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University of California - Irvine
Biological Sciences
Peter A.Bowler

e109 10/24/12 How are the myosin molecules organized? Myosin S1 (“the head”) subfragment crystal structure -is a protein -overall structure of a long tail with two globular heads that rotate and undergo a power stroke -arranged in thick filaments Not all skeletal muscle fibers are exactly the same -Three major types of skeletal muscle fibers: slow-twitch oxidative, fast-twitch glycolytic, fast- twitch oxidative-glycolytic Slow-twitch oxidative muscle fibers: smaller diameter, darker color due to myoglobin (red), fatigue-resistant (lots of myoglobin); more mitochondria; develop tension more slowly; capillary density is greater so has more of a blood supply; for standing, walking, and maintaining posture; get their blood supply from oxidative phosphorylation so they need oxygen (primary fuel); Fast-twitch glycolytic muscle fibers: large diameter, pale color, easily fatigued (b/c run out of ATP quicker); develop tension quicker; don’t have as much myoglobin as slow-twitch muscles; in sprinters; getATP from anaerobic glycolysis -Different fibers are mediated by different properties including myosin types -Sarcomeres are paralleled to longitudinal axis of the muscles  sarcomeres  -sarcomeres are coming in and out of board -not all skeletal muscle fibers are exactly the same Fatigue in a muscle can have a lot of different causes! -Fatigue is that the muscle can no longer sustain or generate contractions as well as it could before -Central fatigue: could be due to psychological effects (lack of motivation) and protective reflexes (undergoing extreme fear) -Peripheral fatigue: • if any issues with the release of the neurotransmitter (like acetylcholine) or receptor activation, then the muscle is not going to contract as well or as forcefully as it usually does • Change in muscle membrane potential • Sarcoplasmic reticulum Calcium leak would lead to lower Calcium release or lower Calcium-troponin interaction, leading to fatigue CNS mediates central fatigue  somatic motor neuron  neuromuscular junction excitation- contraction coupling Calcium signal contraction-relaxation Figure 12-13: review!! understand whole cascade of events Force generated depends on length (muscle length, sarcomere length, overlap of thin and thick filaments) -As muscle lengthens, the sarcomere length increases also Figure 12-15!! -only sarcomeres of intermediate length -There are zero crossbridges in the middle c) -what generates the maximum force is you have the optimal overlap of thin and thick filaments -as the sacromeres get longer, there no longer is any overlap of thin and thick filamentsa t the crosssections, so you can’t undergo force -The normal operating length of the body is around b) , but if you break your arm, the lengths increase muscle twitch = single contraction-relaxation cycle (resulting from 1 action potential from motor neuron) a) Fig 12.16 single twitches: muscle relaxes completely between stimulu -if between these action potentials, if you manipulate the lengths, you might expect a twitch to have a higher or lower tension (higher curve or lower curve) +height of curve is dependent on sacromere length b) summation: stimuli closer together do not allow muscle to relax fully a. stimuli closer together can generate a larger force in the muscle cell i. we’re not talking about the amplitude of the action potential (that’s unchanged). This is in relation to force. c) summation leading to unfused tetanus: stimuli are far enough apart to allow muscle to relax slightly between stimuli a. reach the eventual maximum tension d) summation leading to complete tetanus: muscle reaches steady tension a. fatigue causes muscle to lose
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