Physiology and clinical presentation of muscle disease Flashcards
What is a muscle cell called?
Define sarcolemma, sarcoplasm, sarcoplasmic reticulum and sarcomere
Myocyte - myofibre
- Sarcolemma = muscle cell membrane
- Sarcoplasm = muscle cell cytoplasm
- Sarcoplasmic reticulum= muscle cell endoplasmic reticulum
- Sarcomere= contractile muscle unit formed by myofibrils (contractile proteins)
What is stored in the sarcoplasmic reticulum?
Ca to aid sarcomere contraction
Describe the steps in neuromuscular transmission and muscle contraction
- Neural signal travels down the axon and activated Ca entry terminal axon
- Ca interacts with SNARE proteins outside Acetylcholine vesicles at terminal axon
- Acetylcholine release
- Entry of Na on myofiber -> depolarization current reaches sarcoplasmic reticulum through connecting tubules -> Ca release within the sarcoplasm
- Ca binds to Troponin -> Tropomyosin unleashes Actin -> contraction begins
What substrates are used in muscle metabolism?
Phosphagen system: creatine kinase stores and myokinase system: high intensity short duration exercise
Glycogen main energy fuel
Fatty acids: important for sustained exercise
Branch amino-acids: gluconeogenesis and Tricarboxylic acid cycle substrates: sustained exercise (fueling aerobic capacity)
Lactate: NAD production (glycolysis) or Liver Cori Cycle (gluconeogenesis) - accumulation can be helpful because after exercise it can be quickly transformed into energy
What are the different muscle fibre types? What are the differences between them?
- Differences between muscles : postural vs croup/thigh
- Differences within muscle
- Surface versus Deep (close to bone)
- Differences between breeds
- Training
What clinical signs would you expect in a horse that is unable to utilise fats? Which muscle fibres would be affected?
- poor posture
- recumbency
Type I muscle fibres
How does the type of fuel used change as the duration of exercise increases? How does this correlate to muscle fibre types?
- Type 2x for barrel racing
- TYpe 2 racing
- Type 1 Fatty acids for endurance work
What adaptations do horses have that make them perfect athletes?
Higher muscular oxidative capacity:
* Higher mitochondrial mass
* Higher aerobic enzymatic pool
Use of branch amino-acids to support TCA and gluconeogenesis
Type of training stimulates specific metabolic pathway
- Discipline exercise adaptation
What occurs during muscular oxidative stress? What mechanisms exist to counteract oxidative stress?
High metabolic ratio: multiple metabolic reactions
* ROS mitochondrial resp chain
* Acetyl-carnitines in fatty acid oxidation
* Lactate in glycolysis
- sarcolemma instability releasing CK, AST and troponin which you can measure for assessing muscle damage
Mechanisms to counteract oxidative stress
* Vitamin E (sarcolemma repair)
* Cysteine (respiratory chain, ROS)
* Q10 (Reactive species: TCA, amino-acid and fatty acid oxidation)
What are plasma markers for muscle damage?
- Creatine-Kinase (CK) : sarcoplasm and mitochondria
- Aspartate-transaminase (AST): sarcoplasm
- Troponins: sarcoplasm
- Different isoforms for SK-muscle or cardiac muscle
- Normally, commercial labs only test for Cardiac isoform (CTnl)
- Acetyl-carnitines: mitochondria and sarcoplasm
What is the clinical presentation associated with muscle damage?
- Stiffness, muscle pain, short stride, reluctance to move
- Tachycardia, tachypnea, recumbency, myoglobinuria, weakness
- Paresis of specific muscles, arrythmias, muscle atrophy…
What diagnostic approach should you have for muscle damage? How is it treated?
- Clinical history: age, pasture access, recent exercise, level of activity…
- Physical exam: stance, walking, muscle trembling, temperature, swellings, HR…
- Confirmation: clinical presentation, Dx tests
- Treatment recommendations: control pain, avoid damaging effects of myoglobin release, support muscle cell recovery
