Kin 310 Exercise/Work Physiology

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Kin 310Exercise/Work Physiology

• Office hours - HC 2910
• F 1030-1120
• or by appointment (ryand_at_sfu.ca)
• class email list
• announcements, questions and responses
• inform me of a preferred email account
• class notes will be posted on the web site in
  power point each week
• can be printed up to six per page
• lecture schedule along with reading assignment on
  web site
• www.sfu.ca/ryand/kin310.htm

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Overview

• Discussion of the physiological basis of exercise
  and work
• Cellular bioenergetics
• Providing ATP to meet demand
• Cardiovascular and respiratory compensations and
  capacities
• Limitations and adaptations to training
• Molecular level adaptation
• activity changes the cellular environment -
  stimulating adaptation to better meet demand
• Fatigue - inability to sustain activity level
• description of fatigue in the CNS, the
  neuromuscular junction and the muscle cell
• Ageing - change in physiological capacities -
  impacts of disease and activity level
• Assessment of work load and physical capacity for
  exercise and work
• Exercise and the Environment
• Heat and barometric pressure can create
  additional demands on physiological systems

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Energy Sources and Recovery from Exercise

• Ch 2 Foss and Keteyian - Foxs Physiological
  basis for Exercise and Sport- 6th edition
• all human activity centers around the ability to
  provide energy (ATP) on a continuous basis
• without energy cellular activity would cease
• Main sources of energy
• biomolecules - carbohydrate and fat
• protein small contribution
• lecture will review metabolic processes with an
  emphasis on regulation and recovery

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Energy

• Energy - capacity or ability to perform work
• Work - application of a force through a distance
• Biological work - transport, mechanical and
  chemical work
• Power - amount work performed over a specific
  time (rate of work)
• Transformation of energy - forms of energy can
  be converted from one form to another
• chemical energy in food is transformed into
  mechanical energy of movement or other biological
  work
• Biological energy cycle

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ATP - adenosine tri-phosphate

• Energy harnessed from molecular bonds in
  biomolecules -
• used to resynthesize ATP - Fig 2.2
• only energy released from ATP can be utilized for
  cellular work
• ATP in solution represents immediate source of
  energy available to muscle
• enzyme (eg. ATPase) break high energy bonds
  between phosphate groups
• Forming ADP Pi energy
• Energy used to do biological work
• Eg Calcium ATPase, myosin ATPase
• Reaction is reversible (reform ATP)
• CP -creatine phosphate (phosphocreatine)
• Enzyme CK - Creatine Kinase
• Kinases (eg glycolysis)
• oxidative phosphorylation
• form NADH, FADH2 then form ATP

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Sources of ATP

• Limited quantity of ATP available
• constant turnover (re-synthesis)
• - requires energy
• 3 processes - use coupled reactions
• ATP-PC system (phosphagen)
• energy for re-synthesis from CP
• Anaerobic Glycolysis
• ATP from partial breakdown of glucose
• Limited quantities of glucose
• absence of oxygen
• generates lactate as end product (pH)
• Aerobic System
• requires oxygen
• oxidation of carbohydrates, fatty acids and
  protein
• Krebs cycle and Electron Transport

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Anaerobic sources

• ATP -PC system (fig 2.4)
• high energy phosphates
• energy in CP bond is immediately available
• as ATP is broken down it is continuously reformed
• ADP PC(Creatine Kinase) -gt ATP
• ADP ADP (myokinase) -gt ATP
• CP reformed during recovery
• from ATP formed through aerobic pathways
• Table 2.1 - most rapidly available fuel source -
  very limited quantity
• Depleted with 10 seconds of maximum activity
• Recovers quickly

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Anaerobic Glycolysis

• Incomplete breakdown of glucose or glycogen to
  lactate
• 12 separate, sequential chemical reactions
• breakdown molecular bonds
• couple reaction to synthesis of ATP
• yields 2 (glucose) or 3 (glycogen) ATP
• Rapid but limited production
• Limited glycogen stores
• lactate accumulates -gt acidity -gt fatigue -
  unable to sustain demand
• PFK - phosphofructokinase
• rate limiting enzyme- slow step in reaction -
  inhibited by acidity
• Table 2.2

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Anaerobic Glycolysis

• Pyruvate is final product of glycolysis
• pyruvate is converted to lactate when aerobic ATP
  production can not meet demand for ATP
  utilization
• Inadequate O2 delivery (or high demand)
• enzyme LDH - lactate dehydrogenase
• Redox reaction (Fig 2.6)
• frees up NAD required in glycolysis
• Allows rapid production of ATP through glycolysis
  - until acidity shuts it down
• summary fig 2.7
• glycogen - endogenous fuel
• within muscle
• glucose - exogenous fuel
• comes from blood glucose, released from liver
  glycogen

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Aerobic Sources of ATP

• Acetyl groups - 2 carbon units
• formed from pyruvate and from Beta oxidation of
  free fatty acids
• NAD and FAD - electron carriers
• become reduced when biomolecules are oxidized -
  form NADH, FADH2
• carry these hydrogen atoms to the electron
  transport chain
• donated and passed down chain of carriers to form
  ATP
• Oxidative - phosphorylation
• oxygen is final acceptor of hydrogen, it is
  reduced to H2O
• occurs in mitochondrial membrane system - cristae

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Krebs Cycle

• Fig 2.12 - Krebs Cycle (Citric Acid cycle)
• Key regulatory enzymes
• PDH (pyruvate dehydrogenase),CS (citrate
  synthase), SDH (succinate dehydrogenase)
• NADH - inhibits enzyme activity
• High NADH - indicates ETC is behind in utilizing
  NADH already produced
• Availability of ADP also regulates Krebs cycle
  activity
• ADP and NAD are needed for reactions to occur
• CO2 produced as molecules are oxidized ( H atoms
  are removed)
• Krebs Cycle - produces
• (per acetyl group-2 Carbons)
• 1 GTP (ATP equivalent)
• 3 NADH and 1 FADH2

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ETC

• Electron Transport Chain (ETC)
• H atoms passed down series of electron carriers
  by enzymatic reactions coupled to production of
  ATP
• oxidative phosphorylation
• each NADH - yields 3 ATP
• each FADH2 - yields 2 ATP
• for process to continue, must liberate NAD and
  FAD -
• Process requires oxygen

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Aerobic Glycolysis

• With sufficient oxygen pyruvate moves into
  mitochondria
• Monocarboxylate transporter
• law of mass action
• 1 mole glycogen -
• glycolysis
• 2 moles pyruvate 3 moles ATP
• 2 moles NADH (6 moles ATP after ETC)
• Krebs - per pyruvate molecule
• 4 moles NADH (one from PDH)
• 12 ATP
• 1 mole FADH2
• 2 ATP
• 1 GTP
• Multiplied by 2 30 moles of ATP
• 39 ATP per mole of glycogen

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Fat Metabolism

• Fat and Protein only oxidized
• No anaerobic metabolism
• Fatty acids - 16-18 carbon units
• acetyl groups (2 carbons) broken off chain to
  enter Krebs cycle one at a time
• Beta oxidation Fig. 2.15
• uses 1 ATP for first two carbons only
• produces 1 NADH and 1 FADH2
• acetyl co-A through Krebs/ETC
• Yields 12 ATP
• total of 16 ATP for first acetyl group
• 17 for each remaining acetyl group
• last acetyl group only 12 ATP- as it is not
  produced by beta oxidation
• 1 mole of palmitic acid-138 moles ATP
• Key enzymes - B-HAD, and lipases

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Comparing the Energy Systems

• Table 2.6
• energy capacity - amount of ATP able to be
  produced independent of time
• power - rate of production - time factor
• aerobic - table represents availability from
  glycogen only - fat is unlimited
• Rest
• aerobic - supplies all ATP
• mainly fats and carbohydrates
• some lactate 10 mg/dl in blood
• does not accumulate, but LDH active

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Exercise

• Both anaerobic and aerobic
• relative contribution to ATP production depends
  on
• intensity and/or duration
• state of training
• Dietary factors (replenishment of stores)
• Energy contribution vs time
• (Assumes all out activity for time frame )
• Mcardle, Katch and Katch - Exercise Physiology
• Immediate - phosphagens - major contributor for
  up to 10 sec
• Anaerobic Glycolysis - majro contributor for
  30sec - 2.5 min
• Aerobic metabolism major contributor for 3 min
  onward
• Contribution of energy systems is a continuum,
  not an on or off situation

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Experimental evidence

• Two types of exercise compared in most of the
  following experiments
• near maximal - short duration
• sub maximal - longer duration
• Fig 2.18 glycogen depletion
• activities below 60 (VO2 max) and above 90 -
  limited glycogen depletion
• At 75 significant depletion - leading to
  exhaustion (fatigue)
• 2.18b
• rate of depletion dependant on demand
• Volume of depletion related to duration

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Short duration

• 2-3 minutes high intensity exercise
• fig 2.19 - major energy source CH2O
• ATP and PC will drop rapidly
• restored in recovery (rapidly)
• Aerobic contribution limited by its low power
  output
• also takes 2-3 min to increase output
• oxygen deficit - period during which level of O2
  consumption is below that necessary to supply all
  ATP required by exercise demands
• ATP supplied by anaerobic systems to make up for
  aerobic shortfall
• rapid accumulation of lactate
• 200 mg/dl in blood / muscle

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Prolonged Exercise

• 10 minutes or longer
• Aerobic fat and carbohydrate metabolism are main
  sources of ATP
• CHO dominate up to 20 min
• fats minor but supportive role
• after 1 hr fats become dominant source of ATP
• at lower intensities (lt 60 Hr max) fats also
  have greater contribution
• fig. 2.20
• fatigue during aerobic exercise is not associated
  with lactate, but other factors - discussed later
  in semester
• Fig 2-22 activities require blend of anaerobic
  and aerobic systems
• energy continuum

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Control and Regulation

• Matching provision of ATP to demand is needed so
  performer does not experience early or undue
  fatigue
• Enzymes, hormones, substrates interact to modify
  flow through metabolic pathways of each system
• Table 2.7
• Flow through different pathways is often modified
  by activating and inactivating key enzymes
• Influences over enzymes include
• high vs low energy state of cell(NAD)
• Hormone levels (epinephrine, glucagon)
• amplification of hormone effects
• competition for ADP (between enzymes)
• adequacy of oxygen supply
• power output requirements relative to aerobic
  power (demand)

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Regulation

• In general we observe
• regulation within muscle cell,
• And influences from outside the cell
• both serving to modify regulatory enzymes in each
  pathway
• Fig 2.23
• Energy State regulation
• ADP/ATP ratio
• very quick - tightly linked to rate of energy
  expenditure
• Hormone Amplification
• cAMP 2nd messenger systems - amplification
• Ep and Glucagon - activate phosphorylase -
  glycogen breakdown
• lipase - fat breakdown

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Regulation

• Substrates -
• eg. NADH - buildup
• In cytosol stimulates LDH - frees NAD
• occurs when ETS is maximized
• can not oxidize NADH fast enough
• Also inhibitory in Krebs cycle (DHs)
• eg. Inc Pyruvate
• stimulates PDH - entry into Krebs
• PDH also influenced by phosphorylation
• Fig 6.8 Brooks
• Oxidative State Regulation
• O2 and ADP availability
• O2 stimulates cytochrome oxidase (CO)
• final step in ETC
• low O2 - inhibits Cytochrome Oxidase
• Leads to build up of NADH, FADH2
• key factor is oxygen availability vs demand for
  ATP utilization

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Recovery from Exercise

• Ch. 3
• process of recovery from exercise involves
  transition from catabolic to anabolic state
• breakdown of glycogen and fats to replenishment
  of stores
• breakdown of protein to protein synthesis for
  muscle growth and repair
• Our discussion of recovery will include
• oxygen consumption post exercise
• Replenishment of energy stores
• Lactate metabolism(energy or glycogen)
• Replenishment of oxygen stores
• intensity and activity specific recovery
• guidelines for recovery

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Recovery Oxygen

• Recovery O2 - Net amount of oxygen consumed
  during recovery from exercise
• excess above rest in Litres of O2
• Fast and Slow components
• Based on slope of O2 curve
• first 2-3 min of recovery - O2 consumption
  declines fast
• then declines slowly to resting
• Fig 3.1
• Fast Component - first 2-3 minutes
• restore myoglobin and blood oxygen
• energy cost of elevated ventilation
• energy cost of elevate heart activity
• replenishment of phosphagen
• volume of O2 for fast component area under
  curve
• related to intensity not duration

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Recovery Oxygen

• Slow Component
• elevated body temperature
• Q10 effect - inc metabolic activity
• cost of ventilation and heart activity
• ion redistribution Na/K pump
• glycogen re-synthesis
• effect of catecholamines and thyroid hormone
• oxidation of lactate serves as fuel for many of
  these processes
• duration and intensity do not modify slow
  component until threshold of combined duration
  and intensity
• After 20 min and 80
• We observe a 5 fold increase in the volume of the
  slow component

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Energy Stores

• Both phosphagens (ATP, CP) and glycogen are
  depleted with exercise
• ATP/CP - recover in fast component
• measured by sterile biopsy, MRS
• rate of PC recovery indicative of net oxidative
  ATP synthesis (VO2)
• study of ATP production
• 20-25 mmol/L/min glycogen and all fuels
• during exercise
• CP can drop to 20, ATP to 70
• CP lowest at fatigue, rises immediately with
  recovery
• Fig 3.2 - very rapid recovery of CP
• 30 sec 70, 3-5 min 100 recovery

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Phosphagen Recovery(cont.)

• Fig 3.3
• occlusion of blood flow - no phosphogen recovery
• requires aerobic metabolism
• estimate 1.5 L of oxygen for ATP-PC recovery
• Energetics of Recovery
• Fig 3.4
• breakdown carbs, fats some lactate
• produce ATP which reforms CP
• high degree of correlation between phosphagen
  depletion and volume of fast component oxygen
• Fig. 3.5
• anaerobic power in athlete related to phosphagen
  potential - Wingate test