Exam 3 Physiology of Exercise 2 / II

Professor Bland, Harding University

• Exercising into old age an unusual pattern • Natural tendency to be sedentary • Motivating factors? • Primary aging versus comorbidities of age • Cross-sectional versus longitudinal studies • Medical care, diet, lifestyle factors • Selective mortality • Applicability of findings to larger aged population?

Exercise extends lifespan

longevity (X) < functionality (Y)

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Reasons why we age

Aging of specific systems *Key Image*

Reactive Oxygen Species: Some is good, more is bad = high oxidative stress = high inflammation = poor recovery and reduced strength

ROS

Reduced exercise in age and protein turnover + immune function

Breen et all 2013: 2 weeks of 1400 steps/day:

• insulin sensitivity decreased 43%

• leg FFM decreased 4%

• TNF-alpha increased by 12%

• CRP increased 25%

Neuromuscular Jxn and Age

• Decrease surface area (decrease folds)

• Decrease Ach reeotors

• Decrease Ach pre-synaptic vesicles

• Incerased distance of synaptic cleft

• Peri-synaptic Schwann Cells migrate into synaptic cleft, disrupting signaling

• Mitochondrial dysfunction

Aerobic Fitness

VO2max

• declines faster in sedentary (10%/decade) vs active (5-6%/decade) vs elite athletes (3.6% decline over 25 years), 15%/decade for previously active adults. eclines faster after 75 yrs. Mechanisms?:

• HR decreases

• heart contractility decreases (stiffness)

• SV decreases

Peripheral blood flow

• 10-15% reduction in older individuals (even with exercise)

Lactate threshold

• Absolute LT declines, but at a slower rate than relative LT = LT not a good predictor of performance in older adults.

Muscle Fitness

High variability

• Mass declines 1-2%/yr, then accelerates after 60

• Strength declines 1.5%/yr between 50-60 then 3%/yr >60

Greater type II fiber loss with aging

• higher neural threshold needed for firing

Bone

Aging = decline in BMD and structural integrity

Exercise is protective

• high impact mechanical loading (more so than medium or low)

• Remember muscle-bone cross-talk (myokines and osteokines promote bone remodeling)

Body Composition

• Masters Endurance: 19.7±3.8%

• Masters Power: 16.4±4.4%

• Older control: 24.5±4.6%

• Young Endurance: 15.4±5.2%

• Young Strength/Power: 14.1±3.5%

• Young Control: 17.4±3.0%

VO2 max

• Masters Endurance: 42.0±6.6 mL•kg-1•min-1

• Masters Power: 26.5±2.3 mL•kg-1•min-1

• Older control: 27.1±4.3 mL•kg-1•min-1

• Young Endurance: 60.0±5.4 mL•kg-1•min-1

• Young Control: 43.1±6.8 mL•kg-1•min-1

Strength

• Difficult to compare MVC with various techniques, thus use “standardized mean difference”

• CSA: Not different among MP, ME, OlderC.

Peripheral vs Central Fatigue

Peripheral:

⁃ Internal environment?: Accumulation of protons? Ammonia? Heat?

⁃ Within the muscle?: Pi? SR changes? Inhibition of Ca2+ release? Glycogen/glucose? Decreased conduction velocity?

Central:

⁃ AP blocked? Motor drive? Type III and IV nerve stimulation (stimulate emergency cease response) ?

⁃ Tryptophan/Serotonin/BCAAs? Cytokines? Temperature?

Components of fatigue

“it would be good to remember just one thing in each category”

Functions of Lactate (no need to memorize)

T/F: Lactate causes DOMS

False

T/F: Lactate is responsible for moving H+ to mitochondria to power glycolysis

True, H+ as NADH2

Lactate is what type of functional molecule?

myokine and exerkine

Critical Power = Fatigue Threshold =

The greatest metabolic rate that is powered by the body’s maximum possible oxidative energy provision

• max threshold before switching to anaerobic respiration

• steady state not possible above CP

Muscle Glycogen

• Rapid fuel source – connected with muscle fatigue

  • Depletion = ↓ATP regeneration and ↓EC coupling

    • Even after ATP levels are normal – low glycogen impairs function.

    • May contribute to ↓SR Ca2+ release

  *Low fuel status = fatigue?

• Glycogen Granule

  • Metabolically active with regulating proteins and glycolytic enzymes.

  • Located strategically - subsarcolemmal

Muscle Glycogen Determinants:

￮ CHO intake

￮ Exercise type

⁃ Eccentric ↓ glycogen synthesis

￮ Exercise intensity and duration

⁃ ~40% loss after 3hrs@~31%VO2max and ~70% loss after 2 and 1hrs @~64 and ~84%VO2max (Gollnick, Piehl, and Saltin, 1974)

⁃ ~39% loss after 6 sets of 12RM leg extension (Robergs, et al. 1991)

⁃ May differ between men and women (Wismann and Willoughby, 2006

Na+/K+ Pumps

• Muscle activation results in cellular loss of K+ and increase in Na+

  • Results in interstitial increase in [K+] and change in Na+ gradient

    • Impairs muscle force development

• Therefore – need to maintain Na+/K+ pumps

  • Possible role of ROS in Na+/K+ pump function

• Thus – possible role of anti-oxidants in fatigue

Fatigue

Trait vs State

o Trait (due to exss load3 during past week)

o State (current exercise state)

Training Impulse (TRIMPS)

Carbohydrates

Muscle Glycogen

Rapid fuel source - connected with muscle fatigue

• depletion = decreased atp regeneratioin adn decreased ec coupling

  • even after atp levels are normal, low glycogen impairs fxn

  • low fuel status = fatigue?

  • may contribute to decreased SR Ca2+ release

Glycogen Granule

• metabolically active w regulating proteins and glycolytic enzymes

• located strategically

Muscle Glycogen

• CHO intake

• Exercise type

  • eccentric decreases glycogen synthesis

• Exercise intensity and duration

  • ~40% loss after 3hrs @ ~31% VO2max and ~7-% loss after 2+1 hrs @ 68% VO2max

Na+ / K+ pumps

• Muscle activation results in cellular loss of K+ and increase in Na+

  • results in interstitial increase in K+ and change in Na+ gradient: impairs muscle force development

• Therefore, need to maintain Na+/K+ pumps

  • possible role of ROS in pump fxn

• Thus, possible role of anti-oxidants in fatigue

Relative Energy Deficiency in Sports (REDS)

• Energy Availability (EA) = Energy available for biological function after energy expenditure by fat-free mass

  • (Energy Intake – Exercise Energy Expenditure) ÷ Fat Free Mass.

  • Energy availablilty (EA) of 45 kcals/kg FFM/day = “mantinance”.

• power: weight ratio

• extreme volumes of exercise

REDS effects

REDs: Low Carbohydrate Availability (LCA)

• Impact of not only Low Energy Availability (LEA), but also LCA:

• Acute LCA (<6 days) = negative effect on bone, immune system, iron biomarkers

  • Sometimes even without LEA!

• 3.5 weeks of LCA elevated IL-6 and impaired bone remodeling.

• LCA accelerates REDs outcome

Hydration

• Thirst mechanism

  • Insensitive to hydration status during exercise

  • Time delay between absorption of water (~20 minutes) to blood and quenching of thirst (seconds)

• Performance declines @ ~2-3% loss of body mass

Hydration and Exercise

Impairs aerobic performance.

– temperature → sweat loss → performance

– plasma volume → cardiovascular function

– plasma volume → thermoregulatory function

Effect of dehydration on anaerobic and strength performance is unclear.

Overhydration

• Exercise-associated hyponatremia

  • Low plasma sodium concentration (<135 mmol/L)

  • Excessive intake of fluids

  • Water alone vs sports-drinks

    • Slower absorption

    • Sodium absorbed into intestinal lumen

  • Prevalence

    • Increases with distance running

    • Highest in swimming

    • Slower runners