Module 6 - Hormones role in Exercise

• • Catabolic - energy availability maintaining exercise intensity
  • Anabolic - responding to intensity & build it, & repair (hormones)
• Many hormones impact multiple tissue types, & have diverse effects

  • Eg Testosterone & growth hormone (GH); both stimulate protein synthesis but have other roles
  • Testosterone - in terms of making new glycogen + GH - degated effect in terms of lipids
  • Some hormones are both anabolic & catabolic (eg GH)
  • Peptide & amine hormones tend to act fast, steroids power
• Hormone profiles during & after exercise preserve homeostasis, present or anticipated, eg

  • Prolonged (esp if low CHO, low E availability) &/or sustained competitive exercise increase several catabolic hormones, & suppress insulin
  • AMP can play a role to signal low energy
  • Whereas, activating many motor units (ie short, intensive) tends to cause more anabolic hormone profile, in ex & recovery
• Steroid Hormone:

  • (made on demand)
  • (water insoluble)
  • Requires transport protein in blood
  • Direct action on cell
• Peptide & Amine Hormones:

  • (made in advance)
  • (water soluble)
  • Free
  • Transport easy in blood (but harder to get in cell so,)
  • Secondary response = act on receptor
• Endocrine System Hormones:

  • Steroid hormones
  • Peptide & amine hormones
  • Erythropoietin (EPO)
  • Prostaglandins
• Steroid & Peptide Hormones work differently
• Steroids enter cells & bind at nucleus
• Peptides attach at surface, & act via secondary messengers = intracellular

  • Increase concentration w/ binding of hormone to receptor & amplifies cellular response (eg cAMP)
  • Different from AMP. Created by enzyme in membrane to start cascade of effects to turn on enzymes for response
• Hormones change rates of specific reactions in target cells. Done by changing rates of:

  • Transport across membrane
  • eg insulin increase GLUT4
  • Secretory activity (of other hormones)
  • eg GHIH, GHRH
  • Enzyme activity
  • eg insulin decrease HSL
  • Protein synthesis
  • eg Testerones, IGF-1
  • ALL have exercise & nutrient effect
  • Protein has biggest exercise effect
• Determinants of Hormonal activity:

  • Hormone concentration in blood
  • Hormone - Receptor interaction
• Hormone activity determined by hormone concentration in blood:

  • Rate of secretion (feedback)
  • Rate in inactivation (esp liver) or excretion (kidney)
  • decrease blood flow to lover & kidney in exercise
  • if gets cleared from blood stream quickly
  • Quantity of transport protein (for steroids)
  • how much is bound &/or free
  • Plasma volume (changes)
  • into tissues, PV drops
• Hormone activity determined by Hormone-Receptor Interaction:

  • Blood hormone levels
  • Number of target cell receptors
  • These can rapidly up- or down-regulate!
  • Affinity of binding
  • Receptor sensitivity
• Several factors can acutely change hormone function during exercise:

  • Δ Secretion
  • Δ Plasma volume
  • Δ Antagonist/Binding protein conc
  • Δ Metabolism/clearance
  • Determines cell’s sensitivity to hormone:
  • Δ Receptor sensitivity
  • Δ Receptor density (number/amount)
• Secretion of a hormone can be increase or decrease by several factors eg insulin factors

  • Feedforward control
  • Stress stimulates
  • Sympathetic nerves (SNS)
  • Beta cells
  • Insulin
  • Adrenal medulla
  • Noradrenaline (NAd)
  • Adrenaline (Ad)
  • Which inhibit beta cells
  • Insulin
  • Stress inhibits
  • Parasympathetic nerves (PNS)
  • Beta cells
  • Insulin
  • Negative feedback control
  • Inhibits the release of insulin secretion
• Neuroendocrine pathways of catabolism & anabolism:

  • Hypothalamus (releasing factors) →
  • Anterior Pituitary →
  • Stimulates →
  • Adrenal glands (stress hormones)
  • Catabolic or stress (Exercise)
  • HPA axis

  Or

  • Gonads (sex hormones)
  • Anabolic (Recovery)
  • HPG axis
  • Neg feedback inhibits hypothalamus
• Stress Hormones:

  • Cortisol
  • Adrenaline (Ad)
  • Noradrenaline (NAd)
• Stress hormones are catabolic & suppress anabolism:

  • Hypothalamus
  • Releasing hormones
  • Anterior Pituitary
  • ACTH, GH, Prolactin, LH, FSH
  • Stimulates:
  • Adrenal cortex
  • Cortisol which inhibits
  • Adrenal medulla &
  • Ad & NorAd
  • Anterior Pituitary
  • ACTH, GH, Prolactin, LH, FSH

  Or

  • Gonads: Ovaries/Testes
  • Progesterone, Oestrogen & Testosterone
• Exercise volume, recovery, feeding & life/total stress all important, esp if trying to maintain or accrue muscle
• Hypothalamus release hormones → affect Adrenal release of stress hormones & Gonads
• Cortisol can have neg feedback to not produce more sex hormone

  • also a immunosuppressant
• Hormones increase during exercise (except insulin)
• Hormones decrease after training (except insulin)
• Training enhances receptor sensitivity so don’t need to release as much for same response
• Catecholamines = adrenaline & noradrenaline
• Catecholamine Response to Exercise:

  • Vital, FAST response
  • Increase 2-6 fold (non linear)
  • Mediates actions through 2nd messengers
  • Many effects:
  • CV pressor responses
  • Increase substrate mobilisation
  • Facilitates other catabolic hormones
  • Immune mobilisation
  • Help maintain pressure
  • redistribution of blood flow
  • constricts, hormones in local area inhibit for vasodilation
  • Breaking down glycogen as well as adipose tissue
  • Act w/ other catabolic proteins
• Cardiovascular Effects of Catecholamines:

  • Increase blood pressure (BP) & redistribution of blood flow
  • Increase vasoconstriction
  • Increase heart rate (HR)
  • Increase ventricular contractility
  • Backed up by fluid regulatory hormones
  • Slower acting; ADH, Aldosterone
  • Greater response w/ increase exercise intensity
• Training increase catecholamine response at a given absolute intensity BUT not at same relative intensity
• Adrenaline increases glycogenolysis

  • Adrenaline increase disproportionately w/ exercise intensity
  • Free Calcium, greatly increases glycogenolysis in muscle
• Glycogen Depletion Strongly Dependent on Exercise Intensity

  • Q: Would this be altered by training status? Why?
  • A: Yes, it depends. Even at lower relative intensity trained people will utilise more fats so that means less CHO
  • At high intensity can’t really use fats can’t get ATP fast enough, trained can reach higher intensity so using more glycogen (relative intensity) & as have greater absolute intensity
• Glycogen depletion strongly dependent on exercise intensity

  • Trained utilise more fat, less CHO (even at lower relative intensity)
• Mobilisation of FFA Spares Glycogen at Moderate Intensity:

  • Mobilisation strongly in moderate & prolonged exercise
  • (catecholamines stimulate HSL - that breaks down FFA)
  • Helps sparse glycogen use, maintain [glucose]blood
  • Less FFA mobilisation w/ increase CHO feeding
  • (insulin inhibits HSL)
  • When fed at rest, prior to exercise, during (?)
  • Exercise response varies w/ catecholamine response (catecholamines inhibit insulin)
• Decrease %EE w/ exercise duration (are used first):

  • Muscle triglycerides
  • Muscle glycogen

  Increase %EE w/ exercise duration:

  • Plasma free fatty acids (FFA)
  • Blood glucose
• FFA Mobilisation & Oxidation Influenced by Exercise Intensity
• Very intensive exercise decreases FFA mobilisation despite strong hormonal drive for:

  • Possibly due to decrease blood flow to adipose tissue
  • From catecholamines (as constrict) - less blood to adipose tissue
• Very intensive exercise decrease fat oxidation - even of IMTG in muscle:

  • Higher rate of ATP need & remember, fat uses more O2 / ATP
  • Need ATP from CHO use (glycolysis)
• Low to moderate intensity increases fat oxidation, decreases CHO oxidation
• Fuel Mobilisation by Cortisol & Glucagon:

  • Prolonged or Heavy exercise (decrease energy), stress, exogenous source
  • Cortisol (from adrenal cortex)
  • Increase FFAs (lipolysis)
  • Increase amino acids
  • Which increases gluconeogenesis in pancreas
  • Decrease glucose uptake
  • Glucagon (from pancreas)
  • Increase glycogenolysis
  • Increase gluconeogenesis
  • Increase blood glucose (CNS)
• Prolonged or Heavy exercise (decrease energy), stress, exogenous source

  • Stimulate cortisol that increases amino acids how help w/ CHO availability
  • Provides amino acids to liver for gluconeogenesis
  • Glucagon stimulates breakdown of any glycogen in liver + new glucose (gluconeogensis)
• Control of Cortisol Secretion:

  • Exercise, Bone break, Burns, “Stress” →
  • Higher brain centres →
  • Hypothalamus →
  • ADH, Ad, NAd →
  • Mobilise & activate leukocytes →
  • Pos feedback to hypothalamus

  Or

  • CRH →
  • Anterior pituitary gland →
  • ACTH →
  • Adrenal cortex →
  • Cortisol →
  • Inhibits mobilisation & activation of leukocytes
  • Mobilises tissue amino acids
  • Mobilises free amino acids
  • Stimulates gluconeogenesis
  • Blocks entry of glucose into tissue
  • Neg feedback to Anterior pituitary & Hypothalamus
  • Long term neg affect is mobilise & active leukocytes (immune cells)