Hormonal Control During Exercise

How to mobilize hormones from liver?

1. organ/gland → blood → circulatory system

2. substance released (hormone)

3. target tissue: tissue must have that hormone’s receptor!

steroid hormones

derived from cholesterol, lipid soluble, diffuse through membranes

nonsteroid hormones

made up of proteins/amino acids, not lipid soluble, cannot cross plasma membranes

divided into 2 groups:

1. protein/peptide hormones

2. amino acid derived hormones

what happens to insulin during exercise?

insulin goes down so other hormones can be activated

catecholamines

important for fuel (glucose) mobilization: norepinephrine and epinephrine

in the liver glucagon leads to

gluconeogenesis

what causes changes of hormones during exercise

muscle mass and intensity duration

the largest protein reservoir is

skeletal muscle

hormone sensitive lipase (HSL)

active stimulator of glycolysis

gluconeogenesis

reverse of glycolysis, creation of glucose

growth hormone

gland/location: pituitary gland, anterior lobe (base of brain)

effect on lipolysis (fats)

• increase lipolysis

• increase in liver gluceneogenesis: creation of new glucose

  • only activated during low energy state

• post exercise promotes muscle growth

as intensity or duration of exercise increase, hormone concentration released into the blood increases

during low intensity exercise minimal mass is active, not much change in hormone [ ]

*Note: growth hormone is one the most potent stimulators of HSL enzyme (mobilizing fats)

thyroxine (T4) triiodothyronine (T3)

permits other hormones for fuel mobilization

gland/location: thyroid gland (midline of neck below larynx)

T3 and T4 share similar functions:

• increase basal metabolic rate (BMR)

• increase glucose uptake

• increase glycolysis and gluconeogenesis

• increase lipid mobilization

• plays a role in metabolism

• hyperthyroidism/hypothyroidism

needed for other hormones to function properly

epinephrine and norepinephrine (catecholamines)

released when sympathetic NS is active

gland/location: adrenal medulla (atop of each kidney)

• sympathetic NS innervates adrenal medulla: interaction between NS and endocrine system

• NS active → catecholamines released

• increases liver and muscle glycogenesis: glycogen phosphorylase breaks. down glycogen in liver/muscle to make glucose

• increases lipolysis: HSL breaks down triglycerides into 3FA and glycerol

aerobic training decreases hormone levels at same exercise intensity

cortisol (a glucocoritcoid)

gland/location: adrenal cortex (atop of each kidney)

• increases amino acid mobilization that supports gluconeogenesis

  • from muscle → blood → liver

• increases glycogen breakdown

• increases lipolysis

• anti-inflammatory agent

fuel mobilization during exercise

insulin and glucagon

counter regulatory hormones influenced by glucose [ ]

location: pancreas (behind/below stomach)

insulin: elevated during energy available state ex: after eating

• increases glucose uptake and glycogen storage in muscle and liver

• increase fatty acid uptake and triglyceride storage in muscle, liver, adipocytes

• increases amino acid uptake in cells (protein synthesis)

• inhibits liver gluconeogenesis

glucagon: elevated after prolonged endurance exercise, overnight fasting

• increases liver gluconeogenesis

• increases liver glycogenolysis by activating reversal enzyme

hormone regulation of plasma volume

when active, causes retention of water in kidneys → maintains plasma volume

antidiuretic hormone (ADH)

retention of water in kidneys

playing soccer → sweating → plasma volume: some # of blood cells decrease in water volume (increases blood osmolality which triggers ADH → pituitary gland releases ADH to blood → increase retention of water

activation of ADH: increase in blood osmolality

renin angiotensin-aldosterone (RAA)

causes retention of water in kidneys

running (prolonged exercise) → dehydration: blood volume goes down → causes reduction in kidney blood flow → aldosterone released in kidney → water is retained in kidney

activation of RAA: reduction in kidney blood flow