I have in the past and still do resoundingly endorse Fasted Training. I give explanations in the following thread via discussions, that are worth a quick glance. First, here is a quick explanation with the full fasted-layout:
Here is the Fasted Training Protocol I created for B5150:
Upon Rising: Fasted
USPLabs Recreate™ - 2 caps
USPLabs PowerFULL™ - 3 caps
USPLabs AnabolicPump™ - 1 cap
SupperCissus Rx™ - 1g cap
+30 mins later intra w/o drink:
Xtend BCAA - 12.5g
NutraPlanet Leucine - 7g
NutraPlanet Beta Alanine - 3g
NutraPlanet Creatine Mono - 2.5g
Immediately following last set: 1 P-Slin
Immediate Post Work Out Shake:
Xtend BCAA - 12.5g
NutraPlanet Leucine - 7g
NutraPlanet Beta Alanine - 3g
NutraPlanet Creatine Mono - 2.5g
NutraPlanet KWICK KARB™ (Waxy Maize Starch) - 25 to 30g*
Crushed Oats - 60 - 90g
Second Post Workout Shake/Meal:
Ground oats - 25g*
Whey Protein Isolate - 50g
Throughout the day:
USPLabs PowerFULL™ - 2 caps
USPLabs AnabolicPump™ - 1 to 2 caps as needed
USPLabs Recreate™ - 1 to 2 caps as tolerated
SuperCissus Rx™ - 1g cap x 2
Explanation:
Anabolic Pump is often conceptualized as merely a supplement of glucose homeostasis. While that's true in part, its true identity is one of energy metabolism as a whole; specifically, mitigating energy expenditure and transfer in both fat and muscle cells, via the modulation of energy storage and production mechanisms.
During a long bout of exercise (i.e., an hour long resistance training session) your body's energy homeostasis mechanisms need to take on a more oxidative (the B-oxidation of fatty acids) as opposed to glycolytic (GLUT4 translocation and glucose storage) role. This is due in part to the inability of the body to produce the fuel (glucose) for anabolic processes at the rates needed for anaerobic exercise. In response, your body has in place several mechanisms which prevent the accumulation and synthesis of triglycerides and lipids, and release them into the bloodstream to be oxidized.
These lipolytic processes actually contribute to the majority of energy transaction in a bout of anaerobic exercise - the oxidation of fatty acids and plasma triglycerides, primarily, provide the energy for resistance training.
The reason I mention all this is Anabolic Pump's fascinating ability to regulate one of the vanguards of oxidative and glycolytic energy consumption - AMPk. AMPk works as an essential gate-keeper of energy production, reacting to extracellular fluctuations of various downstream energy messengers (AMP:ATP ratio included). Its activation is responsible for various roles, including all of the above mentioned.
Using such a product in conjunction with fasted cardio simply utilizes energy which would have been stored anyway. The mere presence of AMPk ensures that the liberated fatty acids and triglycerides will be oxidized as it plays a primary role in not only lipolysis, but the inhibition of lipid, triglyceride, and cholesterol synthesis.
In terms of blood glucose, you should have circulating plasma levels which are enough to stave off hypoglycaemia, even with the use of Anabolic Pump. As carbohydrates have not been ingested, the presence of Insulin (the main inducer of hypoglycemia) is not necessarily present. Anabolic Pump works through Insulin-reactive, though not dependent, pathways of energy metabolism. The lipolytic role is also enough to provide ample energy.
Here are the threads:
http://anabolicminds.com/forum/nutrition-health/112791-why-you-shouldnt-2.html
http://anabolicminds.com/forum/supplement-reviews-logs/112127-bigger-faster-stronger-15.html
[pages 15 and 21-23]
An explanation of why AP is beneficial whilst in Ketosis - and, essentially, by fasted training you transiently shift your body into processes that mirror those of Ketosis:
AP also significantly contributes to the processes of Ketosis. Ketosis is the hydrolyzation of stored triglycerides into Fatty Acids, via the process of lipolysis; in fact, Anabolic Pump directly regulates lipogenic processes via AMPk induction, and would significantly contribute to plasma FA levels - thereby used for fuel in the absence of glucose; the inhibition of cholesterol and triglyceride biosynthesis - beneficial because Ketosis is attempting to complete the exact opposite; preventing the redepositing and accumulation of lipids - via exerting transcriptional control over lipid binding genes such as PPAR-y through co-activator inhibition (and its target enzymes); as well as ensuring increased mitochondrial FA oxidation - through inhibiting ACC (acetyl-CoA-carboxylase which inhibits the morphing of acetyl-CoA to malonyl-CoA), as well as directly increasing malonyl-CoA-decarboxylase, and ultimately raising levels of CPT-1; the rate limiting enzyme for mitochondrial FA oxidation.
In all respects, AP contributes to the processes of Ketosis significantly, whereas R-ALA would necessarily be counterintuitive to a Keto-based diet.
and....
Ketosis is simply the process of your body hydrolyzing (chemical breakdown via the interjection of a water molecule to form two end products, or the reaction of a substrate with water) stored triglycerides (fatty acid chains combined with a glycerol, and the body's primary source of stored adipose) to be used as fuel; Ketosis is the recognition by your body of chronic starvation. It therefore causes lipolysis (breakdown of stored triglycerides into respective fatty acids and glycerol molecules) in order to provide fuel in the absence of glucose (your body uses these as fuel via B-Oxidation). AP is beneficial, because it will expedite (speed up) this process due to its direct interconnectivity with many of the above mentioned processes.
a) It increases levels of CPT-1. CPT-1 is the rate-limiting (controls the rate at which a process can occur) enzyme of B-Oxidation (the oxidizing of fatty acids to be used as fuel), and increasing it increases the amount of lipids your mitochondria will use as fuel. This is important, because even during Ketosis where lipolysis (break up of TG into FAs) is occurring, if you do not oxidize (burn) the FAs, they will simply redeposit.
b) On the note of redepositing, AMPk inhibits the accumulation and synthesis of TGs and cholesterol. Why is this beneficial, and tied into the above point? Because if the redepositing of lipids is inhibited, they will be forced to circulate the bloodstream continually; with the increasing of CPT-1, the possibility is increased they will subsequently be oxidized.
Now, as I said, R-ALA is not an anti-lipogenic (compound which inhibits the accumulation, differentiation, or biosynthesis of lipids) and would not assist as greatly as AP would on a "carb-up" during Ketosis. The primary goal of Ketosis is releasing stored triglycerides into the bloodstream to be oxidized: AP accomplishes this. The fundamental step to remaining in Ketosis is low blood sugar levels: AP accomplishes this.
