EXERCISE PHYSIOLOGY EXAM #2

steroid hormone signaling

lipid soluble 

freely diffuses through cell membrane

receptors located within the cell

nonsteroid hormone signaling

secreted from several tissues

lipid insoluble

not freely diffusible

activate second messengers

hypothalamus-pituitary axis (HPA)

links nervous and endocrine systems

hypothalamus innervates pituitary

synthesizes and secretes hormones that stimulate or inhibit pituitary

primary integration center for autonomic nervous system

anterior pituitary: growth hormone

posterior pituitary: ADH

thyroid

T3 and T4

increase metabolic rate

stimulated by TSH released by anterior pituitary during exercise

adrenal glands

catecholamines

• epinephrin

• norepinephrin

• fight or flight

• SNS → 80% E > 20% NE

• increase glycogenolysis

glucocorticoids

• cortisol

  • “stress hormone”

  • increase glucogenesis

pancreas

opposing hormones to balance glucose

insulin

• increase glucose into cells

• increase glycogenesis

• decrease gluconeogenesis

glucagon

• increase glycogenolysis

• increase gluconeogenesis

regulation of carbohydrate metabolism with exercise

regulated by a drop in insulin which rises in glucagon and catecholamines, and activation of glycogenolytic and glycolytic enzymes in muscle ensuring rapid glucose supply at high intensities and maintenance of blood glucose during prolonged exercise

regulation of fat metabolism with exercise

regulated by decreased insulin, increased catecholamines, glucagon, cortisol, and GH, which simulate lipolysis and FFA mobilization. transporters and mitochondrial enzymes regulate uptake and oxidation. fat use increases with duration but decreases at very high intensitiesregulaeed when carbohydrate metabolism predominates

hormones and sweat response/regulation

regulated by sympathetic cholinergic nerves releasing acetylcholine. aldosterone conserves sodium in sweat, ADH helps maintain plasma volume, and catecholamines assist with vasodilation. optimize heat loss while preserving fluid and electrolyte balance during exercise

hormones and prolonged exercise response/regulation

prolonged exercise insulin decreases while glucagon, catecholamines, cortisol, and GH hormone increase to maintain blood glucose and shift fuel use toward fat. aldosterone and ADH increase to conserve fluid and electrolytes, ensuring cardiovascular stability and thermoregulation

factors contributing to O2 deficit and EPOC

increase exercise intensity

increase elevation of metabolism post exercise

increase O2 deficit increases EPOC

effect of intensity and duration

O2 deficit at the start of exercise and relies on anaerobic energy. after exercise, oxygen stays elevated (EPOC) to restore everything

how do we measure exercise metabolism

indirect calorimetry (VO2 and VCO2)

other ones like blood lactate, muscle biopsies, doubled labeled water,, and HR monitoring

respiratory exchange ratio and fuel utilization during exercise

RER = VCO2/VO2

RER indicated balance of fat vs carbohydrate use during exercise. near 0.7 = mostly fat. near 1.0 = mostly carbohydrate. exercise intensity pushes RER up (toward carbs) while longer duration shifts RER down (toward fat)

what are the lactate and ventilatory thresholds

lactate threshold - point where blood accumulates beyond resting levels

ventilatory threshold - point where ventilation increases disproportionately due to CO2 buffering of lactate

mechanisms of lactate threshold

low muscle oxygen

accelerated glucolysis

recruitment of fast-twitch fibers

reduced rate of lactate removal

what is fatigue

decrements in muscular performance with continue effort

inability to maintain required power output to continue muscular work at a given intensity

cause fatigue:

• decrease rate energy delivery

• increase H+ La-

• muscle fiber contractile failure

• neuromuscular control failure

metabolic, muscular, neuromuscular contributors to/mechanisms of fatigue

metabolic

• glycogen/PCr depletion, H+ accumulation

• reduced ATP supply → less force/endurance

muscular

• excitation-contraction coupling failure, cross-bridge dysfunction, fiber damage

• weak contractions, impaired force production

neuromuscular

• reduced motor unit recruitment, neurotransmitter shifts, NMJ fatigue

• lower voluntary activation, increased perception of effort

relationship between glycogen depletion and fatigue

fatigue is related to total glycogen depletion not the rate of depletion

may vary by fiber type/muscle group

limiting ATP supply, impairing muscle contraction, reducing central nervous system function, forcing a less efficient reliance on fat metabolism

carbohydrate availability critical factor in endurance performance

purpose of cardiovascular system

transport, maintain pH, thermoregulation/fluid balance, protection (blood loss & infection)

anatomy and blood flow through valves

1. right atria

2. tricuspid valve

3. right ventricle

4. pulmonary valve

5. pulmonary arteries

6. across lungs

7. pulmonary veins

8. left atria

9. mitral valve

10. left ventricle

11. aortic valve

12. aorta

13. systemic arteries

14. systemic capillaries

15. vena cava

16. right atria

anatomy and blood flow through myocardium vs skeletal muscle

heart relies on coronary circulation and gets most of its blood during relaxation (diastole)

uses systemic arteries and blood flow is more flexible and can recruit more capillaries

anatomy and blood flow through intercalated discs/desmosomes/functional syncytium

intercalated discs - junction between cardiac muscle cells

desmosomes - hold cells together so they don’t pull apart during contraction

functional syncytium - contracts in unison

understand flow of blood from heart to pulmonary and systemic circulation

pulmonary (right side of heart) - superior vena cava → right atrium → right ventricle → pulmonary trunk → right and left pulmonary arteries → arterioles → venules → left atrium

systemic (left side of heart) - left atrium → left ventricle → ascending aorta → coronary arteries → aortic arch → descending aorta → arterioles → venules → right atrium

what is the driving force behind blood flow?

the pressure gradient created by ventricular contraction (heart as a pressure pump)

how do we get blood flow to the heart

blood supply to the heart comes from coronary arteries

blood away from the heart comes from the coronary veins

how do pacemaker cells work/how is the heart rate altered

fire automatically because of the leaky channels

sympathetic input speeds them up (more Ca/Na influx)

parasympathetic input slows them down (more K and less Ca)

break down wigger’s diagram/cardiac cycle

1. ventricular filling period

   1. mitral valve open

   2. aortic valve closed

   3. atrial pressure decreases then small increase

   4. ventricular pressure is same as atrial

   5. aortic pressure decreases

   6. aortic blood flow no change

   7. ventricular volume increases

2. isovolumetric contraction

   1. mitral valve closed

   2. aortic valve closed

   3. atrial pressure no change

   4. ventricular pressure increases

   5. aortic pressure no change

   6. aortic blood flow no change

   7. ventricular volume no change

3. ventricular ejection period

   1. mitral valve closed

   2. aortic valve open

   3. atrial pressure small increase

   4. ventricular pressure increases

   5. aortic pressure increases

   6. aortic blood flow increases

   7. ventricular volume decreases

4. isovolumetric relaxation

   1. mitral valve closed

   2. aortic valve closed

   3. atrial pressure increases

   4. ventricular pressure decreases

   5. aortic pressure decreases

   6. aortic blood flow no change

   7. ventricular volume no change

what determines when you move to the next phase

determined by pressure changes in the chambers relative to each other

valves open when upstream pressure is greater than downstream pressure and valves close when upstream pressure is less than downstream pressure

electrical depolarization triggers contraction which changes the pressure

how is pressure changing in each phase

1. ventricular filling

   1. high pressure in aorta and atrium

2. isovolumetric contraction

   1. higher pressure in atrium or equal

3. ventricular ejection

   1. pressure higher in ventricle

4. isovolumetric relaxation

   1. when pressure is less in ventricle than atria

where is blood moving or not moving during each phase

1. atrial systole

   1. atria → ventricles

2. isovolumetric ventricular contraction

   1. none

3. ventricular ejection

   1. ventricles → arteries

4. isovolumetric ventricular relaxation

   1. atria slowly filling

5. ventricular filling

   1. atria → ventricles

interrogate relationships between cardiac output (SV, HR, MAP, TPR) and (EDV, ESV, preload, contractility, afterload, SNS, etc)

cardiac output = CO = HR x SV

stroke volume = SV = EDV (preload) - ESV (afterload)

SV depends on 3 factors

1. preload (EDV)

   1. stretch of ventricular myocardium

2. contractibility

   1. force of contraction at a given preload

3. after load (ESV)

   1. pressure ventricles must exceed to open semilunar valves

4. HR regulation

   1. SNS increases HR; PNS decreases HR

5. mean arterial pressure

   1. MAP ~ CO x TPR

   2. CO increases → MAP increases

   3. TPR increases → MAP increases

describe Frank-Starling law

the stroke volume increases in response to an increase in the volume of blood filling the heart (EVD/preload) up to a physiological limit

the heart pumps what it receives - more filling → stronger contraction → more blood ejected

form/function of different levels of arterial tree

1. arteries

   1. highest blood pressure

   2. freeways of body

   3. get point A to point B fast

2. arterioles

   1. street lights

   2. control flow of traffic

3. capillaries

   1. get off bus

   2. flow is no that heavy

Pousiells’s Law and its manipulation

change in pressure x pi x radius^4 / 8 x viscosity x length

shorter is easier

longer has more resistance

radius is most important since squared to the 4th

how does the vascular endothelium work/what does it respond to to control blood flow and regulate vessel diameter

it senses flow, pressure, metabolizes, and hormones and in response releases dilator or constrictors. this fine-tunes vessel diameter and ensures tissues get the right amount of blood at the right time

importance of vascular tone

essential for maintaining blood pressure, directing blood flow, protecting microcirculation, and preventing fluid imbalance. too much or too little tone leads to major cardiovascular problems

factors regulating vessel diameter

neural control (norepinephrine/epinephrine

local metabolites

endothelial signals

hormones

myogenic mechanisms

processes of gas delivery/removal

ventilation moves air

pulmonary diffusion exchanges gases with blood

transport carries gases via Hb/plasma

tissue diffusion delivers O2 removes CO2

ventilation again eliminates CO2

mechanics of normal respiration

inspiration = active, driven by diaphragm and external intercostals → thoracic expansion → negative alveolar pressure → air in

expiration = passive, elastic recoil → alveolar pressure above atm → air out

differences between pulmonary vs systemic circulation (pressure and vascular make-up)

pulmonary: low pressure, low resistance, thin-walled vessels, designed for efficient gas exchange without damaging delicate alveoli

systemic: blood flow over long distances and distribute it to all organs

how to measure ventilation

minute ventilation: total air in/out per minute

alveolar ventilation: fresh air reaching alveoli

physiological dead space and CO2 measurements refine accuracy

alveolar ventilation, factors contributing to gas diffusion

alveolar ventilation = (VT - VD) x f determines how much fresh air reaches alveoli

gas diffusion depends on surface area, barrier thickness, partial pressure gradients, diffusion coefficient, and capillary transmit time

movement of gases at lungs and tissues

at the lungs: O2 moves into blood, CO2 moves out to alveoli

at the tissues: O2 moves into cells, CO2 moves into blood

how and why gases move where they do

how: always by simple diffusion down partial pressure gradients

why: O2 moves into blood at lungs and into tissues at capillaries to support metabolism. CO2 moves into alveoli at lungs and into blood at tissues to remove waste and maintain pH balance

O2 cascade

oxygen cascade shows how PO2 falls from 160 mmHg in inspired air → ~100 mmHg in alveoli → ~95 mmHg in arterial blood → ~40 mmHg in venous blood → ~1-5 mmHg at the mitochondria, where it drives cellular respiration

how are O2 and CO2 transported (dissoved, Hb

O2

• ~98% Hb-bound, ~2% dissolved

• dissolved O2 sets PO2; Hb massively increases carrying capacity

CO2

• ~70% bicarbonate, ~20-25% Hb-bound, ~5-10% dissolved

• haldane effect (O2 unloading → increase CO2 uptake) complements Bohr effect

OxyHb dissociation curve

what shifts the curve

why importance

what does the shift favor

right shift → favors O2 unloading to tissues

left shift → favors O2 loading in lungs (but less delivery to tissues)

role of myoglobiin

myoglobin stores and releases O2 within muscle cells, acting as a local reserve and facilitator of O2 delivery to mitochondria, especially during exercise or hypoxia

CO2 and bicarbonate

most CO2 is carried as bicarbonate after being converted inside RBCs. this system allows CO2 transport, pH buffering, and efficient gas exchange at both tissues and lungs

control of ventilation

controlled mainly by medullary and pontine neural centers, adjusted by chemoreceptors sensing CO2, O2, and pH with fine-tuning from reflexes, higher brain inputs, and muscle activity