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How is ATP regenerated?
it is continually rebuilt from ADP + Pi
Which energy system pathway dominates?
the contribution depends mainly on intensity, duration, fuel, and oxygen availability
With regards to hormones, how is fuel mobilized or stored?
Exercise generally increases fuel mobilization and changes insulin/glucagon balance
Key measures of how much energy is being used?
VO2, VCO2, calorimetry, RER, and VO2 max
With regards to fatigue, why does performance fall?
Fatigue is multifactorial and reversible with rest
What changes with training?
Aerobic training improves oxygen delivery/use; anaerobic gains rely heavily on neural, strength and buffering changes
ATP Hydrolysis
ATP → ADP + Pi; releases usable energy for processes such as myosin cross-bridge cycling
Bioenergetics
The study of how energy is transferred and used in biological systems
Catabolism
Breakdown of molecules to release energy
Anabolism
Building larger molecules from smaller units; generally requires energy
Oxidation/Reduction
Oxidation = loss of electrons; Reduction = gain of electrons. ETC reactions alternate these processes.
Enzyme
protein that speeds a chemical reaction without being consumed
Rate-limiting enzyme
Enzyme that exerts major control over the speed of a pathway
Phosphorylation
Addition of a phosphate group; in energy metabolism, it can help form ATP or activate intermediates
Glycogenesis
Formation/storage of glycogen from glucose
Glycogenolysis
Breakdown of glycogen
Gluconeogenesis
Formation of glucose from non-carbohydrate sources including lactate, glycerol, and amino-acid carbon skeletons
Proteolysis/Protein synthesis
breakdown of proteins into amino acids / formation of body proteins from amino acids
Fuel Storage
carbs stored primarily as glycogen in skeletal M and liver
fat stores mainly as triglyceride (TG), a TG contains 3 fatty acids + glycerol
amino acids are the building blocks of proteins & can contribute to metabolism, especially during prolonged exercise or low carb availability
Energy Systems & Muscle Metabolism
all 3 systems operate at the same time. the key issue is which system contributes the greatest share of ATP at a given moment.
System: ATP-PCr
primary fuel/rxn: stored ATP & phosphocreatine (PCr) regenerate ATP via creatine kinase
O2?: no direct O2 requirement
speed/capacity: fastest; very limited stores
best associated w: maximal efforts lasting roughly seconds
System: Glycolysis
primary fuel/rxn: glucose or glycogen → G6P → Pyr; Pyr may become lactate
O2?: can proceed w/out O2
speed/capacity: fast; limited by substrate, H+, and other factors
best associated w: high intensity efforts lasting seconds to minutes
System: Oxidative
primary fuel/rxn: Acetyl-CoA enters Krebs cycle; NADH/FADH2 deliver electrons to ETC; oxidative phosphorylation makes ATP
O2?: yes
speed/capacity: slowest ATP rate; greatest capacity
best associated w: longer duration, lower-to-moderate intensity work
ATP-PCR System
ATP hydrolysis supplies immediate energy. PCr donates its phosphate to ADP to rapidly rebuild ATP.
Creatine kinase is the key enzyme: PCr + ADP + H+ ↔ ATP + creatine.
PCr formation occurs in the mitochondria when ATP supply is adequate; PCr is then available in the cytosol for rapid ATP regeneration.
The system is powerful but short-lived because intramuscular ATP and PCr stores are small.
Glycolysis & Pyruvate fate
The usable carbohydrate form entering glycolysis is glucose-6-phosphate (G6P). Glycogen can enter glycolysis after being broken down and phosphorylated.
Glycolysis occurs in the cytosol and ends with pyruvate. Its rate-limiting enzyme is phosphofructokinase (PFK).
Pyruvate fate depends on exercise intensity, oxygen delivery/use, mitochondrial capacity, and the balance between production and clearance: it can become lactate or be converted to acetyl-CoA.
Lactate is not simply a waste product; it can be transported and oxidized or converted back to glucose in the liver through the Cori cycle.
Oxidative Metabolism
Pyruvate is converted to acetyl-CoA before entering the Krebs (citric acid) cycle.
The Krebs cycle produces NADH and FADH2. These electron carriers deliver electrons to the electron transport chain.
The ETC uses a series of oxidation-reduction reactions to create a proton gradient. ATP synthase uses that gradient to form ATP: oxidative phosphorylation.
NADH produces approximately 2.5 ATP and FADH2 approximately 1.5 ATP.
Carb and Fat Metabolism
Fuel selection shifts with intensity: as exercise intensity rises, the body generally shifts from a greater reliance on fat toward a greater reliance on carbohydrate. This is the crossover concept.
Carbohydrate pathway: Glycogenolysis
Glycogen → glucose-related intermediates; supports blood glucose or muscle energy.
Carbohydrate pathway: Glycolysis
G6P → pyruvate; produces ATP rapidly and can proceed without direct oxygen use.
Carbohydrate pathway: Gluconeogenesis
Lactate, glycerol, and amino-acid substrates → glucose, primarily in the liver.
Carbohydrate pathway: Cori cycle
Lactate from muscle travels to liver, is converted to glucose, and glucose can return to muscle.
Carbohydrate pathway: Glycogenesis
Glucose → glycogen for storage, especially when insulin is elevated.
Fat Metabolism
Lipolysis is the breakdown of triglycerides into fatty acids and glycerol.
Fat circulating in the blood is commonly transported as free fatty acids (FFAs).
Beta-oxidation converts fatty acids into acetyl-CoA, which enters the Krebs cycle.
A triglyceride has three fatty acids; complete oxidation therefore includes ATP from all three fatty acids plus ATP from glycerol. The slides use an example of about 406 total ATP for a triglyceride under their accounting assumptions.
Protein Metabolism
Proteolysis breaks body proteins into amino acids.
Amino acids may be used for protein synthesis or contribute carbon skeletons to energy metabolism after removal/processing of nitrogen
Hormone: Insulin
Class/source: nonsteroid; pancreas
Major exercise-related effects: Promotes glucose uptake, glycogen storage, fatty-acid uptake/triglyceride storage, and amino-acid uptake; inhibits liver gluconeogenesis.
Hormone: Glucagon
Class/source: nonsteroid; pancreas
Major exercise-related effects: Released especially when blood glucose is low; promotes liver glycogenolysis and gluconeogenesis
Hormone: Epinephrine/norepinephrine
Class/source: Amino-acid-derived catecholamines; adrenal medulla
Major exercise-related effects: Sympathetic activation; increases liver and muscle glycogenolysis and lipolysis.
Hormone: Cortisol
Class/source: Steroid glucocorticoid; adrenal cortex
Major exercise-related effects: Increases amino-acid mobilization for gluconeogenesis, glycogen breakdown, and lipolysis; anti-inflammatory.
Hormone: Growth Hormone
Class/source: Peptide; anterior pituitary
Major exercise-related effects: Increases lipolysis and liver gluconeogenesis; supports post-exercise muscle growth.
Hormone: T3/T4
Class/source: Amino-acid-derived; thyroid
Major exercise-related effects: Increase BMR, glucose uptake, glycolysis/gluconeogenesis, and lipid mobilization; support proper action of other hormones.
Hormone: ADH
Class/source: Peptide; posterior pituitary
Major exercise-related effects: Supports water conservation and plasma-volume regulation during fluid loss
Hormone: Aldosterone
Class/source: Steroid; adrenal cortex, RAA system
Major exercise-related effects: Promotes sodium retention; water follows sodium, supporting blood/plasma volume.
Steroid vs. Nonsteroid hormones
Steroid hormones are derived from cholesterol, are lipid-soluble, and can diffuse through cell membranes to influence intracellular receptors and gene expression.
Nonsteroid hormones are not lipid-soluble and cannot cross the cell membrane freely. They act through membrane receptors and intracellular second-messenger pathways. They include protein/peptide and amino-acid-derived hormones.
High-yield hormone patterns
During exercise, sympathetic hormones rise and fuel mobilization increases.
As exercise intensity or duration increases, growth hormone release generally increases.
Aerobic training can reduce catecholamine levels at the same absolute exercise intensity because the exercise is less physiologically stressful.
The endocrine system is regulated by feedback loops. Negative feedback occurs when the response reduces the original stimulus, helping restore a stable internal condition.
Energy Expenditure
Energy expenditure is the rate at which the body uses energy. A food “Calorie” is a kilocalorie (kcal), the heat required to raise 1 kg of water by 1°C.
Direct calorimetry
What it tells you: Heat produced by the body
Strengths & Limits: Accurate over time and useful at rest; expensive, slow, and affected by exercise equipment and sweat
Indirect calorimetry
What it tells you: Energy expenditure estimated from respiratory gases
Strengths & Limits: Uses O2 consumption and CO2 production; best during steady-state oxidative metabolism
VO2
What it tells you: Volume of oxygen consumed per minute
Strengths & Limits: Inspired O2 volume minus expired O2 volume; central measure of aerobic metabolism.
VCO2
What it tells you: Volume of CO2 produced per minute
Strengths & Limits: Expired CO2 volume minus inspired CO2 volume.
RER
What it tells you: VCO2 / VO2
Strengths & Limits: Helps estimate carbohydrate-versus-fat use; values trend higher with greater carbohydrate use.
VO2max
VO2max is the point at which oxygen consumption no longer increases despite further increases in exercise intensity. It is the best single measure of aerobic fitness, but not necessarily the best predictor of endurance performance.
VO2max may be reported as L/min (absolute) or ml·kg−1·min−1 (relative to body mass). Relative VO2max allows fairer comparisons among people of different body sizes, especially for weight-bearing activities.
Lactate Threshold
Lactate threshold is the intensity at which blood lactate accumulation markedly increases because production exceeds clearance. It reflects interaction of aerobic and anaerobic metabolism and is commonly expressed as a percentage of VO2max.
Typical lactate-threshold values of about 50–60% VO2max for untrained people and 70–80% for trained people.
Fatigue
Fatigue is a decrement in muscular performance with continued effort accompanied by tiredness, or the inability to maintain the required power output at a given intensity. It is reversible by rest.
Excess post-exercise oxygen consumption (EPOC)
Replenishes ATP and PCr stores.
Supports continued substrate cycling of glucose and fatty acids.
Maintains an elevated rate of fatty-acid oxidation.
Helps return elevated body temperature toward normal.
Reflects elevated catecholamine levels and other recovery processes
Adaptations to Training
Training adaptations are specific to the systems repeatedly stressed. Aerobic training primarily improves oxygen delivery and aerobic ATP production; anaerobic training improves high-intensity performance through several mechanisms.
Aerobic training adaptation: Increased capillary density
Functional result: Greater oxygen delivery to active skeletal muscle.
Aerobic training adaptation: Increased myoglobin concentration
Functional result: Greater oxygen transport/storage within muscle and improved delivery to mitochondria.
Aerobic training adaptation: Increased mitochondrial density
Functional result: Greater capacity for aerobic ATP production.
Aerobic training adaptation: Increased oxidative capacity
Functional result: Faster rate of aerobic ATP production.
Aerobic training adaptation: Higher lactate threshold
Functional result: Can exercise at a higher percentage of VO2max before substantial lactate accumulation; reflects improved production and clearance.
Aerobic training adaptation: Greater fat oxidation / lower submaximal RER
Functional result: More ATP can be produced through beta-oxidation, reducing reliance on glycolysis at a given submaximal workload.
Aerobic exercise prescription
Frequency: approximately 3–5 days per week.
Duration: approximately 20–30 minutes per day.
Intensity: the most important factor; the textbook recommendation shown is about 70% VO2max.
The muscle must be active and performing work for local adaptations to occur.
Stroke Volume
volume of blood pumped in one heartbeat
SV = EDV - ESV
EDV
volume of blood in the left ventricle before the heart contracts
ESV
volume of blood when the heart contracts (left over)
Cardiac Output (Q)
total volume of blood pumped per minute
Q = HR x SV
3 major functions of blood
transport (O2, nutrients, waste)
temp regulation
pH balance
blood volume
5-6L in men
4-5L in women
whole blood
plasma + formed elements (blood cells)
hematocrit
total percent of volume composed of formed elements
red blood cells
male: 42-45%
female: 38-42%
anemia
less blood cells make you anemic
At rest where is most of the blood?
in the veins
When at rest:
large resorvior of blood is in the splanchnic region
When exercising:
blood moves out of the splanchnic region to the needed muscle
intrinsic control of blood flow
ability of local tissues to constrict or dilate arterioles
Intrinsic Control of Blood Flow
occurs through capillary beds
changes occur because M is contracting
Metabolic mechanisms (VD):
buildup of local metabolic by-products
uses O2, produces, CO2, K+, and H+
Extrinsic Neural Control of Blood Flow
when the sympathetic system gets activated, releases Epi & Norepi which causes catecholamines to bind to receptors and causes smooth M to contract
Redistribution of flow at organ, system level
sympathetic nervous system innervates smooth M in arteries and arterioles:
Baseline sympathetic activity → vasomotor tone
During exercise: increases sympathetic activity → increases vasoconstriction
At rest: decreases sympathetic activity → decreases vasoconstriction (passive VD)
Mechanisms that assist venous return
one-way venous valves
muscle pump
respiratory pump (big changes in thoracic pressure, so big breaths during high intensity exercises)
What system regulates HR
nervous system
HR graph
linear relationship
at rest: total activation of PNS
0-100bpm: gradual withdraw of PNS
100bpm to HR max: gradual increase of SNS
Stroke Volume Graph
venous return and EDV are increasing meaning more blood is going to the heart. more blood into the left ventricle stretches the left ventricle resulting in more forceful contractions (Frank - Starling Mechanism) and thus a decrease in ESV. However, because the heart size (LVEDD) is fixed (it can only get so big) and blood volume is limited, at 60% VO2 max there is a plateau.
LVEDD
left ventricle end diastolic diameter
Cardiac Output Graph
HR = linear relationship
SV = plateau
from rest to 60% VO2 max: HR and SV increasing
from 60% VO2 max to max: only HR increasing
SBP (systolic blood pressure)
determined by increase in Q (cardiac output) x decrease in TPR (total peripheral resistance)
a-VO2 difference
As exercise increases:
arterial content increases
venous content decreases
a-VO2 difference increases
this is because more muscle mass is being recruited which means we need more oxygen
1g of Hb carries
1.34mL of O2
Hb in male and female
male: 15g of Hb/100mL of blood
female: 12.5g of Hb/100ml of blood
to find O2 in blood
multiply grams of Hb by 1.34
example for males: 15 × 1.34 = 20.1 mL of oxygen/ 100mL of blood
Bohr effect
pH and temp can affect how O2 binds to Hemoglobin
lower pH or higher temp results in more O2 being released from hemoglobin which makes O2 get delivered faster and ATP production faster
3 ways CO2 is carried in blood
bicarbonate
dissolved in plasma
bound to Hb (carbaminohemoglobin)
bicarbonate
transports 60-70% of CO2 in blood to lungs
carbonic acid dissociates into bicarbonate (CO2 + H2O → H2CO3 → HCO3- + H+) rxn is catalyzed by carbonic anhydrase
when CO2 gets into lungs, the rxn goes the other way and CO2 is produced
dissolved carbon dioxide
not very efficient
7-10% of CO2 dissolved in plasma
when PCO2 is low in the lungs, CO2 comes out of solution and diffuses into alveoli
Carbaminohemoglobin
20-33% of CO2 transported bound to Hb
does not compete w O2-Hb binding since O2 binds to heme portion of Hb and CO2 binds to protein (globin) portion Hb
getting into lungs: increase in PCO2 → easier CO2-Hb binding
leaving lungs: decrease in PCO2 → easier CO2-Hb dissociation
avg amount of O2 per 100mL of blood
20mL of O2
Pulmonary ventilation in relation to exercise intensity
Ventilation increases before exercise starts due to anticipating & preparing for the exercise (ex: a swimmer or runner waiting for the beeper to go off before starting)
As intensity of exercise increases, so does pulmonary ventilation
Ventilatory rate gets closely matched with the amount of muscle mass in intensity
Pulmonary Diffusion
100% AIr = 79.04% N2 + 20.93% O2 + 0.03 CO2
- Total air P: atmospheric pressure
- individual P: partial pressures
Standard atmospheric P = 760 mmHq
- Daltons Law: total air p = PN2 + PO2 + PCO2
- PN2 = 760 x 79.04% = 600.7 mmHg
- PO2 = 760 x 20.93% = 159.1 mmHg
- PCO2 = 760 x 0.04% = 0.2 mmHg
Regulation of Pulmonary Ventilation
- Primary drive to increase ventilation during exercise (starts in the brain, motor cortex) --> goes into higher brain centers --> Ventilatory control center (Medulla Oblongata) (Peripheral chemoreceptors and Skeletal muscle receptors (chemo receptors and mechanoreseptos that provide feedback for ventilation) also go into control center) --> the control center then goes into respiratory muscles
Central Mechanisms of regulation
Respiratory centers
- inspiratory, expiratory centers
- located in brain stem (medulla oblongata, pons)
- Established in rate, depth of breathing via signals to respiratory muscles
- Cortex overrides signals of necessary
Central chemoreceptors
- stimulated by increase in CO2 in cerebrospinal fluid
- increase rate and depth of breathing, remove excess CO2 from body
Peripheral Mechanisms of Regulation
peripheral chemorceptors (prevents you from stopping your breathing)
- in aortic bodies, carotid bodies
- sensitive to blood PO2, PCO2, H
Mechanoreceptors (stretch)
- in pleaurae, bronchioles, alveoli
- excessive stretch--> reduced depth of breathing
- Hering - Breuer reflex