Exam 3 KIN 340

Chloride shift

-Bicarbonate, which carries a negative charge (anion), diffuses into the plasma -This cannot occur without a counterbalance or an electrochemical imbalance would occur -Therefore, chloride replaces bicarbonate This occurs in tissue capillaries

Links between muscle and systemic physiology

-Biochemical adaptations to training influence the physiological response to exercise: Sympathetic nervous system (↓ E/NE) and Cardiorespiratory system (↓ HR, ↓ ventilation) -Due to: Reduction in "feedback" from muscle chemoreceptors and Reduced number of motor units recruited -Demonstrated in one-leg training studies: Lack of transfer of training effect to untrained leg

Prolonged exercise in a hot environment

- During prolonged submaximal exercise in a hot/humid environment: Ventilation tends to drift upward->Increased blood temperature affects respiratory control center. Little change in PCO2-> Higher ventilation not due to increased PCO2

Arterial blood pressure

- Expressed as systolic/diastolic: old normal was 120/80 mmHg; (115/75 considered ideal) -Systolic pressure: pressure generated during ventricular contraction -Diastolic pressure: pressure in the arteries during cardiac relaxation -Pulse pressure: difference between systolic and diastolic -Mean arterial pressure (MAP): average pressure in the arteries. MAP=DBP+0.33(SBP-DBP)

Regulation of heart rate

- parasympathetic nervous system: via vagus nerve and slows HR by inhibiting SA and AV node -sympathetic nervous system: via cardia accelerator nerves and increases HR by stimulating SA and AV node -low resting Hr due to parasympathetic tone - increase in HR at onset of exercise: initial increase due to parasympathetic withdrawal-->up to 100 beats/min. Later increase due to increased SNS stimulation

O2 transport in the blood

-99% of O2 is transported bound to hemoglobin (Hb): oxyhemoglobin-> Hb bound to O2 and deoxyhemoglobin-> Hb not bound to O2 - amount of O2 that can be transported per unit volume of blood is dependent on the Hb concentration: each gram of Hb can transport 1.34 ml O2 -oxygen content of blood (100% Hb saturation): males: 200ml O2/L blood females: 174 ml O2/L blood

Secondary messengers in skeletal muscle

-AMPK: Glucose uptake, fatty acid oxidation, and mitochondrial biogenesis -PGC-1α: Increases in capillaries, mitochondria, antioxidant enzymes and Activated by p38 and CaMK -Calcineurin: Fiber growth, fast-to-slow fiber type change -mTOR: Protein kinase-major regulator of protein synthesis and muscle size -NFκB: Antioxidant enzymes

Muscle adaptations to anaerobic exercise training

-Anaerobic exercise: Refers to short-duration (i.e., 10-30 seconds) all-out effort which is also referred to as "sprint training" ->Recruits both type I and II muscle fibers to perform the exercise. During exercise lasting 10 seconds or less, the energy is primarily supplied by ATP-PC system. During exercise lasting 20-30 seconds, 80% of energy needed is provided anaerobically whereas remaining 20% is provided aerobically -Anaerobic training increases performance: 4-10 weeks of sprint training can increase peak anaerobic power by 3-28% across individuals

Muscle adaptations to anaerobic exercise training

-Anaerobic training increases performance: a. Sprint training improves muscle buffering capacity by increasing both intracellular buffers and hydrogen ion transporters b. Sprint training also results in hypertrophy of type II muscle fibers and elevates enzymes involved in both the ATP-PC system and glycolysis c. High intensity interval training >30 seconds (at near or above VO2 max) promotes mitochondrial biogenesis

Rest to work transitions

-At the onset of constant-load submaximal exercise: Initially, ventilation increases rapidly-> Then, a slower rise toward steady state - PO2 and PCO2 are relatively unchanged: Slight decrease in PO2 and increase in PCO2. Suggests that increase in alveolar ventilation is slower than increased metabolism

Relationship among pressure resistance and flow

-Blood flow: directly proportional to the pressure difference between the two ends of the system and inversely proportional to resistance blood flow= change pressure/resistance -pressure: proportional to the difference between MAP and right atrial pressure

Hypertension: high blood pressure

-Blood pressure above 140/90 mmHg; new guidelines state 130/80 considered high -Primary (essential) hypertension: cause unknown (multifactorial) and 90% cases of hypertension -Secondary hypertension: result of some other disease process - risk factor for: left ventricular hypertrophy, atherosclerosis/heart attack, kidney damage, and stroke

Why does exercise training improve VO2 max?

-Calculation of VO2 max using the Fick equation: Product of maximal cardiac output and arteriovenous difference VO2 max= HR max x SV max x a-vO2 difference max -Differences in VO2 max in different populations: Primarily due to differences in SV max -Exercise-induced improvements in VO2 max: a. Short duration training (~4 months); 26% increase in VO2 max ->↑SV > ↑a-vO2 (10% increase in SV; 2% improvement in a-vO2 ) -Longer duration training (~28 months); 42% increase in VO2 max ->↑a-vO2 > ↑SV (15% increase in SV; 25% improvement in a-vO2 )

Role of exercise intensity and duration on mitochondrial adaptations

-Citrate synthase (CS): Marker of mitochondrial oxidative capacity -Effect of exercise intensity: 55%, 65%, or 75% VO2 max. Increased CS in oxidative (IIa) fibers with all training intensities -Effect of exercise duration: 30, 60, or 90 minutes, No difference between durations on CS activity in IIa fibers. Increase in CS activity in IIx fibers with higher-intensity, longer-duration training

Can resistance training improve muscle oxidative capacity and increase capillary number?

-Conflicting results of studies: Some studies report a decrease, small increase, or no change in mitochondrial content. Some studies show small increases in capillary number whereas others report a small decrease in capillary number - Reasons for conflicting results: Different frequency and duration of resistance training. Long-term, high-volume training can improve oxidative capacity of muscle

Aging, strength, and training

-Decline in strength after age 50: a. Loss of muscle mass (sarcopenia)-> Loss of both type I and II fibers, Atrophy of type II fibers, Loss of intramuscular fat and connective tissue b. Loss of motor units c.Reorganization of motor units d. Also associated with NSAID use -Progressive resistance training: Causes muscle hypertrophy and strength gains. Important for activities of daily living, balance, and reduced risk of falls

Factors that influence arterial blood pressure

-Determinants of mean arterial pressure (MAP): cardiac output and total vascular resistance MAP= cardiac output x total vascular resistance -Short-term regulation a. sympathetic nervous system b. baroreceptors in aorta and carotid arterial--> increase in BP= decrease SNS activity and a decrease in BP= an increase SNS activity -long term regulation: kidneys via control of blood volume

CO2 transport in blood

-Dissolved in plasma (10%) -Bound to Hb (20%) -Bicarbonate (70%) -At the tissue: H+ binds to Hb, HCO3- diffuses out of RBC into plasma, Cl- diffuses into RBC (chloride shift) -At the lung: O2 binds to Hb (drives off H+) and Reaction reverses to release CO2

Training adaptation-big picture

-Endurance and resistance exercise increases specific muscle proteins: Exercise "stress" activates gene transcription -Process of training-induced muscle adaptation: Muscle contraction activates primary and secondary messengers. Results in expression of genes and synthesis of new proteins-> mRNA levels typically peak in 4-8 hours, back to baseline within 24 hours. Hence, daily exercise is needed to continue training-induced adaptation

Resistance training-induced changes in muscle fiber type

-Fast-to-slow shift in fiber type: a. From type IIx to IIa -> 5-11% change following 20 weeks of training and Small increases occur in type I fibers -Compared to endurance training, resistance training-induced fast-to-slow shifts in fiber type are less prominent

Endurance training-induced change in fiber type and capillarity

-Fast-to-slow shift in muscle fiber type: Reduction in fast myosin, Increase in slow myosin, Extent of fiber type change determined by type of training and genetics -Increased number of capillaries: Enhanced diffusion of oxygen, Increased removal of wastes

Endurance training improves muscle antioxidant capacity

-Free radicals are produced by contracting skeletal muscles: Can contribute to muscle fatigue -Training increases endogenous antioxidants: Protects against exercise-induced oxidative damage and muscle fatigue

Impact of genetics on VO2 max and exercise training responses

-Genetics plays an important role in determining VO2 max: a. Heritability determines ~50% of VO2 max in untrained subjects b. Genetics also plays a key role in determining how individuals respond to exercise training: Average training improvement of VO2 max is 15-20%. Low responders to exercise training achieve only 2-3% improvement of VO2 max. High responders to exercise training can achieve up to a 50% increase in VO2 max. Heritability of training-induced change in VO2 max is 47% -21 genes play a role change in VO2 max with training

Input to the respiratory control center

-Humoral (blood borne) chemoreceptors: a. Central chemoreceptors: Located in the medulla and Sensitive to PCO2 and H+ concentration in cerebrospinal fluid b. Peripheral chemoreceptors: Aortic and carotid bodies and Sensitive to PO2, PCO2, H+, and K+ in blood - Neural input: a.From motor cortex and skeletal muscle receptors ->Muscle mechanoreceptors: Muscle spindles, Golgi tendon organs, joint pressure receptors. Muscle chemoreceptors: sensitive to K+ and H+ concentrations b. Important for regulating breathing during submaximal, steady-state exercise

Endurance exercise-induced signaling events

-Primary Signals: ↑ Ca++, ↑ AMP/ATP, ↑ free radicals -Secondary signals: ↑ Calcineurin, ↑ CaMK, ↑ AMPK, ↑ p38, ↑ NFκB, ↑ PGC-1α -Responses: Fast-to-slow fiber type shift, Mitochondrial biogenesis, Antioxidant enzyme synthesis

Resistance training-induced changes in muscle fiber size

-Hyperplasia: a. Increase in muscle fiber number b. Limited evidence in human studies c. Most evidence indicates that 90-95% of muscle enlargement due to hypertrophy - Hypertrophy: a. Enlargement of both type I and II fibers: Greater degree of hypertrophy in type II fibers b. Increase in myofibrillar proteins c. Increases number of cross-bridges d. Increased ability to generate force

exercise training-induced changes in muscle fuel utilization

-Increased utilization of fat and sparing of plasma glucose and muscle glycogen -Transport of FFA into the muscle: Increased capillary density and Increased fatty acid binding protein and fatty acid translocase -Transport of FFA from the cytoplasm to the mitochondria: Increased mitochondrial number-> Higher levels of CPT I and FAT -Mitochondrial oxidation of FFA: Increased enzymes of β-oxidation->Increased rate of acetyl-CoA formation and High citrate level inhibits PFK and glycolysis

control of ventilation at rest

-Inspiration: Produced by contraction of diaphragm -Expiration: Occurs when diaphragm relaxes due to passive recoil of lungs and chest wall -Respiratory muscle drive is controlled by somatic motor neurons in the spinal cord: Controlled by respiratory control center In medulla oblongata and pons

Exercise training improves acid-base balance during exercise

-Lactate production during exercise -Training adaptations: a. Increased mitochondrial number->Less carbohydrate utilization = less pyruvate formed b. Increased NADH shuttles-> Less NADH available for lactate formation c. Change in LDH type M4->M3H-> M2H2-> MH3-> H4 - Heart form (H4) has lower affinity for pyruvate = less lactate formation

Does the pulmonary system limit exercise performance

-Low-to-moderate intensity exercise: Pulmonary system does not limit exercise tolerance. Diaphragm is highly oxidative and fatigue resistant -High intensity exercise: Not a limitation in healthy individuals at sea level at most exercise intensities ->However, evidence that respiratory muscle fatigue does occur during high intensity exercise (95-100% VO2 max). May be limiting in some elite endurance athletes-> 40-50% experience hypoxemia

Retraining and VO2 max

-Muscle mitochondria adapt quickly to training: Double within 5 weeks of training -Mitochondrial adaptations lost quickly with detraining: Loss of 50% of training gain within 1 week of detraining and Majority of adaptation lost in two weeks -Requires 3-4 weeks of retraining to regain mitochondrial adaptations

Physiological effects of strength training

-Muscular strength: Maximal force a muscle or muscle group can generate-> 1 repetition maximum (1-RM) -Muscular endurance: Ability to make repeated contractions against a submaximal load -Strength training: Percent gain inversely proportional to initial strength-> Genetic limitations exist to gains in strength. High-resistance (2-10 RM) training-> Gains in strength. Low-resistance training (20+ RM) ->Gains in endurance

O2 transport in muscle

-Myoglobin (Mb): Shuttles O2 from the cell membrane to the mitochondria -Mb has a higher affinity for O2 than hemoglobin: Even at low PO2 and Allows Mb to store O2-> O2 reserve for muscle. Buffers O2 needs at onset of exercise until cardiopulmonary system increases O2 delivery -Shape of Mb curve indicates that MB discharges its O2 at very low PO2 values: PO2 in mitochondria of contracting muscle may be as low as 1-2 mmHg

Resistance training-induced changes in the nervous system

-Neural adaptations responsible for early gains in strength: Initial 8-20 weeks - Adaptations include: a. Increased ability to recruit motor units b. Altered motor neuron firing rates c. Enhanced motor unit synchronization d. Removal of neural inhibition

Mechanisms for the impairment of strength during concurrent training

-Neural factors: Impaired motor unit recruitment ->Limited evidence exists to support this concept -Low muscle glycogen content: Due to successive bouts of endurance exercise.Could result in impaired ability to perform a subsequent resistance training bout -Overtraining: No direct evidence exists to prove overtraining contributes impairment of strength gains during concurrent training -Depressed protein synthesis: Endurance training adaptations interfere with protein synthesis-> Via inhibition of mTOR by activation of AMPK

Training reduces the ventilatory response to exercise

-No effect on lung structure - Ventilation is lower during exercise following training: Exercise ventilation is 20-30% lower at same submaximal work rate -Mechanism: Changes in aerobic capacity of locomotor muscles. Result in less production of H+ and Less afferent feedback from muscle to stimulate breathing

Principles of training

-Overload: Training effect occurs when a physiological system is exercised at a level beyond which it is normally accustomed -Specificity Training effect is specific to: Muscle fibers recruited during exercise, Energy system involved (aerobic vs. anaerobic), Velocity of contraction, Type of contraction (eccentric, concentric, isometric) -Reversibility: Gains are lost when overload is removed

Physical characteristics of blood

-Plasma: liquid portion of blood and contains ions, proteins, hormones -cells: a. red blood cells: contain hemoglobin to carry oxygen b. white blood cells: important in preventing infection c. platelets: important in blood clotting -hematocrit: percentage of blood composed of cells

Concurrent strength and endurance training

-Potential for interference of adaptations: Strength training increases muscle fiber size whereas endurance training does not and Depends on intensity, volume, and frequency of training -Numerous studies report that combining strength and endurance training impairs strength gains compared to strength training alone: How much interference occurs depends on intensity, volume, and frequency of endurance training

Resistance training-induced signaling events

-Primary Signals: ↑ Muscle stretch (mechanoreceptor activation) promotes synthesis of phosphatidic acid and activation of the mTOR activator, Ras homolog enrich in brain (Rheb) -Secondary signals: Increases in Phosphatidic acid and Rheb promotes mTOR activation. mTOR activation promotes protein synthesis-> A single bout can increase protein synthesis 50-100% -Responses: Muscle hypertrophy due to increased myofibrillar proteins. Increased number of myonuclei in each fiber-> Derived from satellite cells and Increases in myonuclei may be important to support increased muscle protein synthesis as fiber increases in size

Primary signal transduction pathway in skeletal muscle

-Primary signals for muscle adaptation: a. Mechanical stretch b. Calcium Via calmodulin-dependent kinase c. Free radicals d.Phosphate/muscle energy levels: AMP/ATP ratio activates AMPK -Primary and secondary signals lead to adaptations: Increased protein synthesis -Effect depends on exercise stimulus: Intensity and duration and Resistance vs. endurance training

Ventilation and acid base balacane

-Pulmonary ventilation removes H+ from blood by the HCO3- reaction -Increased ventilation results in CO2 exhalation: Reduces PCO2 and H+ concentration (pH increase) -Decreased ventilation results in buildup of CO2: Increases PCO2 and H+ concentration (pH decrease)

Detraining and VO2 max

-Rapid decrease in VO2 max: ↓ ~8% within 12 days; ↓ 20% after 84 days -↓ SV max: Rapid loss of plasma volume -↓ Maximal a-v O2 difference: ↓ Mitochondria, ↓ Oxidative capacity of muscle-> ↓ Type IIa fibers and ↑ type IIx fibers -Initial decrease (12 days) due to ↓ SV max -Later decrease due to ↓ a-v O2 max

Resistance training improves muscle antioxidant enzyme activity

-Resistance training improves antioxidant capacity in trained muscles: Resistance training-induced increases in muscle antioxidant enzyme activity is similar to the changes observed following endurance exercise training

Detraining and loss of muscle strength and fiber size

-Slow decrease in strength: 31% decrease in strength following 30 weeks detraining and Associated with small changes in fiber size a. Type I fiber size -2% b. Type IIa fiber size: -10% c. Type IIx fiber size: -14% Due primarily to nervous system changes -Retraining results in rapid regain of strength and muscle size: Within 6 weeks after resuming training and Can maintain strength with reduced training for up to 12 weeks

Respiratory control center

-Stimulus for inspiration comes from four respiratory rhythm centers: -In Medulla: preBötzinger Complex and retrotrapezoidal nucleus -In Pons: Pneumotaxic center and caudal pons

Ventilatory control during exercise

-Submaximal exercise a. Primary drive: Higher brain centers (central command) b."Fine tuned" by: Humoral chemoreceptors and Neural feedback from muscle -Heavy exercise : Alinear rise in VE-> Increasing blood H+ (from lactic acid) stimulates carotid bodies. Also K+, body temperature, and blood catecholamines may contribute

Effect of endurance training on performance and homeostasis

-The ability to perform prolonged, submaximal exercise is dependent on the maintenance of homeostasis -Endurance exercise training results in: 1. More rapid transition from rest to steady-state 2. Reduced reliance on glycogen stores 3. Cardiovascular and thermoregulatory adaptations 4. Neural and hormonal adaptations 5. Biochemical changes in muscle

Cardiac output

-The amount of blood pumped by the heart each minute -product of the heart rate and stroke volume: a. Heart rate: number of beats per minute b. stroke volume; amount of blood ejected in each beat Q= HR x SV -depends on training state and gender

Effect of exercise training on lungs

-Training does not alter lung structure -Normal lung exceeds demand for gas exchange ("overbuilt"): Therefore, training-induced adaptation is not required for the lung to maintain blood-gas homeostasis during exercise

Endurance training and VO2 max

-Training to increase VO2 max: Large muscle groups, dynamic activity. 20-60 min, ≥3 times/week, ≥50% VO2 max -Expected increases in VO2 max: Average = 15-20%. 2-3% in those with high initial VO2 max ->Requires intensity of >70% VO2 max. Up to 50% in those with low initial VO2 max-> Training intensity of 40-50% VO2 max -Genetic predisposition: Accounts for about 50% of VO2 max and Prerequisite for very high VO2 max

Stroke volume

-Training-induced increased maximal stroke volume: a. ↑ Preload: (EDV), ↑ Plasma volume, ↑ Venous return, ↑ Ventricular volume b. ↓ Afterload: (TPR) ↓ Arterial constriction, ↑ Maximal muscle blood flow with no change in mean arterial pressure c. ↑ Contractility -Training-induced changes occur rapidly: 11% ↑ in plasma volume, 7% ↑ VO2 max, and 10% ↑ in stroke volume with six days of training

Endurance training increase mitochondrial volume and turnover in skeletal muscle fiber

-Two populations of mitochondria exist in muscle fibers: a Subsarcolemmal are located below sarcolemma b.Intermyofibrillar are located around contractile proteins -Mitochondrial content increases quickly: Depends on intensity and duration of training. Can increase 50-100% within first 6 weeks -Increased mitochondrial volume results in increased endurance performance due to improved bioenergetics homeostasis, decreased glucose utilization, and increased fat metabolism -Endurance exercise training increases mitochondrial turnover in muscle resulting in the removal of damaged mitochondria

incremental exercise-untrained subject

-Ventilation: Linear increase up to ~50-75% VO2 max. Exponential increase beyond this point. Ventilatory threshold (Tvent)-> Inflection point where VE increases exponentially -PO2: Maintained within 10-12 mmHg of resting value

incremental exercise-elite athlete

-Ventilation: Tvent occurs at higher % VO2 max -PO2: Decrease of 30-40 mmHg at near-maximal work-> Hypoxemia. Due to: Ventilation/perfusion mismatch, Short RBC transit time in pulmonary capillary due to high cardiac output

Increased mitochondrial volume and exercise perfomance-details

-[ADP] stimulates mitochondrial ATP production -Increased mitochondrial volume following training: Lower [ADP] needed to increase ATP production and VO2 -Oxygen deficit is lower following training: Same VO2 at lower [ADP] and Energy requirement can be met by oxidative ATP production at the onset of exercise ->Faster rise in VO2 curve, and steady state is reached earlier -Results in: Less lactate and H+ formation Less PC depletion

Airway resistance

-airflow depends on: pressure difference between two ends of airway and resistance of airways airflow= p1- p2/resistance -airway resistance depends on diameter of airway: chronic obstructive pulmonary disease (COPD) and asthma and exercise-induced asthma

Changes in arterial-mixed venous O2 content during exercise

-arteriovenous difference (a-vO2 difference): amount of O2 that is taken up from 100ml blood and increases during exercise due to higher O2 uptake in tissues--> used for oxidative ATP production -fick equation: relationship between cardiac output, a-vO2 difference, and VO2 VO2= Q x a-vO2 difference

Exercise-induced asthma

-asthma results in bronchospasm: narrowing of airways--> increased work of breathing and shortness of breath (dyspnea). many potential causes -exercised-induced asthma: bronchospasm during or immediately following exercise, may impair exercise performance and small change in airway diameter=large increase in resistance

Conducting Zone

-at rest healthy humans breath though the nose -during moderate to heavy exercise, the mouth becomes the major passageway for air -the tracheas branches into two primary bronchi (right and left) which enter each lung: several more branches become forming bronchioles, then branch several more times before becoming alveolar ducts leading into sacs and the respiratory zone -the air is filtered and humidified before it moves to the respiratory zone; regardless of air in the environment, air going to lungs is warm and saturated with water vapor

Transition from rest to exercise and exercise to recovery

-at the onset of exercise: rapid increase in HR, SV, cardiac output and plateau in submaximal exercise -during recovery: decrease in HR, SV, and cardiac output toward resting levels and depend on duration and intensity of exercise and training state of subject

Arm vs leg exercise

-at the same oxygen uptake arm work results in higher a. heart rate: due to higher sympathetic stimulation b. blood pressure: due to vasoconstriction of large inactive muscle mass

Beta-blockade and heart rate

-beta-adrenergic blocking drugs (beta-blockers) a. compete with epinephrine and norepinephrine for beta adrenergic receptors in the heart b. reduce heart rate and contractility--> lower the myocardial oxygen demand -prescribed for patients with coronary artery disease and hypertension -will lower heart rate during submaximal and maximal exercise--> important for exercise prescription

Expiration

-both the lungs and chest wall are elastic return to equilibrium position after expanding during inspiration -passive process during rest

Change in cardiac output during exercise

-cardiac output increase due to: increased HR, linear increase to max -for adults: Max HR=220-age(years) -for children: Max HR=208- 0.7 x age (years) -increased SV: increased, then plateau at 40-60% VO2 max and no plateau in highly trained subjects

prolonged exercise

-cardiac output is maintained -gradual decrease in stroke volume: due to dehydration/reduced plasma volume -gradual increase in heart rate during prolonged exercise (particularly in heat); cardiovascular drift

Circulatory response to exercise

-changes in heart rate and blood pressure -depend on: type, intensity, and duration of exercise--> arm vs leg exercise. Environmental conditions--> hot/humid vs cool

partial pressure of gases

-dalton's law; the total pressure of gas mixture is equal to the sum of the pressure that each gas would exert independently -calculation of partial pressure pair= PO2 + PCO2+ PN2

Inspiration

-diaphragm is the most important muscle of inspiration -only skeletal muscle that is considered essential for life -attaches tot he lower ribs and is innervated by the phrenic nerves -during contraction it forces the abdominal contents downward and forward--> the ribs are lifted outward this happened to reduce intrapleural pressure which allows the lungs to expand. This allows intrapulmonary pressure to drop below atmospheric pressure and air to flow into the lungs

Respiratory muscle and exercise

-do respiratory muscles fatigue during exercise? historically believed that respiratory muscles do not fatigue during exercise. Current evidence suggests that respiratory muscles do fatigue during exercise prolonged (>120min) and high intensity (90-100% VO2 max) -do respiratory muscle adapt to training? yes, increased oxidative capacity improves respiratory muscle endurance and reduced work of breathing.

Emotional influence

-elevated HR and BP in emotionally changed environment due to increase in SNS activity -can increase pre-exercise HR and BP -does not increase peak HR or BP during exercise

Regulation of stroke volume

-end-diastolic volume (EDV): volume of blood in the ventricles at the end of diastole (preload) - average aortic blood pressure: pressure the heart must pump against to eject blood (afterload) -> mean arterial pressure -strength of the ventricular contraction (contractility): enhanced by circulation epinephrine and norepinephrine and direct sympathetic stimulation of heart

End- diastolic volume

-frank-starling mechanism: greater EDV results in a more forceful contraction die to stretch of ventricles -dependent on venous return -venous return increased by: venocontriction--> Via SNS -skeletal muscle pump: rhythmic skeletal muscle contractions force blood in the extremities toward heart and one-way valves in veins prevent backflow of blood -respiratory pump: changes in thoracic pressure pull blood toward heart

Incremental exercise

-heart rate and cardiac output: increases linearly with increasing work rate and reaches plateau at 100% VO2 max -blood pressure: mean arterial pressure increases linearly: systolic BP increases and diastolic BP remains fairly constant -double product (rate-pressure product): increases linearly with exercise intensity and indicates the work of the heart double product= HR x systolic BP

Redistribution of blood flow during exercise

-increased blood flow to working skeletal muscle: at rest 15-20% of cardiac output to muscle and increase to 80-85% during maximal exercise -decreased blood flow to less active organs: liver, kidneys, GI tract -redistribution depends on metabolic rate: exercise intensity

Central command theory

-initial signal to "drive" cardiovascular system comes from higher brain centers due to centrally generated motor signals -fine-tuned by feedback from a. heart mechanoreceptors b. muscle chemoreceptors: sensitive to muscle metabolites (K+,lactic acid) and exercise pressor reflex c. muscle mechanoreceptors: sensitive to force and speed of muscular movement dl baroreceptors: sensitive to changes in arterial blood pressure.

Inspiration and expiration during

-inspiration: during normal, quiet breathing the diaphragm performs most of the work, during exercise, accessory muscles assist in breathing-> external intercostal muscles, pectoralisis minor, scalene muscles, and sternocleidmastoids -expiration: no muscular effector is necessary for expiration to occur at rest. during exercise expiration are those found in the abdominal wall-> rectus abdominus and internal oblique, when these muscles contract the diaphragm is pushed upward and the ribs pull downward. This results in a decrease in volume in the chest.

Function of the respiratory system-big picture

-means of gas exchange between external environment and the body: replacing O2, removing CO2, and regulation of acid-base balance. -ventilation: mechanical process of moving air into and out of lungs -diffusion: random movement of molecules from an area of high concentration to an area of lower concentration

Spirometry

-measurement of pulmonary volumes and rate of expired airflow -useful for diagnosing lung disease: COPD -spirometric tests a. vital capacity b. forced expiratory volume (FEV1): volume of air expired during 1 second during maximal expiration -FEV1/VC ratio: >/equal 80% is normal for healthy individuals

mechanics of breathing

-movement of air occurs via bulk flow: movement of molecules due to pressure difference -inspiration: diaphragm pushes downward, ribs lift outward. Volume of lungs increase and intrapulmonary pressure lowered. -expiration: diaphragm relaxes, ribs pulled downward, volume of lungs decrease, and intrapulmonary pressure raised.

structure of the respiratory system

-organs: a. nose and nasal cavities b. pharynx and larynx c. trachea and bronchial tree d. lungs-> alveoli- site of gas exchange -diaphragm: major muscle of inspiration - lungs are enclosed by membranes called pleura a. visceral pleura: on outer surface of lung b. parietal pleura: lines the thoracic wall c. intrapleural space: intrapleural pressure is lower than atmospheric: prevents collapse of alveoli

Oxygen delivery during exercise

-oxygen demand by muscles during exercise is 15-25x greater than at rest -increased O2 delivery accomplished by: increased cardiac output and redistribution of blood flow from inactive organs to working skeletal muscle

Effect of pH, Temperature and 2-3 DPG on the O2-Hb dissociation curve

-pH: Decreased pH lowers Hb-O2 affinity. Results in a "rightward" shift of the curve ->Favors "offloading" of O2 to the tissues. Bohr effect -Temperature: Increased blood temperature lowers Hb-O2 affinity. Results in a "rightward" shift of the curve - 2-3 DPG: Byproduct of RBC glycolysis. May result in a "rightward" shift of the curve-> During altitude exposure. Not a major cause of rightward shift during exercise

Nitric Oxide is an important vasodilation

-produced in the endothelium or arterioles -promotes smooth muscle relaxation; results in vasodilation and increased blood flow -important in autoregulation with other local factors -one of several factors involved in blood flow regulation during exercise: increased muscle blood flow

blood flow to the lung

-pulmonary circuit: same rate of flow as systemic circuit and lower pressure due to low resistance -when standing most of the blood flow is to the base of the lung due to gravitational force -during exercise, more blood flow to apex.

Respiratory introduction

-pulmonary respiration: ventilation and exchange of O2 and CO2 in the lungs -cellular respiration: O2 utilization and CO2 production by the tissues -purpose of the respiratory system during exercise: gas exchange between the environment and the body. Regulation of acid-base balance during exercise

Electrocardiogram (ECG)

-records the electrical activity of the heart -P-wave: atrial depolarization -QRS complex: ventricular depolarization and atrial repolarization -T wave: ventricular repolarization -ECG abnormalities may indicate coronary heart disease: ST- segment depression can indicate myocardial ischemia

Intermittent exercise

-recovery of heart rate and blood pressure between bouts depend on: fitness level, temperature/humidity, and duration and intensity of exercise

hemodynamics

-resistance depends upon: length of vessel, viscosity of the blood and radius of the vessel (greatest influence on resistance) resistance= length x viscosity/radius^4 -source of vascular resistance: MAP decreases throughout the systemic circulation and largest BP drop occurs across the arterials--> arterioles are called "resistance vessels"

Regulation of local blood flow during exercise

-skeletal muscle vasodilation a. autoregulation: blood increased to meet metabolic demands of tissue. Due to changes in O2 tension, CO2 tension, nitric oxide, potassium, adenosine, and pH b. vasodilation will reduce resistance which will increase blood flow -vasoconstriction to visceral organs and inactive tissues: SNS vasoconstriction and blood flow reduced to 20-30% of resting values

Stroke volume does not plateau in endurance athletes

-stroke volume reaches a plateau at 40-60% VO2 max in untrained subjects: at high HR, filling is decreased and decrease in EDV and SV -stroke volume does not plateau in trained subjects: improved ventricular filling and increase in EDV and SV at high HR

Pulmonary ventilation

-the amount of air moved in or out of the lungs per minute (V) -tidal volume (vt): amount of air moved per breath -breathing frequency (f): number of breaths per minute V=Vt x f -alveolar ventilations (Va): volume of air that reaches the respiratory zone - dead-space ventilation (Vd): volume of air remaining in conducting airways V= Va+ Vd

Heart rate variability

-the time between heart beats: standard deviation of the R-R interval -balance between SNS and PNS: sympathovagal balance -wide variation in the HRV is considered healthy -low HRV is a predicator of cardiovascular morbidity and mortality: in patients with existing cardiovascular disease

Ventilation-perfusion relationship

-ventilation/perfusion ratio (V/Q): indicates matching of blood flow to ventilation and ideal number is 1.0 -apex of lung: underperfused (ratio>1.0) -base of lung: overperfused (ratio<1.0) -during exercise: light exercise improves V/Q ratio and heavy exercise results in V/Q inequality

pulmonary volumes and capacities

-vital capacity (VC): maximum amount of gas that can be expired after a maximum inspiration -residual volume (RV): volume of gas remaining in lungs after maximum expiration - total lung capacity (TLC): amount of gas in the lungs after a maximum inspiration - exercise does not impact any of these volumes

The circulatory system

-works with the pulmonary system: cardiopulmonary and cardiorespiratory system. - purpose of the cardiorespiratory system is to transport O2 and nutrients to tissues, removal of CO2 waste from tissues and regulation of body temperature. - two major adjustments of blood flow during exercise: increased cardiac output and redistribution of blood flow from inactive organs to active muscles. - heart: creates pressure to pump blood - arteries and arterioles: carry blood away from the heart -Capillaries: exchange of O2, CO2 and nutrients with tissues EX: skeletal muscle -veins and venules: carry blood toward the heart.

Arteriovenous O2 difference

-↑ Muscle blood flow: ↓ SNS vasoconstriction -Improved ability of the muscle to extract oxygen from the blood: a. ↑ Capillary density: Slows blood flow through muscle b.↑ Mitochondrial number

Exercise and chromic obstructive pulmonary disease

COPD: increased airway resistance--> due to constant airway narrowing. decreased expiratory airflow -includes two lung diseases: a. chronic bronchitis: excessive mucus blocks airways b. emphysema: airway collapse and increased reistance -increased work of breathing: leads to shortness of breath and may interfere with exercise and activities of daily living

conducting and respiratory zones:

Conducting zone: -conducts air to respiratory zone -humidifies, warms and filters air -components: trachea, bronchial tree, bronchioles Respiratory zone: -exchange of gases between air and blood -components: respiratory bronchioles and alveolar sacs- surfactant prevents alveolar collapse

Electrical activity of the heart

Contraction of the heart depends on electrical stimulation of the myocardium Conduction system: -SA node: pacemaker, initiated depolarization -AV node: passes depolarization to ventricles and briefly delay to allow for ventricular filling. -bundle branches: connect atria to left and right ventricle - Purkinje fibers: spread wave of depolarization throughout ventricles

Pressure changes during the cardiac cycle

Diastole: -pressure in ventricles is low -filling with blood from atria--> AV valves open when ventricular P<atrial P (SV valve closed) Systole: - pressure in ventricles rises -blood ejected in pulmonary and systemic circulation--> semilunar valves open when ventricular P> aortic P (AV valves closed) Heart sounds: -first: closing of AV valves -second: closing of aortic and pulmonary valves

oxyhemoglobin dissociation curve examples

Example: -High PO2 in the lungs results in an increase in arterial PO2 and the formation of oxyhemoglobin: Reaction moves to the right (loading) -A low PO2 in peripheral tissue (skeletal muscle) results in a decrease of PO2 in the systemic capillaries and thus O2 is released from hemoglobin to be used by the tissues: Reaction moves to the left (unloading)

Diffusion of gases

Fick's law of diffusion:The rate of gas transfer (V gas) is proportional to the tissue area, the diffusion coefficient of the gas, and the difference in the partial pressure of the gas on the two sides of the tissue, and inversely proportional to the thickness. V gas= A/T x D X (p1-p2) -Diffusion is for any single gas is greater when surface area large and the pressure is high -Increases in tissue thickness decreases diffusion -Lung is well designed for diffusion of gases across the alveolar membrane into and out of the blood.Remember, capillaries and alveoli are only one cell thick each and large surface area -Lung structure ideal for gas exchange Exercise can increase oxygen uptake and CO2 output by 20-30%

Diagnostic use of the ECG during exercise

Graded exercise test to evaluate cardiac function: -observe ECG during exercise -also observe changes in blood pressure Atherosclerosis: - fatty plaque that narrows coronary arteries -reduces blood flow to myocardium--> myocardial ischemia S-T segment depression: suggest myocardial ischemia

Pulmonary and systemic circuits

Pulmonary circuit: - right side of the heart - pumps deoxygenated blood to the lungs via pulmonary arteries -returns oxygenated blood to the left side of the heart via pulmonary veins Systemic circuit: - left side of the heart -pumps oxygenated blood to the whole body via arteries - returns deoxygenated blood to the right side of the heart via veins.

The cardiac cycle

Systole: -contraction phase -ejection of blood-> 2/3 blood is ejected from ventricles per beat Diastole: -relaxation phase -filling with blood -At rest, diastole longer than systole -During exercise, both are shorter.

Myocardium: muscle of the heart

The heart wall: -epicardium: outer layer -myocardium: middle layer and largest -endocardium: inner layer -Receives blood supply via coronary arteries: high demand for oxygen and nutrients -Myocardial infarction (MI): heart attack. blockage in coronary blood flow results in cell damage. Exercise training protects against heart damage during MI

Oxyhemoglobin Dissociation Curve

deoxyhemoglobin + O2 <--> oxyhemoglobin -The combination of O2 with Hb in the lung (alveolar capillaries) is called loading: The release of O2 from Hb is called unloading These are reversible reactions -Direction of reaction depends on: PO2 of the blood and Affinity/bond strength between Hb and O2 -At the lung High PO2 = formation of oxyhemoglobin and Drives reaction to the right (loading) -At the tissues Low PO2 = release of O2 to tissues and Moves reaction to the left (unloading)

Exercise training protects the heart

regular exercise is is cardioprotective: -reduces incidence of heart attacks -improves survival from heart attack Exercise reduces the amount of myocardial damage from heart attack: -improvements in heart's antioxidant capacity -improved function of ATP-sensitive potassium channels