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Ch.7 Energy Transfer During Physical Activity/Ch.11 Individual Differences…

- - - - No appreciable lactate accumulation occurs with either steady-rate aerobic activity or with brief 5-10sec bouts of all-out effort powered by high energy phosphates
      - The higher the intensity of exercise, the faster the rate of glycogen depletion.
    - - Trained endurance athletes perform steady-rate aerobic exercise at 80-90% of maximum capacity for aerobic metabolism. This favorable response likely relates to three factors:
        
        1) Athelets specific genetic endowment (eg, muscle fiber type, muscle blood flow responsiveness)
        
        2) Specific local training adaptations that favor less lactate production
        
        3) More rapid rate of lactate removal via greater lactate turnover and/or conversion at any intensity of physical activity.
      - Endurance training increases capillary density and the size and number of mitochondria, including the concentration of enzymes and transfer agents in aerobic metabolism.
        
        Such adaptations will help the capacity to generate ATP aerobically through glucose and fatty acid catabolism. Maintaining low lactate level also conserves glycogen reserves to inhibit the processes of muscular fatigue and extend the duration of effort.
      - Sprint-power athletes often achieve 20-30% higher blood lactate levels than untrained counterparts during mammal short-duration exercise. Three mechanisms could explain this:
        
        1) Improved motivation that accompanies training
        
        2) Increased intramuscular glycogen stores that accompany training may allow a greater contribution of energy via anaerobic glycolysis
        
        3) Training-induced increase in glycolytic-related enzymes, particularly phosphofructokinase. The 20% increase in glycolytic enzymes falls well below the two-threefold increase in aerobic enzymes with endurance training.
      - Three factors contribute to differences among individuals in capacity to generate short-term anaerobic energy.; 1) Effects of previous training, 2) capacity to buffer acid metabolites, 3) motivation
        
        Training; In a "classic" 1971 study, researchers determined that trained subjects always exhibit higher levels of muscle lactic acid, blood lactate, and more pronounced muscle glycogen depletion following short-term maximal bicycle ergometer exercise. There was also significant reductions in intramuscular high-energy phosphates with essentially no differences observed between groups.
        
        Anaerobic training might enhance short-term energy capacity by improving the body's alkaline reserve for buffering. This reasoning seems appealing, yet athletes have only a slightly larger alkaline reserve than sedentary counterparts. Additionally, no appreciable change in alkaline reserve occurs following intense physical training. Exercise training most likely confers a buffering capability within the range expected for healthy untrained individuals.
    - - Fast-twitch fibers provide most of the power requirements for all-out effort. The glycogen content of these fibers becomes almost totally depleted because of the activity's anaerobic nature.
        
        In contrast, during moderately intense but more prolonged aerobic activities, slow-twitch muscle fibers become glycogen depleted first.
    - - Recovery from intense training could benefit from active aerobic recovery (cycling, running) to help facilitate lactate removal. Although the precise mechanism for exhaustion during anaerobic activity remains unclear, blood lactate levels provide an objective indication of the relative strenuousness of exercise; they also reflect the adequacy of recovery. Since lactate anions induce a fatiguing effect on skeletal muscle any procedure hat accelerates lactate removal probably augments any subsequent activity.
        
        There's a study on pg173 showing lactate removal rates after 6min supermaximal exercise. There was a passive protocol, active protocol's with 65% VO2max, 35% and 65% VO2max, 35% VO2max. The 35% group did best, the 65% hindered removal the most. The passive group did not have the same rate as the groups containing the 35% protocol. Chart only goes out to 40min, the passive group lagged 15mins behind the 35% only group.
        
        The added lactate removal with active recovery likely results from increased blood perfusion through the "lactate-using" liver, heart and inspiratory muscles. Increased blood flow through the muscles also enhances lactate removal because citric acid cycle metabolism readily oxidizes lactate from muscle.
    - - Lactate serves as an important substrate in energy-storing and energy-generating pathways in different tissues. Lactate measured during or following physical activity does not necessarily reflect absolute levels of anaerobic energy transfer via glycolysis. With increasing intensity, greater lactate production reflects increasing ATP resynthesis from anaerobic pathway.
    - - Testing to measure the short-term system require maximal effort for up to 3min.
        
        Above-normal intramuscular glycogen levels do not affect test performance or final level of blood lactate accumulation.
      - The Katch (all-out stationary cycling of short duration) and Wingate (:30 of super maximal effort on leg-cycle ergometer or arm-crank) tests assume that peak power output reflects the energy-generating capacity of the high-energy phosphates, while average power reflects glycolytic capacity.
      - Large differences exist in anaerobic power when comparing test scores on an absolute basis.
        
        Expressing power output capacity relative to a component of body mass or composition should minimize or even eliminate the gender difference in anaerobic capacity.
        
        Males' greater relative muscle area and metabolic capacity of the fast-twitch fiber type and larger catecholamine response to physical activity may help to explain their larger anaerobic performance.
        
        Female maximal anaerobic performance remains unaffected by variations in menstrual cycle phase.
- - - - This capacity relates to the type I fibers numbers large mitochondria including high levels of enzymes required for aerobic metabolism, particularly fatty acid catabolism.
      - More than likely, the predominance of type I fibers contributes to high blood lactate thresholds observed among elite endurance athletes.
  - - - No appreciable blood lactate accumulates under steady-rate, aerobic metabolic conditions.
      - Oxygen consumption lags behind in the early stages of exercise. It does not instantaneously increase to steady-rate.
        
        This should be a surprise as energy for muscle action comes directly from the immediate anaerobic breakdown of ATP. Even with experimentally increased oxygen availability and increased oxygen diffusion at the tissue level, the initial increase in exercise oxygen consumption is always lower than the steady-rate oxygen consumption.
        
        The oxygen deficit quantitatively expresses the difference between the total oxygen consumption during activity and the total would be consumed had steady-rate oxygen consumption been achieved at the onset.
        
        This oxygen deficit represents the immediate anaerobic energy transfer from the hydrolysis of intramuscular high-energy phosphates and rapid glycolysis until steady-rate energy transfer matches the energy requirements.
        
        Endurance trained persons reach steady-rate sooner with a smaller oxygen deficit than untrained persons or sprint-power athletes.
        
        Three aerobic training adaptations facilitate the rate of aerobic metabolism when exercise begins:
        
        1) More rapid increase in muscle bioenergetics
        
        2) Increase in overall cardiac output
        
        3) Disproportionately large regional blood flow to active muscle complemented by cellular adaptations
    - - As exercise intensity increases, oxygen consumption corresponds with an increase related to the new steady-rate level until maximum oxygen consumption is hit where there is a plateau in oxygen consumption even if exercise intensity increases.
        
        This plateau generally provides assurance that a person has reached maximum aerobic metabolism (ie, achieved "true" VO2max)
        
        Peak oxygen consumption applies when the plateau does not occur or maximum performance is limit by local muscular factors rather than central circulatory dynamics. VO2peak refers to the highest value of oxygen consumption measured during a graded exercise test.
      - Maximal oxygen consumption of elite endurance athletes is almost two-fold that of sedentary persons.
      - VO2max requires integration of high levels of pulmonary, cardiovascular, and neuromuscular function.
      - The six most important factors that influence VO2max include: 1) mode of activity, 2) heredity, 3) state of training, 4) gender, 5) body size and composition 6) age
        
        Mode of activity; the variations in VO2max with different activities reflect the variations in the amount of muscle mass activated in different activities
        
        Heredity; researchers estimate the genetic effect at about 20-30% for VO2max, 50% for maximum heart rate and 70% for physical working capacity. Combining the estimated effects of genetics and familial environment raises the upper limit of genetic determination is about 50% when adjusted for age, gender and body mass and/or body composition.
        
        State of training; A person's state of aerobic training contributes 5-20% of VO2max.
        
        Gender; Females typically score 15-30% below the values of males. Differences in body composition and hemoglobin usually explain the gender difference in VO2max. The average male can generate more aerobic energy because he possess more muscle mass and has less fat than the average female.
        
        Body size and composition; Variations in body mass explain nearly 70% of the differences in VO2max. Adjusting for variation in the muscle mass activated in physical activity provides some explanation of individual differences. Expressing oxygen consumption per unit of appendicular skeletal muscle mass often negates the difference in VO2max between men and women of similar training status.
        
        Age; For adults VO2max declines at about 1% per year after age 25. Despite the apparent aging effect, strong evidence indicates that a person's habitual activity levels exerts far greater influence on aerobic capacity than chronological age.
        
        For children the relative VO2max stays the same from 6-16 about. The improvements/changes are related to changes in muscle mass and fat mass during those years.
        
        VO2max predictions with children are problematic because the age-related performance improvements relate poorly to aerobic capacity. The largest contributions to test scores improvements are increased blood lactate threshold (higher percentage of VO2max sustained during activity) and improved running economy. Both result in faster times.
  - - - Moderate activity requires a longer time to achieve steady-rate oxygen consumption and creates a larger oxygen deficit. Consequently, it takes longer for recovery oxygen consumption to return to pre-activity levels.
      - All-out physical effort does not produce steady-rate oxygen consumption. Such effort demands a larger energy requirement than aerobic processes can supply. Failure to achieve steady-rate oxygen consumption makes it unfeasible to accurately quantify the true oxygen deficit.
      - Trained persons have a faster rate of recovery oxygen consumption than the untrained. More than likely the same training adaptations that facilitate the rapid achievement of steady-rate oxygen consumption also facilitate a rapid recovery process.
    - - All of the physiologic systems activated in physical activity increase their own particular need for oxygen during recovery. Two factors impact recovery oxygen consumption:
        
        1) Level of anaerobic metabolism during physical activity
        
        2) Respiratory, circulatory, hormonal, ionic and thermal adjustments that elevate metabolism during recovery.
        
        Individual factors: resynthesizes ATP and PCr; resynthesizes lactate to glycogen (Cori cycle); oxidize lactate in energy metabolism; restore oxygen to myoglobin and blood; restore thermogenic effects of elevated core temperature; thermogenic effects of hormones (catecholamines); restore elevated heart rate, ventilation, and other physiologic functions
      - One issue with the EPOC computing is that it assumes resting oxygen consumption is static through activity and recovery. This may not be entirely correct. There are two important characteristics of recovery oxygen consumption:
        
        1) Fast component, a single component exponential curve: With mild aerobic activity of relatively short duration and little disruption in body temperature and hormonal milieu, about half the total recovery oxygen consumption occurs within 30s and complete recovery within 2-4min.
        
        2) Slow component, a second phase of recovery in addition to the fast component: Recovery from strenuous activity presents a different picture, presumably because three factors (blood lactate, body temperature and thermogenic hormone levels) increase substantially. Recovery of the slow component can take up to 24hr.
        
        A precise biochemical explanation for the recovery oxygen consumption, particularly the role of lactate, remains elusive.
- - - - Terms such as "speed", "power", and "endurance" must be applied precisely within the context of the specific movement patterns and specific metabolic and physiologic requirements of the activity.