Some Quick Respiratory Defintions:

Tidal Volume= Volume of air moved per breath at rest.

Inspiratory Reserve Volume= The maximal volume of air inspired beyond Tidal Volume (vol. at rest).

Expiratory Reserve Volume= Maximal volume of air expired ability.

Residual Volume= Volume of air remaining in the lungs after Expiratory Reserve Volume

Vital Capacity= Tidal Volume+ Expiratory Reserve Volume+ Inspiratory Reserve Volume

Total Lung Capacity= Residual Volume + Vital Capacity(vol. remaining after expiratory reserve volume + Tidal Volume + Expiratory Reserve Volume + Inspiratory Reserve Volume)

Minute Ventilation (Ve)= volume of air expired per minute (Tidal Vol. x frequency of breaths)

-ex: Oxygen uptake rate (VO2)( ml/kg/min.)

VCO2= Carbon Dioxide production rate

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Our Body’s Blood Distribution @ Rest:

A. Pulmonary Circulation: 9% of total blood volume

B. Heart: 7%

C. Arteries: 13%

D. Tissues:7%

E. Venous Return System: 64%

F. Changes with Exercise:  1. Muscle Pumping Action: muscles pump blood through the venous return system to return blood back to the heart. 2. Nervous System Change: Vasoconstriction helps constrict blood flow back to the heart.

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The Fick Equation:

Volume of blood being moved per minute, and volume of O2 being taken in.

VO2 = Q x (a-vo 2 diff. )      -a-vo2 dif: arterial oxygen content-venous oxygen content in ml. of O2 /100ml of blood.

VO2 = (SV x HR) x ( a-vo2 diff. )

VO2 = ((EDV-ESV) x HR) x (a-vo2 diff.)

-Training Induced Increases in blood volume: Ventricular Volume & Ventricular Wall Thickness tend to increase SV.

Frank-Starling Effect: Ventricles stretch to provide a greater forceful contraction, thus ejecting more volume.  SV changes to affect changes in Q (Cardiac Output)

-You can increase Q with endurance and resistance training.

– SV is the main difference between trained and untrained status of individuals.

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*Factors Affecting HR:

-Following Training: submax HR is lower due to increases in SV.

– Following Trianing, maximum exercise HR may be slightly lower

– influence of SNS (via epinephrine and norepinephrine)-increase strength of contraction and increased HR.

– Following Aerobic Training: mitochondria increase in size and number. ( increase O2 extraction)

– Changes in extraction based on exercise intensity:

A. Rest- extract about 20% of O2 from blood

B. Moderate Exercise- extract about 50% of O2 from blood

C. High Intensity Exercise-extract 75% of O2 from blood.

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The Hemoglobin-Oxygen Dissociation Curve (Hb-O2):

-the amount of oxygen transported in the blood is dependent on the pressure gradient and characteristics of the blood.

– @ sealevel, the saturation  of oxygen in hemoglobin is about 99%. With increasing altitudes, PO2  is lower at about 40% concentrated. This equates to about the same PO2 as in the muscles and tissues, thus O2 doesn’t make it across the gradient much.

– The shift in the curve is influenced by:

1. Increased muscle temperature: means greater gradient and more O2 is transferred in tissues.

2. Increased H+ concentration (decreased pH)

**Practical Application: The Warm up: This allows muscle tissues to be better primed to uptake more O2.

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Anaerobic Threshold:

Practical uses of AeT: (aka: ventilatory threshold or lactate threshold, although not actually the same things)

1. Fitness Appraisal:

2. Aerobic Endurance Preformance Prediction:

3. Exercise Prescription:

A. Limitations: Suppose a cardiac patient—an exercise intensity assigned at 70% Vo2max may be above the person’s anaerobic threshold and, therefore it is too intense to allow exercise to continue for very long.

B. Suppose an Aerobically trained athlete: an assigned 80% VO2max exercise intensity may be too below the person’s anaerobic threshold, and, therefore, it is too easy to stimulate a training effect.

Anaerobic Threshold is a function of: (110,178)

a. Insufficient amount of O2 delivered to the tissues:

b. Increased physical stress of exercise:

c. Icreased sympathethic nervous system of influence:

d. Increased ATP production via anaerobic glycolysis

e. Increased lactic acid formation:

f. Increased H+ concentration:

g. Increased buffering of H+ by sodium bicarbonate:

h. Increased CO2 production is the stimulus for increases in ventilation rate:

Summation: (a) As exercise intensity increases, at some point ventilation increases disproportionately to oxygen consumption (VO2). As intensity increases, the ventilation rate increases thus requiring more O2 to be transported to the working muscles through the blood. After reaching a threshold of ventilation, the need to extract CO2 from the muscles becomes greater than the need to provide O2 to the muscles. Thus with increasing rates of lactic acid being produced by working muscles the greater the volume of CO2 needs to be extracted and disposed of via the venous blood. The point at which this occurs is called the Ventilatory Threshold.

(e)When work rate exceeds about 55%-70% of VO2max at approximately the same point at the VT, more lactate starts to appear in the blood.

(b) The ability to exercise at a high intensity without accumulating lactate is beneficial to the athlete because lactate accumulation contributes to fatigue. The major determinants of successful endurance performance are VO2max and the percentage of VO2max  that an athlete can maintain for a prolonged period,  mostly a determinant of their lactate threshold. Fatigue is usually used to describe decrements of performance with continued effort accompanied by general sensations of tiredness. Fatigue is reversible by rest. Most people believe the fatigue is caused by lactic acid build up, but mounting evidence suggests that lactic acid may actually have beneficial effects on performance.

Fatigue is rarely caused by a single factor but typically by multiple ones at multiple sites. Many questions about fatigue remain unanswered but it has been shown that determinants are likely based on type and intensity of exercise, the fiber type involved, training status, and even diet.

(d) Despite the insufficient oxygen delivery at the onset of exercise, the active muscles are able to generate the ATP needed through anaerobic metabolic pathways. During the initial minutes of recovery, oxygen consumption remains elevated temporarily, and is known as the oxygen debt or EPOC. It is the volume of oxygen consumed above normal levels at rest. After several minutes of rest, heart rate and ventilation begin to decrease.

During intense exercise bouts, the rate of ATP used to provide energy for muscle contractions is rapidly used up and the regeneration of ATP is quickly exhausted after no more than two to three minutes of anaerobic intensity. At exhaustion, ATP may be depleted, and Phosphorus levels increase, which poses as the possible cause of fatigue in this type of exercise. To delay fatigue, the athlete must control the rate of effort through proper pacing to ensure this ATP and the regeneration method of ATP are not exhausted. Training and experience allow an athlete to determine the optimal pace that permits the most efficient use of ATP for the entire event, and thus is why each athlete’s pacing should be completely individualized.

 

(c) The sympathetic nervous system stimulation increases the rate of impulse generation and conduction speed, and thus heart rate. Max. sympathetic stimulation allows the heart rate to increase up to 250bpm, if not for the interference of the parasympathetic nervous system. Sympathetic input also increases the contraction force of the ventricles. The sympathetic system predominates during times of physical or emotional stress. Sympathetic stimulation also triggers release of the hormones epinephrine and norepinephrine which play a part in increasing or decreasing heart rate and contractility during times of stress such as intense exercise.

(f) Recall the misconception of fatigue being the result of lactic acid buildup. Lactic acid accumulates within the muscle fiber only during relatively brief, highly intense muscular efforts. Marathon runners may have near resting levels of lactic acid in their blood at the end of the race, despite feeling fatigued which is likely caused by inadequate energy supply. When not cleared, the lactic acid dissociates, converting to lactate and causing an accumulation of H+ ions. The accumulation of H+ ions causes muscle acidification, resulting in a condition known as acidosis.

(g) Fortunately, the cells and body fluids possess buffers, such as bicarbonate (HCO) that minimize the influence of H+ions. Because of the buffering capacity, the H+ concentration remains low even during the most severe exercise, allowing muscle pH to decrease from a resting 7.1 to no lower than 6.4 at exhaustion.

(h) Lastly, Carbon Dioxide and H2O molecules combine to form carbonic acid. Carbonic acid is unstable and quickly dissociates, freeing a H+ion and forms a bicarbonate ion. The H+ ion consequently binds to hemoglobin. Thus hemoglobin acts as a buffer to remove CO2 away from working muscles and return to the Pulmonary system to be expired via the lungs. The increase in CO2 stimulates the chemoreceptors that signal  the inspiratory center to increase ventilation. Thus the ventilatory threshold reflects the respiratory response to increased carbon dioxide level, and ventilation increases dramatically beyond the VT.