PEES 311 Chapter 13

11. Endurance training results in increased mitochondrial and capillary density in muscle but has no effect on muscle glycolytic capacity. This is an example of what training principle? A. overload B. specificity C. reversibility D. none of the above

B. specificity

3. Cross-sectional studies demonstrate that the physiological variable responsible for the large variation in VO2 max across the normal population is maximal A. heart rate. B. stroke volume. C. arteriovenous O2 difference. D. systolic blood pressure.

B. stroke volume.

15. Four-to-ten weeks of anaerobic training (high intensity exercise lasting 10-30 seconds) can increase the peak anaerobic capacity by ______ across individuals. A. 3-25% B. 30-40% C. 50-60% D. 65-75%

A. 3-25%

32. After a 15-week program of endurance exercise training, which of the following cardiovascular variables does NOT decrease after 14 days of detraining? A. maximal heart rate B. VO2 max C. maximal cardiac output D. maximal stroke volume

A. maximal heart rate

19. Endurance exercise training results in an increased turnover of mitochondria in skeletal muscle. The process of removing old and damaged mitochondria is called______. A. mitophagy B. mitochondrial biogenesis C. mitochondrial proteostasis D. none of the above answers are correct

A. mitophagy

23. Which of the following factors does NOT contribute to the endurance exercise training-induced improvement in stroke volume during exercise? A. increased end-diastolic volume B. increased peripheral resistance C. increased cardiac contractility D. decrease in total peripheral resistance

B. increased peripheral resistance

5. Endurance training has been shown to reduce the oxygen deficit in subjects performing a submaximal exercise. This is due to A. an increased maximal cardiac output. B. increases in the number of mitochondria and capillaries. C. an increased heart rate. D. a greater anaerobic capacity.

B. increases in the number of mitochondria and capillaries.

17. Following an acute bout of endurance exercise training, the rise in the activity of calcinurin, calmodulin kinase, and AMP kinases occurs within _____ following the exercise session. A. seconds B. minutes C. hours D. days

B. minutes

18. Following an acute bout of endurance exercise training, the increase in mitochondrial biogenesis occurs within _____ following the completion of the exercise session. A. seconds B. minutes C. hours D. days

C. hours

20. A single bout of resistance exercise training results in an increase in skeletal muscle protein synthesis. This exercise-induced increase in muscle protein synthesis can occur within _____ following the exercise session. A. seconds B. minutes C. hours D. days

C. hours

40. The initial decrease in VO2 max with detraining occurs because skeletal muscle adaptations (a-vO2 difference) are lost. True or False?

False

29. In theory, concurrent resistance and endurance exercise training can impair muscle protein synthesis following a bout of resistance exercise. The proposed mechanism to explain this inhibition is_____________________________________. A. AMP kinase activation of TSC2 B. AMP kinase activation of mTOR C. AMP kinase activation of PGC-1a D. p38 activation of TSC2

A. AMP kinase activation of TSC2

24. Which of the following endurance training adaptations does NOT result in lower lactate production in the contracting muscles? A. increased glycogen utilization B. increased H4 form of LDH C. increased mitochondrial uptake of pyruvate D. decreased pyruvate formation

A. increased glycogen utilization

31. Which of the following endurance training adaptations assist in maintaining acid-base balance during exercise? A. increased mitochondrial volume in skeletal muscle B. increased M4 form of LDH C. increased lactate production D. increased pyruvate formation

A. increased mitochondrial volume in skeletal muscle

9. During the first 10 weeks of a resistance training program, the initial increase in muscular strength are due primarily to A. neural adaptations. B. muscle fiber hypertrophy. C. muscle fiber hyperplasia. D. Both B and C are correct

A. neural adaptations.

16. The increase in VO2 max that occurs following 4 months of endurance exercise training results from an increase in both maximal cardiac output and maximal a-vO2 difference. Relatively short durations of endurance exercise training (e.g., 1-4 months) increases VO2 max primarily by increasing A. the maximal a-vO2 difference. B. the maximal cardiac output. C. the maximal heart rate. D. both B and C are correct

B. the maximal cardiac output.

25. In resting skeletal muscle fibers, Ras homologue enriched brain (Rheb) activation of mTOR is inhibited by ______. A. phosphatidic acid B. tuberous sclerosis complex 2 (TSC2) C. IGF-1 D. none of the above answers are correct

B. tuberous sclerosis complex 2 (TSC2)

21. Which of the following physiological factors does NOT contribute to the endurance exercise training-induced increase in the maximal a-vO2 difference? A. increased mitochondria volume in the muscle B. increased capillaries in the muscle C. increased hemoglobin in the blood D. increased muscle blood flow

C. increased hemoglobin in the blood

6. The heart rate and ventilatory responses to a fixed submaximal work rate are lower (i.e., lower heart rate and lower minute ventilation) following an endurance training program. This training-induced adaptation is primarily due to changes in the A. central nervous system. B. spinal cord. C. trained skeletal muscles. D. AV node

C. trained skeletal muscles.

2. Endurance exercise training programs (e.g., 3 days/week @ 60% VO2 max for 12 weeks) lasting typically result in a ______% improvement in VO2 max. A. 1-5% improvement in VO2 max B. 5-10% improvement in VO2 max C. 10-15% improvement in VO2 max D. 15-20% improvement in VO2 max

D. 15-20% improvement in VO2 max

14. Following a single bout of resistance exercise training, muscle protein synthesis can remain elevated above baseline for as much as ______ in both trained and untrained individuals. A. 10-15 hours B. 15-20 hours C. 20-25 hours D. 40-50 hours

D. 40-50 hours

37. Following endurance training, maximal cardiac output during exercise is increased due to an increase in the thickness of the left ventricular wall (i.e, ventricular muscle mass increases). True or False?

False

39. The majority of evidence demonstrates that resistance training-induced muscle hypertrophy is the result of muscle fiber hyperplasia. True or False?

False

34. In a "two-legged" maximal cycle ergometer test, if each leg were to vasodilate to the extent experienced in a one-legged VO2 max test, mean arterial blood pressure would fall below normal levels. True or False?

True

35. Research indicates that anyone can increase his or her VO2 max with training, yet a genetic predisposition is required to have a VO2 max comparable to that of an elite endurance athlete. True or False?

True

36. Following endurance training, afterload decreases during maximal exercise because there is a decrease in sympathetic vasoconstrictor activity in the arterioles of the exercising muscles. True or False?

True

38. Reducing the number of motor units required to perform an exercise task may reduce the heart rate and ventilation required to perform the task. True or False?

True

30. Which of the following factors does NOT contribute to the endurance exercise training-induced increases in fat metabolism during exercise? A. slower blood flow in muscle B. increased fat storage in the liver C. increased FFA transporters D. increased beta oxidation enzymes

B. increased fat storage in the liver

10. Which of the following factors contributes to the endurance exercise training-induced improvement in VO2 max?A. increased end diastolic volume B. increased maximal stroke volume C. increased maximal heart rate D. None of the above answers are correct

B. increased maximal stroke volume

13. A single bout of resistance exercise training increases muscle protein synthesis by as much as ______% above resting levels? A. 10-20 B. 50-60 C. 120-150 D. 200-300

C. 120-150

1. The average VO2 max value for the young (e.g., 21 years old) male sedentary population is approximately A. 22 ml · kg-1 · min-1. B. 35 ml · kg-1 · min-1. C. 45 ml · kg-1 · min-1. D. 83 ml · kg-1 · min-1.

C. 45 ml · kg-1 · min-1.

12. High responders to endurance exercise training (i.e., individuals that achieve large increases in VO2 max) can achieve up to______% improvement in VO2 max following a prolonged and intense training program. A. 20 B. 35 C. 50 D. 100

C. 50

4. Heritability (i.e., genetics) determines approximately _____% of VO2 max variability in sedentary adults. A. 25 B. 35 C. 50 D. 90

C. 50

26. Which of the following training adaptations does NOT occur in skeletal muscles following 4-10 weeks of anaerobic exercise training? A. increased muscle buffer capacity B. increased activities of myokinase and creatine phosphokinase C. increased activities of key glycolytic enzymes D. None of the above answers are correct

D. None of the above answers are correct

22. The enhanced capacity of the trained muscle to use fatty acids as a fuel results in A. increased uptake of fatty acids. B. decreased utilization of muscle glycogen. C. sparing of blood glucose. D. all of the above answers are correct.

D. all of the above answers are correct.

28. Several mechanisms have been proposed to explain why concurrent endurance and resistance (strength) training impedes strength development compared to strength training alone. Which of the following mechanisms have NOT been proposed to explain why concurrent training impedes strength development? A. neural factors B. overtraining C. Depressed muscle protein synthesis D. none of above are correct

D. none of above are correct

27. It is well known that resistance exercise training promotes an increase in muscle protein synthesis by activating the mechanistic target of rapamyosin (mTOR) which results in increased protein synthesis. Recent evidence suggests that two signaling molecules interact to directly activate mTOR. These molecules are: A. IGF-1 and Akt B. IGF-1 and phosphatidic acid C. IGF-1 and Ras homologue enriched brain (Rheb) D. phosphatidic acid and Ras homologue enriched brain (Rheb)

D. phosphatidic acid and Ras homologue enriched brain (Rheb)