Response to exercise

Perfusion

 the passage of fluid through the circulatory system or lymphatic system to an organ or tissue usually referring to the delivery of blood to a capillary bed tissue

Hypoxia

low levels of oxygen in body tissues

Sympathetic nervous system

fight or flight response

vasodilation

the widening of blood vessels due to the relaxation of the blood vessel's muscular walls

Vasoconstriction

the constriction of blood vessels, which increases blood pressure.

Total peripheral resistance (TPR)

the amount of force affecting resistance to blood flow throughout the circulatory system)

Systole

Contraction of the heart

Diastole

Relaxation of the heart

Left ventricular ejection fraction (LVEF)

is the central measure of left ventricular systolic function. LVEF is the fraction of chamber volume ejected in systole (stroke volume) in relation to the volume of the blood in the ventricle at the end of diastole (end-diastolic volume).

The sarcoplasmic reticulum (SR)

is a specialized form of the endoplasmic reticulum of muscle cells, dedicated to calcium ion (Ca2+) handling, necessary for muscle contraction and relaxation.

What is the body’s overall goal when responding to exercise?

• Maximise perfusion skeletal muscles and heart

• Maximise perfusion all other areas

• Initiator: muscle hypoxia (low o₂ levels)

• Mediator: sympathetic nervous system

How does the process begin?

Process beings w/muscle contraction

ATP used → O₂ used (need more ATP) therefore local hypoxia in tissues

Vasodilation occurs (blood vessels widening)

Multiple mediators released into plasma

Adenosine generated from ATP usage

Lactate

CO₂ , K⁺

Lowers total peripheral resistance (TRP) (the amount of force affecting resistance to blood flow throughout the circulatory system)

what happens after the sympathetic nervous system is activated regarding the body’s response to exercise?

Increased contractility (Stroke volume) + increased HR

Net result: Increased cardiac output

Increased systolic blood pressure (SBP)

Vasoconstriction in some areas (gut,skin)

Redistributes blood to important areas (heart, muscles)

Blood pressure summary

SBP rises (systolic blood pressure)

More CO = more blood in arteries = more pressure

Primary determinant systolic BP = cardiac output

DBP decreases slightly or stays normal

Local dilation of skeletal muscles

Primary determinant diastolic BP = peripheral resistance (resistance of the arteries to blood flow. Constrict Increase resistance. Dilate, decrease resistance)

Pulse pressure increases

TRP decreases (transient receptor potential)

Ejection fraction

LVEF increases (left ventricular ejection fraction)

More vigorous contraction

Major impact ESV (end systolic volume) decreases 

More preload but less filling time at fast heart rate

faster HR shortens diastole

LESS coronary filling time

Coronary vasodilation → increases blood flow

Only 1 way to get more oxygen

Cannot extract more O₂

Cardiac tissue extracts maximum O₂ from RBC’s (red blood cells)

Cannot extract more to meet increased demand

Preload

Preload - stretching of the heart that occurs with ventricular filling

Preload rises with exercise

Sympathetic stimulation → venous contraction

Increases preload/EDV

Contributes to rise in cardiac output

Along with increased HR and contractility

Lusitropy

Lusitropy - Myocardial relaxation

Opposite of contractility

Increased w/exercise

Contributes to increased preload → increased cardiac output

Key regulatory: phospholamban

Inhibitor: Sarcoplasmic reticulum Ca²⁺ ATPase (SERCA)

Phosphorylated via beta adrenergic stimulation

Stops inhibiting SERCA takes up calcium → relaxation

SERCA

Sarco/endoplasmic reticulum Ca²⁺ ATPase

Sympathetic stimulation → phosphorylated PLB

Inactivated PLB (relieves inhibitory effect)

Allows SERCA to uptake more calcium

Exercise

Rapidly depletes ATP in muscles

•Duration, intensity depends on other fuels

•Short term needs met by creatine

Creatine

Creatine

•Present in muscles as phosphocreatine

•Source of phosphate groups

•Important for heart and muscles

•Can donate to ADP ➜ATP

•Reserve when ATP falls rapidly in early exercise

•Spontaneous conversion creatinine

•Amount of creatinine proportional to muscle mass

•Excreted by kidneys

ATP and creatine

•Consumed within seconds of exercise

•Used for short, intense exertion

•Heavy lifting

•Sprinting

Exercise for longer time requires other pathways

•Slower metabolism

•Result: Exercise intensity diminishes with time

Aerobic exercise

•Long distance running

•Coordinated effort by organ systems

•Multiple potential sources of energy

•Anaerobic exercise

•Sprinting, weightlifting

•Purely a muscular effort

•Blood vessels in muscles compressed during peak contraction

•Muscle cells isolated from body

•Muscle relies on its own fuel stores

Anaerobic exercise

40 yard sprint

•ATP and creatine phosphate (consumed in seconds)

•Glycogen

•Metabolized to lactate (anaerobic metabolism)

•TCA cycle too slow

•Fast pace cannot be maintained

•Creatine phosphate consumed

•Lactate accumulates

Moderate aerobic

 Exercise1-mile run

•ATP and creatine phosphate (consumed in seconds)

•Glycogen: metabolized toCO2 (aerobic metabolism)

•Slower pace than sprint

•Decrease lactate production

•Allow time for TCA cycle and oxidative phosphorylation

•“Carbohydrate loading” by runners

•Increases muscle glycogen content

Intense aerobic exercise

Marathon

•Cooperation between muscle, liver, adipose tissue

•ATP and creatine phosphate (consumed in seconds)

•Muscle glycogen: metabolized toCO2

•Liver glycogen: Assists muscles➜ produces glucose

•Often all glycogen consumed during race

•Conversion to metabolism of fatty acids

•Slower process

•Maximum speed of running reduced

•Elite runners condition to use glycogen/fatty acids

Muscle cramps

•Too much exercise ➜↑ NAD consumption

•Exceed capacity of TCA cycle/electron transport

•Elevated NADH/NAD ratio

•Favors pyruvate ➜ lactate

•pH falls in muscles ➜cramps

•Distance runners: lots of mitochondria

•Bigger, too

Muscle cramps 2.0

•Limited supply NAD+

•Must regenerate

•O2 present

•NADH ➜NAD(mitochondria)

•O2 Absent

•NADH ➜NAD+ via LDH

Fed state

•Glucose, amino acids absorbed into blood

•Lipids b into chylomicrons ➜ lymph➜ blood

•Insulin secretion

•Beta cells of pancreas

•Stimulated by glucose, parasympathetic system

Insulin effects

•Glycogen synthesis

•Liver, muscle

•Increases glycolysis

•Inhibits gluconeogenesis

•Promotes glucose ➜adipose tissue

•Used to form triglycerides

•Promotes uptake of amino acids by muscle

•Stimulates protein synthesis/inhibits breakdown

Insulin in the liver

•Glucokinase (enzyme that facilitates the phosphorylation of glucose → glucose-6-phosphate)

•Found in liver and pancreas

•Induced by insulin

•Insulin promotes transcription

fasting/starvation

•Glucose levels fall few hours after a meal

•Decreased insulin

•Increased glucagon

Cori cycle and Alanine cycle

Hey effect of glucagon

•Glycogen breakdown in liver

•Maintains glucose levels in plasma

•Dominant source glucose between meals

•Other effects

•Inhibits fatty acid synthesis

•Stimulates release of fatty acids from adipose tissue

•Stimulates gluconeogenesis

Malnutrition

•Kwashiorkor (malnutrition characterized by sever protein deficiency)

•Inadequate protein intake

•Hypoalbuminemia → edema

•Swollen legs, abdomen

Marasmus

undernourishment causing a child's weight to be significantly low for their age

•Inadequate energy intake’

•Insufficient total calories

•Kwashiorkor without edema

•Muscle, fat wasting

Hypoglycemia in children

Low blood sugar

•Occurs with metabolic disorders

•Glycogen storage diseases

•Hypoglycemia

•Ketosis

•Usually after overnight fast

•Hereditary fructose intolerance

•Deficiency of aldolaseB

•Build-up of fructose1-phosphate

•Depletion of ATP

•Usually a baby just weaned from breastmilk

Hypoketotic Hypoglycemia

(Hypoketotic hypoglycemia Definition: A decreased concentration of glucose in the blood associated with a reduced concentration of ketone bodies.)

•Lack of ketones in setting of ↓glucose during fasting

•Occurs in beta oxidation disorders

•FFA ➜beta oxidation ➜ketones (beta oxidation)

•Tissues overuse glucose ➜hypoglycemia

Hypoketotic Hypoglycemia

•Carnitine Deficiency

•Low serum carnitine and acylcarnitine levels

•MCADdeficiency

•Medium chain acyl-CoAdehydrogenase

•Dicarboxylic acids 6-10 carbons in urine

•High acylcarnitine levels

a medical condition characterized by low blood sugar levels, with a focus on fatty acid oxidation disorders. It occurs when the body is unable to efficiently break down fats as an energy source, leading to a buildup of toxic by-products and a reduction in energy production