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EXAM 1
Content
Lecture 1: Excitable
Membranes and Action Potentials 1.
Describe, in detail, the structure of the cell membranes. 2.
How does the structure of the cell membrane reveal/influence
the function of that cell? 3.
What type of molecules is the cell membrane most permeable
to, and most impermeable to? Why? 4.
Explain the structure and function of the sodium-potassium
pump. 5.
Provide concentrations for the main electrolytes and charged
molecules that occur within intracellular and extracellular fluid. 6.
Be able to calculate the Nernst Potentials for sodium and
potassium, and more importantly, understand their interpretations. 7.
Be able to define the Nernst Potential. 8.
What determines the resting membrane potential of a cell? 9.
What are the different methods a molecule might be able to
enter or leave a cell? 10.
What are the different types of transport channels in a cell
membrane? 11.
Explain the differences between the sodium and potassium
channels in an excitable membrane. 12.
Be able to draw and label the events (regarding sodium and
potassium channel function and ion flux across the membrane) that happen during
a typical nerve action potential. 13.
Are all membrane potentials and action potentials the same in
all excitable tissues? Explain. 14.
Explain how the action potential crosses a synapse. 15.
Explain how multiple nerve input to a synapse within the CNS
can influence to continued propagation of an action potential. 16.
Explain the importance of the frequency of action potentials
for function within the CNS, as well as for function of the peripheral
somatosensory receptors. 1.
How is the Nervous System arranged from an anatomical
perspective? 2.
How is the Nervous System arranged from a functional
perspective? 3.
Explain the different receptors and neurotransmitters of the
Autonomic Nervous System, and how they differ between the parasympathetic and
sympathetic divisions. 4.
Be able to provide at least some general description of the
complexity of CNS involvement in the development and instigation of movement
patterns. 5.
Be able to locate the motor and somatosensory cortex on a
diagram of the brain. 6.
Explain the segmental distribution of spinal motor nerves. 7.
Provide at least 3 examples of mechano-receptors within the
body. 8.
Explain the basic function of all receptors.
Use one as an example. 9.
What is a receptor potential, and how do receptors sense a
stimulus and convert it to an action potential? 10.
How does the Nervous System signal and interpret the strength
of a stimulus? 11.
Explain some differences between all the nerves in the body,
and how these differences relate to the specific functions of some nerve types. 12.
Be able to explain the multiple functions of the muscle
spindle. 1.
Know the anatomical arrangement and terminology of muscle
from whole muscle to contractile proteins. 2.
Be able to label the structural and regional components of a
sarcomere. 3.
Explain the t-tubule and sarcoplasmic reticulum network and
arrangement within skeletal muscle. 4.
Be able to label diagrams of the different types of
contractile proteins, and their sub-components. 5.
Where is the ATPase enzyme located within skeletal muscle? 6.
What are the components of the myosin heavy chain? 7.
What is the significance of the genetic regulation of the
myosin heavy chain? 8.
Be able to explain the sequence of events, at the molecular
level, of muscle contraction. 1.
Be able to list 3-4 basic differences between the structure
and function of skeletal, cardiac and smooth muscle. 2.
How is cardiac muscle organized to better meet the demands of
the circumferential contraction of the heart? 3.
What are intercollated discs? 4.
If cardiac muscle is not recruited via motor units, how is
the strength of a myocardial contraction regulated? 5.
Be able to label the events that explain the characteristics
of the myocardial action potential. 6.
What are the functional benefits of a more prolonged
myocardial action potential? 7.
How are the contractile proteins of smooth muscle organized? 8.
How does calcium regulate smooth muscle contraction? 9.
Does smooth muscle have a more efficient (ATP cost is less)
contraction mechanism than skeletal or cardiac muscle?
Explain. 1.
What does the term “fiber type” refer to?
How do these differ to motor units? 2.
Know how to explain the procedures involved in myosin ATPase
staining. 3.
Be able to interpret histology sections of stained muscle
when given specific pre-incubation conditions. 4.
What is the PAS stain, and how is it used in research? 5.
Be able to list a table of fiber types, providing all
distinguishing features. 6.
How is the molecular biology of the myosin heavy chain being
used to further our knowledge of muscle fiber types? 1.
Be able to explain the procedure of percutaineous muscle
biopsy. 2.
Be able to list several limitations of the biopsy procedure
when used to quantify muscle fiber type proportions, or changes in muscle
metabolism. 3.
What does research reveal about the needs/limitations of
biopsy for quantifying fiber types? 1.
What is the difference between transcription and translation? 2.
Why is the ATP cost of protein synthesis high?
Explain. 3.
Why is it important to have a sufficient free amino acid pool
in the cytosol of muscle fibers to support protein synthesis? 4.
Can aging muscle (> 60 years old) adapt to chronic
exercise stress? Explain. 5.
Do we ever fully tax the metabolic capacity potential of
skeletal muscle during any exercise condition?
Explain. 1.
What is the definition of fatigue in an exercise context? 2.
Why is differentiating fatigue and the decision to “end
exercise” important in understanding the causes of fatigue? 3.
Contrast mechanisms of fatigue that occur in muscle vs.
within the CNS. 4.
What peripheral factors do you think contribute to central
processes of fatigue and/or the decision to “end exercise”? 5.
How important do you think motor unit recruitment is to the
fatigue of intense exercise? Explain. 6. When humans exercise train, what is that we are training to improve performance? EXAM 2
Content
1.
Is there adequate research evidence to support most of what
is done in resistance training? Explain. 2.
What is an MVC? How is this performed? Explain
the relationship between force of contraction and contraction velocity for
"maximal" effort contractions. 3. What did Young's dissertation research show? 4. Why might palm and/or central cooling improve intense resistance exercise performance? 5.
What research questions needs answers in resistance exercise physiology? 1.
Explain the brief history of muscle biopsy application in
exercise physiology and biochemistry in the U.S. 2.
How
is the muscle biopsy procedure used in exercise physiology and biochemistry? 3. Why is the ATPase enzyme used in histologically identifying fiber types and motor unit expression in human muscle? 4. What other proteins can be used to identify different fiber types? 5. Explain the pH dependency of ATPase staining of human muscle fibers. 6. What are the major limitations of the muscle biopsy procedure and data interpretation. 7. Explain the 3 energy systems of skeletal muscle. 8. Explain the function and capacity limits of the phosphagen system. 9. Explain the Creatine Phosphate Shuttle. 10. Explain the principles behind magnetic resonance spectroscopy. 11. Draw and label rest and post-exercise 31P MRS spectra. Explain how cell pH is calculated. 12. Why is the recovery kinetics of CrP used in assessing muscle metabolic potential? 1. Explain/define the physiological differences between fatigue and the decision to end exercise. 2. What is the potential role of potassium (K+) and the Na+/K+ pump in muscle fatigue? 3. Explain the evidence for a cause-effect connection between available calcium within the cytosol of a muscle fiber and contractile force. What is the role of inorganic phosphate in this response? 4. What evidence is there from 31P MRS that documents near complete exhaustion of the phosphagen system during intense exercise? 5. The following figure is from Spriet's work showing a force "fatigue curve" and contributions from non-mitochondrial energy systems for intense exercise to contractile failure. What does it show that reveals peripheral fatigue as well as an early role for a more CNS based fatigue response?
1. Provide a brief explanation of the historical development of the "central fatigue" construct. 2. If Hill's original model included a CNS component, then why has exercise physiology been more recently focused on muscle metabolism as the cause of exercise-induced fatigue? 3.
List
at least 5 pieces of evidence that Noakes' uses to rationalize the existence of
a Central Governor in the brain. 4. Explain the evidence and physiology behind spinal level processing of afferent feedback that directly alters alpha motor nerve output to contracting muscle. 5. Explain the role and evidence for RPE in fatigue. What do you think? Is this just "F...ing gutless Wympology" creeping into exercise physiology? 6. Why is pacing such a central line of thinking and support for an important role of central fatigue in exercise-induced fatigue? 1. What is your personal assessment of short term intense exercise, fatigue and the decision to end exercise? 2. What are the major obstacles to a viewpoint that is task dependent? 3.
Do you think there is such a thing as a 'Central
Governor" in the brain? Explain. 4. What evidence is there that we are designed to fail/fatigue during intense exercise? 5. What is the main evidence of the physiology of fatigue that you have learned from your manuscript writing? 6. What do you think the near future will reveal about the physiology of exercise and fatigue. 7. Should we in exercise physiology be developing another theory of fatigue?
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