Module 2 - Cardiorespiratory responses to exercise

• A = Alveolar, a = arterial, v = venous
• Hypernoea = increased ventilation
• Hyperventilation = over breathing, decrease CO2 in blood which increases the pH (less H+). Unhelpful offload of CO2
• Regulation of blood by:

  • Pressure
  • Volume
  • Content - gases + glucose
  • Temperature
• Control regulation of blood by:

  • Hydration
  • Hormones, Na
  • Ventilation
  • What we eat (acid:base balance)
  • Glucose (stored & made)
  • Temp (vasoconstriction/dilation)
• Cardiopulmonary function important for:

  • Life & Health
  • Performance
  • Ability to supply O2 to cells (& remove metabolites) governs ability to work
  • O2 consumption increase for athletes
• Ventilation (air flow) increase proportionally more than cardiac output (blood flow)
• Athletes less stressed @ same absolute work rate & achieve higher rates for some factors (eg blood flow)
• Respiratory = oxygenate blood & remove CO2 from cellular respiration. Mediated by ventilation of alveoli
• Trachea --> Bronchi --> Bronchioles --> Terminal bronicoles --> Alveolar ducts --> Alveoli (sacs)
• Alveoli surfactant increase tension
• Respiratory cycle:

  • Inspiration = active (diaphragm, ext. intercostals)
  • Expiration = passive @ rest, active in ex. (ab. muscles + int. intercostals); 6x more air
• Work of breathing rises greatly in exercise

  • ~3% energy usage @ rest
  • ~12-24% energy usage @ max exercise
• Tidal Volume = volume inspired/expired per breath
• Inspiratory Reserve Volume = max inspiration @ end of tidal inspiration
• Expiratory RV = max expiration @ end of tidal expiration
• Total Lung Capacity = volume in lungs after max inspiration
• Residual Lung Volume = volume in lungs after max expiration
• Forced Vital Capacity = max volume expired after max inspiration
• Inspiratory Capacity = max volume inspired following tidal expiration
• Functional RC = volume in lungs after tidal expiration
• Change pressure to control inspiration & expiration
• Min Ventilation (VE) = breathing frequency (fb) * tidal volume (TV)
• Peak VE attained in exercise is below max ventilatory capacity
• FEV1 * (EV1/FVC) = Pulmonary airflow capacity

  • Healthy = ~85% of VC
  • Obstructive LD (emphysema, bronchial asthma)= <40% of VC
  • Obstruction COPD =<70%
  • Some LD - normal FEV1 values
• Anatomical dead space = not involved in gaseous exchange
• As Tidal Volume (TV) becomes larger, dead space does too. BUT the increase in alveolar dead space (VD) is proportionally less than the increase in TV
• Deeper ventilation provides more effective alveolar ventilation than by increased breathing frequency
• Adequate gas exchange bw/ alveoli & blood requires matching alveolar ventilation to pulmonary capillaries
• Mismatch ventilation to perfusion responsible for many gaseous exchange problems in pulmonary disease & possibly intense ex. in highly trained endurance athletes
• Ventilation:Perfusion ratio:

  • Increased physiological dead space from decrease alveolar surface function
• Adequate gas exchange is impossible when dead space >60% of TLV
• 2 Stages dictate exchange of O2 & CO2 bw/ atmosphere & blood:

  1. Avelolar ventilation - mass, drive by pressure gradient
  2. Aveolar-Blood transfer - diffusion of each gas, driven by pressure gradient of each gas
• Anatomical dead space = structural non-alveolar volume

  Physiological dead space = ventilation not used for gas exchange
• Alveolar Ventilation (VA) = (Tidal Volume - Dead Space) * breathing frequency [L/min-1]
• Alveolar Ventilation controlled by:

  • Duration
  • Force (by recruitment & neural frequency)
  • Frequency
  • Resistance (of airways)
• Increase alveolar ventilation more by DEPTH than frequency
• If 'painting' aim to shallow breath to avoid over ventilation
• Ventilation Control by rhythmic respiratory neurons:

  • In medial medulla
  • Active muscles (diaphragm, intercostals)
  • Modified by excitatory & inhibitory stimuli (neural & hormonal)
  • Stimuli act both directly & indirectly
• Ventilation control @ rest:

  • Mainly by chemoreceptors (detect chem state of arterial blood)

  1. Central chemoreceptors = localised medullary neurons; strong sensitivity to CO2 - directly related to pH
  2. Peripheral chemoreceptors = carotid & aortic; limited sensitivity to O2 (only detection for it); Co2, H+, Temp of blood