Cardiovascular_exercise_physiology-Oct_26th-2023 (1).pptx

Cardiovascular exercise physiology Pedro del Corral, PhD, MD Department of Physiology & Pathology Burrell College of Osteopathic Medicine October 26th 2023 1 Objectives: Suggested reading: Guyton’s Medical Physiology 259-262. Powers & Howley Exercise Physiology: Chapter 9: Circulatory responses to exercise 1. Explain the effects of incremental exercise on cardiac output, heart rate, stroke volume, arterial-venous oxygen difference, total peripheral resistance, and blood pressure 2. Discuss the pattern of redistribution of blood flow at rest and during exercise. 3. Identify the factors that regulate local blood flow during exercise. 4. Explain the hemodynamic differences between upper & lower limb exercise. 5. Explain the cardiovascular responses to prolonged exercise 6. Describe the regulation of heart rate during exercise, and describe the effects of exercise on the cardiac cycle 7. List and discuss those factors responsible for regulation of stroke volume during exercise. 8. Discuss the regulation of cardiac output during exercise. 2 Objectives 9. Distinguish between a normal and abnormal BP responses to incremental exercise 10. Explain the blood pressure responses during the post-exercise period including the mechanisms involved 11. Explain the effects of endurance training on maximal oxygen uptake, heart rate, stroke volume, cardiac output (both at rest & maximal exercise) 12. List the typical VO2 max values for various sedentary, active, athletic populations, and disease populations, and indicate the typical change in VO2 max with endurance training programs. 13. Discuss the role of preload, afterload, and contractility in the increase in the maximal stroke volume that occurs with endurance training. 14. Describe the changes in muscle structure that are responsible for the increase in the maximal a-vO2 difference with endurance training. 15. Describe the benefits of assessing cardiorespiratory fitness in the clinical setting, and discuss the “Athletes heart” 16. Calculate stroke volume, cardiac output, ejection fraction, and use the Fick equation to calculate maximal oxygen uptake 3 Human Energy Expenditure • Total Energy Expenditure components: • 1. Resting Metabolic Rate • Multiples of a resting MET are commonly used to estimate the energy expenditure and work performed during various activity tasks. • ~ 0.250 L O2/min or 1.25 calories/min • 2. Thermic effect of food • 3. Physical activity • Reference to muscular work • Measurement of energy expenditure • We will discuss two techniques: • Direct calorimetry • Indirect calorimetry Measurement of energy expenditure 4 Indirect Calorimetry • Measurement of oxygen consumption as an estimate of resting metabolic rate Foodstuffs + O2 Heat + CO2 + H2O • VO2 of 1.0 L•min–1 = ~5 kcal or 21 kJ per minute • Depends on the type of nutrient (carbohydrate or fat) metabolized • How does it work? • Open-circuit spirometry • Determines VO2 by measuring amount of O2 consumed • VO2 = volume of O2 inspired – volume of O2 expired 5 Ergometers Used in the Measurement of Human Work Output and Power Cycle ergometer Bench step Arm ergometer Treadmill 6 Indirect Calorimetry: how do we express it? • 1st Absolute terms (L O2 /min): • • • • 60 kg subject Ventilation (Ve) = 60 L•min-1 Inspired O2 = 20.93% Expired O2 = 16.93% 60 L•min-1 x (20.93% – 16.93%) = 2.4 L•min-1 (absolute terms) • How else can we express this? 7 2nd . Kcal------------------------ 3rd .VO2 (ml•kg • Example (Kcal): • VO2 = 2.4 L•min-1 • 1 L O2 = 5 kcal•L-1 • Ranges from 4.7 kcal•L-1 (fats) to 5.05 kcal•L-1 (carbohydrates) 2.4 L•min-1 x 5 kcal•L-1 O2 = 12 kcal•min-1 -1 •min-1) • Example (ml•kg-1•min-1) • VO2 = 2.4 L•min-1 • Convert to ml • Body weight = 60 kg 2.4 L•min-1 x 1000 ml•L-1 ÷ 60 kg = 40 ml•kg-1•min-1 OR 12 kcal•min-1 x 30 min = 360 kcal 8 4th METs • 1 MET = resting metabolic rate • 3.5 ml•kg-1•min-1 • Example: • VO2 = 40 ml•kg-1•min-1 40 ml•kg-1•min-1 ÷ 3.5 ml•kg-1•min-1 = 11.4 METs • http://www.parvo.com/trueone-2400/ 9 Take home messages • Energy expenditure can be expressed in L•min-1, kcal•min-1, ml•kg1•min-1, and METs. • To convert L•min-1 to kcal•min-1, multiply by 5.0 kcal•L-1. • To convert L•min-1 to ml•kg-1•min-1, multiply by 1000 and divide by body weight in kilograms. • To convert ml•kg-1•min-1 to METs or kcal•kg-1•hr-1, divide by 3.5 ml•kg1•min-1. Exercise 10 Relationship Between Work Rate and oxygen uptake VO2 Relationship Between Work Rate and oxygen uptake VO2 Relationship between work rate and maximal oxygen uptake (VO2max) in subjects with different levels of physical conditioning 11 Transition From Rest to Exercise and Exercise to Recovery • At the onset of exercise: • Rapid increase in HR, SV, cardiac output • How rapid, who, when? • Plateau in submaximal (below lactate threshold) exercise • During recovery • Decrease in HR, SV, and cardiac output toward resting • Depends on: • Duration and intensity of exercise • Training state of subject Figure 4.1: The time course of speed (a); rate of ATP use (b); oxygen uptake (c) 12 Transition From Rest to Exercise to Recovery after long term exercise Circulatory Responses to Exercise 13 Circulatory Responses to Exercise • Changes in heart rate and blood pressure • 1. Depend on: • Type, intensity, and duration of exercise • Arm vs. leg exercise • Environmental condition • Hot/humid vs. cool • 2. Emotional influences • Can increase pre-exercise HR and BP  ↑ HR and BP in emotionally charged environment • Due to increases SNS activity • Does not increase peak HR or BP during exercise O2 Delivery During Exercise 14 Oxygen Delivery During Exercise • Whole body oxygen demand during exercise is 15–25x greater than at rest. How do we accomplish this? VO2 = Q x a–vO2 extraction • Increased O2 delivery accomplished by: • ↑cardiac output (Q) • Redistribution of blood flow • From inactive organs to working skeletal muscle • ↑ a–vO2 extraction Δ in Q from rest to ↑muscular work 15 Changes in Cardiac Output During Exercise: • Cardiac output increases due to: • 1. ↑ HR as power output/metabolic rate increases • Linear increase to max • Max-HR Max HR = 220 – agewith (years) vs decreases aging Q = HR x SV Max HR = 208 – 0.7 x age (years) How is this useful for a physician? Limitations? Stroke volume 16 Changes in Cardiac Output During Exercise: stroke volume (SV) • Cardiac output increases due to: • 2. Increases in SV • Stroke volume reaches a plateau at 40–60% VO2 max in untrained subjects • At high HR, filling time is decreased • ↓ in EDV and SV • Stroke volume does not plateau in trained subjects • Improved ventricular filling • ↑ EDV and SV at high HR Coronary circulation 17 Changes in Cardiac Output During Exercise: Support from Coronary circulation • ↑Q results in increases in the 3 main determinants of myocardial oxygen demand: • heart rate, myocardial contractility, and ventricular work. • ~ 6-fold ↑ in oxygen demands of the left ventricle during heavy exercise is met principally: • coronary blood flow (5-fold), a–vO2 extraction increase modestly (already 70 –80% at rest) • In contrast, in the right ventricle, oxygen extraction is lower at rest and increases substantially during exercise, similar to skeletal muscle, suggesting fundamental differences in blood flow regulation between these two cardiac chambers. Effects of cardiac cycle 18 Changes in Cardiac Output During Exercise: Effect of cardiac cycle on Coronary circulation • During systole, the contracting myocardium generates a high level of intramyocardial pressure that compresses the coronary microvasculature, thereby impeding blood flow • The ability of coronary resistance vessels to dilate in response to increments in myocardial oxygen demand is critical for maintaining an adequate supply of oxygen to the myocardium. • Exercise is the most important physiological stimulus for increasing myocardial oxygen demands. • Implications Sk ms A-V O2 extraction 19 Changes in Skeletal muscle Arterial-Venous O2 extraction During Exercise • Higher arteriovenous difference (a-vO2 difference) • Amount of O2 that is taken up from 100 ml blood • Increase due to higher amount of O2 taken up • Used for oxidative ATP production • As exercise intensity ↑, the venous [Hgb] saturation of blood ↓ as oxygen is extracted and can reach as low as 25% at maximal exercise. • Example: Arterial O2 20 mL/dL, femoral venous O2 concentration 5 mL/dL • AV-O2 difference of 15 mL/dL. • Fick equation • Relationship between cardiac output (Q), a-vO2 difference, and VO2 VO2 = Q x a–vO2 extraction 20 Changes in Arterial-Mixed Venous O2 Content During Exercise 21 Maximal Oxygen uptake (VO2Max) test, Graded/Incremental Exercise test, stress test • What is maximal oxygen uptake? • How do we determine VO2max • Metabolic cart • 1-3 min incremental exercise test: cycle ergometer or treadmill • 12 lead ECG & BP assessment • Relevance • Clinical relevance • https://www.youtube.com/watch?v=s5k7 WPJgCBU • Athletic • https://www.youtube.com/watch?v=3xrIg BgJ1PY 22 Incremental Exercise • Heart rate and cardiac output • Increases linearly with increasing work rate • Reaches plateau at 100% VO2 max • Decrease in vascular resistance & ↑ MAP  ↑ BF • Blood pressure • Mean arterial pressure increases linearly • Systolic BP increases • Diastolic BP remains fairly constant • Double product (Rate-pressure product) • Increases linearly with exercise intensity • Indicates the work of the heart Double product = HR x systolic BP Collective view of the CVS 23 Changes in Cardiovascular Variables During Incremental Exercise Integration & regulation 24 Blood flow • ↑ blood flow is met by vasodilation of resistance vessels in the skeletal muscle, which requires an increase in cardiac output, and is facilitated by an increase in arterial pressure. 25 Redistribution of Blood Flow During Exercise • Total peripheral resistance (TPR) decreases • Increased blood flow to working skeletal muscle • At rest, 15–20% of cardiac output to muscle • Increases to 80–85% during maximal exercise • Skin blood flow • Light & moderate intensity vs high intensity • Decreased blood flow to less active organs • Liver, kidneys, GI tract • Redistribution depends on metabolic rate • Exercise intensity 26 Changes in Muscle and Splanchnic Blood Flow During Exercise 27 Regulation of Local Blood Flow During Exercise • Skeletal muscle vasodilation • Autoregulation • Blood flow increased to meet metabolic demands of tissue • Due to ↓ in O2 tension & pH, and ↑ CO2 tension, nitric oxide, potassium, and adenosine • Vasoconstriction to visceral organs and inactive tissues • SNS vasoconstriction • Blood flow reduced to 20–30% of resting values • Vasculature vessels that play a key role • Small arteries • Arterioles • Capillaries • At rest vs exercise • Sympathetics and sympatholysis • Motor unit recruitment 28 Nitric Oxide Is an Important Vasodilator • Produced in the vascular endothelium • 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 • Increases muscle blood flow 29 Regulation of Heart Rate • ANS: cardiovascular control center – medulla oblongata • Parasympathetic nervous system • Via vagus nerve • Slows HR by inhibiting SA and AV node • Neurotransmitter • Receptors • Membrane potential • Sympathetic nervous system • Via cardiac accelerator nerves • Increases HR by stimulating SA, AV node, ventricles • Neurotransmitter • Receptors • Membrane potential • 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 30 The Cardiac Cycle at Rest and During Exercise Regulation of Stroke Volume 31 Regulation of Stroke Volume • 1. End-diastolic volume (EDV) • Volume of blood in the ventricles at the end of diastole (“preload”) • 2. Average aortic blood pressure • Pressure the heart must pump against to eject blood (“afterload”) • Mean arterial pressure • 3. Strength of the ventricular contraction (contractility) • Enhanced by: • Circulating epinephrine and norepinephrine • Direct sympathetic stimulation of heart 32 Regulation of Stroke Volume: End-Diastolic Volume • A. Frank-Starling mechanism • Greater EDV results in a more forceful contraction • Due to stretch of ventricles • Skeletal muscle myosin • B. Dependent on venous return • Venous return increased by: • Venoconstriction • Skeletal muscle pump • Respiratory pump Venous return 33 Regulation of Stroke Volume: End-Diastolic Volume: Venous return • 1. Venoconstriction • Via SNS • Reflex sympathetic constriction • Smooth muscle • 2. Respiratory pump (∆P) • • • • Thoracic Pressure Abdominal pressure What happens during exercise Blood moves towards the heart • 3. Venous return increased by: • C. Skeletal muscle pump • Rhythmic skeletal muscle contractions force blood in the extremities toward the heart • One-way valves in veins prevent backflow of blood • Type of skeletal muscle contraction • Dynamic • Isometric Average aortic BP 34 Regulation of Stroke volume • 2. Average aortic blood pressure • Pressure the LV must pump against (aorta) to eject blood (“afterload”) • Mean arterial pressure • Relationship between aortic BP and stroke volume • Clinical relevance? Contractility 35 Regulation of Stroke volume: Strength of the ventricular contraction (contractility) • 3. Strength of ventricular contraction • Effects of Sympathetic Stimulation on Stroke Volume • Cardiac accelerator nerves • ↑ inward transport of extracelullar calcium • ↑ cardiac contractility & force production 36 Factors that Regulate Cardiac Output: solid (stimulate) & dotted lines (inhibit) 37 Regulation of cardiovascular adjustments to exercise • 1. Muscle contraction • 2. Vagal withdrawal to the heart • 3. Sympathetic stimulation of the heart • 4. Arteriolar vasodilation in active skeletal muscle coupled to reflex increase in resistance vessels in less active areas • 5. Increase cardiac output to match metabolic needs • What is the signal  Central Command Theory 38 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: • Heart mechanoreceptors • Muscle chemoreceptors • Sensitive to muscle metabolites (K+, lactic acid) • Muscle mechanoreceptors • Sensitive to force and speed of muscular movement • Muscle spindles & Golgi tendon organ • Baroreceptors • Sensitive to changes in arterial blood pressure • Carotid artery • Aortic arch Arm vs leg 39 Arm Versus Leg Exercise: Heart Rate and Blood Pressure • At the same oxygen uptake, arm work results in higher: • Heart rate • Due to higher sympathetic stimulation • Blood pressure • Due to vasoconstriction of large inactive muscle mass Prolonged Exercise 40 Prolonged Exercise • Cardiac output is maintained • Gradual decrease in stroke volume • Due to dehydration and reduced plasma volume • Environmental; effects • Gradual increase in heart rate coupled to a decrease in stroke volume • Cardiovascular drift • Exercise in the heat can bring submaximal HR to maximal levels Hemodynamics - Calculations 41 Hemodynamics - Calculations • Mr Smith is a 58 y.o male presents with angina and is referred for an exercise stress test, his body weight is 176 lb • What is his SV at rest and maximal exercise? Mr. Smith Data Resting-SBP (mmHg) Resting-DBP (mmHg) • The SV = End diastolic volume (ml/beat) – End systolic volume (ml-beat) • The SV (rest) = 119 ml/beat – 54 ml/beat = 65 ml/beat Resting HR (beats/min) • The SV (exercise) = 148 ml/beat – 51 ml/beat = 97 ml/beat Maximal exercise-SBP (mmHg) • Knowing SV, calculate Ejection fraction (%) • EF = SV/EDV *100 • EF (rest) = 65/119 * 100 = 54% • EF (exercise) = 97/148 * 100 = 65% 136 86 79 Resting end-diastolic-volume (ml) 119 Resting end-systolic-volume (ml) 54 Resting arterial-venous oxygen difference (ml O2/dL) 5.1 220 Maximal exercise-DBP (mmHg) 78 Maximal exercise HR (beats/min) 172 Maximal exercise end-diastolic volume (ml) Maximal end-systolic-volume (ml) 148 51 Maximal exercise arterial venous oxygen difference (ml O2/dL) 14.7 42 Hemodynamics - Calculations • Having determined the SV and knowing HR, we can now calculate the Q • Q = SV (ml/beat) * HR (beats/min), in ml/min  convert to L/min • Divide by 1000 119 • Q (rest) = 65 ml/beat * 79 b/min = 5,135 ml/min, convert to L/min: • 5.13 L/min 148 • Q (exercise) = 97 ml/beat * 172 b/min = 16,684 ml/min • 16.68 L/min 43 Hemodynamics - Calculations • Next, we calculate VO2max, having determined the exercise Q and knowing the exercise A-VO2 diff: • VO2max = Q (L/min) * A-VO2 diff (ml of O2/ dL)/100 • To compare individuals, reverse to ml of O2/min and adjust by body weight in kg • VO2max = 16.68 L/min * 14.7 ml of O2/ dL = 2.451 L O2/min 100 • multiply by 1000 and divide by body weight in kg • 2,451 ml/min divided by 80 kg  30.6 ml of O2/kg/min 119 148 • What does this mean? BP responses to exercise? 44 BP response to exercise: Clinical relevance • What constitutes a normal BP change during exercise? • SBP: • Response to each increase in exercise intensity is a rise that approximates 10 ± 2 mmHg per metabolic equivalent (MET) and may plateau at peak exercise. • DBP • Generally ↓ but may not change with increasing intensity, thus overall there is a stepwise increase in pulse pressure from rest to peak exercise. • Normal maximal intensity exercise BP as being • • • • • SBP <210 mm-Hg (men) SBP <190mmHg (women) with DBP o110 mm- Hg (both sexes) SBP cut points may not be applicable in old age. Recommend to stop the test: • Why/who are you testing? • A rapid increase in BP with only limited increases in CO suggests ↑ TPR, impaired vasodilation. • A lack of BP augmentation with exercise suggests inadequate CO unable to 'fill' the dilated exercise circulation. 45 Accordingly, SBP during incremental exercise 450 Systolic Blood Pressure (mmHg) 400 350 300 250 SBP-High SBP-Low SBP-AVG 200 150 100 50 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 METS For a Healthy normotensive 21 MET individual it would reach peak-SBP : High rate:400 mmHg Average rate : 320 mmHg Low rate: 242 mmHg 46 Exercise exaggerated BP response to exercise • Exaggerated SBP response during exercise was first noted in hypertensives, later noted in pre-hypertensives and normotensives. • Exaggerated SBP is a strong predictor of future hypertension, MI, & stroke. Posible mechanisms: • Structural – Atherosclerosis, and Endothelial dysfunctiion • Neuro-endocrine: Catecholamines, angiotensin II, and adrenal corticosteroids (aldosterone, Cortisol) • What are the implications exercise exaggerated BP: • • • • LVH Future HTN Myocardial infarction Stroke The other side of the coin 47 Acute Blood pressure response to exercise: abnormal response - Low • Hypotension during exercise: Inappropriately low BP during exercise is an absolute indication to terminate exercise testing and is defined by the American Heart Association as a drop in SBP >10mmHg (persistently below baseline), despite an increase in workload, when accompanied by any other evidence of ischemia. • Why: major cardiac disease including • • • • severe left ventricular dysfunction, obstruction to aortic outflow severe myocardial ischemia β-blocker medications impairing the normal BP (and heart rate) • Incidence of exercise hypotension is ~2% of treadmill exercise-stress tests. • Value: Exercise hypotension is assumed to be a grave prognostic sign due to the relation with severe disease. Brighter side 48 Acute Blood pressure response to exercise: post exercise period • Post-exercise hypotension (PEH): A single bout of aerobic exercise produces a postexercise hypotension • PEH is the immediate reduction in BP of 5–7 mmHg among people with hypertension that occurs after a single, isolated session of aerobic exercise of varying durations (10 to 50 min) and intensities (40 % up to 100 % of maximum oxygen consumption [VO2max]), and these BP reductions are sustained for up to 24 h after the exercise bout • A bout of aerobic exercise has been found to significantly reduce both the office BP and AMBP of hypertensive individuals. • Mechanisms involved: • 1. Centrally mediated decreases in sympathetic nerve activity with a reduced signal transduction from sympathetic nerve activation into vasoconstriction. • skeletal muscle afferents may play a primary role by resetting of the baroreflex. • Resetting results in reduced sympathetic outflow postexercise, as demonstrated by reduced muscle sympathetic nerve activity in normotensive and hypertensive humans 49 Acute Blood pressure response to exercise: post exercise period - Mechanisms • 2. Peripheral: Sustained postexercise vasodilatation of the previously active skeletal muscle is primarily the result of histamine H1 and H2 receptor activation. • Studies with fexofenadine and ranitidine • Early and late response • What is the clinical relevance of exercise induced hypotension? 50 Why should we assess cardiorespiratory fitness in the clinical setting? • Low levels of cardiorespiratory fitness (CRF) are associated with a high risk of: • cardiovascular disease, all-cause mortality, and mortality rates attributable to various cancers. • A growing body of epidemiological and clinical evidence demonstrates not only that CRF is a potentially stronger predictor of mortality than established risk factors such as smoking, hypertension, high cholesterol, and type 2 diabetes mellitus, but that the addition of CRF to traditional risk factors significantly improves the reclassification of risk for adverse outcomes. AHA Scientific Statement, Circulation, 2016 The effects of Endurance Training on the cardiovascular system 51 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 • Prerequisite for very high VO2 max 52 Range of VO2 Max Values in the Population 53 VO2 Max – Timing effect • Calculation of VO2 max • Product of maximal cardiac output and arteriovenous difference VO2 max = HR max x SV max x (a-vO2) max • Differences in VO2 max in different populations • Primarily due to differences in SV max • Improvements in VO2 max • ~50%  SV and ~50%  a-vO2 • Shorter duration training (4 months) •  SV >  a-vO2 • Longer duration training (28 months) •  a-vO2 >  SV 54 Progression of VO2 Max Changes With Training 55 Cardiac pressure volume curves Mostly due to cardiac chamber compliance 56 Arteriovenous O2 Difference • 1.  Muscle blood flow • SNS vasoconstriction • 2. Improved ability of the muscle to extract oxygen from the blood • A. Capillary density • Slows blood flow through muscle • B. Mitochondrial number & Size • Diffusion distance Athletes Heart 57 Athletes heart • Endurance training  changes in cardiac structure (all chambers) and function. • The physiologic hypertrophy • Stimulus for cardiac chamber enlargement is repetitive volume challenge for the heart incurred during training. • At least 4 to 5 sessions per week of moderate aerobic • Changes in left and right ventricular morphology can be seen as early as 3 months, with the left ventricle displaying increases in mass (concentric hypertrophy) followed by enlargement (eccentric hypertrophy) with continued training. • Ventricular enlargement leads to a higher end-diastolic volume reserve • ↑stroke volume during exercise can be accomplished using the Starling mechanism 58 Athletes heart • The larger cardiac chambers are also associated with a more compliant or “flexible” ventricle. • For any given filling pressure, the athlete’s heart is much larger and distensible than the heart of a nonathlete. • The high compliance of the ventricular chamber distinguishes the physiologic adaptation to chronic exercise training from pathologic conditions that can also be associated with cardiac hypertrophy, such as: • uncontrolled hypertension and systolic heart failure. Detraining and VO2 Max 59 Detraining and in changes in Maximal oxygen uptake • 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 • 21st to 84 days 60 Detraining: The Dallas Bedrest and training Study • In 1966, 5 healthy 20-year-old men were studied extensively at baseline, after 3 weeks of bedrest, and after 8 weeks of intensive dynamic exercise training. • Results of this investigation were published in 1968 as a supplement to Circulation in the now widely cited Dallas Bedrest and Training Study. • In the present study, a 30-year follow-up has been carried out on the 5 subjects previously studied in 1966. 61 Detraining: The Dallas Bedrest and training Study 62

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