ch3 - bioenergetics of exercise and training Flashcards
what is catabolism associated with?
release of energy
are exergonic reactions catabolic or anabolic or neither?
catabolic
what do endergonic reactions include?
anabolic processes and the contraction of muscle
through what intermediate molecule are exergonic and endergonic reactions derived?
ATP
what is atp composed of?
adenosine and three phosphate groups
adenosine is the combination of what chemicals?
adenine (a nitrogen-containing base) and ribose (a five-carbon sugar)
the breakdown of one molecule of ATP to yield energy is known as?
hydrolysis, because it requires one molecule of water
what is the hydrolysis of ATP catalyzed by?
an enzyme called adenosine triphosphatase (ATPase)
what is crossbridge recycling?
the process that occurs after myosin ATPase catalyzes ATP hydrolysis
what other enzymes catalyze ATP at other locations?
calcium ATPase for pumping calcium into the sarcoplasmic reticulum, sodium-potassium ATPase for maintaining the sarcolemmal concentration gradient after depolarization
what equation depicts the reactants (left), enzyme (middle), and products (right) of ATP hydrolysis
ATP + H2O ADP + Pi + H+ + Energy
hydrolysis of ADP does what?
cleaves the second phosphate group and yields adenosine monophosphate
how does ATP store energy?
in the chemical bonds of the two terminal phosphate groups, which classifies it as a high-energy molecule
where do ATP-producing processes occur?
in the cell
how does the glycolytic system depend on oxygen?
it doesn’t, neither does the phosphagen system
where do the glycolytic and phosphagenic systems occur?
in the sarcoplasm of a muscle cell
where do the oxidative and aerobic mechanisms occur in muscle cells?
in mitochondria
what do mitochondria require for aerobic mechanisms?
oxygen as the terminal electron acceptor
which of the three macronutrients can be metabolized for energy without oxygen?
carbohydrate, which is critical during anaerobic metabolism
which energy system is active during anaerobic exercise?
all three energy systems are active at any given time, it’s an issue of contribution percentage (modulated by intensity and duration)
what chemical process does the phosphagen system rely on?
hydrolysis of ATP and breakdown of another high-energy phosphate molecule called creatine phosphate (CP), also called phosphocreatine (PCr)
what enzyme catalyzes the synthesis of ATP from CP and ADP?
phosphocreatine / creatine kinase
what is the reaction for catalyzing the synthesis of ATP from CP and ADP?
ADP + CP
what does creatine phosphate do for the ADP–>ATP process
supplies a phosphate group that combines with ADP to replenish ATP, a reaction that provides energy at a high rate
what is the downside of the PCr reaction?
because CP is stored in relatively small amounts, the phosphagen system cannot be the primary supplier of energy for continuous, long-duration activities
how much ATP does the body store?
approximately 80 to 100 g (about 3 ounces) of ATP at any given time, which does not represent a significant energy reserve for exercise
what’s the lowest ATP a body can have?
not zero, because ATP stores cannot be completely depleted due to the necessity for basic cellular function
how much ATP does the body store?
80 to 100 g (about 3 ounces) of ATP at any given time
what are the implications of the amount of stored ATP?
it does not represent a significant energy reserve for exercise, and ATP stores cannot be completely depleted due to the necessity for basic cellular function.
When muscle fatigue causes ATP to be reduced by 50-60% of preexercise levels, how does phosphagen system fix this?
by using the creatine kinase reaction to maintain the concentration of ATP; under normal circumstances, skeletal muscle concentrations of CP are four to six times higher than ATP
which type of muscle fibers contain higher concentrations of CP?
type II, therefore individuals with higher percentages of Type II fibers may be able to replenish ATP faster through the phosphagen system
what is the adenylate kinase reaction?
2ADP ATP + AMP
why is the adenylate kinase reaction important?
because a product of the adenylate kinase (myokinase) reaction is AMP, and AMP is a powerful stimulant of glycolysis
what are the reactions of the phosphagen system controlled by?
the law of mass action / mass action effect
what does the law of mass action / mass action effect control?
the reactions of the phosphagen system
what is a consequence of the phosphagen system having enzyme-mediated reactions?
the rate of product formation is greatly influenced by the concentrations of the reactants
as ATP is hydrolyzed to yield the energy necessary for exercise, there is a transient increase in what?
ADP concentrations (as well as Pi/phosphorus) in the sarcolemma
transient sarcolemma increases in ADP produces what effect?
increases rate of the creatine kinase and adenylate kinase reaction to replenish the ATP supply
for how long will the ATP hydrolysis to increase the rate of ADP concentrations in sarcolemma continue?
the process will continue until (a) the exercise ceases or (b) the intensity is low enough that it does not deplete CP stores and it allows glycolysis or the oxidative system to become the primary supplier of ATP and rephosphorylate the free creatine
after ATP hydrolysis ends and the exercise ceases or glycolysis/oxidative can become primary supplier of ATP (and rephosphorylate the free creatine), what occurs?
the sarcoplasmic concentration of ATP will remain steady or increase, which will slow down or reverse the directions of the creatine kinase and adenylate kinase reactions. as a result, these reactions/equations are often referred to as near-equilibrium reactions that proceed in a direction dictated by the concentrations of the reactants due to the law of mass action
why is the ATP resynthesis rate during glycolysis is not as rapid as with the single-step phosphagen system?
because the process of glycolysis involves multiple enzymatically catalyzed reactions
why is the capacity to produce ATP higher in the glycolytic system than in CP?
due to a larger supply of glycogen and glucose compared to phosphagenic
what is the end result of glycolysis?
pyruvate
what are the two ways pyruvate may proceed?
- Pyruvate can be converted to lactate in the sarcoplasm. 2. Pyruvate can be shuttled into the mitochondria.
how does ATP resynthesis occur at a faster rate when pyruvate is converted into lactate?
via the rapid regeneration of NAD+
what is a limitation of the ATP resynthesis (during pyruvate–>lactate) due to rapid regeneration of NAD+?
limited in duration due to the subsequent H+ production and resulting decrease in cytosolic pH; this process is sometimes called anaerobic glycolysis (or fast glycolysis)
what process is aerobic or slow glycolysis?
when pyruvate is shuttled into the mitochondria to undergo the Krebs cycle, the ATP resynthesis rate is slower because of the numerous reactions, but can occur for a longer duration if the exercise intensity is low enough.
At higher exercise intensities, what happens to pyruvate and NADH?
they will increase above what can be handled by pyruvate dehydrogenase and will then be converted into lactate and NAD+
why might the term aerobic/anaerobic glycolysis be inaccurate?
because glycolysis itself does not depend on oxygen
how do energy demands affect the use of pyruvate?
the fate of pyruvate is ultimately controlled by the energy demands within the cell. if energy demand is high and must be transferred quickly, as during resistance training, pyruvate is primarily converted to lactate for further support of anaerobic glycolysis. if energy demand is not as high and oxygen is present in sufficient quantities in the cell, pyruvate can be further oxidized in the mitochondria.
what catalyzes the formation of lactate from pyruvate?
the enzyme lactate dehydrogenase
what is a mistaken belief about the formation of lactate from pyruvate?
that the end result is the formation of lactic acid.
why is lactate, rather than lactic acid, the product of the lactate dehydrogenase reaction?
due to the physiological pH (i.e., near 7) and earlier steps in glycolysis that consume protons
what are the functions of proton (H+) accumulation during fatigue?
reduces the intracellular pH, inhibits glycolytic reactions, and directly interferes with muscle’s excitation-contraction coupling
how might proton (H+ accumulation interfere with excitation-contraction coupling
possibly by inhibiting calcium binding to troponin or by interfering with crossbridge recycling
how does the decrease in pH affect cell energy systems?
inhibits the enzymatic turnover rate of the cell’s energy systems
what is exercise-induced decrease in pH referred to?
metabolic acidosis, and may be responsible for much of the peripheral fatigue that occurs during exercise, although the role of metabolic acidosis in peripheral fatigue has been questioned recently
what other factors might play a role in peripheral fatigue?
increased interstitial K+ concentration and Pi that impairs Ca++ release
what other mechanisms might be responsible for H+ accumulation?
the simple hydrolysis of ATP
what alternate theory has been posed toward lactate?
that lactate itself actually works to decrease metabolic acidosis rather than accelerate it
how is lactate used as an energy substrate?
in Type I and cardiac muscle fibers and in gluconeogenesis—the formation of glucose from noncarbohydrate sources—during extended exercise and recovery
what is the resting concentration of lactate in blood and in muscle?
normally there is a low concentration of lactate in blood and muscle. The reported normal range of lactate concentration in blood is 0.5 to 2.2 mmol/L at rest and 0.5 to 2.2 mmol for each kilogram of wet muscle (muscle that has not been desiccated).
what factors affect lactate production?
lactate production increases with exercise intensity and appears to depend on muscle fiber type. maximal rate of lactate production for Type II muscle fibers is 0.5 mmol•g−1•s−1 and for Type I muscle is 0.25 mmol•g−1•s−1 (so, type II = double type I)
what might be the reason type II fibers produce so much more lactate than type I?
a higher concentration or activity of glycolytic enzymes than in Type I muscle fibers
what is the highest lactate accumulation, and at what point does severe fatigue occur?
highest possible concentration of lactate accumulation is not known, and severe fatigue may occur at blood concentrations between 20 and 25 mmol/L; another showed blood lactate concentrations greater than 30 mmol/L following multiple bouts of dynamic exercise (so, between 20->30 mmol/L)
what other factors affect lactate accumulation besides exercise intensity and fiber type?
exercise duration, state of training, and initial glycogen levels
what chemical state does blood lactate concentration reflect?
the net balance of lactate production and clearance as a result of bicarbonate (HCO3−) buffering
how does HCO3 − minimize the disruptive influence of H+ on ph?
by accepting the proton (H2CO3)
how do methods of oxidation involve lactate?
lactate can be transported in the blood to other muscle fibers to be oxidized or it can be cleared by oxidation within the muscle fiber in which it was produced
what is a hepatic method to clear lactate, what does it convert to, and what is this called?
lactate can be transported in the blood to the liver, where it is converted to glucose. this process is referred to as the Cori cycle
how long do blood lactate concentrations typically return to preexercise values?
within an hour after activity, depending on the duration and intensity of exercise, training status, and type of recovery (i.e., passive versus active)
what is the effect of light activity on lactate during the postexercise period?
clears lactate faster; light activity during the postexercise period has been shown to increase lactate clearance rates. (for example, an active recovery following a 200-yard (182.9 m) maximal-effort swim resulted in the greatest lactate clearance in comparison to a passive recovery in competitive swimmers. in addition, both aerobically trained and anaerobically trained athletes have faster lactate clearance rates than untrained people.)
when do peak blood concentrations occur?
approximately 5 minutes after the cessation of exercise, a delay frequently attributed to the time required to buffer and transport lactate from the tissue to the blood
given two scenarios: high intensity intermittent and low-intensity continuous, which would result in greater blood lactate accumulation?
greater following high-intensity, intermittent exercise (e.g. resistance training, sprinting) than following lower-intensity, continuous exercise
how would you infer that resistance training results in alterations of lactate response similar to those from aerobic training?
trained people experience lower blood lactate concentrations than untrained people when exercising at an absolute workload (same resistance); these alterations include (1) lower blood lactate concentration at a given workload in trained individuals (2) higher blood lactate concentrations in trained individuals during maximal exercise
what is the net reaction for glycolysis when pyruvate is converted to lactate?
Glucose + 2Pi + 2ADP –> 2Lactate + 2ATP + H2O
when would pyruvate not be converted into lactate?
when oxygen is present in sufficient quantities in the mitochondria; pyrvuate is then transported there along with two molecules of reduced nicotinamide adenine dinucleotide (NADH) produced during glycolytic reactions (reduced refers to the added hydrogen)
how does acetyl coenzyme A enter mitochondria?
from pyruvate, which converts to acetyl CoA through the pyruvate dehydrogenase complex
what is a consequence of the pyruvate –> acetyl CoA conversion?
the loss of a carbon as CO2, and acetyl-CoA can then enter the Krebs cycle for further ATP resynthesis
what happens after acetyl CoA enters the Krebs cycle?
the NADH (nicotinamide adenine dinucleotide) molecules enter the electron transport system, where they can also be used to resynthesize ATP
the net reaction for glycolysis when pyruvate is shuttled to the mitochondria may be summarized as what?
Glucose + 2Pi + 2ADP + 2NAD+ –> 2Pyruvate + 2ATP + 2NADH + 2H2O
what are the two primary mechanisms for resynthesizing ATP during metabolism?
- Substrate-level phosphorylation 2. Oxidative phosphorylation
what is phosphorylation?
the process of adding an inorganic phosphate (Pi) to another molecule
ADP + Pi –> ATP is what?
the phosphorylation of ADP to ATP
the resynthesis of ATP in the electron transport chain is also called what?
oxidative phosphorylation
substrate-level phosphorylation refers to what?
direct resynthesis of ATP from ADP during a single reaction in the metabolic pathways.
in glycolysis, what are the two steps that result in substrate-level phosphorylation of ADP to ATP?
I. 1,3-bisphosphoglycerate + ADP + Pi phosphoglycerate kinase –> 3-phosphoglycerate + ATP II. Phosphoenolpyruvate + ADP + Pi + Pyruvate kinase—> Pyruvate + ATP
what is the gross number of ATP molecules that are resynthesized as a result of substrate-level phosphorylation during glycolysis?
four
in glycolysis, the reaction that converts fructose-6-phosphate to fructose-1,6-bisphosphate is catalyzed by what?
the enzyme phosphofructokinase [PFK]
in glycolysis, what is required for the reaction that converts fructose-6-phosphate to fructose-1,6-bisphosphate to occur?
the hydrolysis of one ATP molecule.
in glycolysis, what are the two possible sources of glucose?
blood glucose and muscle glycogen
what are the requirements for when blood glucose enters the muscle cell?
- it must be phosphorylated to remain in the cell and to maintain the glucose concentration gradient 2. the phosphorylation of one molecule of blood glucose, which is catalyzed by hexokinase, also requires the hydrolysis of one ATP
how does glycogenolysis (breakdown of muscle glycogen) differ from blood glucose
due to the help of the enzyme glycogen phosphorylase, the glucose is already phosphorylated, and it does not require the hydrolysis of ATP
when glycolysis begins with one molecule of blood glucose, what is the net result?
two ATP molecules are used and four ATP are resynthesized, which results in a net resynthesis of two ATP molecules
what is the net resynthesis of ATP from muscle glycogen?
only one ATP is used and four ATP are resynthesized, which yields a net resynthesis of three ATP molecules
what is the function of stimulating the rate of glycolysis?
the rate of glycolysis is stimulated to increase during intense muscle actions by high concentrations of ADP, Pi, and ammonia and by a slight decrease in pH and AMP, all of which are signs of increased ATP hydrolysis and a need for energy
in contrast to the stimulation of glycolysis, how is glycolysis inhibited?
glycolysis is inhibited by markedly lower pH, ATP, CP, citrate, and free fatty acids, which are usually present at rest (a slight decrease in pH increases glycolysis, but if pH continues to decrease significantly it will inhibit the rate of glycolysis)
what more specific factors contribute to the regulation of glycolysis?
the concentrations and turnover rates of three important glycolytic enzymes: hexokinase, PFK, and pyruvate kinase
why are hexokinase, PFK, and pyruvate kinase regulatory enzymes in glycolysis?
each has important allosteric (meaning “other site”) binding sites
when does allosteric regulation occur?
when the end product of a reaction or series of reactions feeds back to regulate the turnover rate of key enzymes in the metabolic pathways. consequently, this process is also called end product regulation or feedback regulation
when does allosteric inhibition occur?
when an end product binds to the regulatory enzyme and decreases its turnover rate and slows product formation (in contrast, allosteric activation occurs when an “activator” binds with the enzyme and increases its turnover rate)
how is glucose-6-phosphate phosphorylated?
through catalyzation by hexokinase
how is hexokinase allosterically inhibited?
by the concentration of glucose-6-phosphate in the sarcoplasm
what are the consequences of the higher concentration of glucose-6-phosphate?
the higher the concentration of glucose-6-phosphate, the more hexokinase will be inhibited
how does glucose move around a cell once it’s been phosphorylated?
it can’t; the phosphorylation of glucose commits it to the cell so that it cannot leave
what is the function of the PFK reaction (fructose-6-phosphate → fructose 1,6-bisphosphate)?
commits the cell to metabolizing glucose rather than storing it as glycogen
why is phosphofructokinase the most important regulator of glycolysis?
because it is the rate-limiting step
how does the activity of the glycolytic pathway decrease?
through PFK activity
how does PFK activity decrease the activity of the glycolytic pathway?
reduces the conversion of fructose-6-phosphate to fructose 1,6-bisphosphate and, subsequently, decreases activity of the glycolytic pathway
ATP is an allosteric inhibitor of what?
phosphofructokinase
how does PFK activity decrease?
by elevated intracellular ATP concentrations
what is the function of adenosine triphosphate as it relates to the PFK and the glycolytic pathway?
Adenosine triphosphate is an allosteric inhibitor of PFK; therefore, as intracellular ATP concentrations rise, PFK activity decreases and reduces the conversion of fructose-6-phosphate to fructose 1,6-bisphosphate and, subsequently, decreases activity of the glycolytic pathway
what is an allosteric activator of PFK?
AMP, and it is also a powerful stimulator of glycolysis
what is another way to stimulate phosphofructokinase aside from AMP?
the ammonia produced during high-intensity exercise as a result of AMP or amino acid deamination (removing the amine group from the amino acid molecule) can also stimulate PFK
what is the final regulatory enzyme in glycolysis?
pyruvate
how does the conversion of phosphoenolpyruvate to pyruvate (the final step) occur?
through catalyzation by pyruvate kinase
what is pyruvate kinase allosterically inhibited and activated by?
allosterically inhibited by ATP and acetyl-CoA (the latter is a Krebs cycle intermediate), and allosterically activated by high concentrations of AMP and fructose-1,6bisphosphate
what is the ventilatory threshold?
the breaking point in the relationship between ventilation and VO2
what does the lactate threshold represent and correspond with?
a significantly increased reliance on anaerobic mechanisms for energy production to meet demand; the LT corresponds well with the ventilatory threshold (breaking point in the relationship between ventilation and VO2) and is often used as a marker of the anaerobic threshold.
when does the lactate threshold typically begin?
at 50% to 60% of maximal oxygen uptake in untrained individuals and at 70% to 80% in aerobically trained athletes
what is the onset of blood lactate accumulation?
a second increase in the rate of lactate accumulation at higher relative intensities of exercise.
when does the OBLA occur?
when the concentration of blood lactate reaches 4 mmol/L
breaks in the lactate accumulation curve may correspond to what?
points at which intermediate and large motor units are recruited during increasing exercise intensities (the muscle cells associated with large motor units are typically Type II fibers, which are particularly suited for anaerobic metabolism and lactate production)
what would cause lactate accumulation to occur later at a higher exercise intensity?
some studies suggest that training at intensities near or above the LT or OBLA pushes the LT and OBLA to the right
why might training near LT or OBLA cause them to occur later?
reduced catecholamine release at high exercise intensities and increased mitochondrial content that allows for greater production of ATP through aerobic mechanisms
what might allow an athlete to perform at higher percentages of maximal oxygen uptake?
shifting the LT or OBLA curves to the right
what are the primary energy substrates of the oxidative system?
primarily carbohydrate and fats as substrates
when does use of protein occur by the oxidative system?
during long-term starvation and long bouts (>90 minutes) of exercise
what is the fat/carb ratio for ATP production at rest?
at rest, approximately 70% of the ATP produced is derived from fats and 30% from carbohydrate
how does substrate use shift as the intensity of exercise increases?
there is a shift in substrate preference from fats to carbohydrate; during high-intensity aerobic exercise, almost 100% of the energy is derived from carbohydrate if an adequate supply is available, with only minimal contributions from fats and protein
during prolonged, submaximal, steady-state work, how does energy substrate use shift?
there is a gradual shift from carbohydrate back to fats, and to a very small extent protein
NADH stands for what?
nicotinamide adenine dinucleotide + hydrogen
FADH2 stands for what?
flavin adenine dinucleotide
substrate-level phosphorylation is in contrast to what other kind?
oxidative phosphorylation
when does oxidative metabolism of blood glucose and muscle glycogen begin?
with glycolysis.
when would pyruvate not be converted to lactate but transported to mitochondria?
if oxygen is present in sufficient quantities; it is converted into acetyl CoA then
the citric acid cycle is also known as what?
tricarboxylic acid cycle and the Krebs cycle
what continues the oxidation of the substrate from glycolysis, and produces two ATP indirectly from guanine triphosphate (GTP)?
the Krebs cycle / citric acid cycle, it does this via substrate-level phosphorylation for each molecule of glucose
before one molecule of glucose is produced, what is produced from two pyruvate molecules?
six molecules of NADH and two molecules of reduced flavin adenine dinucleotide (FADH2)
what is the function of hydrogen atoms in FADH2 and NADH?
these molecules transport hydrogen atoms to the ETC to be used to produce ATP from ADP
what is the ETC’s function of NADH and FADH2?
the ETC uses the NADH and FADH2 molecules to rephosphorylate ADP to ATP
how is a proton concentration gradient formed through hydrogen atoms?
the hydrogen atoms from NADH and FADH are passed down a series of electron carriers known as cytochromes to form a proton concentration gradient; cytochromes are proteins with heme bonded to them
what does the proton concentration gradient do?
provides the energy for ATP production, with oxygen serving as the final electron acceptor (resulting in the formation of water)
why would NADH and flavin adenine dinucleotide differ in their ability to produce ATP?
because they enter the ETC at different sites
what is the ATP produced by one molecule of NADH and one molecule of FADH2?
one molecule of NADH can produce three molecules of ATP; one molecule of FADH2 can produce two molecules of ATP
oxidative phosphorylation?
the process in which ATP is formed as a result of the transfer of electrons from NADH or FADH2 to O2 by a series of electron carriers
the oxidative system begins with what?
glycolysis, and includes the Krebs cycle and ETC
the oxidative system gets how much ATP from one molecule of blood glucose?
approximately 38 ATP
if the initiation of glycolysis by the oxidative system is in muscle glycogen, what is the net ATP production and why?
39, since the hexokinase reaction is not necessary with muscle glycogenolysis
how much ATP synthesis does oxidative phosphorylation account for compared to substrate level?
over 90% of ATP synthesis compared to substrate-level phosphorylation
how are fats used by the oxidative system?
triglycerides stored in fat cells can be broken down by an enzyme, hormone-sensitive lipase, to produce free fatty acids and glycerol
breaking down triglycerides to produce free fatty acids and glycerol does what?
releases a portion of the total free fatty acids from the fat cells into the blood, where they can circulate and enter muscle fibers and undergo oxidation
how would fat cells undergo oxidation?
by entering muscle fibers and circulating, which happens when the breakdown of triglycerides and glycerol releases a portion of the total free fatty acids from the fat cells into the blood
how are intramuscular sources of free fatty acids produced?
by storing limited quantities of triglycerides in the muscle along with a form of hormone-sensitive lipase
what happens when free fatty acids enter the mitochondria?
they undergo beta oxidation, a series of reactions in which the free fatty acids are broken down, resulting in the formation of acetyl-CoA and hydrogen protons
what happens when acetyl CoA and hydrogen protons are formed from the breakdown of free fatty acids?
the acetyl-CoA enters the Krebs cycle directly, and the hydrogen atoms are carried by NADH and FADH2 to the electron transport chain
what is the result of beta oxidation carrying NADH and FADH to the electron transport chain
hundreds of ATP molecules
how can 300 ATP molecules be yielded by the oxidative system
breakdown of a single triglyceride molecule containing three 16-carbon chain free fatty acids (palmitic acid) can be metabolized by beta oxidation to yield over 300 ATP molecules (>100 ATP per palmitic acid)
what is the oxidative potential of fats, proteins, and carbs?
proteins < carbs < fats, in this order (and fats are way higher)
what is protein oxidation?
the oxidative system’s breakdown of protein to its constituent amino acids by various metabolic processes
after protein is broken down into its constituent aminos by the oxidative system, how is it utilized?
converted into glucose (gluconeogenesis), pyruvate, or various Krebs cycle intermediates to produce ATP
is gluconeogenesis the production of glucose from protein?
not quite; gluconeogenesis is the metabolic process by which organisms produce glucose for catabolic reactions from non-carbohydrate precursors
what percentage of ATP do amino acids produce in short-term and long-term exercise?
minimal during short-term exercise but 3% to 18% of energy requirements during prolonged activity
what are the major amino acids that are oxidized in skeletal muscle?
primarily leucine, isoleucine, and valine (BCAAs); alanine, aspartate, and glutamate may also be used
how are nitrogenous waste products of amino acid degradation eliminated?
through the formation of urea and small amounts of ammonia
why is the elimination of nitrogenous waste products through ammonia significant?
because ammonia is toxic and is associated with fatigue
the rate-limiting step in the Krebs cycle is what?
the conversion of isocitrate to a-ketoglutarate, a reaction catalyzed by the enzyme isocitrate dehydrogenase
isocitrate dehydrogenase is stimulated and inhibited by what?
stimulated by ADP and allosterically inhibited by ATP
the reactions that produce NADH or FADH2 also influence what?
the regulation of the Krebs cycle
if NAD+ and FAD2+ are not available in sufficient quantities to accept hydrogen, what occurs?
the rate of the Krebs cycle is reduced
when GTP accumulates, what occurs?
the concentration of succinyl CoA increases, which inhibits the initial reaction (oxaloacetate + acetyl-CoA → citrate + CoA) of the Krebs cycle
what is the initial reaction of the Krebs cycle?
oxaloacetate + acetyl-CoA → citrate + CoA
the electron transport chain is inhibited and stimulated by what?
inhibited by ATP and stimulated by ADP
how is exercise intensity defined?
a level of muscular activity that can be quantified in terms of power (work performed per unit of time) output
what do short high intensity activities rely on?
fast glycolysis and phosphagen energy system
what do low intensity activities rely on?
slow glycolysis and the oxidative energy system
what is the range of time for athletic activities?
1 to 3 seconds (e.g., snatch and shot put) to more than 4 hours (long-distance triathlons and ultramarathons)
does intensity matter more for energy system contribution, or does duration?
the degree to which anaerobic and oxidative systems contribute to the energy being produced is determined primarily by the exercise intensity and secondarily by exercise duration
what are energy substrates?
molecules that provide starting materials for bioenergetic reactions
what are the energy substrates?
phosphagens (ATP and CP), glucose, glycogen, lactate, free fatty acids, and amino acids
fatigue is associated with depletion of what energy substrates?
phosphagens and glycogen; depletion of substrates such as free fatty acids, lactate, and amino acids typically does not occur to the extent that performance is limited
creatine phosphate can decrease how much during the first stage of high-intensity exercise of short and moderate duration (5-30 seconds)?
50-70%, and almost completely depleted as a result of very intense exercise to exhaustion
during experimentally induced fatigue, how might concentrations of ATP decrease from preexercise levels?
might only slightly or might up to 50% to 60%
how is intramuscular ATP concentration sustained during exercise?
as a consequence of CP depletion and the contribution of additional ATP from the myokinase reaction and oxidation of other energy sources, such as glycogen and free fatty acids
when does postexercise phosphagen repletion occur and how?
in a relatively short period; largely as a result of aerobic metabolism, although glycolysis can contribute to recovery after high-intensity exercise
complete postexercise resynthesis of ATP and CP occur when?
ATP: within 3 to 5 minutes, CP: within 8 minutes
how might aerobic endurance training affect resting concentrations of phosphagens?
may increase resting concentrations of phosphagens and decrease their rate of depletion at a given absolute submaximal power output but not at a relative (percentage of maximum) submaximal power output.
how have short-term studies of sprint and six months of resistance or explosive training affected resting phosphagens?
have not shown alterations in resting concentrations of phosphagens, but total phosphagen content can be larger following sprint training due to increases in muscle mass, and resistance training has been shown to increase the resting concentrations of phosphagens in the triceps brachii after five weeks of training
why might resting phosphagens increase in some resistance training studies but not others?
due to selective hypertrophy of Type II fibers, which can contain a higher phosphagen concentration than Type I fibers
how much glycogen is stored in the liver and muscle respectively?
70-100g in liver and 300-400g in muscle
can training and dietary manipulations influence resting glycogen?
yes, anaerobic training (including sprinting and resistance training) and stereotypical aerobic endurance training can increase resting muscle glycogen concentration with concomitantly appropriate nutrition.
during high intensity exercise, which source of glycogen (liver or muscle) is used more?
muscle, and the rate of glycogen depletion is related to exercise intensity
when would liver glycogen be more important?
during low-intensity exercise, and its contribution to metabolic processes increases with duration of exercise
how does exercise intensity affect glycogenolysis (the breakdown of glycogen) at 50%, 75%, and 100% of maximal oxygen uptake?
0.7, 1.4, and 3.4 mmol * kg^-1 * min^-1, respectively
when does glycogen become an increasingly important energy substrate?
at relative intensities of exercise above 60% of maximal oxygen uptake; the entire glycogen content of some muscle cells can become depleted during exercise
at what intensity are relatively constant glucose concentrations maintained and why?
below 50% of maximal O2 uptake, as a result of low muscle glucose uptake
when do blood glucose concentrations below 50% maximal O2 fall?
as duration >90min, but rarely below 2.8mmol/L; when duration >90, liver glycogen depletion may result in substantially decreased blood glucose
when might exercise-induced hypoglycemia occur?
when blood glucose <2.5 mmol/L
what does impact does blood glucose around 2.5 to 3.0 mmol/L have on carbohydrates?
reduced liver carbohydrate stores and causes decreased carbohydrate oxidation and eventual exhaustion
how much glycogen depletion does high intensity intermittent exercise cause?
20% to 60% with relatively few sets
phosphagen is primarily the limiting factor in exercise with high resistance and few sets, but when is glycogen the limiting factor?
resistance training with many total sets and larger total amounts of work
how might glycogen limit performance despite not being there?
selective muscle fiber glycogen depletion (more depletion in Type II fibers), which can also limit performance
how are intensity and glycogenolysis related?
generally the greater the intensity the faster the rate of glycogenolysis, BUT it appears that when the total work performed is equal the absolute amount of glycogen depletion is the same regardless of the intensity
repletion of muscle glycogen during recovery is accomplished how?
postexercise carbohydrate ingestion; repletion appears to be optimal if 0.7 to 3.0 g of carbohydrate per kilogram of body weight is ingested every 2 hours following exercise
ingesting 0.7 to 3.0 g of carbohydrate per kilogram of body weight will replenish muscle glycogen when and at what rate?
at 5 to 6 mmol/g of wet muscle mass per hour during the first 4 to 6 hours following exercise; muscle glycogen may be completely replenished within 24 hours, provided that sufficient carbohydrate is ingested
what factors would make glycogen take longer to replenish?
if the exercise has a high eccentric component (associated with exercise-induced muscle damage); more time may be required to completely replenish
what bioenergetic factors may be limiting factors?
for many activities glycogen; for primarily anaerobic activities, the effect of metabolic acidosis on limiting contractile force; increased intracellular inorganic phosphate, ammonia accumulation, increased ADP, and impaired calcium release from the sarcoplasmic reticulum
the ability of working tissues to use oxygen is called what?
oxygen uptake
how does oxygen uptake increase during low-intensity exercise with a constant power output?
oxygen uptake increases for the first few minutes until a steady state of uptake (oxygen demand equals oxygen consumption) is reached
what is oxygen deficit?
at the start of an exercise bout, some of the energy must be supplied through anaerobic mechanisms because the aerobic system responds slowly to the initial increase in the demand for energy; this anaerobic contribution to the total energy cost of exercise is the oxygen deficit
what terms exist for postexercise oxygen uptake?
oxygen debt, recovery O2, and xcess postexercise oxygen consumption (EPOC). EPOC is the oxygen uptake above resting values used to restore the body to the preexercise condition.
what is the relationship between oxygen deficit and EPOC?
the oxygen deficit may influence the size of the EPOC, but the two are not equal
when do aerobic mechanisms provide much of the energy for work?
if the exercise intensity is above the maximal oxygen uptake that a person can attain
if aerobic mechanisms are active, what can you infer about exercise duration?
it will decrease
what kind of sport requires maximal sustained effort to exhaustion or near-exhaustion?
competitive middle-distance sprints (400 m to 1,600 m)
what is the metabolic profile of most sports?
very similar to those of a series of high-intensity, constantor near-constant-effort exercise bouts interspersed with rest periods, such as American football, basketball, and hockey. In this type of exercise, the required exercise intensity (power output) that must be met during each exercise bout is much greater than the maximal power output that can be sustained using aerobic energy sources alone
what kind of benefit would aerobic power provide athletes in most sports?
increasing aerobic power through primarily aerobic endurance training – while simultaneously compromising or neglecting anaerobic power and anaerobic capacity – is of little benefit to athletes in these sports (it would be of little benefit for a baseball player to run miles during training rather than focusing on exercises that improve anaerobic power and capacity)
how does interval training work?
emphasizes bioenergetic adaptations for a more efficient energy transfer within the metabolic pathways by using predetermined intervals of exercise and rest periods (i.e., work-to-rest ratios)
what are the nine HIIT variables that can be manipulated to achieve the most precise metabolic specificity?
- intensity of the active portion of each duty cycle, 2. duration of the active portion of each duty cycle, 3. intensity of the recovery portion of each duty cycle, 4. duration of the recovery portion of each duty cycle, 5. number of duty cycles performed in each set, 6. number of sets, 7. rest time between sets, 8. recovery intensity between sets, and 9. mode of exercise for HIIT.
what factors should a S&C professional consider when designing a HIIT program?
aerobic/anaerobic durations and intensities, desired training adaptations are periodization, number of exercise sessions per day and week, how to juggle HIIT sessions in conjunction with other training sessions (e.g. team practice)
how would properly spaced work-to-rest intervals allow more work to be accomplished at higher exercise intensities with the same or
less fatigue than during continuous training at the same relative intensity? in one study, 2:1, 1:1, and 1:2 work-to-rest ratios were used with the same running intensity for a total duration of 30 minutes, however, the subjects were able to complete 4.14 miles (6.66 km), 3.11 miles (5.00 km), and 2.07 miles (3.33 km), respectively, all while working aerobic capacity in a manner similar to that in the continuous running condition
six sessions of four to seven 30-second maximum cycling efforts interspaced with 4 minutes of recovery is what work-to-rest ratio?
1:8
what improvements would interval training bring?
muscle oxidative potential, muscle buffering capacity, muscle glycogen content, and time-trial performance, as well as doubled aerobic endurance capacity
what’s the summary of guidelines for work-to-rest ratios?
few studies provide definitive guidelines; information of ratios between 40s:20s, 30s:30s, and 30s:20s is mixed. outcomes include total work, time to exhaustion, metabolic values (VO2Max/Lactate concentration).
what variables are considered when determining proper work to rest ratio?
knowledge of the time intervals, intensity of work, and recovery periods for each of the energy systems (e.g. complete resynthesis of CP may take up to 8 minutes, which suggests that short-duration, high-intensity exercise requires greater work-to-rest ratios due to the aerobic mechanisms that replete phosphagen stores)
what are the most important HIIT factors to consider?
the intensities and durations of the active and recovery portions of each duty cycle
how should HIIT sessions be optimized?
they should maximize the time spent at or near VO2max; specifically, the cumulative duration and intensity of the active portions of the duty cycles should equate to several minutes above 90% of VO2max
what are the beneficial adaptations of HIIT?
oxidative muscle fiber adaptation and myocardial hypertrophy. also increases in VO2max, proton buffering, glycogen content, anaerobic thresholds, time to exhaustion, and time-trial performance.
what is an example of HIIT’s comparable results?
one study reported equivalent improvements in muscle buffering capacity and glycogen content for HIIT at 250% of VO2peak during four to six 30-second cycling sprints compared to continuous cycling for 90 to 120 minutes at 65% of VO2peak over six total training sessions. 750 kJ cycling time trials decreased in both groups by 10.1% and 7.5% in the HIIT and long, slow endurance training groups, respectively. Thus, HIIT provided performance and physiological adaptations equivalent to those of long, slow endurance training, but in a time-efficient manner.
what is the pro/con of cross training / combination training?
relationships in power recovery in the first 10 seconds of a cycling sprint, the resynthesis of PCr, and endurance fitness (VO2max); however, aerobic endurance training may reduce anaerobic performance capabilities, anaerobic energy production capabilities, and hypertrophy/strength gains (studies are mixed on all of this)
what are the mechanisms by which combination training might inhibit gains?
may increase training volume to a level that may result in overtraining in comparison to aerobic and anaerobic training alone; also might be by (a) decreasing rapid voluntary activation, (b) chronically lower muscle glycogen levels that can limit intracellular signaling responses during resistance training, and (c) and fiber type transition to slow-twitch fibers
