Challenges to the Cardiovascular System II
Comparison of Resistance and Endurance Training Responses
- Foundational Principle: Resistance exercise alone does not improve the functional capacity of the cardiovascular system (CVS).
- Study Data on Left Ventricular (LV) Dimensions: Morganroth et al. (Ann J. Intern Med 1975) compared cardiac parameters across different athletic profiles (n=57 subjects total):
* Untrained (n=16):
* LV mass:211g
* LV wall:10.3mm
* LV vol:101ml
* SV (Stroke Volume):(70)ml
* College runners (n=15):
* LV mass:302g
* LV wall:11.3mm
* LV vol:160ml
* SV:116ml
* World class runners (n=10):
* LV mass:283g
* LV wall:10.8mm
* LV vol:154ml
* SV:113ml
* College wrestlers (n=12):
* LV mass:330g
* LV wall:13.7mm
* LV vol:110ml
* SV:75ml
* World class shot putters (n=4):
* LV mass:348g
* LV wall:13.8mm
* LV vol:122ml
* SV:68ml
Detraining and the 'Use It or Lose It' Principle
- Coyle EF et al. (1984) Study: Examined the time course of loss of adaptations after stopping prolonged intense endurance training.
* Subject Profile: Runners or cyclists who trained for 10-12 months.
* Training Protocol: 5imes1 hour sessions/week at 70-80% VO2extmax.
* Observation Period: Cardiovascular variables were monitored over 84 days of detraining after cessation of regular exercise.
* Results:
* Heart Rate (HR) increased.
* All other measured variables decreased: Cardiac Output (CO), Stroke Volume (SV), O2 extraction, and VO2extmax.
- Kemi et al. (2004) Findings: Aerobic fitness is directly associated with cardiomyocyte contractile capacity and endothelial function during both training and detraining phases.
Cardiovascular Adaptations in Extreme Environments: Space and Bed Rest
- Cardiac Atrophy: Prolonged bed rest and spaceflight lead to cardiac atrophy (Perhonen et al., 2001).
- Comparative Metrics (Pre-flight vs. In-flight):
* Pre-flight (supine):
* HR:61±2bpm
* SV:131±2ml
* CO:8.0±0.2L/min
* In-flight:
* HR:70±5bpm
* SV:93±2ml
* CO:6.5±0.4L/min
Physiological vs. Pathological Cardiac Hypertrophy
- Functional (Physiological) Hypertrophy:
* Normal adaptation of the heart to chronic pressure or volume overload.
* Result: Improved cardiac function.
- Pathological (Pathophysiological) Hypertrophy:
* Maladaptation of the heart resulting in decreased cardiac work and increased afterload.
* Origins: Can be congenital (e.g., hypertrophic cardiomyopathy) or acquired (e.g., hypertension).
* Progression: Initially acts as a compensation for reduced cardiac function; however, it leads to an increase in cardiac work and ultimately results in cardiac failure.
Pathophysiological Challenges to Cardiovascular Function
- Reduced Blood Volume (Preload reduction):
* Haemorrhage.
* Burns.
* Diarrhoea/Vomiting.
* Dehydration.
- Reduced Venous Return (Preload reduction):
* Sepsis.
* Anaphylaxis.
* General Anaesthesia.
- Pump Dysfunction (Increased Afterload / Reduced Emptying):
* Systemic hypertension.
* Arrhythmia.
* Myocardial infarction (MI).
* Heart failure.
* Valve disease.
Consequences of Inadequate Cardiac Output and Mortality Statistics
- Primary Systemic Effects:
* Inadequate O2 distribution and CO2 removal.
* Hypotension and circulatory collapse.
- UK Mortality Data (ONS/The Guardian):
* Circulatory Diseases (Total): 158,084 deaths (−1.1%
* Specific Circulatory Causes:
* Cerebrovascular diseases (brain haemorrhage): 43,363
* Chronic ischaemic heart disease: 43,957
* Acute myocardial infarction (heart attack): 25,960
* Other heart diseases: 24,718
* High blood pressure (hypertensive): 4,726
* Diseases of arteries, arterioles, and capillaries: 10,029
* Diseases of veins, lymphatic vessels, and lymph nodes: 4,094
* Chronic rheumatic heart diseases: 934
* Non-Circulatory Comparisons:
* Cancer: 141,446 (+0.7%
* Respiratory diseases: 30,857
* Bronchitis, emphysema, and chronic lung disease: 23,870
* Diabetes: 5,223
Heart Transplantation and Upregulation of Cardiac Output during Exercise
- Surgical Connections: A donor heart is installed by connecting the Aorta, Pulmonary artery, Superior vena cava, and Inferior vena cava.
- Control Mechanisms for Cardiac Output Upregulation:
1. Input from 'central command'.
2. Decreased parasympathetic activity.
3. Increased sympathetic activity.
4. Autonomic reflexes.
5. Direct effects of local signals: temperature, pH, O2, CO2, adenosine, NO, Mg2+, K+.
6. Feedback from activation of receptors in joints and muscles at the onset of exercise.
- Analytical Question: Students are prompted to consider what cardiovascular changes would occur specifically in a heart-transplant recipient (whose heart is denervated) during exercise.
VO2 Max: Aerobic Capacity and Determinants
- Definition: The maximum ability of the body to utilize oxygen during exercise. It serves as an indicator of maximum aerobic capacity (ATP synthesis).
- Limiting Factors:
* The combined ability of the cardiovascular and pulmonary systems to transport oxygen to the muscular tissue system.
* The chemical ability of the muscular cellular tissue system to use oxygen in breaking down fuels.
- Metabolic Demand Pathway: Ventilation → Diffusion across respiratory membrane → Pulmonary blood flow → Carriage of gases by blood → Systemic blood flow → Blood tissue gas exchange.
- Determinants of VO2max:
* Training status.
* Gender.
* Size, stature, and body composition.
* Heredity.
* Muscle fibre type.
* Haematocrit.
- VO2max Ranges for International Athletes (ml⋅kg−1⋅min−1):
* Cross-country skiing: Men 69-95, Women 56-74.
* Long-distance running: Men 65-80, Women 55-72.
* Rowing: Men 58-74, Women 48-68.
* Cycling: Men 56-72.
* Football: Men 54-70, Women 48-68.
* Figure skating: Men 42-54.
* Untrained: Men 38-52, Women 30-46.
- Correlation with Cardiac Output: There is a close linear relationship between maximal cardiac output (COmax) and maximal oxygen consumption (VO2max). Values for sedentary individuals typically cluster around 14-22L/min CO and 2.0-3.0L/min VO2, while endurance athletes can reach 38-40L/min CO and 5.0-6.0L/min VO2.