Study/data Re Carbs & Insulin Post Work-Out.
Carbless PWO - "insulin sensitivity and insulin
Background (Post-Exercise state)
Under ordinary circumstances ingestion of a meal induces a transient increase in muscle protein synthesis (MPS) followed by muscle protein breakdown (MPB). In this manner tissue is maintained but there is no net protein synthesis thus no anabolism.
The general consensus from research in this area is that exercise induces protein degradation as well as protein synthesis. Ingestion of protein during this time period strongly tips the balance of degradation versus synthesis to that of overall protein synthesis.
"The metabolic basis for skeletal muscle growth lies in the relationship of muscle protein synthesis to muscle protein breakdown. Muscle hypertrophy occurs only from net protein synthesis; that is, when muscle protein synthesis exceeds breakdown.... resistance exercise, has a profound effect on muscle protein metabolism, often resulting in muscle growth. Acutely, resistance exercise may result in improved muscle protein balance, but, in the absence of food intake, the balance remains negative (i.e., catabolic). ...Amino acid availability is critical to the control of muscle protein metabolism. Thus, a meal or a supplement containing protein or amino acids will influence muscle protein. ...[and if] ingested after exercise should result in muscle anabolism." - Tipton, Kevin, et al., Ingestion of Casein and Whey Proteins Result in Muscle Anabolism after Resistance Exercise, Med Sci Sports Exerc. 2004 Dec;36(12):2073-81
So the message is simply that if you workout and you eat you will have net protein synthesis. Lets take food completely out of the equation and look at what happens after you workout.
If a special window is created how long does it last?
The same authors (Tipton, et al.) from the previous study years prior did something interesting. They examined1 the muscle protein synthesis rate and the muscle protein breakdown rate over the 48 hour period following resistance exercise. They discovered that exercise significantly increased the synthesis rate for a period exceeding 48 hours. The muscle protein synthesis rate in their experiment was measured as 112% above base at the 3 hour post-exercise time period; 65% above base at the 24 hour post-exercise time period and 34% above base at the 48 hour post-exercise time period.
They found that muscle protein breakdown rate was also increased 31% at 3 hours post-exercise and 18% 24 hours post-exercise but had returned to baseline at the 48 hours post-exercise time period.
Based on their observations they concluded that the act of resitance exercise results in an increase in muscle net protein balance that persists beyond 48 hours.
But what they did that was so interesting to me is that their study was undertaken in the absence of food. Exercise was performed and subsequent measurements were taken in the fasted state. The authors mentioned that other studies did not find as long a post-exercise increase in muscle protein synthesis rate as they did. In particular in the other differing study the increase in the rate of protein synthesis was only elevated 14% above baseline at 36 hours post-exercise leading those authors to conclude that "muscle protein synthesis rate was initially increased but then sharply decreased at the 36 hour post-exercise time period." This contrasts with the findings of the aforementioned Tipton study which still found protein synthesis rate strongly elevate (34%) 48 hours post-exercise.
So why the difference between studies?
In my opinion the difference is attributable to the fact that the subjects of the other study where in the fed-state at all measured time periods. The fed state included carbohydrates, protein and fats.
This is significant enough in my opinion to underscore. The rate of protein synthesis is strongly elevated throughout the 48 hour period following exercise and beyond in the absence of food. With the ingestion of food the rate of protein synthesis begins with a strong elevation but markedly declines after the first day and is practically over by the 36 hour mark. Extrapolating a bit it appears that the 60 hour mark w/o food is equivalent to the 36 hour mark with food. This amounts to a 66% more prolonged time period of elevated protein synthesis.
We can not banish protein from our post workout time period because we need the substrate. It is nice to have increased the rate of protein synthesis but without the raw materials that come from ingested protein (i.e. amino acids) there will be no increase in the amount of muscle protein synthesized. No we can not banish protein...
...so the questions becomes can we banish carbohydrates in the post-workout environment and accrue an overall benefit to muscle anabolism? Will we accrue a net benefit to a reduction in nutrient storage in adipose tissue? Is it possible that carbohydrates are the component of "food" that is responsible for a less prolonged elevated protein synthesis rate?
Before we can even begin to explore those types of questions we need to first examine specifically the increase in insulin sensitivity and insulin responsiveness that occurs immediately after exercise and how the timing of carbohydrate ingestion can determine the extent to which an increase in insulin sensitivity and insulin responsiveness remains active in muscle tissue.
1 - Mixed Muscle Protein Synthesis And Breakdown After Resistance Exercise In Humans, Stuart M. Phillips, Kevin D. Tipton, Asle Aarsland, Steven E. Wolf, And Robert R. Wolfe, Am. J. Physiol. 273 (Endocrinol. Metab. 36): E99- El07, 1997.
Exercise induces an increase in muscle insulin sensitivity and may induce an increase in muscle insulin responsiveness.
The action of insulin on glucose transport is described in the literature in terms of two distinct concepts: insulin sensitivity and insulin responsiveness. 2 These two concepts can also can be used to more loosely describe the actions of insulin on muscle tissue as they relate to increasing transport of amino acids and increasing the activity of insulin within muscle. They are not used to described an enhanced binding affinity for the insulin molecule to the receptor. This tighter binding is a distinct and further method the body utilizes to increase the actions engendered by insulin and it does so following a fast.
Insulin sensitivity is defined as the "concentration of insulin required to cause 50% of its maximal effect on glucose transport. An increase in insulin sensitivity results in a shift in the insulin dose-response curve to the left with a decrease in the insulin concentration required to cause 50% of the maximal response." 3
Insulin responsiveness is defined as the "increase in glucose transport induced by a maximally effective insulin concentration. Thus an increase in insulin responsiveness results in a larger increase in glucose transport in response to a maximally effective insulin stimulus, with a proportional upward shift of the dose response curve.3
So to state things simply, if there is an increase in insulin sensitivity less insulin will do more.
If there is an increase in insulin responsiveness then the upper limit to what insulin is normally capable of doing is increased. This state could be called supra-normal or in terms of The Flintstones "the Bam Bam effect".0
Post workout increased insulin action
The act of contracting a muscle in a workout induces an increase in the permeability of muscle to glucose. Insulin is not needed for this glucose uptake to occur.4 This action is short-lived and reverses rapidly when the contractions end. This phenomenon is replaced by an increase in sensitivity and responsiveness of muscle glucose uptake to insulin which may persist.5-7
Increased insulin sensitivity in muscle after exercise occurs in response to the exercise event itself. It does not require glycogen depletion to initiate it. It happens without regard to glycogen depletion. However the duration of this enhanced insulin sensitivity will be determined by subsequent glycogen super-compensation.7
Increased insulin responsiveness on the other hand does require glycogen depletion. It will not occur without it. The exercise event itself is not sufficient to trigger an increase in insulin responsiveness.7 The increase in exercise-induced responsiveness comes to an end before glycogen is restored to preexercise levels. 8
In essence there are two distinct mechanisms by which sensitivity and responsiveness are increased and there are two different levels of glycogen repletion by which their increase returns to normal.
What effect does carbohydrate ingestion post-exercise have on increased insulin action?
Several studies early on established clearly that prevention of glycogen supercompensation (i.e. refilling of glycogen stores above resting base levels) after glycogen-depleting exercise results in the persistence of the exercise-induced increase in insulin action on muscle. 8-10 More recent studies have confirmed these findings and found that the explanatory mechanism primarily centers on the "persistence of the adaptive increase in GLUT4." 11
One of the pioneer studies, the Cartee study8 had a primary purpose, to determine the effect of carbohydrate deprivation on the persistence of increased insulin sensitivity and responsiveness after exercise. They found that those animals fed carbohydrates showed no increase in insulin responsiveness at 3 hours post-exercise. Only the muscles of the fat-fed (i.e. carbohydrate free) animals showed a continued increase in insulin responsiveness at 3 hours post-exercise. The magnitude of the responsiveness elevation equaled 25%. These results almost mirror those found in a previous study using fasted animals. In that study the increase in responsiveness at the 3 hour mark was 22%. 12
So here we have a correlation between the fasted-state and the fat-fed (i.e. no carb) in regard to the increase in insulin responsiveness 3 hours post-exercise. This contrasts with those fed carbohydrates who exhibited no increase in insulin responsiveness. Carbohydrate feeding prevents an increase in responsiveness.8
In regard to insulin sensitivity, they found that in animals fed carbohydrates, the increase in post-exercise insulin sensitivity was lost by the the 18 hour mark. To reiterate the carbless group continued to enjoy increased insulin sensitivity for at least 48 hours.
The study found that while a small portion of the increased insulin effect was attributable to the increase in insulin responsiveness most of the effect came from increased insulin sensitivity. This increase in sensitivity endured unchanged for 48 hours in the fat-fed (no carb) group.8 These results mirrored the persistence displayed in a similar study that fasted the animals. 12
The study found that total caloric intake had no significant effect on exercise-induced insulin sensitivity. 8 There was minimal glycogen resynthesis in the carbless (fat-fed) group at the 3 hour post-exercise mark. By 18 hours muscle glycogen concentration had increased two-fold. By 48 hours glycogen concentration in muscles had returned to resting fasting control value.8 Compensation after two full carbless days had been achieved but super-compensation had not yet occurred.
Insulin and increased transport
The same study examined the effect of exogenous insulin. When muscles from exercised animals were treated with low amounts of insulin there was a strong increase (two-fold) in transport activity. "This effect persisted essentially unchanged for 18 and 48 hours in the fat-fed and the 18 hour fasted rats but had reversed by 18 hours in carbohydrate-fed rats." 8
This underscore the need to have some amount of insulin around in order to maximize insulin's utility.
There is a need for some physiological amount of insulin in the post-exercise environment.
Another study investigated the reversal of the exercise-induced increase in muscle permeability to glucose in regard to insulin and found, "that 1) the exercise-induced increase in permeability to glucose reverses rapidly in rat epitrochlearis muscles incubated in vitro in the absence of insulin, and 2) this rapid reversal is not dependent on glucose transport, glycogen synthesis, or protein synthesis. Our studies on muscles incubated in vitro provide evidence that the prolonged persistence, i.e., slow reversal, of the increase in muscle permeability to glucose seen in vivo after exercise depends on the presence of a low concentration of insulin."13
My conjecture is that even in the absence of carbohydrate ingestion there is enough insulin present to maintain the increase. However there may not be sufficient amounts to maximize the increase in transport activity.
0 - Dat just being silly
2 - Ivy JL and Holloszy JO. Persistent increase in glucose uptake by rat skeletal muscle following exercise. Am J Physiol Cell Physiol 241: C200â€“C203, 1981
3 - Holloszy, John O., Exercise-induced increase in muscle insulin sensitivity, J Appl Physiol 99: 338â€“343, 2005
4 - Holloszy, J. O., S. H. Constable, And D. A. Young, Activation of glucose transport in muscle by exercise, Diabetes/Metab. Rev. 1: 409-423,1986.
5 - Richter, E. A., L. P. Garetto, M. N. Goodman, And N. B. Ruderman, Enhanced Muscle Glucose Metabolism After Exercise: Modulation By Local Factors, Am. J. Physiol. 246 (Endocrinol. Metab. 9): E476-E482,1984.
6 - Wallberg-Henriksson, H., S. H. Constable, D. A. Young, And J. 0. Holloszy, Glucose Transport Into Rat Skeletal Muscle: Interaction Between Exercise And Insulin. J. Appl. Physiol. 65: 909- 913,1988.
7 - Zorzano, A., T. W. Balon, M. N. Goodman, And N. B. RudErman, Glycogen Depletion And Increased Insulin Sensitivity And Responsiveness In Muscle After Exercise. Am. J. Physiol. 251 (Endocrinol. Metab. 14): E664-E
8 - Cartee Gregory D. et al., Prolonged increase in insulin-stimulated glucose transport in muscle after exercise, Am. J. Physiol. 256 (Endocrinol. Metab. 19): E494-E499, 1989
9 - Fell RD, Terblanche SE, Ivy JL, Young JC, and Holloszy JO, Effects of muscle glycogen content on glucose uptake by muscle following exercise, J Appl Physiol 52: 434â€“437, 1982.
10 - Young JC, Garthwaite SM, Bryan JE, Cartier L.J., and Holloszy JO. Carbohydrate-feeding speeds reversal of enhanced glucose uptake in muscle after exercise, Am J Physiol Regul Integr Comp Physiol 245: R684â€“R688, 1983.
11 - Pablo M. Garcia-Roves, Prevention of glycogen supercompensation prolongs the increase in muscle GLUT4 after exercise, Am J Physiol Endocrinol Metab 285: E729â€“E736, 2003
12 - Allberg-Henriksson, H., S. H. Constable, D. A. Young, and J. 0. Holloszy, Glucose Transport Into Rat Skeletal Muscle: Interaction Between Exercise And Insulin, J. Appz. Physiol. 65: 909- 913,1988.
13 - Young, D.A., et al., Reversal of the exercise-induced increase in muscle permeability to glucose, Am. J. Physiol. 253 (Endocrinol. Metab. 16): E331-E335, 1987
Is there a benefit to muscle protein synthesis from prolonging insulin sensitivity?
Intuitively the answer is "of course". I can point to the known effects of insulin on protein metabolism and argue that all of that will be enhanced.
The authors Roy and Tarnopolsky expressed the belief that while a "more rapid rate of muscle glycogen recovery may be of benefit to an individual performing multiple work-outs per day...an enhanced postexercise insulin response would be of benefit to an athlete performing resistance exercise, since it may attenuate muscle protein degradation and/or increase muscle protein synthesis."14
The authors in the Cartee study underscore the loss of potential for insulin's positive effect on protein metabolism by concluding "Our results provide evidence that carbohydrate feeding speeds reversal not only of the increase in muscle glucose transport induced by exercise but also the increased susceptibility of muscle to the action of insulin that becomes evident after the activation of glucose transport by exercise has partly reversed." 8
14 - Roy and Tarnopolsky, Effect of glucose supplement timing on protein metabolism after resistance training, J Appl Physiol 82: 1882-1888, 1997
Exercising in fully repleted glycogen state is important
This is just a quick note to emphasize that repletion or super-compensation of muscle glycogen needs to take place prior to initiating the following exercise session. From, Influence of muscle glycogen availability on ERK1/2 and Akt signaling after resistance exercise in human skeletal muscle, Andrew Creer, et al., J Appl Physiol 99: 950â€“956, 2005
"...two potential cellular pathways have been implicated for cellular growth and development in response to muscle contraction: extracellular signal-regulated kinase (ERK1/2) and Akt intracellular signaling pathways. Once stimulated (phosphorylated), these pathways lead to phosphorylation of the downstream targets responsible for activation of transcriptional and translational factors that serve as the molecular basis for muscle adaptation."
"In conclusion, on the basis of the present findings, it appears that mechanical stress associated with exercise is a powerful stimulator of ERK1/2 and p90rSk phosphorylation, independent of glycogen concentration. However, muscle glycogen availability appears to play a role in regulation of the Akt pathway, inasmuch as Akt phosphorylation was elevated only after RE (resistance exercise) in the HCHO (high carb) trial. Thus the present findings suggest that although the ERK1/2 pathway may be unaffected by muscle glycogen, exercising in a glycogen-depleted or malnourished state may disrupt mechanisms involved with protein translation through the Akt pathway. In this manner, adaptations to an acute bout of exercise may be blunted."