Respiratory Exchange Ratio (RER)

.• RatiobetweenCO2.released(VCO2) and oxygen consumed

(VO2)

.• RER=VCO2/VO2

• Usually0.78to0.80atrest

Respiratory Exchange Ratio

Limitations:

• Does not take PRO into account

• CO2 exchange not as constant as O2 use

– CO2 can change with different breathing patterns

– This occurs at intense/max exercise when lactate/acid build up increases exhalation of CO2

Due To Limitations,best at rest or steady state exercise

• Typical values:

– Rest: 0.78 - 0.80

– Increases with greater exercise intensity – Indicative of greater reliance on CHO

Isotopes:element with atypical atomic weight 

Isotopes – Radioactive or nonradioactive

Isotopes – Traced throughout the body

Isotopes – Good for long-term measure

Isotopes – Can convert into energy expenditure

• Carbon 13 – infused, selectively traced to determine distribution and movement

• Doubly labeled water (deuterium: 2H) - ingested, monitor rate at which substance leaves body in urine, saliva, and blood

Calorimetry

Key Points

• Direct calorimetry measures heat production

• Indirect calorimetry measures O2 consumption & CO2 production

• RERatrest=0.78to0.80

• RERforfat=0.70

• RER for carbohydrate = 1.0

• Isotopes used to determine metabolic rate over long periods of time

Basal Metabolic Rate (BMR

BMR: minimum amount of energy required by body to sustain basic cellular function,

i.e., for living

BMR is  measured in supine position,thermoneutral environment,after 8hr sleep and 12 hr fast

BMR Affected by:

• Fat-free mass (FFM)

• Body surface area (BSA)

• Age – gradual decline w/age, ↓ FFM

• Stress – psychological stress ↑ activity of SNS

• Hormones - Thyroxine & epinephrine both ↑ BMR 

• Body temperature – higher w/ higher temperature

RMR:

• Similar to MR(within 5-10%)

• Easier To Measure(stringent conditions not met) • Ranges from 1,200 - 2,400 kcal/day

Food energy equivalents:

CHO: 4 kcal/g

Fat: 9 kcal/g

Protein: 4 kcal/g

Energy per liter of oxygen consumed

CHO: 5.0 kcal/L Fat: 4.7 kcal/L Protein: 4.5 kcal/L

Metabolic Rate During Submaximal Exercise

• Metabolism ↑ in direct proportion to ↑ in exercise intensity

• During exercise at a constant power output (work rate) VO2 ↑ from resting value to steady-state within 2-3 minutes

• Linear ↑ in VO2 with ↑ in work rate

Maximal Oxygen Uptake (VO 2max

• Maximal capacity for O2 consumption during maximal exertion
  – Point at which O2 consumption does not ↑ w/ added work

• Best measurement of aerobic fitness

• Increases w/ training (plateaus at 8-12 weeks)

• Usually expressed relative to body weight (ml · kg-1 · min-1)

• Normally active untrained college-aged students = 38-42 (women); 44-50 (men)
  – Due to differences in FFM and hemoglobin

• Declines in active people after age 25-30 by ~ 1% per year

• Best measurement of aerobic fitness

• NOT best predictor of endurance performance

• Even w/ plateau at 8-12 weeks, performance can ↑
  – More training allows competition at higher percentage of V• O2max

Key points:

BMR minimum energy to sustain life

• RMR more often measured

• Can calculate caloric expenditure from VO2 and RER

• VO2max highest oxygen consumption with maximal work

Estimates of anaerobic effort include

• Excess post-exercise oxygen consumption (EPOC)

• Lactate threshold

O2 demand > O2 consumed in early exercise

• Body incurs O2 deficit

• Occurs when anaerobic pathways are used for ATP production

O2 consumed > O2 demand in early recovery

• Excess postexercise O2 consumption (EPOC)

Factors Responsible for EPOC

• Rebuilding depleted ATP and PCr supplies

• Clearing lactate

• Replenishing O2 supplies borrowed from Hb and myoglobin

• Removing accumulated CO2

• Increased metabolic and respiratory rates due to ↑body temperature

Lactate Threshold

• Point when blood lactate begins to accumulate above rest, usually with ↑ exercise intensity

• Production exceeds clearance

• Expressed as %VO2max

• Lactate Accumulation = fatigue

  • –  Ability to exercise hard without accumulating lactate
    beneficial to athletic performance

  • –  Compare two athletes with same VO2max

  • –  One with higher lactate threshold = better endurance performance

Lactate threshold (LT) (%VO2max):

• One of best determinants of an athlete’s pace in endurance events

• UT typically have LT around 50% - 60% VO2max

• Elite athletes reach LT around 70% - 80% VO2max

There is no clear V• O2max-like method for measuring anaerobic capacity

Imperfect but accepted methods include 

• Maximal accumulated O2 deficit

• Wingate anaerobic test

• Critical power test

Economy of Effort 

As athletes become more skilled, they use less energy for given pace •

• Is true independent of VO2max

• Body learns energy economy with practice

Multifactorial phenomenon

• Better form is more economical

• Economy increases with distance of race

• Varies with type of exercise (running vs. swimming)

Successful Endurance Athletes

1. High VO2max

2. High lactate threshold (as % V• O2max)

3. High economy of effort

4. High percentage of type I muscle fibers

• EPOC - metabolic rate above resting level after exercise

• Lactate threshold - point when lactate production exceeds ability to clear or remove lactate

• Calculations of energy expenditure ignore anaerobic aspects

• Higher lactate threshold indicative of endurance performance

• Endurance performance capacity also associated w/ high economy of effort

Definitions of fatigue

1. Decrements In Muscular Performance With continued effort, accompanied by sensations of tiredness

2. Inability To Maintain Required Power Output To continue muscular work at given intensity

Complex phenomenon influenced by

• type/intensity of exercise

• fiber type

• training status, diet

Four major causes of fatigue:

1. Energy delivery (ATP-PCr, anaerobic glycolysis, and oxidation)

2. Accumulation of metabolic by-products (e.g., lactate, H+)

3. Failure of muscle contractile mechanism

4. Alterations in the nervous system

PCr depletion
– Coincides with fatigue – Offset by pacing

Glycogen depletion (“hitting the wall”)
– Reserves are limited so can deplete quickly
– Depletion correlated with fatigue
– Occurs more quickly with high intensity exercise
– Pattern depends on duration & intensity of activity
– Selective to muscle groups involved in activity
– Depletion of liver glycogen to increase blood glucose 

Muscle Glycogen and Fatigue

• Fibers recruited first or most often deplete fastest • Type I fibers w/ moderate endurance exercise

• Pattern depends on intensity of activity

  • Type I fibers recruited first (light/moderate intensity)

  • Type IIa fibers recruited next (moderate/high intensity)

  • Type IIx fibers recruited last (maximal intensity)

• Selective to muscle groups involved in activity

• Depletion of liver glycogen to increase blood glucose

  • Muscle glycogen not enough for prolonged exercise

  • Hypoglycemia associated with fatigue

• Some muscle glycogenolysis required to maintain Krebs cycle and ETC

• As glycogen declines, FFA metabolism increases

Inorganic phosphate (Pi)

• Impairs contraction and reduces Ca+ release from SR

Heat (especially ambient temperature)

• ↑ CHO utilization, so ↑ rate of glycogen depletion

• High muscle temps may impair muscle function

• Time to fatigue affected by ambient temperature

• Muscle pre-cooling can prolong time to exhaustion

• Lactic acid is Produced w/ short-duration high intensity exercise produce lactic
  acid & H+

• Too much lactic acid results in acidosis (low muscle pH)

Buffers help muscle pH, but sometimes not enough

• Minimize drop in pH

• Cells don’t function well in acidic environment

• If intracellular pH < 6.9, slows glycolytic enzymes, ATP synthesis

• If pH = 6.4, prevents glycogen breakdown, result = exhaustion

Failure may occur at neuromuscular junction, preventing muscle activation

• Possible causes:

• ACh synthesis and release

• Altered ACh breakdown in synapse

• Increase in muscle fiber stimulus threshold • Altered muscle resting membrane potential

• Fatigue may inhibit Ca2+ release from SR

CNS undoubtedly plays role in fatigue but not fully understood yet

• Fiber recruitment has conscious aspect

• Stress of exhaustive exercise may be too much

• Subconscious or conscious unwilling to endure more pain

• Discomfort of fatigue = warning sign

• Elite athletes learn proper pacing, tolerate fatigue

Muscle Soreness

• Results From Exhaustive Or High-intensity exercise, especially performed for first time

• Can be felt anytime

– Acute soreness during and immediately after exercise

– Delayed-onset soreness one to two days later

Acute Muscle Soreness

• Felt during or immediately following strenuous or novel exercise

• – Accumulation of metabolic by-products (H+)

• – Tissue edema (plasma fluid into interstitial space) – Edema Acute muscle swelling

• Disappears in minutes to hours

DOMS: delayed-onset muscle soreness

• – Appears one to two days after exercise bout

• – Ranges from stiffness to severe, restrictive pain

• Major cause of DOMS: eccentric contractions

• – Example: Level-run pain < downhill-run pain

• – NOT caused by blood lactate concentrations

Structural Damage Indicated By Muscle Enzymes In blood

• – Concentrations 2 to 10 times after heavy training

• – Onset of DOMS parallels onset of muscle enzymes in blood

• SarcomereZ-disks-anchor points for contractile proteins (transmit force when fibers contract)

• – Z-disk, myofilament damage seen after eccentric work

Inflammation And Soreness Connected

• –  White blood cells (WBC) defend body against foreign materials and pathogens

• –  WBC count increases with soreness, but not that simple
  • Substances Released Initiate Inflammation – Neutrophils, cytokines, oxygen free radicals (?) – Released substances stimulate pain nerve
  • Macrophages(immune cell)
  – remove cell debris
  – later associated with muscle regeneration

Muscle Soreness: Sequence of Events in DOMS

1. High tension in muscle  structural damage to muscle, cell membrane

2. Membrane damage disturbs Ca2+ homeostasis in injured fiber

• Inhibits cellular respiration, activates enzymes Z-disks degraded

3. After few hours, circulating neutrophils

4. Products of macrophage activity, intracellular contents accumulate (e.g., histamine, kinins, K+) 

• Stimulate free nerve endings  pain

5. Fluid and electrolytes shift into the area, creating edema

DOMS reduced muscle force generation

• Loss Of Strength Results From Three Factors:

• –  Physical disruption of muscle

• –  Failure in excitation–contraction coupling (apparently most important)

• –  Loss of contractile protein

• –  See figure 5.15 in your text

Must reduce DOMS for effective training

• Three strategies can reduce DOMS

1. – Minimize eccentric work early in training

2. – Start with low intensity and increase gradually

3. – Start with high-intensity, exhaustive training (soreness bad at first, much less later on)

• Factors associated with DOMS potentially important in stimulating hypertrophy

Muscle Cramps

Exercise-associated muscle cramps (EAMC)

• –  During, immediately after exercise

• –  Control between muscle and motor neuron altered

• –  Localized to overworked muscle

• –  Linked to lack of conditioning, improper training, and depletion of muscle energy stores
  • Note:allassocw/fatigue

• –  Treated with stretching

Heat cramps

• – Often associated with large sweat and electrolyte losses, especially sodium and chloride

• – Coupled with dehydration

• – Treatment: high-sodium solution, ice, massage