Kinesiology 1088A/B Lecture Notes - Motor Program

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4 Sep 2014

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Functions of imagery (paivio, 1985) he argued that imagery is more than a vision in your head. We can use thoughts in training (1) cognitive (used more in training) Skills (2) motivational (success and feeling in competition) Sport situation imagery type (1 of 5 above) outcome. What we"re doing when we"re imaging is setting up a blueprint we create certain pathways of neural engagement within our body. This particular muscle has to be innervated needs to occur so i can execute . So through setting up this blueprint plan, we already have a pathway established when we go to execute the movement (b) psychoneuromuscular theory. Neuromuscular impulses identical to actual performance; reduced amplitude. Says that the impulses (although lower in amplitude) and the sequences of firing are going on, not necessarily in a pathway but certain muscles need to be innervated in a certain way.

Related Questions

A justification for job training programs is that they improve worker productivity. Suppose that
you are asked to evaluate whether more job training makes workers more productive. However,
rather than having data on individual workers, you have access to data on manufacturing firms in
Ohio. In particular, for each firm, you have information on hours of job training per worker
(training) and several non-defective items produced per worker hour (output).
(i) Carefully state the ceteris paribus experiment underlying this policy question.
(ii) Does it seem likely that a firm's decision to train its workers will be independent of worker
characteristics?
(iii) Name a factor other than worker characteristics that can affect worker productivity.
(iv) If you find a positive correlation between output and training, would you have convincingly
established that job training makes workers more productive?

ultramarinehare933

Consider the following abstracts about intervention to improve memory, one real, and one fictitious:

Memory enhancement in healthy older adults using a brain plasticity-based training program: A randomized, controlled study
Mahncke HW et al. PNAS August 15, 2006 vol. 103 no. 33 12523-12528
Normal aging is associated with progressive functional losses in perception, cognition, and memory. Although the root causes of age-related cognitive decline are incompletely understood, psychophysical and neuropsychological evidence suggests that a significant contribution stems from poorer signal-to-noise conditions and down-regulated neuromodulatory system function in older brains. Because the brain retains a lifelong capacity for plasticity and adaptive reorganization, dimensions of negative reorganization should be at least partially reversible through the use of an appropriately designed training program. We report here results from such a training program targeting age-related cognitive decline. Data from a randomized, controlled trial using standardized measures of neuropsychological function as outcomes are presented. Significant improvements in assessments directly related to the training tasks and significant generalization of improvements to nonrelated standardized neuropsychological measures of memory (effect size of 0.25) were documented in the group using the training program. Memory enhancement appeared to be sustained after a 3- month no-contact follow-up period. Matched active control and no-contact control groups showed no significant change in memory function after training or at the 3-month follow-up. This study demonstrates that intensive, plasticity-engaging training can result in an enhancement of cognitive function in normal mature adults.

Memory enhancement in healthy older adults using genetic modification also protects against Alzheimerâs Disease.1
I M Genius, Prestigious Journal 1 (1): 1-10
Inserting extra copies of the gene NR2B, which encodes the NMDA receptor, leads to improved memory and also prevents onset of Alzheimerâs Disease. Two chemical signals are needed to trigger this nerve cell receptor, which means that it plays a key role in forming associations. For instance, if you touch a flame, the visual signal and pain signal arrive to the brain at roughly the same time, activating NMDA receptors and creating a memory. Healthy adults were given extra copies of the gene and these were rigged so that genesâ activity would increase over time as the adults aged. Earlier studies had revealed that in young animals, NMDA receptors are activated even by signals that arrive somewhat far apart, facilitating learning. As an animal ages, though, the signals must travel more in step to trip NMDA receptors and cement memories. Adults treated with the NR2B gene had significant improvements in assessments directly related to the training tasks and significant generalization of improvements to nonrelated standardized neuropsychological measures of memory (effect size of 0.25). In addition, adults treated with the genes showed lower levels of onset of Alzheimerâs Disease compared with matched controls.

For discussion

Are these interventions therapy or enhancement? (Is age-related loss of memory a disease?)

Are there morally significant differences between the methods (cognitive training versus genetic

modification)?

What are the potential harms and benefits from using these interventions?

What are your views on the moral permissibility of the interventions?

How would your responses change if the interventions were for increasing muscle mass and performance in elite athletes?

grayleopard228

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

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Kinesiology 1088A/B Lecture Notes - Motor Program

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