Logan Steele
Fast-twitch muscle fibres, also known as type 1, are very vascular, meaning they have greater blood flow, which allows faster delivery of nutrients and removal of waste products. These fast-twitch fibres are also called red fibres. Scientists have discovered a genetic switch that increases muscle blood supply, which could be good news for people with heart disease, frailty, peripheral vascular disease, and other medical problems where exercise could be beneficial but is not possible. This discovery could also help treat critical limb ischemia (CLI), a devastating condition that can lead to muscle wasting and amputation due to blocked blood flow to the skeletal muscle. CLI is often linked to risk factors such as diabetes, obesity, and smoking. Additionally, understanding the gene network that controls high vascular supply to muscles could promote improved muscle performance and fitness, especially for those who cannot exercise.
| Characteristics | Values |
|---|---|
| Fast-twitch muscles | Can make you go fast, but only for a short while |
| Slow-twitch muscles | Can make you go long and slow |
| Slow-twitch muscle fibers | Also called type 1, very vascular, greater blood flow, sometimes called red fibers |
| Fast-twitch muscle fibers | Fast-twitch B fibers |
| Slow-twitch muscle fibers | Slow-twitch A fibers |
| Phenotypic switching of vascular smooth muscle cells | Hallmark of atherosclerosis or vascular restenosis |
| Aortic vascular smooth muscle cells (VSMCs) | Associated with coronary heart disease |
| Phenotypic switching of VSMCs | Regulated by miR-145 |
| Phenotypic switching of VSMCs | Occurs in the 'normal region' of the aorta |
| Phenotypic switching of VSMCs | Occurs in aortic aneurysm (AA) |
| Phenotypic switching of VSMCs | Occurs in vascular aging |
| Phenotypic switching of VSMCs | Occurs in atherosclerosis (AS) |
| Phenotypic switching of VSMCs | Occurs in aortic aneurysm (AA) |
| Phenotypic switching of VSMCs | Occurs in vascular injury |
| Phenotypic switching of VSMCs | Occurs in hypertension |
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What You'll Learn
Fast-twitch vs slow-twitch muscle fibres
All humans are born with a mix of slow and fast-twitch muscle fibres, also called type 1 and type 2 muscle fibres. The proportion of these muscle fibres depends on genetics, age, and fitness. For instance, people who are good at endurance sports tend to have a higher number of slow-twitch fibres, while people who excel at sprinting tend to have a higher number of fast-twitch fibres.
Slow-twitch muscle fibres are involved in low to moderate-intensity activities like walking, jogging, and running long distances. They are also called "red fibres" due to their rich blood supply and high myoglobin content, which is an oxygen-binding protein that gives muscles their reddish colour. These fibres rely on aerobic respiration to produce energy, which is a combination of glycolysis and the Krebs cycle. This process is slower than anaerobic respiration but produces much more energy, allowing slow-twitch fibres to be fatigue-resistant.
On the other hand, fast-twitch muscle fibres are necessary for speed and power. They are used for high-intensity activities like sprinting, jumping, powerlifting, and soccer. These fibres rely on carbohydrates stored in the muscles and anaerobic respiration to produce energy quickly. However, this process is limited, causing fast-twitch muscles to fatigue more quickly.
With age, fast-twitch muscles degenerate more rapidly than slow-twitch muscles, and the neuro input to these muscles declines. Therefore, it is important to maintain fast-twitch muscles through higher-intensity exercises and resistance training with heavier weights.
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Critical limb ischemia (CLI)
CLI is a clinical syndrome of ischemic pain at rest or tissue loss, such as non-healing ulcers or gangrene, related to peripheral artery disease. It is a serious condition that requires immediate treatment to restore blood flow to the affected area and prevent limb loss. The number one priority is to preserve the limb and prevent amputation. Treatment options for CLI include rehabilitative exercise, surgical bypass of blood vessels, medications to prevent clots, reduce blood pressure, and lower cholesterol, endovascular treatments (minimally invasive), and surgery to repair or replace arteries. Endovascular procedures used to treat CLI include angioplasty, where a tiny balloon is inserted through a puncture in the groin and inflated using a saline solution to open the artery, and atherectomy to remove plaque buildup. Hybrid surgical techniques such as iliac stenting and common femoral endarterectomy are also used to reduce operative risk.
Diagnosis of CLI involves identifying and locating the cause of blockages using methods such as auscultation, ankle-brachial index (ABI), Doppler Ultrasound, CT angiography, and Magnetic resonance angiography (MRA). Defining specific cut points for the clinical diagnosis of CLI can be challenging due to the overlap in values among patients who progress to major amputation or cardiovascular events. However, rest pain or non-healing wounds may suffice as a definition to justify the use of expensive technology such as angiography and revascularization, which are fundamental to the treatment of CLI.
CLI affects a significant number of people, with an estimated 2.8 to 3.5 million US citizens suffering from the condition in 2010, according to a report by THE SAGE GROUP. Risk factors for CLI include diabetes, obesity, smoking, high blood pressure, and high cholesterol. CLI is a severe complication of PAD that requires prompt treatment to improve patient outcomes and prevent major medical complications.
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Genetic switches and muscle blood supply
Skeletal muscle is composed of two types of fibers: slow-twitch and fast-twitch. Slow-twitch muscle fibers have a dense supply of blood vessels, allowing for faster delivery of nutrients and removal of waste products. On the other hand, fast-twitch muscle fibers have fewer blood vessels. The percentage of fast and slow-twitch fibers is largely genetic, but training can influence their strength, power, and efficiency.
Scientists have discovered a genetic switch that can increase the number of blood vessels in skeletal muscle. This discovery was made by researchers at the University of Texas Health Science Center at Houston (UTHealth) and the Salk Institute for Biological Studies. The genetic switch, known as the estrogen-related receptor gamma (ERR gamma), converts fast-twitch muscle fibers into slow-twitch fibers with a dense supply of blood vessels. This conversion results in a significant increase in muscle blood supply, as measured by imaging and angiography.
The identification of the ERR gamma vascular switch opens up potential therapeutic avenues for treating critical limb ischemia (CLI) and other cardiovascular diseases linked to defective blood supply. CLI is a devastating condition that affects millions of people worldwide and can lead to muscle wasting, infections, severe pain, and even amputation. The disease is linked to the blockage of blood flow to the skeletal muscle, and current treatment options include rehabilitative exercise and surgical bypass of blood vessels. The discovery of the ERR gamma vascular switch offers hope for a new approach to restoring blood supply in skeletal muscle without traditional intervention.
Additionally, the ERR gamma vascular switch has implications beyond the treatment of CLI. According to Ronald M. Evans, Ph.D., senior author and investigator at the Howard Hughes Medical Institute, understanding the gene network that specifies high vascular supply to muscle gives us a powerful tool to promote improved muscle performance and fitness, especially for those who cannot work out. This is good news for people with heart disease, frailty, peripheral vascular disease, and other medical conditions where exercise could be beneficial but is not possible.
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Phenotypic switching of vascular smooth muscle cells
Vascular smooth muscle cells (VSMCs) are the major cell type in the arterial vessel wall. They have a contractile phenotype that maintains the normal vessel structure and function under physiological conditions. In response to stress or vascular injury, VSMCs can switch to a less differentiated state (synthetic phenotype) to acquire the proliferative, migratory, and synthetic capabilities for tissue reparation.
Phenotypic switching of VSMCs is regulated by miR-145. Switching of VSMCs from a contractile phenotype to an adverse proliferative phenotype is a hallmark of atherosclerosis or vascular restenosis. Aortic VSMCs from patients with atherosclerosis-associated coronary heart disease (CR) had lower SMC-specific contractile marker expression and higher proliferation compared to patients with non-atherosclerosis-associated valvular disease (VL).
The phenotypic plasticity of VSMCs is central to vessel growth and remodeling but also contributes to cardiovascular pathologies. Imbalances in VSMCs phenotypic switching can result in a variety of cardiovascular diseases, including atherosclerosis, in-stent restenosis, aortic aneurysms, and vascular calcification.
New technologies, including fate mapping, single-cell transcriptomics, and genetic and pharmacologic inhibitors, have provided fundamental new insights into the biology of VSMCs. Understanding the molecular mechanisms that underlie the remarkable plasticity of VSMCs may lead to novel approaches to treat and prevent cardiovascular disease and restenosis.
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Vascular smooth muscle contraction
Vascular smooth muscle is responsible for the control of total peripheral resistance, arterial and venous tone, and the distribution of blood flow throughout the body. The smooth muscle cells are small, mononucleate, and spindle-shaped, and they are usually arranged in helical or circular layers around large blood vessels.
The smooth muscle cell directly drives the contraction of the vascular wall and hence regulates the size of the blood vessel lumen. The contractile response of vascular smooth muscle is the product of myosin light chain kinase (MLCK) and myosin light chain phosphatase (MLCP) activation. In smooth muscle, this process is initiated by a calcium (Ca2+)-mediated change in the thick (myosin) filaments. All smooth muscle cells, regardless of the stimulus, produce force or contraction through cross-bridge cycling between actin and myosin filaments.
The contractile phenotype in vascular smooth muscle predominates, and vascular smooth muscle contraction is regulated by vasoactive peptides such as angiotensin II and endothelin-1. Angiotensin II promotes the maintenance of systemic pressure through various mechanisms in the cardiovascular and renal systems. It is also crucial to salt and water homeostasis. However, this peptide is implicated in several cardiovascular conditions, such as hypertension, atherosclerosis, and heart failure.
The potential across the plasma membrane of vascular smooth muscle is an important determinant of the contractile state of vascular smooth muscle. This is because both the entry of Ca2+ into the cell and the extrusion of Ca2+ from the cell are voltage-dependent. Depolarization increases Ca2+ influx and decreases Ca2+ efflux. Tyrosine phosphorylation, or mitogen-activated protein kinase (MAPK), has been associated with increased levels of AT1 receptor activation.
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Frequently asked questions
Fast-switch muscle refers to fast-twitch muscle fibres, which are responsible for powerful, explosive movements. They are used for short periods of activity and are the opposite of slow-twitch muscle fibres, which are used for endurance.
A muscle being vascular refers to the density of blood vessels within it. Slow-twitch muscle fibres are very vascular, meaning they have greater blood flow, which allows faster delivery of nutrients and removal of waste products.
Vascularity in muscles is important for maintaining healthy blood flow and preventing diseases caused by blocked blood flow, such as critical limb ischemia (CLI) and atherosclerosis. CLI can lead to muscle wasting and even amputation. Atherosclerosis is caused by the switching of vascular smooth muscle cells from a contractile phenotype to a proliferative phenotype, leading to a blockage in blood flow.
