of triiodothyronine on mitochondrial energy coupling in human skeletal muscle

>Given the disproportionate increase in TCA cycle flux compared with ATP synthesis, these data suggest that T₃ promotes increased thermogenesis in part by promoting mitochondrial energy uncoupling in skeletal muscle.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC209375/

The ω6-fatty acid, arachidonic acid, regulates the conversion of white to brite adipocyte through a prostaglandin/calcium mediated pathway

>Brite adipocytes are inducible energy-dissipating cells expressing UCP1 which appear within white adipose tissue of healthy adult individuals. Recruitment of these cells represents a potential strategy to fight obesity and associated diseases.

>Methods/Results

>Using human Multipotent Adipose-Derived Stem cells, able to convert into brite adipocytes, we show that arachidonic acid strongly inhibits brite adipocyte formation via a cyclooxygenase pathway leading to secretion of PGE2 and PGF2α. Both prostaglandins induce an oscillatory Ca++ signaling coupled to ERK pathway and trigger a decrease in UCP1 expression and in oxygen consumption without altering mitochondriogenesis.

>Conclusion

>Our results suggest that dietary excess of ω6 polyunsaturated fatty acids present in Western diets, may also favor obesity by preventing the “browning” process to take place.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4264041/

>>132252

I DO NOT

All arms baby. Goal: keep arms on body, start lifting.