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6 Apr 2019

Multiple Choice,

To understand the relationship between anxiety and performance

A. increased muscle soreness contributed to inferior performance

B. We must understand the intensity and direction

C. We understand increased coordination difficulties contributed to inferior performance

D. a and c

E. b and c

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Nelly Stracke
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8 Apr 2019

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Related questions

Skeletomuscular system

A) Know the types of bone tissue, and the location and function of each

B) Know the basic components and functions of the axial and appendicular skeletons

C) Understand why the hollow tube structure of bones is structurally sound

D) Understand why skeletons should not frighten you, but zombies are still a scary idea

E) Understand the principle of antagonism between muscle groups

F) Know the cycle of actin and myosin binding to cause muscle contraction

G) Know the basic units of a muscle: fascicles, muscle fibers, myofibrils, sarcomeres

21. Aerobic training would decrease submaximalheart rate, which is beneficial for aerobic performance because

a. it saves energy used by heart beats.

b. it gives longer time for ventricular filling.

c. a and b.

d. None of above.

22. Aerobic training would ________ anaerobicpower during maximal exercise.

a. delay onset of

b. facilitate onset of

c. rely on

23. Compared to untrainedindividuals, trained endurance athletes have

a. higher maximal heartrates.

b. higher resting cardiacoutputs.

c. higher resting heartrates.

d. higher maximal strokevolumes.

24. What is the likely outcome oflow volume, low intensity training?

a. increased aerobiccapacity

b. increased anaerobiccapacity

c. increased aerobic andanaerobic capacity

d. little improvement in eitheraerobic or anaerobic capacity

25. Which of the followingstatements explaining the increase in SV after aerobic training iscorrect?

a. reload, contractility, andafterload increase

b. preload, contractility, andafterload decrease

c. preload and contractilityincrease, afterload decreases

d. preload decreases,contractility and afterload increase


26. When motor units contract moresynchronously,

a. muscles cannot sustainsteady forces anymore

b. muscles increase the rate offorce development

c. the ability to generateforce is impeded

d. a single motor neuron nowinnervates several motor units

27. In general, whole-muscle hypertrophy in humans most likely resultsfrom

a. mostly fiberhyperplasia

b. entirely fiberhyperplasia

c. mostly fiberhypertrophy

d. equal contributions of fiberhypertrophy and fiber hyperplasia

28. Overload can be achieved by

a. increasing intensity.

b. increasing recovery time.

c. a certain type of training.

d. All of above.

29. Resistance training increases forceproduction by

a. neural adaptation followed by intramuscular adaptation.

b. intramuscular adaptation followed by neural adaptation.

c. simultaneous neural and intramuscular adaptation.

30. Training causesan increase in stroke volume due to all of the following except

a. increased filling time.

b. increased left ventricular volume.

c. increased cardiac and arterial stiffness.

d. improved intrinsic contractile function.

31. The risk of DOMS after a giventraining session can be reduced by which trainingstrategy?

a. train at high intensity withboth resistance and anaerobic training components

b. train with primarily intenseeccentric exercise

c. reduce eccentric componentof muscle action

d. employ more downhillexercise in the training program

32. After anaerobic training, thecross-sectional areas of ______ are larger than before thetraining.

a. type I fibers

b. type II fibers

c. type I and type IIfibers

33. Aerobic training would cause __________cardiac hypertrophy, which is increased ______________.

a. concentric, the diameter of left ventricle.

b. eccentric, the diameter of left ventricle.

c. concentric, the wall thickness.

d. eccentric, the diameter and wall thickness of leftventricle.

34. InFartlek training, ___________ is changed based on

1. Bacterial transcription termination VS. Eukaryotic transcription initiation

a. What is required for Rho-independent termination? How does each sequence feature contribute to the mechanism of termination?

b. What is required for Rho-dependent termination?

c. How does Rho differ from other helicases we discussed in Chapter 28? How is it similar?

d. Do you understand the difference between core promoter elements and regulatory elements? Do you understand the difference between core transcription factors and regulatory transcription factors?

e. What are the major features of the TATA-binding protein-DNA interaction? How does this interaction lead to dsDNA destabilization?

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