Kines 350 Exam 4

List each of all the exercise adaptations from training

Respiratory and Cardiovascular Adaptations

1. Better pH balance (less production of lactate and H+ ions)

2. Lower resting heart rate (larger blood volume and SV)

3. Higher SV (more blood volume, contractility, and less afterload)

4. Increased capillary density (offloads more O2)

5. Improved minute ventilation (V/Q ratio)

6. More Type I fibers (aerobic metabolism)

7. 
   

Cellular Adaptations

1. Increase in mitochondrial mass (make more ATP)

2. Higher Aerobic enzyme activity (Isocitrate Dehydrogenase and Cytochrome Oxidase RLE increase)

Muscle Adaptation

1. More Type II fibers (faster muscle recruitment)

2. 
   

Why do we have exercise adaptations?

As we increase endurance training and and intensity our body adapts to maintain homeostasis during training.

How much percentage can our VO2max increase with endurance training?

about 15-20%

Smaller increase in individuals that initially have a higher VO2max (smaller gap to keep improving)

True or False Genetics on VO2max are 50% are determined by genetics.

True, genetics determines about 50% of VO2max in sedentary adults, they also play a key role in determining the training response.

Low responders-2-3%

Average responders- 15%-20%

High responders- 50%

What is the initial cardiovascular adaptation VO2max of short duration training? Long term?

Short duration (approx. 4 months) increase in SV is a dominant factor to increase VO2max

Long term- both increase in SV and a-VO2 difference

How does endurance training improve Stroke Volume?

Stroke volume is determined by

1. Contractility- improves cardiac muscle contraction

2. Preload- increase blood volume, increases venous return, increases preload

3. Decrease in afterload- peripheral resistance to pump more blood out

How does our arteriovenous O2 difference increase after endurance training?

We have an increase in capillary density

• slows down blood flow through muscle to offload O2 to muscle more

Increase in mitochondrial number

• mitochondria use O2 in ETC, increase ATP production, uptake O2 more

• increases mitochondrial turnover (mitophagy=breakdown of mitochondria)

• utilization of fat as a fuel

• less glycolysis metabolism (less lactate production, less PC depletion)

True or False endurance training promotes a fast-to-slow shift in muscle fiber type and increased capillarization

True, fast twitch fibers reduce, and increase in slow twitch fibers (slow twitch aerobic metabolism, endurance training fibers)

How does endurance training change utilization of fuel?

Endurance training uses fat metabolism more, sparing plasma glucose and muscle glycogen in the body for brain functions

• FFA travel to muscle more

• mitochondrial oxidation of FFA, which increases in beta-oxidation

How does endurance training improve antioxidant capacity?

training increases endogenous antioxidant enzymes

• improves removal of free radicals that cause oxidative damage

How does endurance training improve acid-base balance?

Pyruvate+NADH➛lactate+NAD+

• NADH if not producing lactate goes directly to ETC, to increase ATP production

• less carb utilization=less pyruvate formed

• less H+ moving into bloodstream

Acid base balance: moves lactate threshold up as VO2max increases

How does endurance training and resistance training promote protein synthesis in fibers? Does specific muscle adaptive responses depend on exercise stimulus?

Exercise stress activates gene transcription, they reduce miRNA which decrease protein synthesis by blocking mRNA

Yes, Primary and Secondary signals lead to muscle adaptations that increase protein synthesis

• resistance vs endurance training

• intensity and duration of training

What are primary signals responsible for exercise-induced adaptation?

Mechanical/Hormonal Input

1. Mechanical stretch (resistance training) increase

2. Calcium (endurance training) increase

3. AMP/ATP (endurance training) increase

4. Free Radicals (endurance) increase free radicals

What are secondary signals responsible for exercise-induced adaptation?

Intracellular Signaling

1. Kinases promote glucose uptake, mTOR (protein kinase) major regulator of protein synthesis and increases muscle size and strength

2. Angiogenesis (forms new blood vessels)

3. Regeneration and a fast-to-slow shift in fiber type

How does hormone adaptation changes after training? How does the one-leg training study help us determine this?

• Sympathetic nervous system (decreases Epinephrine/Norepinephrine)

• Cardiorespiratory system (decrease HR and decrease ventilation)

If we only train one leg, we see exercise adaptations for that one leg and the other untrained leg because unilateral strength training yields neural strength gains in the untrained contralateral limb via central nervous system spillover.

How does training improve homeostasis during exercise and reduce “feedback” from muscle chemoreceptors

There is less change within muscles, which means less feedback to cardiovascular control center which means we can lower HR and Ve to maintain homeostasis from disruption

How is detraining (stopping training) affect VO2max?

there is an initial rapid decrease in VO2max of about 8% within 12 days

SV decreases after loss of plasma volume, HR increases

Decrease in Mitochondria, reduces a-VO2 difference and oxidative capacity

• switch from Type I fibers back to Type IIx fibers

How does retraining affec VO2max?

Retraining can quickly adapt the body again

• Muscle mitochondria can double within 5 weeks of retraining

Mitochondrial adaptations lost quickly with detraining

• Loss of about 50% of training gain within 1 week of detraining

What kind of exercises can improve anaerobic training? What kind of adaptations can happen in anaerobic training?

Types of Exercise

• Sprint interval training (SIT)

• High intensity interval training (HIIT)

Adaptations

• sprint training improves muscle buffering capacity (bodies ability to clear out acid H+ accumulation) and hypertrophy and Type IIa and IIx muscle fibers and elevates enzymes involved in ATP-PC system and glycolysis to increase rate of production

What are physiological effects to strength training-defintions

1. Muscular strength-max force increases

2. Muscular endurance-frequency and repeated contractions against sub max load

3. Strength training-high resistance increases muscle strength and low resistance training increases muscle endurance

How does aging result in loss of both muscle mass and strength?

As we get older our muscle mass decreases the greatest after 50

We see a loss of

• loss of muscle mass (sarcopenia)

• atrophy type II fibers and type 1

How does strength training increase our muscle strength?

As strength training increases, our nervous system gets better at firing motor units to muscle fibers, increases our muscle fiber size/function.

True or False neural adaptations to resistance training are responsible for early gains in muscle strength

True, neural adaptations increase strength and mass of specific fibers during the first 2-8 weeks of training.

Evidence is that muscular strength increases in the first 2 weeks as muscle fiber size stays the same

include

• increase number motor units recruited

• increase firing rate of motor units

• increased synchronization

• improved neural transmission in neuromuscular junctions- synaptic vesicles release more acetylcholine

How does resistance training improve muscle fiber force production?

An increase in muscle fiber specific tension in type I fibers, increase in calcium sensitivity-resulting in a greater number of cross-bridges

Go from muscle fiber IIx to IIa to increase fatigue threshold

How does resistance training improve muscle mass?

Hypertrophy- increase in cross-sectional area of muscle fibers (single muscle fibers get bigger such as actin, myosin, and troponin)

How does resistance training improve protein synthesis?

1. Protein synthesis is the major reason why muscle mass increases, resistance training increases protein synthesis much faster than non resistance trainers.

2. mRNA increases which increases ribosome number and capacity of muscles to utilize them.

3. Increases mTOR which inhibits an inhibitor (TSC2) to increase Rheb and increase PA molecules for protein synthesis

Overall resistance training activates mTOR to increase muscle hypertrophy

What is the supplement for mTOR?

Whey protein, which can independently promote small increases of protein synthesis but a sedentary individual does not result in much of an increase in hypertrophy.

MUST TRAIN to see RESULTS

How does the length of training activate each protein synthesis signal?

As weeks continue…

1. Increase in protein synthesis (first couple of weeks)

2. Increase in mTOR (continues training)

3. Increase in Rheb and PA (prolonged training)

Can hormones affect muscle hypertrophy?

Yes, hormones such as, Insulin growth factor 1 and growth hormone can link with mTOR and increase protein synthesis

they are not required to increase muscle hypertrophy

True or False taking drugs like acetaminophen and ibuprofen negatively affect our muscle hypertrophy

False, they have been proven to have no such effect

What is the role of satellite cells in resistance training adaptations? How is this related to older indivuals?

Satellite cells are stem cells located in between the sarcolemma and basal lamina that produce myonuclei

in resistance training they produce more myonuclei as muscle mass increases to maintain the ratio as protein synthesis increases.

Older individuals can have an improved satellite cell activation but are limited compared to younger individuals

Is genetic influence also a major factor for resistance training adaptations?

Yes, genetics play a huge role in resistance training adaptations, about 80% of the differences are contributed by genetics, about 47 genes play a key role

• Many hypertrophy-linked genes are directly linked to mTOR pathway and are activated via strength-training

• So the response between individuals who strength train vary a lot

How is detraining affected in resistance training compared to endurance training?

Detraining in resistance training is slower and retraining is much faster than in endurance training.

How does blood flow restriction therapy improve muscular hypertrophy?

An inflated cuff partially restricts arterial flow and inhibits venous return,

• increase w/ the low load to increase in muscle strength

• increases metabolites to increase muscle strength and hypertrophy

How long of inactivity does it take for muscles to start atrophying?

20-30 days of muscle inactivity can result in 20-30% reductions in muscle fiber size

• conservation of muscle mass is dependent upon protein synthesis

  • if we do not use our muscles, we will synthesize proteins for somewhere else in the body

What happens during concurrent strength and endurance training? What mechanisms explain this impairment of strength gains resulting from concurrent training?

Potential for interference in training adaptations, can counteract each other.

• concurrent strength and endurance training impairs strength gains compared to strength training alone

Mechanisms:

• neural factors- impaired motor unit recruitment

• overtraining- no direct evidence exists to prove overtraining is impairing

• depressed protein synthesis- endurance training cell signaling can interfere with protein synthesis via increase in TSC1/2 which inhibits mTOR

What BMI is considered underweight, normal, overweight?

Underweight: <18.5 kg/m squared

Normal: 18.5-24.9 kg/m squared

Overweight: > 30 kg/m squared

KEEP IN MIND: BMI does not provide details of body composition

• muscular individuals could be classified as obese

What are methods of testing body composition?

1. Underwater weighing

   • divides body into fat free mass and fat mass, more lean people sink, not that accurate SEE=+- 2.7%

2. Air displacement plethysmography

   • Bod-Pod uses air displacement, also not that accurate

3. Dual energy x-Ray absorptiometry (DEXA)

   • two x-ray beams are used to determine whole body and regional estimates of lean tissue, bone density, and fat, most accurate SEE=+-1.8%, disadvantage include expensive and certified medical personnel must perform the scan

4. Bioelectrical impedance analysis (BIA)

   • detects electric current and measures lean tissues since it is a good conductor, fat tissue is a bad conductor of electricity, less accurate SEE= +-3.5% to 5%

5. Sum of skinfolds

   • pinches subcutaneous fat (20-70%), not too accurate SEE=3.5%

True or False there is no body fat % that is considered obese, only BMI?

True, there is age related guidelines of body fat percentage

MEN

• young adults: 8-22%

• middle age: 45-64%

• elderly: 10-23%

WOMEN

• young adults: 20-35%

• middle: 24-38%

• elderly: 25-35%

Women have more body fat percentage than men

What is important about healthy weight loss?

the key to successful weight management program lies in the understanding body energy stores

• change in body macronutrient energy stores=energy intake-energy expenditure (REE+PA/E+TEF)

No diet plans are better than others, do what works best for you, reducing one type of macronutrient does not change weight

The best weight loss is caloric deficit with exercise

How does macronutrient energy storage reflect body stores carbs, protein, and fat.

CHO-primarily stored in liver and skeletal muscles-total mass of CHO stores is relatively small, water is stored with CHO and we get bloating.

Proteins exist as numerous cellular proteins, proteins are not stored as fuel sources

Fat stores as triglycerides primarily in white adipocytes, three different types

• white-most abundant

• beige-produces lots of heat

• brown-for thermoregulation

True or False we are starting to reduce obesity across the U.S

True, the U.S has been known being one of the largest obese countries, studies have shown that the use of GLP-1 have improved the numbers and we are are seeing a decline in obesity

What is counterintuitive about low energy diets in loss of both fat and fat free mass?

The loss of lean mass is not the goal, because it decreases our metabolic rate which means we cannot burn and use calories as efficiently, therefore it is counterintuitive because we might think we are losing weight when we really are not losing anything.

What is Rhabdomyolysis?

A serious and life threatening condition from extreme rapid muscle deterioration, when a muscle fiber dies, releasing its contents into the bloodstream, the accumulation of K+ and Ca+2 in the extracellular fluid can cause major electrical shock and stop the heart

What kind of factors affect athletic performance?

1. Energy Production- anaerobic and aerobic production

2. Diet-carb and water intake

3. CNS function- arousal and motivation

4. Environment- altitude, heat, and humidity

5. Strength/skill- practice, natural body type and muscle fiber type

How can we test fatigue?

Using the wingate test, not very accurate,. We use the cycler to increase resistance to show how much time we can perform exercise to show when fatigue sets in. After a recovery of 10 min we see we reach the same power initially due to ATP PC replenishment.

Where can we see fatigue? What is the ultimate cause of fatigue?

We see fatigue in the

• Central fatigue- spinal cord and psyche

  • Central Nervous System- signals from higher brain centers to alpha motor units (rate of firing) and signals back to higher brain centers

• Peripheral fatigue- muscle sarcolemma, cross bridges, actin-myosin cite

  • golgi tendon organs limits response to CNS, slows down firing of alpha motor units

  • neural factors, mechanical factors, and energetics of contractions

The ultimate cause of fatigue is the number of cross-bridges decrease, do not produce max muscle force

What is Central Fatigue?

Reductions in:

• motor units activated

• motor unit firing frequency

• excessive training can reduce performance and is related to serotonin activity

Altered by:

• increasing motivation

• physical and mental diversion

What neural factors are related to fatigue?

Neuromuscular junction:

• not the site of fatigue

Sarcolemma and transverse tubules

• altered muscle membrane to conduction and action potentials- can disrupt sodium potassium pump

  • inability of Na+/K+ pump to maintain action potential amplitude

• An action potential block in t-tubules

  • reduced sarcoplasmic reticulum Ca+ release

What mechanical factors are related to fatigue?

Cross-bridge cycling and tension development depends on:

• arrangement of actin and myosin

• Ca+ binding to troponin-exposes actin site but if Ca+ then not enough Ca+2 to bind to troponin, decrease in cross-bridges

High H+ concentration may contribute to fatigue

• reduce in forces per cross-bridges

• reduce the force generated at a given Ca+ concentration

  • H+ interferes with Ca+ binding troponin

What energetics of contraction contribute to fatigue?

imbalance between ATP requirements and ATP generating capacity- accumulation of Pi which inhibits maximal force and reduces cross-bridge cycling

Rate of ATP utilization is slowed faster than the rate of ATP generation

muscle fiber recruitment increases as exercise intensity increase

• type 1, type 2a, type 2x up to

  • 40% VO2max type 1 fibers recruited

  • Type 2a fibers recruited at 40 to 75% VO2max

  • exercise >75% VO2max requires 2x fibers- if we rely on type IIx fibers, we fatigue more quickly b/c of increased H+ and lactate production

What are some factors that limit all-out anaerobic performance?

As exercise intensity increases, muscle fiber recruitment progresses from type 1, type IIa, type IIx

Types:

• Ultra short-term performance

• Short-term performance

How does ultra-short term performance relate to anaerobic fatigue?

an event that is <10 seconds at high power events

• dependent on type II fibers

• motivation, skill, arousal

• primary energy source is anaerobic

How does short term performance relate to anaerobic fatigue?

Ultra short-term performance

• events lasting 10-180 seconds

• where shift from anaerobic and aerobic metabolism

  • mixed slow and fast twitch fibers

• fueled primarily by anaerobic glycolysis

  • resulting in elevated levels of H+ and lactate

• ingestion of buffers may improve performance

Factors limiting all-out aerobic preformance?

As the duration of an all-out performance increases, more demand is placed on the aerobic sources of energy, based on exercise duration

Types:

• moderate-length performance

• intermediate-length performance

• long-term performance

How does moderate-duration performance affect fatigue?

events lasting 3 to 20 minutes

• a high VO2max is advantages

  • high max stroke volume

  • high arterial oxygen content (extraction of O2)

• require energy expenditure near VO2max

  • type 2x fibers recruited

Intermediate-duration performance affects fatigue?

events lasting 21-60 minutes

• predominantly aerobic

important factors:

• running economy and exercise efficiency

  • high percentage of type 1 muscle fibers

• environmental factors

• state of hydration

• lactate threshold

Long-term performances affect on fatigue?

Event lasting 1-4 hours

• environmental factors more important

• maintaining rate of carbohydrate utilization

  • muscle and liver glycogen stores decline

• consumption of fluids and electrolytes

• diet also influences performance

Factors affecting performance in ultra-endurance events

• 166 km mountain run, Triple Iron Triathlon, etc.

• Most important variables

  • VO2max

  • %VO2max that can be sustained

• Metabolic response

  • fat oxidation is higher after event

  • consistent with exercise at <60% VO2max

• Potential for hyponatremia-low blood sodium

Elite marathoners possess…

A VO2max at which a runner can maintain performance - 4.0L/min

• influenced by running economy

  • genetics and intense training are both needed