Aerobic Fitness & Training Adaptations

• Why to Train Aerobic Fitness:

  • Health & wellness
  • Extreme environments
  • Help prevent, & also treat several conditions
• Why to Train Aerobic Fitness:

  • Performance
  • Sport (endurance, & most team sports; increase energy role, & aid recovery)
  • Energy utilising during those events or in recovery
  • If recovery quickly get anaerobic systems back
  • Industry
  • Recreational
• Why to Train Aerobic Fitness:

  • Extreme environments
  • Help deal with:
  • Heat
  • Altitude
  • Space
  • Bedrest
  • Rough terrain
  • Expeditionary
  • Have higher value (aerobic fitness) so doesn't drop as badly
• Integration of Physiological Systems:

  • Working together = integrate response
  • All comes back to energy (ATP)
  • ATP demand stimulates demands of these systems
  • Utilising & depleting energy substrates
  • Aerobic energy demand, demanding on mitochondria
  • H+ ion from breaking down ATP
  • Neuro-endocrine responses to exercise (catecholamines, anabolic sex hormones)
  • Multi-factorial responses
• Main concepts for improving aerobic fitness & performance:

  • 3 main ways to increase ‘aerobic fitness’

  1. Increase VO2 max (aerobic power)
  2. Maximal capacity to utilise oxygen
  3. Increase ‘Anaerobic’ threshold
  4. Determines… (max sustainable power)
  5. Increase Endurance capacity
  6. (max duration)
• Main concepts for improving aerobic fitness & performance:

  • Increase threshold & capacity >> max
  • Can sustain sub maximal at a higher intensity (at same relative VO2 max)
  • So, can sustain exercise at higher proportion of higher upper limit of oxygen use, for longer
• Concepts for improving ‘aerobic fitness’ to a lesser extent:

  • Increase efficiency (~economy)
  • More efficient use less energy
  • Decrease O2 & energy needed at matches speed or power
  • Decrease heat load, dehydration, glycolysis
  • Generally a long term & small (5-10%) effect of training
  • Important performance factor amongst athletes at similar level in technical movements (eg swimming) & in prolonged events
  • Little bit change can make a difference
  • How to measure? Energy use or VO2 at steady state power (for efficiency) &/or speed (for economy)
• Rare for someone to excel in all factors/determinants:

  • Even among elite athletes in same sport
  • 1000s of genetic determinants for each of:
  • So many genes contribute to physiology
  • Individual differences
• Factors / Determinants of Aerobic Fitness:

  • VO2 max
  • Haemoglobin mass
  • Heart size & function
  • Blood volume
  • Economy
  • Anthropometry
  • Technique
  • Exercise capacity (distance)
  • Muscle fibre composition
  • Energy substrates
  • ‘Sustainable’ threshold
  • Muscle mitochondrial content & function
  • Sweat gland function
  • Lung function
  • Vascular system structure & function
• Illustration of these effects:

  • Max aerobic increases then plateaus
  • If have low VO2 max will have a lot of room to move/more to gain
  • Aerobic endurance:
  • Able to sustain for longer happens faster & to a greater extent
  • Often difference here - ability to sustain a high intensity
• Why measure max aerobic power?

  • Major determinant (& predictor) of endurance “performance in many contexts"
  • Powerful & brief, eg 2 km rowing (~80% predictor)
  • Prolonged steady state (eg marathon)
  • Prolonged intermittent (eg mtb, football)
  • Ultra-endurance (eg adventure racing)
  • Occupational capabilities (eg police, fire, military)
  • Most prolonged (length of life = longevity)
• Why measure max aerobic power?

  • Sets the upper limit for producing & utilising ATP aerobically
  • Tests the response capabilities of almost all systems in body
  • Assess suitability / risk for surgery
  • Inform exercise prescription & monitoring training outcomes (intensity)
• Procedure for measuring max aerobic power:

  • Indirect, sub/maximal methods
  • Sub max for sedentary & clinical populations in particular
  • Some may not want to go to max as: feel uncomfortable or not motivated too
  • Duration must allow full activation of aerobic metabolism in muscle & O2 delivery by blood
  • Usually incremental power (or speed)
  • Usually 8-12 min duration
  • If longer may fatigue without reaching VO2 max
  • For an elite athlete may go on longer to get to max
  • Measure VO2 (& rate of CO2 production)
  • To predict RER
• Criteria to see if reach VO2 max, usually at least 2 of:

  • Fatigue
  • Plateau VO2 despite increase intensity
  • Don’t always see plateau some athletes may stop once in anaerobic
  • HR within 10 bpm of age-predicted max
  • eg 220 - age or better 201 - 0.7 * age
  • Also day to day variation
  • RER >1
  • RPE > 18/20
• Many ways to measure non/sustainable thresholds:

  • Max ‘sustainable’ pace, eg for 30 min
  • Develop a critical power curve
  • Ventilatory thresholds (2 thresholds/peaks)
  • From stepped-intensity or ramped-intensity protocols
  • First increase in VE / VO2 indicates VT1 (1st peak), below which prolonged exercise, slow oxidative motor units (largely Type 1 fibres) predominate
  • Lactate curves
  • Informally: RPE (~<15/20)
  • Pretty loose & less reliable than measuring physiological response
• Training to increase aerobic power (VO2 max) & threshold

  • VO2 = Cardiac Output (Qc) * O2 Extraction
  • = SV * HR * (caO2 - cvO2 difference)
  • O2 Delivery O2 Extraction
  • Central Peripheral
  • O2 Delivery: enhanced by HR, SV
  • O2 Extraction: capillarisation = in muscle + what's happening in muscle in terms of bio changes
  • Combo of these play a role in enhance aerobic power in more training
• Factors that influence Oxygen (O2) delivery - to muscles:

  1. Alveolar ventilation
  2. Tidal volume, breathing frequency
  3. Cardiac Output
  4. Heart rate (HR)
  5. Stroke volume (SV); Heart size & strength
  6. Oxygen carrying capacity
  7. Haemoglobin [Hb]. Red Blood Cell (RBC) Volume, Blood Volume
  8. More RBC, more Hb
  9. Blood volume increased 1st then - more RBC & Hb
  10. Capacity of arteries & arterioles
  11. Capillarisation
• Ventilation. Is it trainable? Yes & No

  • Decrease VE at a given VO2
  • Deeper breaths (help alveolar ventilation)
  • (Therefore decrease ventilatory equivalent than untrained) - in trained
  • Increase respiratory muscle resistance to fatigue
  • Maybe important in very hard sustained or repeated exercise
  • Respiratory training devices may be useful? (lack data in athletes)
  • In terms of breathing deeper, harder faster training respiratory muscles
• Ventilation. Is it trainable?... Yes & No

  • Little effect on VE at max effort (not as trainable)
  • Indicates that pulmonary ventilation isn’t normally a “limiting factor”, except
  • Obstructive pulmonary disorders
  • Some elite endurance athletes
  • With very high ability to utilise O2 then yes it may be limiting but typically it’s not
  • Extended strenuous exercise
  • For maximal endeavours (VO2 max) - is more the ability to utilise that oxygen (that is a limiting factor)
• Heart Stroke Volume Increase due to several local factors:

  • Increase left ventricle capacity
  • Increases end diastolic volume
  • Increase left ventricle mass (~20%)
  • Allows increase contractility (force generated)
  • Increase compliance
  • Faster/greater relaxation (filling)
  • Less passive resistance to shortening
  • Increase capillarisation (in heart itself)
  • Increase antioxidant capacity in heart
  • (Superoxide dismutase)
  • Protects cells against prolonged ischaemia & reperfusion
• Ventricular Wall Thickness, Volume & Mass

  • Those that require high aerobic component compared to those that don’t
  • Rowing, soccer, canoeing = high
  • Diving, volleyball, fencing = low
• Stimulus & Suggested Training:

  • Pressure?... concentric hypertrophy
  • Intensity (>90% VO2 max?)
  • Volume?... larger chamber (EDV)
  • Training volume (?)
  • ‘Homeostasis’ (Heat, ROS, H+, Ca2+)
  • Metabolic, oxidative species may play a role in remodelling heart
  • Intensity (>90% VO2 max?)
  • Metabolic efficiency? Of heart it self
  • Training volume
• A few weeks including RHIE (HIT; 85-100% VO2 max) is especially effective for increase ventricular contractility & cardiac output
• External factors that increase SV with aerobic training:

  • Increase Preload due to:
  • Increase blood volume
  • Increase venous return
  • Increase time for filling (decrease HR)
  • At rest & submax exercise
  • Due to decrease SNS & increase PNS
  • Increase contractility
  • As HR lower allows more time for filling

  
  

  
  

  
  

  • Increase Preload means more stretch so stronger contraction
  • (Frank Starlin
• External factors that increase SV w/ aerobic training:

  • Decrease Afterload (~BP) due to:
  • = or decrease TPR
  • Decrease SNS at rest & exercise
  • Increase arterial capacities
  • Increase arteriole reactivity
  • Endothelial function better
  • Increased capillarisation
  • Of muscle, of skin?
  • Also reducing the resistance more place for the blood to go
  • Decrease Afterload (decrease arterial BP) allows higher ejection fraction since less work needed to eject blood
  • Easier to eject blood, less pressure to get blood back into circulation
• HR shows useful adaptations:

  • Lower HR rest, & all submax intensities
  • Likely increase PNS & decrease SNS
  • No change in HR max
  • Lower HR rest is more valuable that higher max
  • Gives more multiples of increase to HR max
  • More filling time (increase SV)
  • Heart doing less work so lower oxygen (O2) & energy demand
  • Gives bigger range in which can function
• HR shows useful adaptations:

  • 3 ways to use HR (eg 120 bpm):
  • %HR max, eg 63% of HR max:
  • (%HR max = HR / HR rest * 100)
  • To give indication of strain related to max
  • %HRRange, eg 44% HRR
  • (%HRR = (HR - HR rest) / (HR max - HR rest) * 100)
  • Indication of strain, better if can use range as is their HR capacity
  • More related to strain they are going to have
• Adaptations can’t be separated, as are so integrated (linked) with one another
• Blood Volume (BV) is very trainable; increase has large advantages:

  • Lots of evidence
  • Cross sectional data
  • VO2 max vs BV
  • Linear relationship with increasing RBC volume with increase VO2 max
• Blood Volume (BV) is very trainable; increase has large advantages:

  • BV = Plasma Volume (PV) + Red Cell Volume (RBC)
  • Increase Plasma Volume (PV)
  • Increase venous return
  • Increase stroke volume (SV)
  • Greater volume helps flow to periphery for thermoregulation
  • Increase thermoregulation
  • Off-sets increase viscosity of increase red cell volume
  • Takes only 1 day to become clearly measurable!
  • A measurable difference
• Blood Volume (BV) is very trainable; increase has large advantages:

  • BV = Plasma Volume (PV) + Red Cell Volume (RBC)
  • Increase Red Cell Volume (RCV)
  • Increase O2 delivery
  • Decrease demand for periphery blood flow
  • Takes ~ 3 weeks to become measurable/apparent
  • PV & RBC (eventually) increase to similar extent, so do NOT get more O2 per L blood
• Blood Volume (BV) is very trainable; increase has large advantages:

  • Interventions
  • Red cell withdrawal
  • Red cell infusions (blood doping)
  • Carbon monoxide
  • Binds to Hb, blocking O2 binding
  • Shows decrease in saturation available
  • Training effect on BV
• “Athletic Anaemia” occurs early in increase training load:

  • Appearance of anaemia due to plasma volume increase faster than red blood cell volume increase (Dilution, not actually anaemia)
  • PV volume increase earlier on may have low Hb (dilution effect)
  • Haemoglobin concentration [Hb] & Hematocrit [Hct] decrease
  • Both indicators of RBCs
  • Hct = RCV / BV
  • Not really a problem if low RBC per BV if know are in training stage
• Plasma Volume: What causes it, & how to achieve it?

  • Acute decrease BV
  • Aldosterone
  • Heat (metab., environ.)
  • (Decrease Central Venous Pressure)
  • Long duration activity?
  • (Decrease Arterial Pressure)
  • (Conserve Na+ & H2O)
  • Dehydration?
  • Acute increase Osmolality
  • ADH (conserve H2O)
  • Contractile Activity (causes fluid shifts)
  • Increase Albumin synthesis
  • Upright during recovery
• Red Blood Cell Volume: What causes it & how to achieve it?

  • (Renal) Hypoxia
  • Erythropoietin (EPO)
  • Very prolonged increase in PV?
• Training & increase systemic vascular capacity:

  • Main changes
  • Larger arteries & arterioles (trained limbs, gut, skin, … brain?)
  • Some new networks of arteries & arterioles(?) (cardiac)
  • More capillaries (= ‘angiogenesis’)
  • One of the biggest effects
  • How much blood can be held in vascular space
  • V_GF = ventricular growth factor
• Training & increase systemic vascular capacity

  • How?
  • Metabolic signals locally
  • Shear stress in blood vessels is regulated (in acute regulation)
  • Exercise puts high shear stress on vessel wall:
  • Increase Nitric Oxide (NO) production…
  • … increase vessel dilation (NO-dependent dilation)
  • & stimulates vessel proliferation (capillarisation)
• Training & increase systemic vascular capacity:

  • What training is best?
  • Wide range of interval & continuous training effective (that can be used)
• Capillarisation enhances delivery & extraction:

  • Aids exchange: (from more capillaries)
  • Decrease diffusion distance
  • Increase time for exchange
  • Increase blood flow in tissue
  • Related to:
  • Fibre size
  • Bigger fibres need more capillaries
  • Need more O2, energy to contract
  • Fibre type (mitochondrial density)
  • Oxidative fibres need more capillaries
  • Density is ~500 capillaries/mm2
• Peripheral Factors that influence O2 extraction & utilisation:

  1. Myoglobin
  2. Fibre size & type
  3. Mitochondria
  4. Mitochondrial volume:
  5. Size
  6. Number
  7. Cellular location/arrangement
  8. Of new mitochondria → eg could come all together
  9. Oxidative enzyme concentrations