When lifting any weight, you’ve got a concentric (hard) and eccentric (easy) phase. For instance, as you lower into a squat, you’re performing an eccentric action. When you return to standing, that’s concentric. And, according to research published in the European Journal of Applied Physiology, eccentric work is far better at triggering hypertrophy.
This is why I never understand why girls who don’t want to “get bulky” are told by trainers to do 3 sets of 10-12 (or 5 sets of 1,000 reps of bicep curls with a 1 lb pink dumbbell). While it’s difficult for women to gain any sort of size lifting in ANY rep range, if we were trying to gain muscle size, that’s EXACTLY what we would want to do (as it would be causing sarcoplasmic hypertrophy).
While most of these muscle building supplements can be taken at any time of the day, some are best to include in your pre-workout routine. Citrulline malate, in particular, is one that should be taken about an hour ahead of your workout. Because this supplement boosts performance, taking it ahead of your workout will maximize its effect, making sure you get the most out of the supplement.
Other supplements could easily have been included here, but these are considered the most useful and effective for the majority of bodybuilders and athletes. Although food should always come first, supplements offer an effective alternative for getting nutrients that either aren't available in sufficient quantity in food or are in foods that you may not be eating.

Contrary to certain rumors that animal-based protein is more suitable to trigger muscle growth than plant-based protein, a study by Mangano et al. (2017) could not provide any evidence for this. In contrast, if combined properly, plant-based protein can even have a higher biological quality. A combination of one part wheat protein (e.g. seitan) and two parts soy protein (e.g. tofu) has thus been favored by many bodybuilders. Some bodybuilders, such as Patrik Baboumian and Robert Cheeke, follow a strict vegan diet.[37]
To do dips, place your hands at shoulder-width apart on a bench, with your body and feet stretched out in front of the bench. Slowly bend your elbows and lower your body down so that your butt nearly touches the floor. Lift back up with your arms to starting position; repeat, doing 3 x 8. If this isn't a high-intensity set for you, increase the resistance by lifting one foot off the floor.
In young rats given creatine in the diet at 2% of the diet for eight weeks, supplementation appears to increase bone mineral density (BMD) in the lumbar spine with a nonsignificant trend to increase BMD in the femur.[426] Despite the trend, the femur appeared to be 12.3% more resistant to snapping from mechanical stress associated with increased thickness.[426] Menopausal rats (ovarectomized) experience similar benefits, as supplementation of creatine (300mg/kg) for eight weeks during ovarectomy is able to increase phosphorus content of the bone and other biomarkers of bone health, although bone stress resistance was not tested.[427]
In regard to the blood brain barrier (BBB), which is a tightly woven mesh of non-fenestrated microcapillary endothelial cells (MCECs) that prevents passive diffusion of many water-soluble or large compounds into the brain, creatine can be taken into the brain via the SLC6A8 transporter.[192] In contrast, the creatine precursor (guanidinoacetate, or GAA) only appears to enter this transporter during creatine deficiency.[192] More creatine is taken up than effluxed, and more GAA is effluxed rather than taken up, suggesting that creatine utilization in the brain from blood-borne sources[192] is the major source of neural creatine.[193][192] However, “capable of passage” differs from “unregulated passage” and creatine appears to have tightly regulated entry into the brain in vivo[193]. After injecting rats with a large dose of creatine, creatine levels increased and plateaued at 70uM above baseline levels. These baseline levels are about 10mM, so this equates to an 0.7% increase when superloaded.[193] These kinetics may be a reason for the relative lack of neural effects of creatine supplementation in creatine sufficient populations.