Exercise Phys - Exam 2

cardiovascular responses to acute exercise

increased blood flow to working muscles; involves altered heart function and peripheral circulatory adaptations.

Normal RHR ranges

untrained - 60-80, trained - as low as 30-40 BPM

Things affecting RHR

Neural tone, temperature, altitude

Heart rate Anticipatory response

HR increases above RHR just before start of exercise; due to decrease vagal tone (parasympathetic) and an increase in epinephrine and norepinephrine

Heart rate during exercise

Directly proportional to intensity

Max Heart Rate

highest HR achieved in all-out effort to volitional fatigue, slight decline with age, highly reproducible.

Steady State HR

Point of plateau, optimal HR for meeting circulatory needs at given submax; intensity and steady state HR increase together, adjustment to new intensity can take 2-3 min

Heart Rate Variability

Measure of HR rhythmic fluctuation both at rest and exercise; analyzed with respect to frequency not time.

HR variability due to

continuous changes in sympathetic and parasympathetic balances

HR variability influenced by

core temp, sympathetic nerve activity, reparatory rate

Stroke Volume

How much blood is pumped out of the heart each beat; major determinant of endurance capacity

Stroke volume determined by

Volume of venous blood returned to heart, ventricular distensibility, ventricular contractability, aortic/pulmonary artery pressure.

Preload

How much blood starts in the ventricles (EDV)

Afterload

Amount of pressure in the aortic valve

Stroke volume during exercise

Increases with intensity to 40-60% of VO2max (then levels off); beyond that = plateau to exhaustion (but HR keeps increasing); elite endurance athletes are possible exception.

Stroke Volume and standing

Max exercise SV about double standing SV; but max exercise SV only slightly > supine SV; supine SV way higher than standing; due to easier path for blood back to heart (supine EDV > standing EDV)

Factors increasing SV

increased preload (Frank-Starling), increased contractility (inherent ventricle property), decreased afterload (decreased Aortic R)

Frank-Starling Mechanism

increased stretch due to increased EDV → increased contraction strength

Inherent Ventricle Property

Increase in NE or Epinephrine → increased contractility

Stroke volume changes at low intensities

Increased preload (due to increased venous return & EDV)

Stroke Volume Changes at higher intensities

Increase in HR → less filling time → decreased EDV → decreased SV; leads to plateau at high intensities

Mechanisms to combat decreasing SV at high intensity

Increase in contractility, decreased afterload via vasodilation

Cardiac Output

Q = HR x S; increases with increase in intensity; plateus near VO2 max

Normal Cardiac Output values

Resting = ~5L/min

Untrained Qmax ~20 L/min

Trained Qmax 40 L/min

Fick Principle

calculation of tissue O2 consumption dependent on blood flow and O2 extraction (a-v O2 difference)

BP during endurance exercise

Increase in MAP, systolic BP increase proportional to intensity, diastolic BP decreases slightly until max (when it increases)

MAP =

Q x TPR (Total peripheral Resistance); increase in Q = slight decrease in TPR (vasodilation)

Rate-Pressure Product

HR x SBP (think reps x weight)

Resistance Exercise and MAP

Periodic large increases in MAP, up to 480/350 mmHg (@ isometric point), most common during Valsalva maneuverV

Valsalva Maneuver while lifting

Holding in breath while pushing hard

Working and Nonworking muscles and VD vs VC

Working Muscles = VD, nonworking muscles = VC

Blood flow Redistribution

Increase in Q → increase in available blood; blood flow redirected to areas with greatest metabolic needs

Away from splanchnic and kidneys by VC

Local Vasodilation

local VD permits additional blood flow to exercising muscles; triggered by metabolic and endothelial byproducts, and Po2 and Pco2

Skin VD during exercise

As temp increases skin VD occurs, heat loss permitted through skin

Cardiovascular drift

gradual increase in HR and decrease in SV during prolonged exercise

Cardiovascular Drift causes

skin blood flow increased, plasma volume decreased, venous return/preload decreased (all 3 decrease SV); HR drifts up to compensate for SV decrease to maintain Q

(A-V) O2 difference

arterial O2 content - mixed venous O2 content (active and inactive tissues)

O2 extraction at muscles

Resting ~ 6mL O2/100mL blood

Max exercise ~16-17 mL O2/100 mL blood

Upright Exercise and plasma volume

Leads to a decrease in Plasma volume (compromise of exercising); increased MAP → increase capillary hydrostatic pressure; sweating further decreases plasma volumes

Hemoconcentration

decreased plasma volume leads to hemoconcentration; Hemocrit increase up to 50%

Net effects of Hemoconcentration

RBC concentration increase, Hemoglobin concentration increase, O2 carrying capacity increase

CV system responds to exercise

complex, fast, finely tuned

CV system priority during exercise

Maintenance of BP (through fluid balance, VC & VD); BP prioritized before other needs

Central command theory

Preemptive increase in HR and BP in preparation for exercise, before any actually happens

Central Regulation

Stimulation for rapid changes in HR, Q, BP during exercise; Precedes metabolic buildup in muscles, HR increases within 1s of onset exercise

Central Command

Higher brain centers; coactivation of motor and cardiovascular centers

Ventilation during exercise

Immediate increase in ventilation; before muscle contractions, anticipatory response from central command

Second phase of increase in ventilation

Gradual; driven by chemical changes in arterial blood, increase in co2 and H+ sensed by chemoreceptors, right arterial stretch receptors

Ventilation increase in relation to metabolic needs

Proportional; low intensity only tidal volume increases

high intensity both tidal volume and rate increase

Ventilation recovery after exercise

Takes several mins, may be regulated by blood pH, Pco2, temp

Exercise induced Asthma

Lower airway obstruction (coughing, wheezing, dyspnea (shortness of breath)); more water evaporated from airway surface, disruption of airway epithelium and injury of microvasculature

Dyspnea

Shortness of breath; common with poor aerobic fitness, caused by inability to adjust to high blood Pco2 and H+, fatigue in respiratory muscles despite drive to increase ventilation

Hyperventilation

Anticipation/anxiety about exercise; increase Pco2 gradient between blood and alveoli, decrease blood Pco2 → increase blood pH → decreased drive to breathe

Ventilation and energy metabolism

Ventilation matches metabolic rate, ventilatory threshold

Ventilatory equivalent for O2

VE/Vo2 (L air breathed/L air consumed) per min; index of how well control of breathing is matched to body’s O2 demands

Ventilatory threshold

Point where L air breathed > L O2 consumed; associated with lactate threshold and increase in Pco2

Estimating Lactate threshold

excess lactic acid + sodium bicarb = excess sodium lactate, H2O, Co2; anerobic threshold

Ventilatory limitations on performance

usually not limiting factor, respiratory muscles very fatigue resistant and account for 10% of Vo2 and 15% of Q during heavy exercise; airway R and gas diffusion normally not limiting factors @ sea level

Elite endurance athletes exercising @ high intensities (ventilation)

Ventilation possibly limiting factor, ventilation-perfusion mismatch, exercise-induced arterial hypoxemia (EIAH)

Acid-base balance

@ Rest - 7.1-7.4, slightly alkaline (higher = alkalosis)

@ exercise - 6.6-6.9, slightly acidic (lower = acidosis)

Physiological mechanisms that control pH

Chemical buffers (bicarb, phosphates, proteins, hemoglobin); increase in ventilation helps H+ bind to bicarb, kidneys remove excess H+ from buffers

Active recovery and pH

Active recovery facilitates pH recovery

passive = 60-120 min

Active = 30-60 min

Cardiovascular recovery from acute exercise

Postexercise hypotension (aerobic and resistance)

Postexercise hypotension (aerobic)

aerobic exercise; driven by peripheral vasodilation, can last for several hours, histamine is important mediator

Postexercise hypotension (resistance)

Resistance exercise; driven by decreased cardiac output