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Transcript of Energía(/(ATP( Aminoácidos( - vet.unicen.edu.ar · Fuentes(de(ATP(durantela...
MÚSCULO Trabajo –> Movimiento
Termogénesis
Reserva (depósito) de aminoácidos (Nitrógeno)
EsqueléGco (ME)
Diversidad histológica y en la fisiología de la contracción
Contracción de las miofibrillas
Síntesis y degradación de proteínas (recambio proteico)
Equilibrio iónico (Na+, K+) de membranas
Energía / ATP
Crecimiento -‐> Retención de proteínas (Nitrógeno)
Aminoácidos
Liso (ML) Cardíaco (MC) Depósito (USO LOCAL) de glucosa como glucógeno
Síntesis y degradación de glucógeno
Glucosa
OXIDACIÓN DE CARBOHIDRATOS Y LÍPIDOS
Capacidad oxidaGva: Gpos de fibras musculares y músculos
LENTAS, OXIDATIVAS
RÁPIDAS, OXIDATIVAS Y GLICOLÍTICAS
RÁPIDAS, GLICOLÍTICAS
FIBRAS
LENTOS ROJOS
RÁPIDOS ROJOS
RÁPIDOS BLANCOS
MÚSCULOS O2
O2
ESPECIES
CABALLOS Y OVEJAS VACAS Y CONEJOS
CERDOS
POLLOS
O2
O2
GLUCOSA
ÁCIDOS GRASOS
CUERPOS CETÓNICOS ACETATO
Krebs H+ H+
ATP
CO2 CALOR
Recambio proteico
Temblor
Movimiento Postura
Mantenimiento celular
Glucogenogénesis Glucogenolisis
CALOR
CALOR
Aporte O2 ≥ Requerimientos O2 (ME, ML, MC)
G6P
GLUCÓGENO
PIRUVATO LACTATO
ATP
Movimientos de alta demanda de energia por unidad de Gempo
Aporte O2 < Requerimientos O2 (ME)
O2
CALOR
GLUCÓGENO MUSCULAR LACTATO (MC)
HÍGADO
GLUCOSA
CORAZÓN
CO2
ATP
PIR
G6P
GLUCÓGENO
LP-‐TAG AGL ACETATO GLUCOSA
AGL
CETÓNICOS
GLUT4
AGL ACIL-‐CoA
ACoA
ACIL-‐CoA
ATP
FOx
H+
ADP
H++ e-‐
ATP
ATP
AMP G6P
PIR
Krebs AOA PIR
GLUCÓGENO
LAC
ATP
LAC
[ATP] EN MÚSCULO < 1 SEGUNDO DE CONTRACCIÓN
CreaGna-‐P
ADP
CreaGna
ATP CREATINA-‐P
25 mM
ATP 4mM
∆G’= -‐12 KJ/mol
¿Cuál es el sustrato que manGene la contracción en los primeros momentos?
449
16 CHAPTER
O U T L I N E
16.1 Glycolysis Is an Energy-Conversion Pathway in Many Organisms
16.2 The Glycolytic Pathway Is Tightly Controlled
16.3 Glucose Can Be Synthesized from Noncarbohydrate Precursors
16.4 Gluconeogenesis and Glycolysis Are Reciprocally Regulated
Glycolysis and Gluconeogenesis
The first metabolic pathway that we encounter is glycolysis, an ancient pathway employed by a host of organisms. Glycolysis is the sequence of
reactions that metabolizes one molecule of glucose to two molecules of pyruvate with the concomitant net production of two molecules of ATP. This process is anaerobic (i.e., it does not require O 2 ) because it evolved before substantial amounts of oxygen accumulated in the atmosphere. Pyruvate can be further processed anaerobically to lactate ( lactic acid fermentation ) or ethanol ( alco-holic fermentation ) . Under aerobic conditions, pyruvate can be completely oxidized to CO 2 , generating much more ATP, as will be described in chapters 17 and 18. Figure 16.1 shows some possible fates of pyruvate pro-duced by glycolysis.
Because glucose is such a precious fuel, metabolic products, such as pyruvate and lactate, are salvaged to synthesize glucose in the process of gluconeogenesis. Although glycolysis and gluconeogenesis have some enzymes in common, the two pathways are not simply the reverse of each other. In particular, the highly exergonic, irreversible steps of glycolysis are bypassed in gluconeogenesis. The two pathways are reciprocally regulated so that glycolysis and gluconeogenesis do not take place simultaneously in the same cell to a significant extent.
Usain Bolt sprints to a win in the 200-meter finals at the Olympics in London in 2012. Glucose metabolism can generate the ATP to power muscle contraction. During a sprint, when the ATP needs outpace oxygen delivery, as would be the case for Bolt, glucose is metabolized to lactate. When oxygen delivery is adequate, glucose is metabolized more efficiently to carbon dioxide and water. [Christophe Karaba/epa/Corbis.]
A. Low O2 (last seconds of a sprint)
B. Normal (long slow run)
Muscle fiber
Glucose Pyruvate
CytoplasmMitochondrion
ATP
ATP
ALactate
BCO2 + H2O
Glycolysis
GlycolysisDerived from the Greek stem glyk-, “sweet,” and the word lysis, “dissolution.”
CreaGna ADP
ATP
Contracción muscular
A
B
C
DP-‐CreaGna
O2
Fuentes de ATP durante la contracción muscular en el ejercicio.
Glucosa Piruvato Lactato
Citoplasma Mitocondria
Fibra muscular
Glicólisis AGL
D
Fuentes de ATP durante la contracción muscular en el ejercicio.
The amount of ATP in muscle suffices to sustain contractile activity for less than a second. Creatine phosphate in vertebrate muscle serves as a res-ervoir of high-potential phosphoryl groups that can be readily transferred to ADP. Indeed, we use creatine phosphate to regenerate ATP from ADP every time that we exercise strenuously. This reaction is catalyzed by cre-atine kinase . Creatine kinase
Creatine phosphate 1 ADP ! ATP 1 creatine
At pH 7, the standard free energy of hydrolysis of creatine phosphate is 2 43.1 kJ mol 2 1 ( 2 10.3 kcal mol 2 1 ), compared with 2 30.5 kJ mol 2 1 ( 2 7.3 kcal mol 2 1 ) for ATP. Hence, the standard free-energy change in forming ATP from creatine phosphate is 2 12.6 kJ mol 2 1 ( 2 3.0 kcal mol 2 1 ), which corresponds to an equilibrium constant of 162.
Keq 5
[ATP][creatine][ADP][creatine phosphate]
5 e2¢G89y2.47 5 e12.6y2.47 5 162
In resting muscle, typical concentrations of these metabolites are [ATP] 5 4 mM, [ADP] 5 0.013 mM, [creatine phosphate] 5 25 mM, and [cre-atine] 5 13 mM. Because of its abundance and high phosphoryl-transfer potential relative to that of ATP, creatine phosphate is a highly effective phosphoryl buffer. Indeed, creatine phosphate is the major source of phosphoryl groups for ATP regeneration for a runner during the first 4 seconds of a 100-meter sprint. The fact that creatine phosphate can replenish ATP pools is the basis of the use of creatine as a dietary supple-ment by athletes in sports requiring short bursts of intense activity. After the creatine phosphate pool is depleted, ATP must be generated through metabolism (Figure 15.7).
TABLE 15.1 Standard free energies of hydrolysis of some phosphorylated compounds
Compound kJ mol21 kcal mol21
Phosphoenolpyruvate 261.9 214.81,3-Bisphosphoglycerate 249.4 211.8Creatine phosphate 243.1 210.3ATP (to ADP) 230.5 2 7.3Glucose 1-phosphate 220.9 2 5.0Pyrophosphate 219.3 2 4.6Glucose 6-phosphate 213.8 2 3.3Glycerol 3-phosphate 2 9.2 2 2.2
FIGURE 15.7 Sources of ATP during exercise. In the initial seconds, exercise is powered by existing high-phosphoryl-transfer compounds (ATP and creatine phosphate). Subsequently, the ATP must be regenerated by metabolic pathways.
ATP
Creatine phosphateAnaerobic
metabolism(Chapter 16)
Aerobic metabolism(Chapters 17 and 18)
Seconds Hours
Ener
gy
Minutes
43115.2 ATP: Currency of Free Energy
EnergÍa para la contracción
Fosfato de CreaWna
Metabolismo aeróbico
Metabolismo anaeróbico
GLUT4
INSULINA y EJERCICIO
Ejercicio
GLUT4 Insulin
Na Na Na
CAPTACIÓN DE GLUCOSA
DESCANSO
POSTPRANDIAL
GLUCÓGENO
GS
G6P
PIR
ACoA
CO2
FFK
PDH
AGL ACIL-‐CoA
ACIL-‐CoA
ATP
FOx
H+
ADP
H++ e-‐
ATP Krebs
MAL-‐CoA ACoA
ACAC2
-‐
-‐
ICDH
+
DESCANSO
GLUCÓGENO
GS
G6P
PIR
ACoA
CO2
FFK
PDH
AGL ACIL-‐CoA
ACIL-‐CoA
ATP
FOx
H+
ADP
H++ e-‐
ATP Krebs
MAL-‐CoA ACoA
ACAC2
-‐
-‐
EJERCICIO
-‐
ICDH
t/D
ATP/ADP
t/D
+
t/D
+
+
+
+
EJERCICIO
GLUCÓGENO
GS
G6P
PIR
ACoA
CO2
FFK
PDH
AGL ACIL-‐CoA
ACIL-‐CoA
ATP
FOx
H+
ADP
H++ e-‐
ATP Krebs
MAL-‐CoA ACoA
ACAC2
-‐
-‐
EJERCICIO
-‐
ICDH
t/D
ATP/ADP
t/D
+
t/D
+
+
+ ADRENALINA
+
+
ADRENALINA
+
EJERCICIO
LIPÓLISIS
GLUCÓGENO
GS
G6P
PIR
ACoA
CO2
FFK
PDH
AGL ACIL-‐CoA
ACIL-‐CoA
ATP
FOx
H+
ADP
H++ e-‐
ATP Krebs
MAL-‐CoA ACoA
ACAC2
-‐
INSULINA
-‐
ICDH
+
+
LUEGO DEL EJERCICIO + CONSUMO DE CARBOHIDRATOS
-‐
GLUCÓGENO
GS
G6P
PIR
ACoA
CO2
FFK
PDH
AGL ACIL-‐CoA
ACIL-‐CoA
ATP
FOx
H+
ADP
H++ e-‐
ATP Krebs
MAL-‐CoA ACoA
ACAC2
-‐
-‐
ICDH
PERÍODO POSTASORTIVO
GLUCAGON
+
LIPÓLISIS
100
Descanso Liviano
25% VO2 max 2-‐3 min
Contribución a la oxidación (%)
50
AGL CETÓNICOS GLUCOSA
Liviano 25% VO2 max
60 min
Moderado 65% VO2 max
60 min
Intenso 85% VO2 max
30 min
Intenso 85% VO2 max 60-‐120 min
OXIDACIÓN DE LÍPIDOS Y CARBOHIDRATOS DURANTE EL EJERCICIO EN HUMANOS
J.F. Hocquette et al. / Livestock Production Science 56 (1998) 115–143 119
Glucose is extracted by muscle through facilitated Within resting muscles, glucose can follow severaldiffusion via transmembrane glucose transporters, metabolic pathways: (1) direct oxidation, (2) gly-mainly the insulin-sensitive isoform (glucose trans- colysis to L-lactate, which is then released to theporter No. 4: GLUT4). The rate-limiting role of circulation, (3) glycogen synthesis, which constitutesglucose transport in glucose homeostasis and a major fate of glucose (Pethick, 1984) and (4) fattyglycogen deposition within muscle cells was demon- acid synthesis, in particular in intramuscular adiposestrated by several in vivo and in vitro approaches tissue (Smith and Crouse, 1984). At steady state, the(for review, see Hocquette et al., 1996a). The glucose uptake by muscle (corrected for lactate andmajority of GLUT4 is inside the cell in the basal pyruvate output) if completely oxidized could con-state, from where it can be rapidly translocated to the tribute 31–57% of resting muscle energy expenditureplasma membrane following stimulation either by in sheep (Pethick, 1984, Fig. 3), 31–41% in humansinsulin or by exercise. The regulation of GLUT4 (Elia et al., 1988; Mandarino et al., 1993) and
14expression and activity in skeletal muscles differs probably more in pigs (Lindsay, 1981). Using C-among cattle, goats (Hocquette et al., 1995), sheep glucose tracers, only 18–26% of extracted glucose in(Sasaki, 1994), pigs (Hocquette et al., 1996b) and sheep is promptly oxidized to CO with the remain-2rats (for reviews, see Girard et al., 1992; Hocquette der of the glucose carbon probably passing throughet al., 1996a). The recent cloning of GLUT4 probes pools which turnover more slowly (glycogen, pro-in pigs (Chiu et al., 1994), sheep (Bennett et al., tein) before being oxidized. Glycogen can be mobil-1995) and cattle (Abe et al., 1997) will allow further ized either for glycolysis or for oxidative catabolism.understanding of the regulation of glucose transport Glycolysis is controlled by PFK activity, which isin domestic animals. inhibited by an excess of ATP or lactate (Regen et
Fig. 3. The maximum potential contribution of metabolites to oxidation in resting or exercising hindlimb skeletal muscle of sheep, assumingcomplete oxidation. The absolute utilisation of nutrients was calculated using data based on arterio–venous measurements after havingaccounted for recycled metabolites. Then, the respective contribution (in %) of each energy-yielding substrate was estimated as the ratio ofnutrient use to total oxygen consumption on an energy basis. The estimates represent the mean of the exercise period (Pethick, 1984; Pethicket al., 1987; Harman, 1991; Harman and Pethick, 1994).
USO DE SUSTRATOS ENERGÉTICO POR EL MÚSCULO EN OVEJAS
AGL
CETÓNICOS
ACETATO
GLUCOSA
NIVEL DE EJERCICIO
Descanso
Contribución a la oxidación (%)
(103 mol of ATP at best) are insufficient to provide the 150 mol of ATP needed for this grueling event. Much larger quantities of ATP can be obtained by the oxidation of fatty acids derived from the breakdown of fat in adipose tissue, but the maximal rate of ATP generation is slower yet than that of glycogen oxidation and is more than 10-fold slower than that with creatine phosphate. Thus, ATP is generated much more slowly from high-capacity stores than from limited ones , accounting for the different velocities of anaerobic and aerobic events. Fats are rapidly consumed in activities such as distance running, explaining why extended aerobic exercise is beneficial for people who are insulin resistant.
Is i t possible to determine the contribution of each fuel as a function of exercise intensity? The percentage contribution of each fuel can be measured with the use of a respirometer, which measures the respiratory quotient (RQ), the ratio of CO 2 produced to O 2 consumed. Consider the complete combustion of glucose :
C6H12O6 1 6 O2 ¡ 6 CO2 1 6 H2O Glucose
The RQ for glucose is 1. Now consider the oxidation of a typical fatty acid , palmitate :
C16H32O2 1 23 O2 ¡ 16 CO2 1 16 H2O Palmitate
The RQ for palmitate oxidation is 0.7. Thus, as aerobic exercise intensity increases, the RQ will rise from 0.7 (only fats are used as fuel) to 1.0 (only glucose is used as fuel). Between these values, a mixture of fuels is used (Figure 27.12).
What is the optimal mix of fuels for use during a marathon? As suggested above, this is a complex question that varies with the athlete and level of train-ing. Studies have shown that, when muscle glycogen has been depleted, the power output of the muscle falls to approximately 50% of maximum. Power output decreases despite the fact that ample supplies of fat are available, sug-gesting that fats can supply only about 50% of maximal aerobic effort. Indeed, depletion of glycogen stores during a race is referred to as “bonking” or “hit-ting the wall , ” with the result that the athlete must greatly reduce the pace.
How is an optimal mix of these fuels achieved? A low blood-sugar level leads to a high glucagon/insulin ratio, which in turn mobilizes fatty acids from adipose tissue . Fatty acids readily enter muscle, where they are degraded by b oxidation to acetyl CoA and then to CO 2 . The elevated acetyl CoA level decreases the activity of the pyruvate dehydrogenase complex to block the conversion of pyruvate into acetyl CoA. Hence, fatty acid oxidation decreases the funneling of glucose into the citric acid cycle and oxidative phosphorylation. Glucose is spared so that just enough remains available at the end of the marathon to increase the pace as the finish line draws near . The simulta-neous use of both fuels gives a higher mean velocity than would be attained if glycogen were totally consumed before the start of fatty acid oxidation. It is important to bear in mind that fuel utilization is only one of many factors that determine running ability.
If carbohydrate-rich meals are consumed after glycogen depletion, glycogen stores are rapidly restored. In addition, glycogen synthesis continues during the consumption of carbohydrate-rich meals, increasing glycogen stores far above normal. This phenomenon is called “super compen-sation” or, more commonly, carbo-loading.
81527.4 Effects of Exercise
RQ
A
B
Maximal aerobiceffort
Light aerobiceffort
100%
Carbohydrate utilization
50%
0%
100%
Fat u
tiliz
atio
n
50%
0%
1.0
0.9
0.8
0.7
FIGURE 27.12 An idealized representation of fuels use as a function of aerobic exercise intensity. (A) With increased exercise intensity, the use of fats as fuels falls as the utilization of glucose increases. (B) The respiratory quotient (RQ) measures the alteration in fuel use.
(103 mol of ATP at best) are insufficient to provide the 150 mol of ATP needed for this grueling event. Much larger quantities of ATP can be obtained by the oxidation of fatty acids derived from the breakdown of fat in adipose tissue, but the maximal rate of ATP generation is slower yet than that of glycogen oxidation and is more than 10-fold slower than that with creatine phosphate. Thus, ATP is generated much more slowly from high-capacity stores than from limited ones , accounting for the different velocities of anaerobic and aerobic events. Fats are rapidly consumed in activities such as distance running, explaining why extended aerobic exercise is beneficial for people who are insulin resistant.
Is i t possible to determine the contribution of each fuel as a function of exercise intensity? The percentage contribution of each fuel can be measured with the use of a respirometer, which measures the respiratory quotient (RQ), the ratio of CO 2 produced to O 2 consumed. Consider the complete combustion of glucose :
C6H12O6 1 6 O2 ¡ 6 CO2 1 6 H2O Glucose
The RQ for glucose is 1. Now consider the oxidation of a typical fatty acid , palmitate :
C16H32O2 1 23 O2 ¡ 16 CO2 1 16 H2O Palmitate
The RQ for palmitate oxidation is 0.7. Thus, as aerobic exercise intensity increases, the RQ will rise from 0.7 (only fats are used as fuel) to 1.0 (only glucose is used as fuel). Between these values, a mixture of fuels is used (Figure 27.12).
What is the optimal mix of fuels for use during a marathon? As suggested above, this is a complex question that varies with the athlete and level of train-ing. Studies have shown that, when muscle glycogen has been depleted, the power output of the muscle falls to approximately 50% of maximum. Power output decreases despite the fact that ample supplies of fat are available, sug-gesting that fats can supply only about 50% of maximal aerobic effort. Indeed, depletion of glycogen stores during a race is referred to as “bonking” or “hit-ting the wall , ” with the result that the athlete must greatly reduce the pace.
How is an optimal mix of these fuels achieved? A low blood-sugar level leads to a high glucagon/insulin ratio, which in turn mobilizes fatty acids from adipose tissue . Fatty acids readily enter muscle, where they are degraded by b oxidation to acetyl CoA and then to CO 2 . The elevated acetyl CoA level decreases the activity of the pyruvate dehydrogenase complex to block the conversion of pyruvate into acetyl CoA. Hence, fatty acid oxidation decreases the funneling of glucose into the citric acid cycle and oxidative phosphorylation. Glucose is spared so that just enough remains available at the end of the marathon to increase the pace as the finish line draws near . The simulta-neous use of both fuels gives a higher mean velocity than would be attained if glycogen were totally consumed before the start of fatty acid oxidation. It is important to bear in mind that fuel utilization is only one of many factors that determine running ability.
If carbohydrate-rich meals are consumed after glycogen depletion, glycogen stores are rapidly restored. In addition, glycogen synthesis continues during the consumption of carbohydrate-rich meals, increasing glycogen stores far above normal. This phenomenon is called “super compen-sation” or, more commonly, carbo-loading.
81527.4 Effects of Exercise
RQ
A
B
Maximal aerobiceffort
Light aerobiceffort
100%
Carbohydrate utilization
50%
0%
100%
Fat u
tiliz
atio
n
50%
0%
1.0
0.9
0.8
0.7
FIGURE 27.12 An idealized representation of fuels use as a function of aerobic exercise intensity. (A) With increased exercise intensity, the use of fats as fuels falls as the utilization of glucose increases. (B) The respiratory quotient (RQ) measures the alteration in fuel use.
RQ= CO2/O2 = 1
RQ= CO2/O2 = 0,7
¿QUÉ SUSTRATO OXIDAMOS?
GLUCOSA
PALMÍTICO
(103 mol of ATP at best) are insufficient to provide the 150 mol of ATP needed for this grueling event. Much larger quantities of ATP can be obtained by the oxidation of fatty acids derived from the breakdown of fat in adipose tissue, but the maximal rate of ATP generation is slower yet than that of glycogen oxidation and is more than 10-fold slower than that with creatine phosphate. Thus, ATP is generated much more slowly from high-capacity stores than from limited ones , accounting for the different velocities of anaerobic and aerobic events. Fats are rapidly consumed in activities such as distance running, explaining why extended aerobic exercise is beneficial for people who are insulin resistant.
Is i t possible to determine the contribution of each fuel as a function of exercise intensity? The percentage contribution of each fuel can be measured with the use of a respirometer, which measures the respiratory quotient (RQ), the ratio of CO 2 produced to O 2 consumed. Consider the complete combustion of glucose :
C6H12O6 1 6 O2 ¡ 6 CO2 1 6 H2O Glucose
The RQ for glucose is 1. Now consider the oxidation of a typical fatty acid , palmitate :
C16H32O2 1 23 O2 ¡ 16 CO2 1 16 H2O Palmitate
The RQ for palmitate oxidation is 0.7. Thus, as aerobic exercise intensity increases, the RQ will rise from 0.7 (only fats are used as fuel) to 1.0 (only glucose is used as fuel). Between these values, a mixture of fuels is used (Figure 27.12).
What is the optimal mix of fuels for use during a marathon? As suggested above, this is a complex question that varies with the athlete and level of train-ing. Studies have shown that, when muscle glycogen has been depleted, the power output of the muscle falls to approximately 50% of maximum. Power output decreases despite the fact that ample supplies of fat are available, sug-gesting that fats can supply only about 50% of maximal aerobic effort. Indeed, depletion of glycogen stores during a race is referred to as “bonking” or “hit-ting the wall , ” with the result that the athlete must greatly reduce the pace.
How is an optimal mix of these fuels achieved? A low blood-sugar level leads to a high glucagon/insulin ratio, which in turn mobilizes fatty acids from adipose tissue . Fatty acids readily enter muscle, where they are degraded by b oxidation to acetyl CoA and then to CO 2 . The elevated acetyl CoA level decreases the activity of the pyruvate dehydrogenase complex to block the conversion of pyruvate into acetyl CoA. Hence, fatty acid oxidation decreases the funneling of glucose into the citric acid cycle and oxidative phosphorylation. Glucose is spared so that just enough remains available at the end of the marathon to increase the pace as the finish line draws near . The simulta-neous use of both fuels gives a higher mean velocity than would be attained if glycogen were totally consumed before the start of fatty acid oxidation. It is important to bear in mind that fuel utilization is only one of many factors that determine running ability.
If carbohydrate-rich meals are consumed after glycogen depletion, glycogen stores are rapidly restored. In addition, glycogen synthesis continues during the consumption of carbohydrate-rich meals, increasing glycogen stores far above normal. This phenomenon is called “super compen-sation” or, more commonly, carbo-loading.
81527.4 Effects of Exercise
RQ
A
B
Maximal aerobiceffort
Light aerobiceffort
100%
Carbohydrate utilization50%
0%
100%
Fat u
tiliz
atio
n
50%
0%
1.0
0.9
0.8
0.7
FIGURE 27.12 An idealized representation of fuels use as a function of aerobic exercise intensity. (A) With increased exercise intensity, the use of fats as fuels falls as the utilization of glucose increases. (B) The respiratory quotient (RQ) measures the alteration in fuel use.
GRASAS CARBOHIDRATOS
Trabajo aeróbico liviano Trabajo aeróbico intenso
(ejempl: 25% VO2 max) (ejemplo: 85% VO2 max)
SÍNTESIS Y DEGRADACION DE PROTEÍNAS EN MÚSCULO
PROTEÍNAS
Síntesis
Degradación
AMINOÁCIDOS
ATP ADP
AA
SÍNTESIS Y DEGRADACION DE PROTEÍNAS EN MÚSCULO
PROTEÍNAS
Síntesis
Degradación
AMINOÁCIDOS
INSULINA
ATP ADP
AA
+
-‐
INSULINA
Roedores jóvenes y lechones
Rumiantes Humanos
POSTPRANDIAL
SÍNTESIS Y DEGRADACION DE PROTEÍNAS EN MÚSCULO
PROTEÍNAS
Síntesis
Degradación
AMINOÁCIDOS
INSULINA
ATP ADP
AA
POSTABSORPTIVO
AYUNO
SÍNTESIS Y DEGRADACION DE PROTEÍNAS EN MÚSCULO
PROTEÍNAS
Síntesis
Degradación
AMINOÁCIDOS
ATP ADP
AA
+
HORMONA DE CRECIMIENTO
+
LARGO PLAZO CRECIMIENTO