topic 12: training 1 and 2 - ex phys

VO2max

increases by working large muscle groups and dynamic activity — 20-60 min ≥3 times a week ≥50% VO2max

• smaller increase in individuals with high initial VO2max

• VO2max = HRmax x SV max x (a-vO2)max

• CO increases → SV increases → preload increases

  • post-CO after training is higher mainly due to SV

stroke volume

changes occur rapidly over days of training

increases preload: increases PV, venous return, ventricular volume, decrease HR

• frank starling: greater stretch due to more preload

increases contractility: increases left ventricular volume

decreases afterload: decreased TPR due to decreased SNS vasoconstriction — increases max blood flow with no change in MAP

a-vo2 difference

increases muscle blood flow and decreases SNS vasoconstriction to decrease afterload

• improved ability of muscle to extract O2 from the blood

• increases capillary density

  • decreases diffusion distance to the mitochondria

  • slower blood flow for greater cross-sectional area

  • redistribution to active organs

• increases mitochondrial number

  • increases muscle fiber ability to use O2

  • increases BV

• more myoglobin — transport O2 from cell membrane to mitochondria

• over training: total BV increases, lower hematocrit (RBC over BV), less O2 carried (sports anemia)

fiber type

shift in fast to slow (type 2 to type 1) in muscle fiber type bc of more mitochondria for oxidative metabolism

• CV adaptations, skeletal adaptations, genetics

• increased capillaries → SLOWER blood flow and more diffusion of O2 and remove wastes

• increases myoglobin content by 80%

• increases oxidative enzymes (SDH, citrate synthase) → enhanced glycogen sparing

mitochondrial content

increased mitochondria increases endurance performance due to shift in aerobic metabolism

• less reliance on glycolysis, ATP-Pc, lactate and H+

  • lactate threshold is greater in trained — can maintain high intensities

• increased mitochondria turnover: more mitochondria used = more remade

  • mitophagy: cleanup and recycling

• O2 uptake: the longer it takes to reach aerobic met, longer it takes to reach steady state

  • endurance trained have less O2 debt and can reach steady state faster — more capillaries, mitochondria, enzymes, type 1, etc

increased mitochondria

in skeletal muscle fiber, fuel utilization, and acid-base balance

pH:

• increased FFA oxidation and decreased PFK activity → decreased pyruvate → decreased lactate and H+ → blood pH maintained

• increase uptake of pyruvate and NADH → decreased lactate and H+ → blood pH maintained

less CHO used = less pyruvate

increased NADH shuttles = less NADH to make lactic acid to regenerate NAD+

fuel utilization

increases utilization of fat and sparing plasma glucose and muscle glycogen

• increased transport of FFA into muscle — from increased capillary density, fatty acid binding protein, and fatty acid translocase

• fatty acid → plasma → cytoplasm → mitochondria = higher carnitine pal and translocase

• increased enzymes of beta oxidation — increasing acetyl-CoA

  • high citrate inhibits PFK and glycolysis

• RER: more CHO used, using less O2 but making more CO2

  • training decreases RER

muscle antioxidant capacity

training increases endogenous antioxidants produced by the body to sequester free radicals

• free radicals: produced by contracting muscles and can damage the binding of actin and myosin — need little amounts for signaling and immune

• improves fibers ability to remove radicals

• protect against exercise-induced oxidative damage and muscle fatigue

• blood vessel →← lipid membrane → muscle fiber (cystolic/mithcondrial)

  • cytosolic: SOD (superoxide dimutase), CAT (catylase), Vit C (in catylase wth exogenous forms)

  • mitochondrial: SOD, CAT

exercise stimulus

exercise stimulus → transcription → translation → protein → mitochondria → antioxidants, muscle fiber types, etc.

• transcription: unwinding DNA and produce genetic code → forms messenger RNA in nucleus

• translation: messenger RNA from nucleus to cytoplasm is read → protein

• ex: increase in PV bc stimuli increases transcription factors

transduction pathway

from endurance training

increases Ca2+

• → increases calcineurin → fast to slow fiber type shift

• → increases CaMK → increases PGC-1a → fast to slow fiber type shift, mitochondrial biogenesis, synthesis of antioxidant enzymes

increases AMP/ATP

• → increases AMPK → increases PGC-1a → fast to slow fiber type shift, mitochondrial biogenesis, synthesis of antioxidant enzymes

increases free radicals

• → increases NFxB → synthesis of antioxidant enzymes

• → increases p38 → increases PGC-1a → fast to slow fiber type shift, mitochondrial biogenesis, synthesis of antioxidant enzymes

primary signals

as endurance training increases

• Ca2+ increases: released from SR for contraction, elevated for longer duration

• AMP/ATP increases: ATP breakdown to ADP and AMP

• free radicals increase: oxygen consumption in mitochondria produces byproducts

secondary messengers

from the primary signals and send to skeletal muscle

• AMPK: senses energy state of exercising muscle, promotes glucose uptake

• PGC-1a: mitochondrial biogenesis, capillarization, synthesis of antioxidant enzymes

• mTOR: protein kinase — major regulator of protein synthesis and muscle size

peripheral feedback

untrained: small and low count of mitochondria → more group 3 and 4 afferent signals (lactate, H+) → cardiorespiratory control centers → high HR and VE over time

trained: large and high count of mitochondria → less group 3 and 4 afferent signals (lactate, H+) → cardiorespiratory control centers → mid HR and VE over time

central command: endurance trained have less stimulus from the brain to CV control center → low HR and VE

anaerobic training

sprint interval training (SIT): severe exercise lasting 10-30s (>100% VO2max)

• energy supplied by ATP-Pc system and glycolysis

high intensity interval training (HIIT): very heavy exercise lasting 60-240s (80-100% VO2max)

• energy required to perform 60 s — 70% anaerobic, 30% aerobic

results in improved anaerobic performance

• increased muscle buffer capacity: H+ accumulation inhibits actin and myosin crossbridge and Ca2+ to troponin

• muscle fiber hypertrophy

• increased anaerobic bioenergetic capacity in trained muscle

neural adaptations

neural adaptations and NS changes responsible for early gains in resistance strength training

• initial 8-20 weeks

• neural steps to a contraction: GTO senses tension → afferent signal → to spinal cord and motor cortex → decision to perform a movement → motor neuron axon → NMJ of skeletal muscle

• increased ability of recruiting motor units, firing rate, synchronization, transmission across NMJ

• cross education: training in one limb transfers to the other limb (ex: adaptations in good leg will transfer to injured leg)

muscle fiber type

resistance training-induced changes in muscle fiber type

• increase force production: more contractile proteins (type 2) and Ca2+ sensitivity (type 1)

• shift from fast to slow fibers (from type 2x to type 2a)

• hyperplasia: increased number of fibers

  • satellite cell activation: repair microinjuries due to mechanical stress of lifting

• hypertrophy: increase muscle proteins (actin and myosin) due to more sarcomeres

  • increases muscle mass

• increases muscle antioxidant capacity, tendons and ligament strength, and bone mineral content

muscle protein synthesis

resistance training-induced increase in muscle protein synthesis

• untrained: rate to muscle strength and hypertrophy is longer and less elevated than trained

• post exercise: increase in mRNA → increase ribosome → increase mTOR (takes minutes to activate) → increase protein synthesis (takes hours)

hypertrophy

due to resistance training

increased anabolic hormones is NOT required

• IGF-1, GH, testosterone can increase activation but not required

• stims mTOR

• mTOR pathway is stimulated by mechanical contraction (actin and myosin)

• leucine amino acid in supplement/diet + resistance training = muscle protein synthesis

anti-inflammatory drugs do NOT negatively impact

• can take for soreness but not in long term

• CAN decrease muscle strength — inflammation needed for repair but can impair recovery

satellite cells: ratio of myonuclei to cytoplasm domain

• muscle repair, can increase muscle mass and protein synthesis

• hypertrophy increases contractile protein volume in cytoplasm and needs more support from satellite cells

80% genetic variation

atrophy

prolonged inactivity of skeletal muscle due to decreased protein synthesis and increased protein breakdown

• muscle protein balances with inactive and active muscles

• inactive (ex: sedentary): decreased protein synthesis, increase in protein degredation

• active (ex: trained): increased protein synthesis, decreased protein degredation

• skeletal muscle inactivity → increased radical production from mitochondrial dysfunction = oxidative stress → decreased protein synthesis

concurrent strength

combining strength and endurance training impairs strength gains and aesthetic physiques

• 1RM squat over weeks: strength athletes see more improvement in strength than concurrent and endurance athletes

• resistance: increases mechanoreceptor activation → increases mTOR → hypertrophy

• endurance: increases AMPK → increases TSC1/2 → blocks mTOR → interferes with protein synthesis

• instead do alt days and 6h bt exercises

  • aerobic training activates AMPK that contradict pathways activated by resistance training mTOR

• depends on training, intensity, modality, volume, frequency, integration

• other factors:

  • limited neural evidence on impaired motor recruitment

  • no evidence on overtraining effects