Cardiac Muscle Puns

Basically what the title says. Would be grateful if anyone could explain how cardiac muscles behave phsyiologically as a syncytium.

I’m a doctor doing postgraduation in physiology. And I’m preparing for an upcoming presentation on action potential. I’m still doing my research and am a bit confused. So, I thought it would be nice to get some help from you all.

TPR said it is uninucleate, but i found this thread. can someone confirm? Thank you

https://www.reddit.com/r/Mcat/comments/gfelzd/is_cardiac_muscle_multinucleate_or_uninucleate/

Hi Reddit! I’m Sian Harding, Professor of Cardiac Pharmacology at Imperial College London. My research focuses on what happens to the cardiac muscle during heart failure.

What is heart failure?

Heart failure in humans is a syndrome characterised by fatigue, breathlessness and water retention. It happens after recovery from an initial cardiac injury and affects more than 500,0000 people in the UK alone, accounting for up to 40% of all deaths worldwide.

Cardiac injury is often due to heart attack but can also be a consequence of genetic defects, infection or chemotherapy. It has a poor prognosis, with mortality similar to some of the worst cancers. Suffering from heart failure means to be at high risk of shorter life expectancy and generally reduced quality of life.

The cardiac muscle cell, or cardiomyocyte, is the building block of the heart. Deterioration of myocyte function during the development of heart failure is a process that is distinct from the original injury to the heart and may be the result of the body's attempt to produce maximum work from a damaged muscle. Characterisation of the functional alterations to the myocyte, and the molecular processes underlying them, has led to ideas for specific treatments for the failing heart.

About my research

My research at the National Heart & Lung Institute is centred on the cardiomyocyte and its role in heart failure. Starting with simply understanding what happens in heart failure and the effects on myocardial function, to developing models and systems around that.

We use several different animal species (mice, rabbits, rats) to either mimic the heart failure syndrome as a whole, for example by tying off part of the heart muscle under anaesthesia, or to imitate just part of it such as the high catecholamine levels.

My research group was also among the first to do work on isolated human cardiomyocytes. Our understanding from this work leads to involvement in gene therapy trials and more recently in using pluripotent stem cells to produce genotype-specific cardiomyocytes.

This allows the possibility of gene editing and creating engineered heart tissue. It can be a really powerful tool for looking at larger scale characteristics like arrhythmia.

About animal research

Research involving animals forms an important element of our work but is not undertaken lightly. My commitment towards the Reduction, Refinement and Replacement principles is evident

I understand its facilitated by nodes, but like to my understanding since there isn't any acetylcholine to signal depolarization how do muscle cells know when to contract?

I know there are gap junctions or something but still a little confused by this

Medical student here. I was studying some anki decks and struggling to understand this question even after searching.

I know afterload is approximated by MAP but what is meant exactly by velocity of shortening and why is it maximal when afterload is zero?

Any help would be appreciated

Serna JDC, Caldeira da Silva CC, Kowaltowski AJ. Functional changes induced by caloric restriction in cardiac and skeletal muscle mitochondria [published online ahead of print, 2020 May 27]. J Bioenerg Biomembr. 2020;10.1007/s10863-020-09838-4. doi:10.1007/s10863-020-09838-4

https://doi.org/10.1007/s10863-020-09838-4

Abstract

Caloric restriction (CR) is widely known to increase life span and resistance to different types of injuries in several organisms. We have previously shown that mitochondria from livers or brains of CR animals exhibit higher calcium uptake rates and lower sensitivity to calcium-induced mitochondrial permeability transition (mPT), an event related to the resilient phenotype exhibited by these organs. Given the importance of calcium in metabolic control and cell homeostasis, we aimed here to uncover possible changes in mitochondrial calcium handling, redox balance and bioenergetics in cardiac and skeletal muscle mitochondria in response to six months of CR. Unexpectedly, we found that CR does not alter the susceptibility to mPT in muscle (cardiac or skeletal), nor calcium uptake rates. Despite the lack in changes in calcium transport properties, CR consistently decreased respiration in the presence of ATP synthesis in heart and soleus muscle. In heart, such changes were accompanied by a decrease in respiration in the absence of ATP synthesis, lower maximal respiratory rates and a reduced rate of hydrogen peroxide release. Hydrogen peroxide release was unaltered by CR in skeletal muscle. No changes were observed in inner membrane potentials and respiratory control ratios. Together, these results highlight the tissue-specific bioenergetic and ion transport effects induced by CR, demonstrating that resilience against calcium-induced mPT is not present in all tissues.

Reference: https://www.sciencedirect.com/science/article/pii/S1525001604014686#:~:text=Genetic%20defects%20in%20lysosomal%20acid,in%20cardiac%20and%20skeletal%20muscles.

Petrick HL, Brunetta HS, Pignanelli C, et al. In vitro ketone-supported mitochondrial respiration is minimal when other substrates are readily available in cardiac and skeletal muscle [published online ahead of print, 2020 Jul 31]. J Physiol. 2020;10.1113/JP280032. doi:10.1113/JP280032

https://doi.org/10.1113/jp280032

Abstract

Key points: Ketone bodies are proposed to represent an alternative fuel source driving energy production, particularly during exercise. Biologically, the extent to which mitochondria utilize ketone bodies compared to other substrates remains unknown. We demonstrate in vitro that maximal mitochondrial respiration supported by ketone bodies is low when compared to carbohydrate-derived substrates in the left ventricle and red gastrocnemius muscle from rodents, and in human skeletal muscle. When considering intramuscular concentrations of ketone bodies and the presence of other carbohydrate and lipid substrates, biological rates of mitochondrial respiration supported by ketone bodies are predicted to be minimal. At the mitochondrial level, it is therefore unlikely that ketone bodies are an important source for energy production in cardiac and skeletal muscle, particularly when other substrates are readily available.

Abstract: Ketone bodies (KB) have recently gained popularity as an alternative fuel source to support mitochondrial oxidative phosphorylation and enhance exercise performance. However, given the low activity of ketolytic enzymes and potential inhibition from carbohydrate oxidation, it remains unknown if KBs can contribute to energy production. We therefore determined the ability of KBs (sodium DL-β-hydroxybutyrate, β-HB; lithium acetoacetate, AcAc) to stimulate in vitro mitochondrial respiration in the left ventricle (LV) and red gastrocnemius (RG) of rats, and in human vastus lateralis. Compared to pyruvate, the ability of KBs to maximally drive respiration was low in isolated mitochondria and permeabilized fibres (PmFb) from the LV (∼30-35% of pyruvate), RG (∼10-30%), and human vastus lateralis (∼2-10%). In PmFb, the concentration of KBs required to half-maximally drive respiration (LV: 889 μm β-HB, 801 μm AcAc; RG: 782 μm β-HB, 267 μm AcAc) were greater than KB content representative of the muscle microenvironment (∼100 μm). This would predict low rates (∼1-4% of pyruvate) of biological KB-supported respiration in the LV (8-14 pmol·sec-1 ·mg-1 ) and RG (3-6 pmol·sec-1 ·m

But that does not make them a living being. The "beating heart" criteria as a measure is deeply ignorant. It seems predicated on the assumption that a clump of cells is imbued with an eternal human spirit. I am disappoint the press is not calling BS on this type of magical thinking.

From what I understand, a heart right axis deviation can occur when the diaphragm is more distally to the apex of the heart so the heart isn't sitting on the diaphragm as normal (I've been told this can occur with tall people). So I was thinking that this position theoretically stretches the heart more than usual due to gravity, and thus affecting the muscle contraction. Or is there too insignificant changes in position to make a difference?

Reference: https://www.sciencedirect.com/science/article/pii/S1525001604014686#:~:text=Genetic%20defects%20in%20lysosomal%20acid,in%20cardiac%20and%20skeletal%20muscles.

Because you're always in my heart