Chapter 47

1. A sarcomere is bounded by the Z lines and consists of overlapping actin and myosin filaments. The actin filaments are anchored on the Z lines and do not extend all the way to the middle of the sarcomere. The myosin filaments are anchored on the M band at the center of the sarcomere but do not extend all the way to the Z lines. Thus there are regions where the actin and myosin filaments do not overlap (i.e., the I band and the H zone). When the muscle, hence the sarcomere, contracts, the myosin filaments move along the actin filaments toward the Z lines. As a result, the I band gets narrower. At the same time, the actin filaments move closer to the M band, so the H zone gets narrower.

2. One subunit of troponin anchors it to tropomyosin filaments. One subunit of troponin binds to the actin filament. One subunit binds Ca²⁺. When Ca²⁺ binds to the troponin subunit, it causes a conformational change in the troponin, resulting in the tropomyosin filament pulling away from the myosin-binding site of the actin. Actin–myosin binding results in contraction of the sarcomere.

3. Rigor mortis is due to the loss of ATP that is required to break actin-myosin cross bridges. With the cessation of breathing and circulation at death, muscles do not receive oxygen and glucose from the blood and production of ATP through oxidative metabolism ceases. However, some ATP can continue to be produced by anaerobic metabolism, and the muscles with the most glycogen will be able to sustain anaerobic metabolism longer.

4. By destroying acetylcholinesterase, Malathione prevents the breakdown of acetylcholine released at the motor end plates, and as a result there is continuous and extreme activation of the muscle cell motor endplates. Action potentials continue to be fired in the muscle cell membranes resulting in tonic release of Ca²⁺ into the sarcoplasm and sustained activation of actin/myosin cross bridge formation.

5. Gap junctions enable sheets of cardiac or smooth muscle to contract as a unit. That makes it possible for cardiac muscle cells to work together to pump blood or smooth muscle cells to exert a unified function such moving food through the gut. The individual control over skeletal muscle fibers enables fine control over complex movements.

1. A skeletal muscle is made up of many muscle fibers. Each muscle fiber is innervated by one motor neuron constituting a motor unit, but one motor neuron may form synapses with multiple muscle fibers. The nervous system can alter the frequency of action potentials in one motor unit, and it can increase the number of motor units activated in the same muscle.

2. Postural muscles must remain continuously contracted for long periods of time, but they are not generally used for quick, powerful movements.

3. The energy source for the sprint comes primarily from preformed ATP and creatine phosphate along with some contributions from glycolysis. These sources of ATP are rapidly mobilized. The longer 10-kilometer run requires production of ATP through oxidative metabolism, which requires O₂ transport and many more enzymatic reactions. It is therefore a slower source of ATP that cannot sustain as high a workload.

1. Arthropods have external skeletons and therefore cannot grow without shedding (molting) their exoskeletons.

2. Since astronauts are losing bone mass, it is reasonable to hypothesize that the activity of their osteoclasts has increased, or the activity of their osteoblasts has decreased. It is possible that these changes are being induced by altered activity of their osteocytes in response to lack of weight-bearing stresses on their bones.

3. If the joint has a large force arm relative to the load arm, it can generate great pressures. If the force arm is short relative to the load arm, the end of the load arm can move over a large distance very quickly but cannot exert much pressure. Thus a larger force arm:load arm ratio for the jaw joint enables the jaws to apply great pressure over a small distance, whereas the smaller force arm:load arm ratio for the elbow enables the lower arm to move quickly over a larger distance but does not enable it to apply great pressure.

1. 

2. The jump takes 50 ms (see Figure B), and the shortening in terms of muscle lengths is 7.5 mm/33.6 mm = 0.22 ML. So, velocity of muscle contraction in ML/sec = 0.22/.05 sec = 4.4.

3. The power generated by the jumping muscle is maximal at the observed mean jumping velocity.

1. If the workout capacity goes up with cooling, that suggests that the heat extraction is enabling more work, or in other words, decreasing muscle fatigue that otherwise limits workout capacity.

2. Cooling increased the work capacity for each workout in comparison to the previous workout, and over time, the rate of change of capacity was much greater with cooling than without. This difference in rate of change indicates that increasing work capacity (Figure A) leads to increased rate of conditioning (Figure B).

1. In both groups muscle glycogen fell to about 25 percent of its resting value by the point of fatigue. There were no significant differences (P > 0.05) in muscle glycogen at any time point in the two groups. Thus over 3 hours both groups depleted their muscle glycogen at about the same rate. Blood glucose in the placebo group fell steadily after the first hour, but blood glucose did not fall in the glucose-fed group, and blood glucose levels were significantly different in the two groups after the first hour. Both groups had similar levels of carbohydrate oxidation for the first 2 hours, after which the placebo group had declining carbohydrate oxidation levels that were significantly different from those of the glucose-fed group.

2. The difference between the two groups in time to fatigue was significant, and therefore the data show that carbohydrate feeding delayed muscle fatigue. Carbohydrate feeding also maintained blood glucose levels and the rate of carbohydrate oxidation. In addition, the data show that up until hour 3, this effect does did not involve a slowing of muscle glycogen depletion.

3. For the glucose-fed group, there was no significant decline in muscle glycogen between hour 3 and 4, indicating that other sources of fuel were being metabolized once muscle glycogen was depleted. A possible explanation for these effects of carbohydrate feeding is that it enabled the subjects to support more of their metabolic work with carbohydrates. We can hypothesize that the placebo group had to compensate sooner with fuel sources other than carbohydrates.

4. The body uses a mixture of carbohydrate and fats as fuel for ATP production via oxidative metabolism. Fats are slower to be mobilized than carbohydrates. The blood FFA data indicate that the placebo group began to depend more on FFA metabolism after 1 hour of exercise, but the glucose-fed group did not increase utilization of FFAs until between 3 and 4 hours of exercise. At that time the subject depended less on muscle glycogen. Overall, the carbohydrate feeding extended the time that the subject could exercise without increasing utilization of FFAs.

5. Suggest eating small snacks composed of simple sugars periodically during runs to prolong the time to fatigue.