ch5 - adaptations to anaerobic training programs Flashcards

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1
Q

what kind of anaerobic adaptations exist?

A

changes to the nervous, muscular, connective tissue, endocrine, and cardiovascular systems.

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2
Q

what is the most common kind of anaerobic adaptation study?

A

in the early to intermediate stages of training (i.e. 4 to 24 weeks)

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3
Q

how is augmented neural drive thought to occur?

A

via increased agonist muscle recruitment, improved neuronal firing rates, and greater synchronization in the timing of neural discharge during high-intensity muscular contractions; a reduction in inhibitory mechanisms (i.e. from Golgi tendon organs) is also thought to occur with long-term training

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4
Q

where does increased motor unit adaptation begin?

A

in the higher brain centers, where the intent to produce maximal levels of muscular force and power causes motor cortex activity to increase; as force developed rises, or whenb a new exercise or movement is being learned, primary motor cortex activity elevates in an effort to support the enhanced need for neuromuscular function

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5
Q

where/how are adaptation to anaerobic training methods reflected?

A

by substantial neural changes in the spinal cord, particularly along the descending corticospinal tracts

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6
Q

how do we know that recruitment of fibers is a limiting factor in strength?

A

in untrained individuals or in those rehabilitating from injury, electrical stimulation has been shown to be more effective than voluntary activations in eliciting beneficial gains. research has shown that only 71% of muscle tissue is activated during maximal efforts in untrained populations.

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7
Q

what does a motor unit consist of?

A

the alpha motor neuron and the muscle fibers that it activates; a motor unit may innervate <10 muscle fibers for small, intricate muscles or >100 fibers for large, powerful trunk and limb muscles.

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8
Q

Increased force with greater firing rates reflects what?

A

the summation of successive muscle contractions, whereby action potentials temporarily overlap

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9
Q

how does summation influence force production?

A

With increased motor unit firing rates, the muscle fibers are continually activated by subsequent action potentials before they have time to completely relax following a prior action potential. The summation of overlapping action potentials is expressed as augmented contractile strength. These firing rates represent an adaptive mechanism shown to improve following heavy resistance training.

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10
Q

in terms of motor units, what are gains in strength and power of agonist muscles generally associated with?

A

(a) an increase in recruitment; (b) an increased rate of firing; (c) greater synchronization of neural discharge, which acts to coordinate the activity of multiple muscles in synergy; or (d) a combination of all these factors.

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11
Q

what are motor units high in the recruitment order primarily used for?

A

high force, speed, or power production

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12
Q

do some muscle fiber types (e.g. type I, II) get larger with resistance training, or all?

A

all muscle fibers get larger because for the most part they are all recruited to some extent in order to produce the higher levels of force required to lift progressively heavier loads

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13
Q

once a motor unit is recruited, less activation is needed in order for it to be rerecruited. why might this have implications for strength and power training?

A

the high-threshold motor units may be more readily reactivated subsequent to prior recruitment.

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14
Q

under what circumstances do exceptions to the size principle exist – i.e. an athlete is able to inhibit the lower-threshold motor units and in their place activate higher-threshold motor units?

A

when force production is required at very high speeds for the expression of muscular power (e.g. olympic weightlifting, plyometrics, agility/interval training)

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15
Q

what is the reasoning behind the selective recruitment principle?

A

it would be very difficult for athletes to generate enough angular velocity and power to attain maximal height for the vertical jump if they had to recruit the entire slow-twitch motor unit pool before activation of the fast-twitch units (there simply is insufficient time to recruit all of the motor units in order and still perform an explosive jump)

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16
Q

is selective recruitment learned?

A

selective recruitment appears to be an intrinsic neural mechanism favoring explosive exercise, but using specific training methods may enhance selective recruitment

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17
Q

how does size affect muscle activation?

A

as muscle size increases it does not require as much neural activation to lift a given load; this shows the importance of progressive overloading to promote the continual recruitment of an optimal amount of muscle tissue

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18
Q

is rate of firing important for muscle adaptation?

A

yes, high firing rates from the onset of ballistic muscle contraction are especially critical to increased rates of force development, and the increase in firing rate (vs. recruitment) appears to be dependent on muscle size, such that smaller muscles rely more on an increased firing rate to enhance force production whereas larger muscles depend more on recruitment. anaerobic training can play a role in enhancing firing rates of recruited motor units.

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19
Q

how might training improve firing rates?

A

resistance training may result in a more synchronized pattern (i.e., the firing of two or more motor units at a fixed interval) of activation during the exertion of large forces, rather than the customary asynchronous pattern usually common to motor function; synchronization is potentially more critical to the timing of force production and less significant with regard to the overall level of force developed.

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20
Q

why is the NMJ significant?

A

it represents another potential site for neural adaptation following anaerobic training – following both high- and low-intensity running, the NMJ was found to increase in its total area. High-intensity training, however, resulted in more dispersed, irregular-shaped synapses and a greater total length of nerve terminal branching compared to low-intensity training. In another study, greater end-plate perimeter length and area, as well as greater dispersion of acetylcholine receptors within the end-plate region, were also found after seven weeks of resistance training. anaerobic training appears to induce beneficial morphological changes in the NMJ that are conducive to enhanced neural transmission capabilities.

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21
Q

how does anaerobic training affect reflex?

A

causes positive changes in the reflex (i.e., muscle spindle or stretch reflex) response of the neuromuscular system and enhances the magnitude and rate of force development via this reflex. resistance training in particular has been shown to increase reflex potentiation by between 19% and 55%. resistance-trained athletes (weightlifters, bodybuilders) are found to have greater reflex potentiation in the soleus muscle compared to untrained individuals.

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22
Q

what are the types of EMG used and why?

A

surface EMG and intramuscular (needle or fine wire) EMG

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23
Q

what are the pros/cons of surface EMG?

A

surface EMG requires placement of adhesive electrodes on the surface of the skin where they are able to monitor a large area of underlying muscle. Surface EMG is often more effective for monitoring superficial muscle, as it is unable to bypass the action potentials of superficial muscles and detect deeper muscle activity. however, the more body fat an individual has, the weaker the EMG signal is likely to be with use of this methodology.

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24
Q

what are the pros/cons of intramuscular EMG?

A

the skin surface is numbed, and a needle electrode, or a needle containing two fine-wire electrodes, is inserted through the skin and positioned into the belly of the muscle itself. Fine-wire electrodes emphasize a specificity of assessment in that they are located in a muscle of interest and accurately record localized motor unit action potentials (85). Because of its invasiveness, intramuscular EMG is primarily adopted in research settings or under clinical conditions.

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25
Q

what factors confound EMG readings?

A

not sure if e.g. increased recruitment, discharge rate, or synchronization, or golgi tendon organ inhibition

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26
Q

during what portion of a training program do neural adaptations dominate?

A

6 to 10 weeks.

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27
Q

do neural adaptations stop if the athlete ‘gets used to’ hypertrophy gains?

A

no, neural adaptations will contribute to the performance improvements through progressive overload

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28
Q

for what kinds of activities are neural factors most important?

A

very high training intensities (>85% of 1-repetition maximum [1RM]) and training programs designed to elicit muscular power..

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29
Q

what do EMG studies say about cross-education and how do we know?

A

strength in the untrained limb may increase up to 22%, with an average strength increase of approximately 8%; the increase in strength of the untrained limb is accompanied by greater EMG activity in that limb, thereby suggesting that a central neural adaptation accounts for the majority of strength gains.

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30
Q

what is the opposite of cross-education?

A

a bilateral deficit in untrained lifters; force produced when both limbs contract together is lower than the sum of the forces they produce when contracting unilaterally.

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31
Q

what kinds of activities might have neural-limiting cocontraction antagonist muscle group activity?

A

ballistic movements that require high levels of joint stability, or when people are unfamiliar with a task and require more inherent stability

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32
Q

other than size and fiber type changes, what are the biochemical/ultrastructural components of muscle adaptation?

A

muscle architecture, enzyme activity, and substrate concentrations

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33
Q

what is the biological process of hypertrophy?

A

there is an increase in the net accretion (increase in synthesis / reduction in degradation / both) of the contractile proteins actin and myosin within the myofibril, as well as an increase in the number of myofibrils within a muscle fiber. In addition, other structural proteins such as titin and nebulin are synthesized proportionately to the myofilament changes. The new myofilaments are added to the periphery of the myofibril and result in an increase in its diameter. The cumulative effect of these additions is an enlargement of the fiber and, collectively, the size of the muscle group itself.

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34
Q

what pathways does mechanical deformation activate?

A

the protein kinase B-mammalian target of rapamycin (mTOR) pathway, the adenosine monophosphate activated protein kinase pathway, and the mitogen-activated protein kinase pathway

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35
Q

how does the akt/mTOR pathway directly regulating adaptations to resistance training?

A

when muscle fibers contract, akt/mTOR signaling increases dramatically, and this response is critical for increasing muscle protein synthesis and subsequent growth (a process known as myogenesis)

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36
Q

what factors influence protein synthetic rates?

A

carbohydrate and protein intake, amino acid availability, timing of nutrient intake, mechanical stress of the weight training workout, muscle cell hydration levels, and the anabolic hormonal and subsequent receptor response

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37
Q

what is the sequence of protein synthesis?

A

(a) water uptake, (b) noncontractile protein synthesis, and (c) contractile protein synthesis – and concurrently, reduced degradation acts to maintain the size of fibers by reducing net protein loss

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38
Q

lifting of heavy loads, the inclusion of eccentric muscle actions, and low to moderate training volumes are examples of what?

A

mechanical factors for hypertrophy

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39
Q

what is the order of most oxidative to least oxidative fibers?

A

I, Ic, IIc, IIac, IIa, IIax, and IIx, with a concomitant myosin heavy chain (MHC) expression (i.e., MHC I, IIa, and IIx)

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40
Q

how do type IIx change to IIa?

A

by changing their myosin adenosine triphosphatase (ATPase) isoform content, which then goes to an intermediate fiber Type IIax and then to a IIa

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41
Q

detraining is likely to have what effect on type II fibers?

A

an increase in Type IIx fibers and a reduction in Type IIa fibers, with a possible overshoot of Type IIx fibers (i.e., higher IIx percentages than observed pretraining)

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42
Q

why is transformation from type II to I probably not possible?

A

differing MHC isoforms and relative oxidative enzyme content

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43
Q

what effect do larger pennation angles have on protein/CSA?

A

larger pennation angles can accommodate greater protein deposition and allow for greater increases in CSA

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44
Q

how does anaerobic exercise affect blood pH?

A

reduces it substantially / acidizes it

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45
Q

how might adaptation affect pH?

A

more exposure to increased H+ concentration –> buffering capacity can improve –> increased capacity then allows an athlete to better tolerate the accumulation of H+ within the working muscle, resulting in delayed fatigue and greater muscular endurance (HIIT performed above the lactate threshold has been shown to increase buffering capacity by 16% to 38%)

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46
Q

how does CP, ATP, and glycogen content change following resistance training?

A

study reported 28% increase in resting CP, 18% increase in ATP concentrations and 112% glycogent content after five months of resistance training

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47
Q

axial skeleton is what?

A

skull-cranium, vertebral column, ribs, and sternum

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48
Q

appendicular skeleton is what?

A

shoulder girdle, pelvis, and bones of the upper and lower extremities

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49
Q

why is the rate of bone adaptation different in axial vs appendicular skeleton?

A

differing amounts of trabecular (spongy) bone and cortical (compact) bone

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50
Q

why is trabecular bone able to respond more rapidly to stimuli than cortical?

A

less dense, greater surface area-to-mass ratio, softer, weaker, more flexible and therefore more inclined to adaptive change

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51
Q

what is the MES for bone adaptation?

A

approximately 1/10 of the force required to fracture bone.

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52
Q

how does high intensity anaerobics affect collagen?

A

increase in collagen fibril diameter + number of covalent cross-links within hypertrophied fiber + increase in the number of collagen fibrils + increase in packing density of collagen fibrils

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53
Q

why are single-joint/machine exercises contraindicated for bone growth?

A

these exercises have a machine stabilize the body rather than promoting skeletal support

54
Q

how does training variation affect bone+collagen growth?

A

human skeleton compensates for new strain patterns experienced by the bone –> the direction of the collagen fibers within the bone matrix may change to conform to the lines of stress experienced by the bone –> changing the distribution/direction of the force vectors by varying exercise presents a unique stimulus for new bone formation within a given region of bone+collagen

55
Q

at what repetition amount will further bone growth be unlikely to occur?

A

more than a total of 30 to 35 repetitions

56
Q

what is procollagen?

A

the parent protein of collagen, synthesized and secreted by fibroblasts, consisting of three protein strands twisted around each other in a triple helix

57
Q

what are fibroblasts?

A

the most common cells found in the connective tissue of animals and act as stem cells in the synthesis of the extracellular matrix, as well as playing a critical role in wound healing

58
Q

what is the arrangement of collagen filaments called?

A

microfibril; as bone grows, microfibrils become arranged into fibers, and the fibers into larger bundles

59
Q

how may collagen be arranged?

A

longitudinally: tendons or ligaments, sheets with the layers in different directions: bone, cartilage, and fascia.

60
Q

what is the composition of tendons and ligaments?

A

packed parallel arrangements of collagen bundles with relatively few cells; small number to make a low requirement for oxygen and nutrients in these tissues. ligaments contain elastin in addition to collagen because some stretch is needed within a ligament for normal joint motion.

61
Q

is the connection of tendon and bone weak?

A

no, tendons and ligaments attach to bone with great strength, allowing the maximal transmission of forces

62
Q

what is fascia?

A

the fibrous connective tissues that surround and separate the different organizational levels within skeletal muscle; fascia has sheets of fibrocollagenous support tissue, containing bundles of collagen fibers arranged in different planes, to provide resistance to forces from different directions. fascia within muscles converges near the end of the muscle to form a tendon through which the force of muscle contraction is transmitted to bone.

63
Q

why is tendon metabolism slower than muscle and what are the implications?

A

due to poorer vascularity and circulation; the increase in blood flow to skeletal muscle via exercise is not paralleled by the same flow perfusion in tendons (this limited vascularity has implications for regeneration and is the reason tendons can take significant amounts of time to heal following injury)

64
Q

what are the sites for increasing growth and load-bearing capacity?

A

junctions between tendon and bone surface, within tendon or ligament, and in network of fascia within skeletal muscle

65
Q

what adaptations increase tendon’s ability to withstand greater tensional force?

A

(1) an increase in collagen fibril diameter (2) a greater number of covalent cross-links within the hypertrophied fiber (3) an increase in the number of collagen fibrils (4) an increase in the packing density of collagen fibrils

66
Q

adaptations of tendon stiffness from resistance training?

A

15% to 19% increase in achilles tendon stiffness from 8-week studfy but heavy loads (80% of 1RM) increase tendon stiffness while light loads (20% of 1RM) do not

67
Q

what are the main functions of cartilage?

A

(1) provide a smooth joint articulating surface (2) act as a shock absorber for forces directed through the joint (3) aid in the attachment of connective tissue to the skeleton

68
Q

how does cartilage get its own blood?

A

it doesn’t; it lacks its own blood supply and must depend on diffusion of oxygen and nutrients from synovial fluid (which is why cartilage does not easily repair itself following injury)

69
Q

what is another word for hyaline cartilage

A

articular cartilage (found on the articulating surfaces of bones)

70
Q

where is fibrous cartilage found

A

in the intervertebral disks of the spine and at the junctions where tendons attach to bone

71
Q

what are the main functions of cartilage?

A

(1) provide a smooth joint articulating surface (2) act as a shock absorber for forces directed through the joint (3) aid in the attachment of conective tissue to the skeleton

72
Q

what does the nutrient supply to articular cartilage via diffusion from synovial fluid tell us about joint health?

A

movement about a joint creates changes in pressure in the joint capsule that drive nutrients from the synovial fluid toward the articular cartilage of the joint, while immobilization of a joint prevents proper diffusion of oxygen and essential nutrients throughout the joint. immobilization = death of the healthy cells (chondrocytes) within cartilage and a resorption of the cartilage matrix. cartilage undergoes atrophy, or thinning, when external loading is removed (e.g., postoperative immobilization and paraplegia)

73
Q

what is the association between hydrogen ion accumulation and GH/cortisol?

A

it’s thought that hydrogen ion accumulation may be a primary factor influencing growth hormone and cortisol release.

74
Q

for how long after workout does resistance training upregulate AR content?

A

within 48 to 72 hours after

75
Q

how does downregulation of AR occur post-RT?

A

significant downregulation of AR content 1 hour after the workout; AR protein content may initially downregulate prior to upregulation. consumption of a protein-carbohydrate supplement before and after the workout attenuates this AR downregulation.

76
Q

during a lift, when is blood pressure highest?

A

during concentric phase of each repetition than during the eccentric phase, especially at the “sticking point” of an exercise

77
Q

during a lift, when are stroke volume and cardiac output the highest?

A

mostly during the eccentric phase, especially when Valsalva is used

78
Q

what factors influence the degree to which blood flow is increased in the working muscles?

A

(a) intensity of resistance, (b) the length of time of the effort (i.e., number of reps), and (c) size of the muscle mass activated

79
Q

how is blood flow affected during muscular contraction?

A

peripheral blood flow within the muscle is impeded during a set, but increases during the subsequent rest period (reactive hyperemia); lack of blood flow –> increase in metabolites such as hydrogen ions and reduction in pH = stimulus for muscle growth

80
Q

how does rate-pressure product (heart rate X systolic blood pressure; a measure of myocardial work) change with resistance training?

A

either remain constant or decrease following resistance training

81
Q

how does stroke volume change w/ resistance training?

A

increase in absolute magnitude, but not relative to body surface area or lean body mass (in other words, stroke volume will increase as lean tissue mass increases during long-term resistance training)

82
Q

how is oxygen extraction affected by resistance training?

A

generally not improved with resistance training using heavy loads and low volume; enhanced to a greater extent with continuous aerobic exercise, perhaps slightly with resistance if high volume and short rest periods

83
Q

how are cardiac dimensions changed by resistance training?

A

increased left ventricular wall thickness and mass, but the increase disappears when expressed relative to body surface area or lean body mass

84
Q

why might cardiac dimensions change from resistance training?

A

exposure to intermittently elevated blood pressures and increases in intrathoracic pressure in addition to accommodating changes from increases in lean body mass and body size

85
Q

an athlete’s heart is more likely to show what dimensions

A

greater than normal absolute posterior left ventricular and intraventricular septum wall thickness

86
Q

would weightlifters have greater than normal absolute left and right ventricular end-diastolic and end-systolic volumes?

A

no, have been reported in bodybuilders but not weightlifters, so high-volume training may increase absolute left ventricular volumes more

87
Q

What Performance improvements Occur Following Anaerobic exercise?

A
  1. muscular strength 2. power 3. local muscle endurance 4. body composition (probably) 5. flexibility (maybe) 6. aerobic capacity (maybe in untrained but probably not otherwise) 7. motor performance e.g. jumping
88
Q

what is the strength increase by training status with resistance training?

A

40% untrained, 20% moderate, 16% trained, 10% advanced, 2% elite

89
Q

what is the optimal load for power output in jump squat?

A

0%RM (bodyweight) but 30-60% squat 1RM in power athletes

90
Q

at what percent RM is peak power in the squat maximized?

A

56%

91
Q

at what percent RM is peak power in the power clean maximized?

A

80%

92
Q

at what percent RM is peak power in the ballistic bench press throw maximized?

A

46% to 62%

93
Q

what are the skeletal muscle adaptations to anaerobic muscular endurance training?

A

fiber type transitions from type IIx to type IIb, increases in mitochondrial and capillary numbers, buffering capacity, resistance to fatigue, and metabolic enzyme activity

94
Q

what body composition changes from anaerobic training?

A

reduce body fat by up to 9%, increase lean tissue mass, daily metabolic rate, and energy expenditure from exercise

95
Q

how should anaerobics be applied to flexibility trainiong?

A

a combination of resistance training and stretching appears to be the most effective method to improve flexibility with increasing muscle mass

96
Q

what is the status of anaerobic training and VO2max?

A

5% to 8% increase in untrained; no increase but if there is it’ll be through circuit training / high volume / short rest

97
Q

motor performance changes from anaerobic training?

A

increase running economy, vertical jump, sprint speed, tennis serve velocity, swinging and throwing velocity, and kicking performance

98
Q

how to balance combination training?

A

increasing recovery period between type of training; 2x resistance training + 2x aerobic endurance training > two days of combined (25% vs. 13% leg press 1RM)

99
Q

what is most affected by concruent high intensity resistance and aerobic endurance training?

A

power development

100
Q

what are the first signs of NFOR?

A

decreased performance, increased fatigue, decreased vigor, and hormonal disturbances

101
Q

how long can overtraining syndrome last?

A

6 months or more

102
Q

Acute anaerobic exercise results in what changes?

A

increased cardiac output, stroke volume, heart rate, oxygen uptake, systolic blood pressure, and blood flow to active muscles.

103
Q

what is a predominant feature of OTS?

A

inability to sustain high-intensity exercise when training load is maintained or increased

104
Q

What are the symptoms anaerobic overtraining?

A

• Unexplained underperformance • Persistent fatigue • Increased sense of effort during training • Disordered sleep patterns • Loss of appetite

105
Q

What testing-related question helps indicate anaerobic overtraining?

A

are the athlete’s scores in maximal exercise tests, sport-specific performance tests, or vital signs assessments (heart rate, blood pressure) poorer than on previous tests or poorer than normal/baseline

106
Q

What training program errors might indicate anaerobic overtraining?

A

• Training volume increased significantly (<5%) • Training intensity increased significantly • Training monotony present • High number or frequency of competitions

107
Q

What lifestyle factors may indicate anaerobic overtraining?

A

• Psychological signs and symptoms (disturbed Profile of Mood States [POMS], higher than normal rating of perceived exertion [RPE]) • Social factors (family, relationships, finances, work, coach, team) • Recent or multiple time zone travel

108
Q

What are the exclusion criteria of anaerobic overtraining?

A

• Confounding illnesses • Anemia • Infectious diseases • Muscle damage (high creatine kinase levels) • Endocrine disorders (diabetes, catecholamines, adrenal, thyroid) • Major eating disorders • Biological abnormalities (C-reactive protein, creatinine, decreased ferritin) • Musculoskeletal injury • Cardiologic symptoms • Adult-onset asthma • Allergies

109
Q

for how long are acute concentrations of testosterone, gh, and cortisol raised post-resistance training?

A

for up to 30 minutes in men

110
Q

functions of catecholamines?

A

epinephine, norepinephrine, and dopamine are important for force production, muscle contraction, energy availability and augmentation of other hormones such as testosterone

111
Q

short term resistance training has been shown to decrease RHR how much?

A

between 5% and 12%. longitudinally, no change or reductions of 4% to 13%.

112
Q

a chronically resistance trained athlete is more likely to have what kind of HR profile?

A

average and lower than resting have been reported compared to untrained people

113
Q

why might bodybuilders have greater absolute left ventricular volume?

A

possibly due to aerobic training.

114
Q

how does bodybuilder cardiac output and stroke volume compare to powerlifters?

A

greater; stroke volume and cardiac output may be greater per absolute workload as a result of training (probably due to decreased afterload on left ventricle, which increases cardiac output and decreases myocardial oxygen consumption)

115
Q

does ventilation rate limit resistance training?

A

generally no; is either unaffected or only moderately improved by it

116
Q

what ventilatory adaptations occur from anaerobics?

A

increased tidal volume and breathing frequency with maximal exercise; with submaximal activity though, breathing frequency is often reduced while tidal volume is increased.

117
Q

an aerobic athlete who trains with heavy resistance will likely get what effect on aerobic power?

A

no adverse effects, despite expected cellular changes; might enhance performance

118
Q

how would an athlete mitigate short term overreaching?

A

tapering; can lead to beneficial strength and power gains

119
Q

how long does nonfunctional overreaching last?

A

weeks or months

120
Q

what are the two types of overtraining?

A

sympathetic and parasympathetic

121
Q

how does psychology affect nonfunctional overreaching vs overtraining?

A

overtraining has serious altered psychological states, which may be brought on by endocrine shifts; many athletes sense OTS before it actually happens due to psych symptoms

122
Q

what does detraining entail?

A

decrements in performance and loss of adaptations following cessation of anaerobic training

123
Q

a trained athlete and recreational lifter would have to wait how long before effects of detraining are observed?

A

usually four weeks or more – in recreational lifters, six weeks

124
Q

how does detraining effect strength relative to baseline?

A

rarely lower than pretraining values; shows that resistance training has a residual effect when the stimulus is removed

125
Q

a powerlifter could expect what kind of atrophy from seven months no training?

A

an average of 37.1% atrophy was observed in all fiber types (from one study)

126
Q

what are the demographics of overtrained athletes?

A

77% were involved in sports requiring high levels of strength, speed, or coordination

127
Q

anaerobic is more likely to contribute to which type of overtraining?

A

sympathetic

128
Q

aerobic is more likely to contribute to which type of overtraining?

A

parasympathetic

129
Q

what kind of endocrine decrements does overtraining have?

A

decreased LH and free testosterone; lowered post-exercise testosterone

130
Q

can resting testosterone/cortisol be used as an indicator of overtraining?

A

no; it indicates only physiological strain of training and can’t be used for diagnostic purposes