Heart Basics -Size, Force of Contraction, Amount of Blood Moved(Rest & Active) SV, Q Valves, SA Node, AV Node, Bundle of HIS, Purkinje Fibers, Intercalated discs. -The two atria receive blood into the heart; the two ventricles send blood from the heart to the rest of the body. - Absolute values of Qmax range from 14 to 20 L/min in untrained people, 25 to 35 L/min in trained individuals, and 40 L/min or more in large endurance athletes.

Heart Basics -The left ventricle has a thicker myocardium due to hypertrophy resulting from the force with which it must contract. - Cardiac tissue has its own conduction system through which it initiates its own pulse without neural control.

Chapter 10

-The autonomic nervous system or the endocrine system can alter heart rate and contraction strength. -PNS acts through the vagus nerve to decrease heart rate and force of contraction. -SNS is stimulated by stress to increase heart rate and force of contraction. -Epinephrine and norepinephrine—released due to sympathetic stimulation—increase heart rate. -Aorta – Artery – Arteriole – Capillaries – Venuoles – Vein – Vena Cava

Chapter 10

Cardiovascular Adaptations to Training Left ventricle size and wall thickness increase -Stroke volume increases -Resting and submaximal heart rates decrease -Blood volume increases -Blood pressure does not change or slightly decreases -Cardiac output is better distributed to active muscles

Cardiovascular Adaptations to Training Less Cardiac Drift - Gradual decrease in stroke volume and systemic and pulmonary arterial pressures and an increase in heart rate. Occurs with steady-state prolonged exercise or exercise in a hot environment. * Neurogenic Factors or Peripheral Influences

STROKE VOLUME AND TRAINING

Heart Terminology -Polarization – The Muscle contains a negative and positive charge but isn’t currently contracting Depolarization – The muscle is actively contracting Repolarization – The muscle is preparing to contract once again. Best case scenario is.2 second Premature Atrial Contractions – (PAC’s) – Not as serious as PVC but may require Beta Blockers * Beta Blockers – Block Epinephrine & Norephinephrine * Calcium Blockers - Premature Ventricular contractions (PVC’s)—feel like skipped or extra beats – May require Beta Blockers – Can lead to death

Heart Terminology Continued EF = SV/EDV Averages 60% at rest – Decreases with exercise -May lead to Pulmonary Edema if the heart is weak or diseased. Bradycardia—resting heart rate below 60 bpm Tachycardia—resting heart rate above 100 bpm Ventricular tachycardia—three or more consecutive PVCs that can lead to ventricular fibrillation in which contraction of the ventricular tissue is uncoordinated

Q =

Dyspnea—shortness of breath. During exercise this is most often caused by inability to readjust the blood PCO 2 and H + due to poor conditioning of respiratory muscles Cholinergic Fibers (Dilation) SNS Baroreceptor – Dilates peripheral vasculature and slows the heart (PNS)

How does your body get more oxygen to the working muscles? Increased blood flow to capillary beds Utilization of the large amounts of unused O2. *Remember your body generally extracts 20-25% of the usable O2 from blood.

Bodily Positions Specific exercise elicits specific adaptations creating specific training effects Upper Body vs. Lower Body Pg. Supine vs. Erect Erect or Declined Measuring Heart Rate To Determine Stroke Volume

Establishing Training Intensity Train at a percentage of VO2max Difficult and confusing for the untrained practitioner Train at percentage of Maximum Heart Rate (HRmax) Generally use 70% **The way I prefer is known as the Karvonen (HRR)

How long before improvement occurs? Muscle – 6-8 weeks Hypertrophy – 1-2 weeks neuromuscular efficiency Aerobic Endurance – Changes in VO2max in as little as 1 week Pg. 369 (Eccentric Hypertrophy) BP should drop 6-10 mmHg How long before I lose what I’ve gained? SV & Q diminish at approximately 40% of gains at 2 months of no exercise.

Muscle Strength – CV Conditioning – Measurable loss at 72hrs.