KINE 3012 Lecture Notes - Lecture 12: Cardiac Muscle, Stroke Volume, Cardiac Output

• School: York University
• Department: Kinesiology & Health Science
• Course: KINE 3012
• Professor: Michael Connor

Document Summary

Fra(cid:374)k- starli(cid:374)g mecha(cid:374)is(cid:373: frank-starli(cid:374)g: stre(cid:374)gth of heart"s systolic co(cid:374)tractio(cid:374) is directly proportio(cid:374)al to its diastolic expansion. It only effect hr: nep & ep (sympathetic system) affects both sv & hr. Regulation of sv: sympathetic stimulation increases ca2+ concentration, strength of contraction depends on ca2+ concentration, with sympathetic stimulation the curve shifts left. This means with any edv given, the sv is higher. This is because nep & ep increase amount of ca2+ released from sr. Greater amount of intracellular calcium to allow more myosin & actin contraction. Increase strength of contraction means greater actin & myosin interaction. I(cid:374)crease sy(cid:373)pathetic acti(cid:448)ity, there"s greater effect o(cid:374) sv. If cardiac muscle not relaxing, its not filling. With sympathetic activity- on contraction: (cid:449)/sy(cid:373)pathetic there"s (cid:373)ore calciu(cid:373)- results in faster & stronger contractions & faster relaxation. In the vascular system, nep & ep have different effects b/c different receptors. Nep & ep have same effect b/c same receptors.