I am studying for step1. I got really confused by the different types of receptors/ naming of currents related to potassium in the action potentials of the cardiac myocytes.
phase 1 : transient potassium efflux. according to electrochemical gradiant. through which channels?
phase 2 : which channels are responsible for K+ efflux, and Ca++ influx counteraction during plateau. I read It's voltage gated. Is it the same in phase 1? is it the delayed rectifier type? what does that actually mean?
phase 3 : delayed rectifier potassium channels? are they the only ones responsible for the repolarization? as I read in another source that Inward rectifier channels are also responsible.
phase 4 : what actually is I(k1) is it through inward rectifier channels?
I got lost in some of the details so please if anybody can explain to me or give an accurate resource. as I read some contradicting ones out there. thanks in advance.
Grab a cup of coffee cuz this is a long one.
A program review that isnt SBS/RP/Smolov! Thats a new one! This is for bodybuilding purposes and i know a majority of you train for strength, but i enjoy the training discussions on this sub so i thought this would be a great place for this.
First and foremost: My spreadsheet for the program which includes the podcast episode this program is based off of by Alex Kikel. The guts of this program is pretty much set up how its described, but I made adjustments based off how I like to train and taking things i learned that work for me through many years of different programs. Particularly big influences in this are John Meadows, Broderick Chavez, Justin Harris, Joe Bennett, and Mike Israetel.
For those that dont want to waste their time listening to the podcast, its rather simple and i shall write it out.
Phase 1:Alarm/Glycolytic Upregulation (Volume Accumulation). You start at 80 sets a week and add 5 sets a week until you reach peak volume of 120 sets. Load only increases when designated reps are hit on all sets.
Phase 2: Alactic Improvement ("Strength" Block). Priority is to increase load as often as possible, rather than reach the top end of rep scheme.
Phase 3: Myocyte Maturation ("Intensity" Block). Added drop sets throughout the rest of the training block. Work through rep ranges again rather than prioritizing load.
All of this is accomplished throughout 16 weeks, followed either by a deload and a restructure or how im going through it with a "bridge." More on this later. Alex Kikel used big science words and biology and physiology to come up with how the training program is worded and set up, but i think it really can just be named more simply with the terms i put in parentheses. He also puts a disclaimer in his podcast that he knows hes not using the words exactly correctly but it gets his point across of what theyre trying to achieve, just in case anyone was about to have a hissy fit about the terminology which is also why i just think my terms leave less headache.
Background Info:
Age: 29, training since 21 so about 8 years on the dot today.
Height: 5'10, but used to say i was 6' back in college.
Start of blast: 300mg/600mg/3ius Test/Deca/GH (M-F only)
Mid Blast: 250mg/600mg/50mg/2ius Test/Deca/Adrol/GH (M-F only)
End Blast: 250mg/600mg/300mg/2ius Test/Deca/Mast
... keep reading on reddit β‘In my understanding, action potential means depolarization. It depends on Na influx and represented by QRS complex
Action potential duration means the time from depolarization to repolarization. It depends on K channels and is represented by QT interval. It also determines the effective refractory period.
And conduction velocity is the speed with which this action potential/depolarization wave transfers to next cells. It depends on the magnitude(?) of the Na influx during phase 0.
Am I understanding it correct? Really grateful for any response.
Hi everyone, I have a question that came up while researching inactivation gates on Na+ channels.
From reading Goldin (2003) "Mechanisms of sodium channel inactivation," it seems that some Na+ channels have a time-dependent inactivation channel that closes during the depolarization phase of an action potential. My question specifically pertains to the mechanics of these inactivation gates during a state of extracellular hyperkalemia. In this paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/, on figure 3 we see an overlaid cardiac action potential of a normal potential and one that occurs in hyperkalemia. I understand from the GHK equation that hyperkalemia would cause an elevation in cell resting membrane potential, but what I am having trouble understanding is why the peak reached by both actions potentials are the same, to ~+30mV. The authors state that "The membrane potential at the onset of depolarization determines the number of sodium channels activated during depolarization, which in turn determines the magnitude of the inward sodium current and the Vmax of the action potential. " Linking this with my understanding of the inactivation gates, I understand this statement to mean that in a higher than normal cell resting potential environment, less Na channels are able to participate in an action potential due to failure to "reset" the inactivation gate, which is directly dependent on cell repolarization. If there are less Na channels participating in phase 0 of the action potential and if inactivation gates are time-dependent, why then, do both phase 0s reach +30mV? Shouldn't the hyperkalemia AP be lower than +30mV because less total Na+ influx would have been achieved before inactivation gates closed due to less Na channel participation?
Iβm designing an experiment where I need to simulate an action potential to a single cardiac myocytes to stimulate calcium fluctuations.
https://www.sciencedirect.com/science/article/pii/S0003986118305447
Highlights
- The ketone body Ξ²-hydroxybutyrate can be utilized by the heart.
- Its effects on single cell excitation-contraction coupling has not been studied.
- Acute perfusion of Ξ²-hydroxybutyrate does not affect excitation-contraction coupling.
- Culturing myocytes with Ξ²-hydroxybutyrate improves excitation-contraction coupling.
Abstract
Ξ²-hydroxybutyrate is the primary ketone body produced by the body during ketosis and is used to meet its metabolic demands. The healthy adult heart derives most of its energy from fatty acid oxidation. However, in certain diseases, the heart alters its substrate preference and increases its ketone body metabolism. Little is known about the effects of Ξ²OHB on ventricular myocyte excitation-contraction coupling. Therefore, we examined the effects of ketone body metabolism on single cell excitation-contraction coupling during normoxic and hypoxic conditions. Myocytes were isolated from adult rats, cultured for 18β―h in RPMI 1640, RPMI 1640 no glucose, and M199, HEPES with/without various amount of Ξ²OHB added. To simulate hypoxia, myocytes were incubated at 1%O2, 5% CO2 for 1β―h followed by incubation at atmospheric oxygen (21%O2,5% CO2) for 30β―min before recordings. Recordings were obtained using an IonOptix system at 36Β±1α΅ C. Myocytes were paced at 0.5, 1, 2, 3, and 4β―Hz. We found that exposure to Ξ²OHB had no effect on excitation-contraction coupling. However, culturing cells with Ξ²OHB results in a significant increase in both contraction and calcium in RPMI 1640 media. Dose response experiments demonstrated 0.5β―mM Ξ²OHB is enough to increase myocyte contraction in the absence of glucose. However, Ξ²OHB has no measurable effects on myocytes cultured in a nutrient rich media, M199, HEPES. Therefore, Ξ²OHB improves single cell excitation-contraction coupling, is protective against hypoxia, and may
... keep reading on reddit β‘https://onlinelibrary.wiley.com/doi/abs/10.1002/jcp.26427
>Abstract
>This study was conceived to evaluate the effects of three different diets on body composition, metabolic parameters and serum oxidative status. We enrolled three groups of healthy men (omnivores, vegetarians and vegans) with similar age, weight and BMI and we observed a significant decrease in muscle mass index and lean body mass in vegan compared to vegetarian and omnivore groups, and higher serum homocysteine levels in vegetarians and vegans compared to omnivores. We studied whether serum from omnivore, vegetarian and vegan subjects affected oxidative stress, growth and differentiation of both cardiomyoblast cell line H9c2 and HβH9c2 (H9c2 treated with H2O2 to induce oxidative damage). We demonstrated that vegan sera treatment of both H9c2 and HβH9c2 cells induced an increase of TBARS values and cell death and a decrease of free NO2β compared to vegetarian and omnivorous sera. Afterwards, we investigated the protective effects of vegan, vegetarian and omnivore sera on the morphological changes induced by H2O2 in H9c2 cell line. We showed that the omnivorous sera had major antioxidant and differentiation properties compared to vegetarian and vegan sera. Finally, we evaluated the influence of the three different groups of sera on MAPKs pathway and our data suggested that ERK expression increased in HβH9c2 cells treated with vegetarian and vegan sera and could promote cell death.
>The results obtained in this study demonstrated that restrictive vegan diet could not prevent the onset of metabolic and cardiovascular diseases nor protect by oxidative damage.
Dear sultans of stain, kings of the cross section, Going through a paper, I found the above statement. It raised some skepticism. Any thoughts from the community on the validity of this? I tried to find stained images of muscle cells that included red blood cells, but only found a very low quality image, anyone have any images to validate this?
Both adipogenesis and myogenesis are anabolic processes, but the body defaults to the former with an energy excess. Only when faced with physical stress, the body prefers the latter. This is mostly controlled by the hormones Myostatin and Follistatin - Myostatin promoting adipogenesis, and Follistatin promoting myogenesis. Resistance exercise inhibits Myostatin signalling to promote myogenesis and suppress adipogenesis.
Having higher lean/muscle mass is healthier in almost every way than having higher fat mass. Myocytes, unlike adipocytes, aren't cytotoxic to tissues, so while high fat mass provokes a disease-like state of systemic inflammation and insulin resistance, high fat mass protects from such state.
If so, why doesn't the body default to myogenesis?
