Metabolism - Calcium And Exercise

Front 1

Explain the significance of maintaining serum calcium levels within set limits

Back 1

Calcium plays a critical role in many cellular processes including hormone secretion (insulin), muscle contraction, nerve conduction, exocytosis and the activation and inactivation of many enzymes(proteases - necrosis/apoptosis). It also acts as an intracellular secondary messenger in response to protein hormones binding to surface receptors. Therefore it is very important to regulate the free ionized calcium plasma concentration, as this is the active form, within set limits 1-1.3m.M. Above this concentration you are at risk of hypercalcaemia and below you are at risk of hypocalcaemia.
- 50% ionised calcium
- 45% protein bound ( 80% to albumin)
-5% complexed with citrates, phosphates etc

Common laboratory tests measure total adjusted calcium which includes that which is bound to albumin and other plasma proteins.
- the total adjusted calcium reg range is 2.10-2.6 mmol/L

Front 2

List the hormones involved in the control of calcium levels in serum

Back 2

Parathyroid hormone – increase calcium plasma concentration - a single chain polypeptide hormone secreted from chief cells within the 4 parathyroid glands which sit on the posterior wall of the thyroid gland, 1 pair on each lobe.
Calcitriol – Vitamin D – increase calcium concentration - made from D3 and D4 derived in the diet and in the body from direct contact with UV light. Hydroxylation in the liver and the kidney form calcitriol. PTH regulates conversion in kidney.
Calcitonin – decreases plasma calcium by stimulating osteoblast activity - secreted from parafollicular cells in connective tissue septa of the thyroid gland

Front 3

Describe the hormonal regulation of serum calcium

Back 3

Low plasma free calcium levels stimulate PTH secretion and synthesis (transcriptional and post transcriptional levels) in chief cells. PTH targets bone which is stimulates osteoclast activity so that bone matrix is resorped and Ca2+ andPi are released from, hydroxyapatite crystals , into the circulation. PTH also targets the kidney where it increases reabsorption of calcium ions at the distal proximal tuble. Reabsorption of Pi is inhibited by PTH to prevent calcium phosphate stones forming. PTH also regulates the hydroxylation of inactive forms of Vit D3 and D4 in the kidney to form calcitriol, which stimulates reabsorbtion of calcium in kidneys as well. In the gut calcitriol increases the uptake of calcium ions and in the bone, along with PTH, increases osteoclast activity. Therefore the plasma free calcium level is increased. Negative feedback mechanism from calcium levels to PTH control regulation. The short term regulation of serum calcium is under the control of PTH but the long term regulation is controlled by calcitriol.
Calcitonin activates osteoblast activity, increasing bone density and reducing plasma calcium concentration. It is not vital, however may be during pregnancy to preserve the maternal skeleton.

Front 4

Explain the interaction of parathyroid and vitamin D

Back 4

The active form of vitamin D – calcitrol is synthesised from the hydroxylation of vitamin D3 and D4 in the liver and the kidney. D3 – cholecalciferol, is made in the skin from contact with UV light and from dairy products. D4 – ergocalciferol, is made by yeast and fungi and is put into margarine.. Hydroxylation of D3 in the liver is not regulated and forms 25-hydroxyvitamin D which can stay for 2 weeks. Hydroxylation of 25-hydroxyvitamin in the kidney is regulated by PTH which increases the activity of C1 hydroylase. PTH and Calcitirol both work together to increase plasma calcium concentration by increasing absorbtion of calcium in GI tract, increasing renal tubule reabsorbtion of calcium thus reducing calcium lost in urine and increases osteoclast activity. However they both do this in different ways. PTH’s main role in the kidney is to decrease the reabsorbtion of Pi, reducing serum phosphate concentration and therefore hydroxyapatite crystals dissolve out of the bone. Calcitriol regulation is long term and increases phosphate reabosorption in the gut along with calcium.

Front 5

Explain the regulation of parathyroid hormone and vitamin D

Back 5

Vitamin D – calcitriol has a half life of 0.25 days, a few hours. and is then excreted in urine. It is made into its hormonally active form by PTH increasing the activity of C1 hydroxylase in the kidney, converting 25-hydroxyvitaminD3 into calcitriol.
Parathyroid hormone is regulated by negative feedback mechanism from serum calcium concentration. High levels of calcium bind to specic receptors on chief cells to reduce PTH release.

Front 6

Describe hypercalcaemia - causes, symptoms and treatment

Back 6

Hypercalcaemia
Causes – high levels of Vit D, overactive parathyroid,- adenocarcinoma ( tumour of a gland), ectopic tumour - humeral hypercalcaemia > breast, prostate, myeloma tumour elsewhere which is releasing PTH related peptide shares the same actions as PTH except for acting c1 hydroxlase so doesn’t increase calcitrol concentration
Signs of chronic hypercalcaemia - groans, moans, bones, stones and phyciatric overtones:
Constipation, fatigue, weakness, depression, osteoporosis – decreased bone density, kidney stones,(renal calculi) confusion. High blood pressure- increased volume in blood due to calcium.

Treatment – fluids to replace excess lost in urine, bisphosphonates and calcitonin increase osteoblast activity, primary hyperparathyroidism -> removal of benign tumour in one of the parathyroid glands

Front 7

Describe Hypocalcaemia - causes, symptoms and treatment

Back 7

Causes – vit d deficiency, hypoparathyroidism, retension of phosphate (renal failure)
Signs and symptoms – hyperexcitabilty in the nervous system including NMJ resulting in paraesthesis (pins and needles), tetany (muscle spasms), paralysis and convulsions( rapid contractions and relax) Convulsions of the respiratory muscle can cause death.
Treatment - increase vit D in diet. Hypoparathyroidism very rare caused by removal of parathyroid gland during thyroidectomy.

Front 8

What tests would you order for someone with high levels of serum calcium?

Back 8

- Request parathyroid hormone test – if assay shows high levels of hormone, hypercalcaemia is due to high activity of the parathyroid gland
- Abdominal radiography which show extensive faeces throughout the colon and calcification over renal areas.
- If PTH assay is low then request a PTHrP (parathyroid hormone related peptide) which has the same affects on kidney and bone as PTH however does not activate c1 hydroxyvitamin D and so does not stimulate calcitriol formation. PTH levels will be low because the increased serum calcium will, by negative feedback, inhibit PTH secretion.
- PTHrP is released from tumours which may be ‘Particular Tumours Love Killing Bone’ –prostate, thyroid, renal, breast tumour. Look for lung cancer with a chest X ray – biopsy.

Front 9

Where is calcium located in the body?

Back 9

Most calcium is located in the bone 1kg. Calcium deposition in bone is matched by bone resorption, liberating minerals, at 280mg/day. The extracellular fluid only has 1g of calcium of which 45% is free and the active form, 45% is bound to protein, 10% is bound to small organic anions.
It is the free ionized calcium in plasma that is physiologically active. However laboratory tests meaure total calcium which includes that which is bound to proteins. The levels are then corrected depending on the level of albumin in the blood to determine if free calcium is within the set limits. Net intestinal uptake is 175mg/day. Daily intake is around 800-1200mg. In CA2+ balance urinary secretion is the same as the net absorption.

Front 10

What are the main acute and chronic regulators of serum calcium.

Back 10

Acute regulator is parathyroid hormone.
Chronic regulator is calcitriol.

Front 11

What would a high alkaline phosphatase level indicate?

Back 11

Alkaline phosphatases are found mainly in the liver, bone, bile duct, kidney and placenta.
Elevated alkaline phosphatases may suggest a blockage in the bile duct or increased bone turnover as osteoblasts release this enzyme(seen in paget’s disease). Elevated levels are normal during pregnancy and children.

Front 12

Describe the positions of the pituitary gland and adrenal glands and their size relative to gender.

Back 12

Pituitary gland is located at the base of the brain suspended from the hypothalamus by a stalk. The land weighs 0.5-0.9g and is larger in females due the effect of oestrogen on lactotrophs.
The adrenal glands are a pair of multifunctional endocrine glands that cap the upper poles of the kidneys and lie against the diaphragm. They are small and have a combined weigh of 6-8g. This weight is slightly less in females, maybe due to concentration of male sex hormones testosterone, androgens.

Front 13

Describe the adrenal cortex.

Back 13

The adrenal cortex surrounds the adrenal medulla and lies underneath the connective tissue capsule. It has long inverted U shaped lines of cells and 3 layers:
Zona glomerulosa – relatively small cells, like a hair pin, in the outermost zone secrete mineralocorticoides eg aldosterone stimulates Na+ reabsorption in the kidney in exchange for K+ . Over secretion of aldosterone increases Na+ and water retention and loss of K+ causing hypertension and muscle weakness. Under secretion of aldosterone causing hypotensions eg addison’s disease.
Zona fasciculata – relatively large cells, in the middle zone that produce glucocorticoids eg cortisol that have a number of important functions including the regulation of carbohydrate metabolism.
Zone reticularais – relatively small cells in a network, that secrete glucocorticoids and small amounts of androgens – male sex hormones which stimulate the growth and development of male genital tract and male secondary sexual characteristics including height, body shape, facial and body hair, lower voice pitch, increased muscle protein.
Oestrogen stimulates growth and development of female genital tract, breasts and female secondary characteristics eg broad hips, accumulation of fat in breasts and buttocks, body hair distribution – decrease circulating cholesterol levels.

Front 14

List the hormones produced by the pituitary and adrenal glands together with their function

Back 14

ANTERIOR PITUITARY:
- ACTH – Produced in corticotrophs - adrenocorticotrophic hormone stimulates s the zona fasciculata to secrete cortisol in response to stress – hyperglycaemia, infection, exercise, cold, emotional stress and shock - trauma, burns, haemorrhage
- TSH – produced in thyrotrophs - thyroid stimulating hormone stimulates the thyroid gland to synthesise and secrete thyroid hormones, T3 and T3. Trophic effects of the hormone are to increase vascularity and increase number and size of follicular cells which could lead to enlargement of gland, goitre. A goitre may or may not be overactive ie cause thyrotoxicosis.
- Growth hormone – produced in somatotrophs (largest no. Of cells) – targets all cells for growth and development
- LH & FSH – Produced in gonadotrophs – LH is responsible for ovulation, FSH in males stimulate spermatogenesis and in females it stimulate maturation of follicles
- Prolactin – produced in the lactotrophs – stimulates milk production in mammary glands
ADRENAL GLAND HORMONES:
- Glucocorticoids- eg cortisol is released from the zona fasciculata from the adrenal cortex and its secretion is controlled by ACTH in response to stress and shock
- Mineralcorticoids- eg aldosterone are released from the zona glomulosa in the adrenal cortex, controlled by the rennin angiotensin system. It regulates the body’s sodium and potassium levels.
- Androgens released from zona reticularis which are male hormones
- Catecholamines eg the hormone adrenalin is released from adrenal medulla and increases the impact of the sympathetic nervous system preparing the body for flight or fight by increasing heart beat and force of contraction, increasing glycogenolysis and lipolysis, bronchodilation, diversion of blood to muscles and away from skin and GI tract.

Front 15

Describe in general terms the structure of the steroid hormones

Back 15

The steroid hormones are produced in all 3 layers of the adrenal cortex. They are hydrophobic molecules derived from cholesterol. Cholesterol ester is stored as lipid droplets in steroid producing cells, which have abundant SER and mitochondria. Steroids are not stored but are synthesised on demand. Cholesterol ester > cholesterol (c27) > progesterone (c21) > either aldosterone (c21), cortisol (c21) or androgen (c19).
Steroids differ from other streroids in the number of C atoms, presence of functional groups and distribution of C=C double bonds. All steroids are lipophillic an ar synthessised from cholesterol via progesterone in a series of enzyme catalysed reactiond

Front 16

Explain how the steroid hormones affect their target tissues

Back 16

They are transported in the blood bound to transport carrier proteins eg albumin, to target cells where they diffuse across the plasma membrane where they bind with a cytoplasmic receptor which then translocates the complex to the DNA binding domain where they attach and stimulate the transcription of a particular gene.
The major transport carrier for cortisol is transcortin and carries 90% of serum cortisol, 10% being free and biologically active.

Front 17

Explain how cortisol secretion is controlled by ACTH & CRF

Back 17

The HPA axis is stimulated in response to stress eg hyperglycaemia, cold, infection, emotional stress or shock eg trauma, burns, and haemorrhage ( physical, chemical and emotional stressors). CRF (corticotrophin releasing factor) is released from the hypothalamus, travels down the hypophyseal portal vessels to corticotrophs in the anterior pituitary gland where it stimulates the release of ACTH into the circulation. ACTH interacts with corticotrophin receptors on the surface of zona fasciculate and zona reticularis to secrete glucorticoids. The binding increase the intracellular concentration of cAMP, the secondary messenger which activates cholesterol esterase, increasing the conversion of cholesterol ester to cholesterol; it also stimulates other steps in the synthesis of cortisol from cholesterol. Increase of cortisol in blood inhibits the release of CRF and ACTH from the hypothalamus and anterior pituitary respectively by negative feedback inhibition. Cortisol is secreted following a circadian rhythm, highest in morning and lowest in middle of the night.

Front 18

Describe in general terms the structure and functions of adrenaline

Back 18

Adrenaline is a catecholamine which is synthesised in the adrenal medulla , a modified sympathetic ganglion, from tyrosine converted to dopa which is then converted to dopamine and then noradrenalin and methlyation occurs to form adrenalin. Adrenalin is an amino acid derived hormone which heightens the effects of the sympathetic nervous system, preparing the body for flight or fight. It is stored in vesicles in adrenal medulla nerve cells and is released upon sympathetic nervous stimulation in response to stress. The hormone mobilises nutrients, increases glycogenolysis and lipolysis in cells, inhibits insulin, increases mental alertness, increases heart rate and force of heart contraction and causes bronchodilation.

Front 19

What causes overproduction of adrenalin.

Back 19

Overproduction of adrenalin by the adrenal medulla, usually due to a tumour (phaeochomocytoma) which may cause hypertension, anxiety, palpitations, pallor, sweating and glucose intolerance.

Front 20

Explain how ACTH can lead to increased pigmentation in certain areas of the body

Back 20

Pigment (melanin) production from melanocytes is activated by the hormone MSH. ACTH is formed from the post translational processing of POMC ,a large polypeptide hormone(241amino acids), along with many other peptides including melanocyte stimulating hormone. The MSH 13 amino acid sequence lies within the ACTH sequence. Therefore ACTH has sequence homology with melanocyte stimulating hormone and when ACTH is in excess it has MSH like activity. If ACTH is in excess eg in addison’s disease, excess pigmentation can occur.

When MSH is released to activate the appetite, it is acting as a neurotransmitter and therefore does not enter the blood stream and does not cause pigmentation.
ACTH has a short half life in circulation and is released in pules that follow a circadian rhythm , peaking at early hours of the morning and lowest levels seen in the middle of the night.

Front 21

Describe the main actions of cortisol

Back 21

Cortisol is a steroid hormone secreted from large cells in the zona fasciculate in the adrenal cortex. It is released in response the stress eg hyperglycaemia, cold, emotional stress, exercise and infection and also in response to shock eg burns, haemorrhage and trauma.
The metabolic actions of cortisol include increasing all metabolite substrates by increasing proteolysis, lipolysis and gluconeogenesis, decreasing amino acid uptake and protein synthesis, increases glycogenolysis and decreases uptake of glucose by non glucose dependant cells and inhibits the secretion of insulin. Very high concentrations of cortisol eg in cushing’s syndrome, increase lipogenesis causing central obesity and moon face.
Cortisol also directly affects the cardiac muscle, bone and the immune system.

Front 22

Explain the effects of over secretion of cortisol

Back 22

Over secretion of cortisol:

Signs and symptoms: increased lipogenesis in adipose tissue causing increased central adiposity, moon face and weight gain, thinning of skin causing purple striae, increased proteolysis in muscles and hepatic gluconeogenesis which may cause hyperglycaemia and associated glycosuria, polyuria and polydipsia, thin arms and legs from muscle wasting, immunosuppressive, anti inflammatory and anti allergic reactions of cortisol leading to increased susceptibility to infections and produce acne, back pain and collapse of ribs due to osteoporosis caused by disturbances of calcium metabolism and loss of bone matrix protein – collagen, mineralcorticoid effects of excess cortisol causing hypertension due to sodium and fluid retension.
Cause: cushing’s syndrome – increased secretion of glucocorticoids due to increased activity of the adrenal cortex due to tumour (adenoma) or disorders in the secretion of ACTH caused by pituitary adenoma or ectopic secretion of ACTH.
Also signs and symptoms could be due to long term treatment with glucocorticoids for various chronic inflammatory conditions.
Treatment: remove tumour

Front 23

Explain the effects of Under secretion of cortisol:

Back 23

Causes – addison’s disease - decreased activity of the adrenal cortex caused by auto immune destruction of the adrenal cortex affecting mineralocorticoids and glucocorticoids or disorders in pituitary or hypothalamus, leading to decreased secretion of ACTH or CRF which only affects glucocorticoids. (mineralocorticoids are only regulated by rennin angiotensin system)

Signs and symptoms: insidious onset of symptoms - weight loss, tiredness, extreme muscular weakness, anorexia, abdominal pain and occasional dizziness, dehydration, increased pigmentation due to ACTH-mediated melanocyte stimulation, hypotension due to decreased sodium and fluid uptake in kidneys, hypoglycaemic episodes especially on fasting.

Front 24

How would you expect a patient suffering with addison’s disease to react to a stress such as trauma or a severe infection.

Back 24

Release of glucocorticoids is the usual response to stress. Patients with addison’s syndrome may therefore not respond appropriately. The stress could therefore precipitate an Addisonian crisis with nausea and vomiting causing extreme dehydration due to lack of aldosterone to activate water resorption. hypotension, confusion, fever, pain and coma.
This is a Clinical emergency and must be treated with intra venous cortisol and fluid replacement immediately.

Front 25

Explain how cortisol can have weak mineralocorticoid and androgen effects

Back 25

The effects of cortisol are mediated by binding to the cytoplasmic receptors in the target cell. All steroid hormone receptors have a similar basic structure with hormone and DNA binding domains. The hormone binding domain in Glucocorticoid receptors has over 60% sequence homology with the hormone binding domains in mineralocorticoid and androgen receptors. Therefore cortisol can bind to these receptors to a limited extent, stimulating their partial activation.

Front 26

What are the clinical tests for adrencocortical function?

Back 26

1. Measurement of plasma cortisol and the 24 hr urinary excretion of cortisol and its breakdown products ( 17 hydroxysteroids)
2. ACTH plasma levels
3. Dynamic tests: dexamethasone, a potent synthetic steroid is given orally.
If adrenocortical function is normal, ACTH and cortisol secretion is suppressed.
If cushing’s syndrome due to pituitary adenoma – cortisol secretion is reduced by more than 50% ( pituitary is insentive to cortisol but more sensitive to dexamethasone)
However cushing’s syndrome caused by adrenal gland adenoma or an ectopic secretion of ACTH suppression does not occur.
4. Synacthen – synthetic analogue of ACTH – given intramuscularly
Normally increases plasma cortisol by more than 200nmol/l. Abnormal response – addison’s disease

Front 27

Describe the metabolic and hormonal response to pregnancy

Back 27

The mother supplies everything that is needed for the growing foetus throughout pregnancy eg nutrients, vitamins, minerals, oxygen and water. The rate of nutrient transfer across the placenta is dependent on the nutritent concentration in maternal blood. During the first 20 weeks of pregnancy metabolic changes occur to increase maternal nutrient stores, especially TAG stores, ready for more rapid growth of the foetus, birth and subsequent lactation. Increasing levels of insulin promote an anabolic state in the mother that results in increased nutrient storage. During the second half of pregnancy, the nutrient demands by the foetal-placental unit increase and so the concentration of nutrients in the maternal circulation is kept relatively high to meet the demands for the foetus as well as the maternal tissues. The nutrient concentration in maternal circulation is kept high by reducing maternal utilisation of glucose by making fatty acids the main substrate, delaying the maternal disposal of nutrients after meals and by releasing fatty acids from stores built up in first half of pregnancy. Production of Anti- insulin hormones increases faster than insulin and so the insulin/anti insuling ratio falls. Anti- insulin hormones are produced by the foetal-placental unit eg oestrogen, progesterone and placental lactogen. The decreased insulin/anti insulin ratio coupled with increased availability of fatty acids in the liver promote the production of ketone bodies which are used as fuel by the foetal brain.

Front 28

Explain the hormonal basis of gestational diabetes

Back 28

The rate of insulin secretion usually increases as pregnancy proceeds by Beta cell hyperplasia, beta cell hypertrophy and increased rate of insulin synthesis in beta cells. In some woman the maternal pancreas fails the reach the metabolic demands of pregnancy and the pancreas fails to release the increased amounts of insulin required. Therefore blood glucose increases and gestational diabetes results. After birth when the metabolic demands of pregnancy are removed and hormone levels change, the pancreas can respond adequately and diabetes disappears. Women who experience gestational diabetes are more likely to develop type 2 diabetes mellitus later in life.

Front 29

What are the Problems associated with gestational diabetes:

Back 29

• Excess foetal growth
• Macrosomia – excessive birth weight
• Difficult delivery

Front 30

Describe the metabolic and hormonal response to a marathon.

Back 30

Marathon: long distance, 26 miles
- Aerobic
- Uses all fuel molecules
- First muscle glycogenolysis
- When muscle glycogen exhausted, circulating blood glucose is metabolised ( liver glycogenolysis and gluconeogenesis replaces that used by muscle)
- When blood glucose falls, fatty acids are beta oxidised. – cortisol mobilises fats
- Fall in insulin/ anti-insulin ratio – increases glycogenolysis in liver, gluconeogenesis in liver, lipolysis in adipose tissue. It has no affect on ketogenesis as insulin not low enough.
- Adrenaline and noradrenalin inhibit insulin secretion
- Adrenaline, noradrenalin and growth hormone increase rapidly whereas glucagon and cortisol increase gradually.
Which muscles fibres are best suited to marathon runners?
Type 1 – slow oxidative – more mitochondria, slower fatigue, slow contraction

Front 31

Describte the metabolic and hormonal response to medium intensity exercise.

Back 31

Medium intensity: 1500m
- Half aerobic/ half anaerobic
- ATP, C-P and anaerobic glycogen metabolism are used first
- ATP is then produced aerobically from glycogen in muscle
- Anaerobic metabolism of glycogen and produces lactate


Type IIA – fast oxidative, lots of mitochondria, moderate fatigue resistance

Front 32

Describe the metabolic and hormonal response to high intensity exercise.

Back 32

High intensity: 100m sprint
- Muscle ATP and CP are used initially
- Anaerobic glycogen metabolism as oxygen supply to skeletal muscles is inadequate
- Lactate and H+ build up, H+ accumulation causes fatigue
- Controlled by nervous system – noradrenalin and some endocrine systems - adrenalin

Type IIb – fast anaerobic – few mitochondria, fast fatigue

Front 33

Describe how H+ accumulation in muscles impairs muscle function.

Back 33

H+ inhibits glycolysis, interferes with actin/myosin interaction and causes sarcoplasmic reticulum to bind calcium, inhibiting contraction.

Front 34

What are the benefits of using muscle glycogen over circulating glucose during exercise.

Back 34

The availability of glycogen is not affected by blood supply, there is no need for membrane transport into muscle cells, it’s already there, produces glucose 6 phosphate without using ATP ( Glycogen phosphorylase uses Pi), mobilisation can be very active as it is branched so has many sites for enzyme attack and glycogen phosphorylase activity can be changed rapidly by a mixture of covalent modification and allosteric activation.

Front 35

What factors limit the use of fatty acids in muscle?

Back 35

Rate of lipolysis, limited capacity of transport carrier proteins, rate of fatty acids uptake into muscles and into muscle mitochondria, fatty acid oxidation requires more oxygen/mole of ATP produced than glucose and fatty acids can only be metabolised under aerobic conditions.

Front 36

Explain the benefits of exercise

Back 36

Training improves exercise capacity by adapting cardiovascular and musculo-skeletal systems:

Cardiovascular:
- More 2,3- bisphosphoglycerate in blood ( reduces affinity of haemoglobin for O2 so more is released to muscles)
- Heart beats slower for same cardiac output
Skeletal muscle:
- Increased GLUT 4 in cell membrane
- Increased glycogen storage
- Increased mitochondria and oxidative enzymes in mitochondria
- Increased number and size of muscle fibres
- Increased vasculation of muscles- improves o2 supply
- Increased myoglobin - ability to store O2 in muscles

Benefits:
- Increase in muscle proteins and decrease in adipose stores
- Glucose tolerance improves so muscle glycogenesis increases
- Insulin sensitivity of tissues increases
- Blood triglycerides decrease – decreased VLDL, LDL and increased HDL
- Blood pressure falls
All of the above are very important in diabetics.
- Psychological effects – feeling of well being

Front 37

Compare the muscle in a sprinter and a marathon runner.

Back 37

The fibre composition of muscle is largely genetically determined.
Long distance runners (marathon) have 70% red muscle – type 1.
Sprinters have 70% white muscle – type 2

Red muscle: slower contraction, slower exhaustion, good capillary supply, lots of mitochondria, high fatty acid oxidation, high oxidative capacity, high myoglobin content, low glycosidic capacity.
Red muscle is needed for low intensity and high endurance exercise.

White muscle: faster contraction, faster exhaustion, poor capillary supply, few mitochondria, low fatty acid oxidation, high glycosidic capacity, low oxidative capacity, low myoglobin content.
White muscle is needed for high intensity and low endurance exercise.