Post-Exercise Nutrition Primer

Post-Exercise Nutrition Primer

Maximizing the anabolic and performance effects of exercise


Picture of Dr. Mauro Di Pasquale
Dr. Mauro Di Pasquale

Mauro Di Pasquale, B.Sc..(Hons); M.D is a licensed physician in Ontario, Canada. For the past 30 years he has specialized in sports medicine and the treatment of obesity.

There is no doubt that the timing and type of protein intake after exercise is crucial for increasing skeletal muscle protein synthesis and an overall net balance.1 Exercise provides an adaptive response so that the body is able to make use of any nutrition supplied post exercise. 


Nutrient intake on its own provides a storage response so that if one is fed or receives an infusion of mixed amino acids after a fasted period, protein synthesis increases, whereas protein breakdown remains the same or decreases slightly, which is different from the response after exercise. 


Without nutrient intake after exercise, protein synthesis and protein breakdown are increased, but net balance does not become positive as it does after amino acid intake after fasting. Because of the exercise stimulus, when amino acids are provided after exercise protein synthesis increases more than what normally occurs after exercise or AA feeding alone, and protein breakdown remains similar to exercise without feeding. Thus, the provision of AA enhances protein synthesis and leads to a positive net protein balance and an overall increase in protein accretion.2


In addition, while the increase in protein synthesis after feeding is a transient storage phenomenon, physical exercise stimulates a longer-term adaptive response. Providing nutrition after physical activity takes advantage of the anabolic signaling pathways that physical activity has initiated by providing amino acid building blocks and energy for protein synthesis. 


Insulin has a Jekyll and Hyde type of action, depending on the general state of the body and food availability, especially carbs. Since insulin’s effects on protein, fats, and carbs can vary depending on the tissues involved and several other variables, it’s important not to take the view that what happens in skeletal muscle or any other tissues universally happens in the whole body. 


Glycogen compensation and super compensation (after glycogen depleting exercise) after exercise requires a substantial carbohydrate load that results in a quick and large increase in glycogen levels in both liver and skeletal muscles. Once the stores are full, or even super full, the stimulus declines dramatically. However, if no carbohydrates are given post exercise, the muscle will maintain a capacity to fully compensate or super compensate glycogen until enough carbs are either available through the diet or by gluconeogenesis to fill the glycogen stores as much as possible.3


Overemphasis on Post Exercise Carbohydrate Intake 

Because of the over-emphasis placed on maintaining glycogen stores to maximize exercise performance, much of the research has centered around the effects of post exercise carbs, and post-exercise carbs combined with protein,4 and the effects these have on glucose transporters (GLUT1, GLUT2, GLUT4), glucose metabolism, including levels of hexokinase and glycogen synthase, and insulin,5,6 there’s not much out there dealing with just the use of protein and fat after exercise.


The usual advice is that carbs, with some protein thrown in, are a necessary part of post-exercise nutrition regardless of diet that you’re following, including a low carb diet.7,8,9,10,11 However, that’s not true. In fact, the use of carbs post-training can be counterproductive, and eliminating post training carbs can have added anabolic and fat burning effects. That’s because the intake of carbs after exercise blunts the post exercise insulin sensitivity. That means once muscle has loaded up on glycogen, which it does pretty quickly on carbs, insulin sensitivity decreases dramatically. 


This statement runs counter to present thinking and research about post-exercise nutrition. As such, let’s take it step by step so that I can make my reasons for the above statements clear and easier to understand. 

Dr. Di Pasquale practiced what he preached. He was the Canadian powerlifting champion for eight years and won the World Championships in 1976.

Muscle Glycogen and Insulin Action 

First, it’s well known that a single session of exercise increases insulin sensitivity for hours and even days.12,13 It’s also known that bouts of resistance and endurance exercise result in a significant decrease in glycogen and that total energy content and CHO content are important in the resynthesis of muscle and liver glycogen.14 

Glucose uptake and glycogen synthesis are enhanced in the presence of insulin following an acute exercise bout that lowers the muscle glycogen concentration and activates glycogen synthase.15,16 

Muscle glycogen concentration dictates much of this acute increase in insulin sensitivity after exercise.17 Therefore, an increased availability of dietary carbohydrate in the hours after exercise and the resultant increase in muscle glycogen resynthesis reverses the exercise-induced increase in insulin sensitivity.18

Dissociation of Insulin’s Effects on Glucose and Protein Metabolism 

Along with glucose uptake, amino acid uptake, and protein synthesis also increase. As well, the use of fatty acids as a primary fuel also rises after exercise since glycogen resynthesis takes priority over the use of glucose for aerobic energy. 

However, as liver and muscle glycogen levels get replenished, insulin sensitivity decreases, as does amino acid uptake, protein synthesis and the use of fatty acids as a primary fuel. Fatty acids, preferably from the breakdown of body fat, can provide the fuel needed secondary to the prolonged increased metabolic rate that occurs after vigorous exercise, especially resistance training.19,20

By increasing insulin levels and not providing carbs, you shunt your body’s metabolism to the use of more fatty acids for energy while at the same time keeping muscle glycogen levels below saturation and amino acid influx and protein synthesis elevated for a prolonged period of time post exercise. 

In essence, by limiting glycogen synthesis you prolong the beneficial effects of insulin on protein synthesis and degradation and decrease the dampening effects of insulin on fatty acid breakdown and oxidation. At the same time although you delay glycogen synthesis you still maintain the capacity for rapidly increasing glycogen stores once you increase your carb intake. 

This increased capacity for glycogen synthesis, and everything that goes with it, can persist for several days if the muscle glycogen concentration is maintained below normal levels by carbohydrate restriction. By keeping carbs low and protein and energy high after training, you can increase protein synthesis over a prolonged period of time and get long term anabolic effect.21 

A study looked at the effects of post training carbohydrate deficit while keeping calorie intake constant, on insulin action and on fat oxidation. The study showed that carbohydrate deficit post-exercise resulted in increased fat oxidation and enhanced insulin action. The enhanced insulin action was proportional to the degree of carbohydrate deficit – i.e. the further the post exercise carbs were decreased, the greater the insulin action.22

Insulin and Nutrient Delivery to Skeletal Muscle 

As mentioned above in the discussion on insulin, we’ve seen that one of insulin’s actions is to increase microvascular (nutritive) perfusion of muscle, which is enhanced by exercise.23,24 This enhancement is crucial to maximizing the anabolic effects of exercise and targeted nutrition. 

For example, a review looked at the effects of insulin on the vascular system and on nutrient delivery to muscle.25 The paper points out the fact that that there are two flow
routes in muscle: one in intimate contact with the muscle cells (myocytes) and able to exchange nutrients and hormones freely and thus regarded as nutritive, and a second with essentially no contact with myocytes and regarded as nonnutritive (felt to provide blood to muscle connective tissue and adjacent fat cells, but not muscle cells). 

The point to take home here is that in the absence of increases in bulk flow to muscle, say after a training session, insulin may act to switch flow from nonnutritive to the nutritive route. This capillary recruitment results in an increase in nutritive blood flow so that muscles that have been stressed and are undergoing an adaptive response will have what they need to recover and grow. 


This information is another piece of the anabolic puzzle. Putting it all together can give us ways to dramatically improve body composition – increase muscle mass and decrease body fat. In my view, the best way to do this is to figure out ways to increase the potent anabolic effects of insulin, both on nutritive delivery to the muscle cells and into the muscle cells, while at the same time minimizing the undesirable effects on body fat. 

One of these ways is to increase insulin in a pulsed manner along with an increase in amino acid availability, but minimal carbs, at the times when the body is primed for growth and repair, for example in that window of opportunity that exists for several hours after training. It would also be desirable to maintain elevated androgen levels, and increase growth hormone (GH) and insulin-like growth factor-I (IGF-I) levels at the same time as insulin, in order to further enhance the anabolic effects of insulin and decrease, and actually reverse, the undesirable effects of insulin on fat metabolism.

The bottom line is that the key to maximizing body composition, and to increase performance in fat-adapted athletes is to keep carbs low and energy and protein intake high for several hours or even more after exercise.


1 Tipton, KD, Ferrando AA, Phillips SM, Doyle D Jr, Wolfe RR. Post exercise net protein synthesis in human muscle from orally administered amino acids. Am. J. Physiol. 1999;276:E628-634. 

2 Miller BF. Human muscle protein synthesis after physical activity and feeding. Exerc Sport Sci Rev. 2007;35(2):50-5. 

3 Garcia-Roves, P.M., D.H. Han, Z. Song, T.E. Jones, K.A. Hucker, and J.O. Holloszy. Prevention of glycogen supercompensation prolongs the increase in muscle GLUT4 after exercise. Am. J. Physiol. Endocrinol. Metab. 2003;285:E729-E736,. 

4 Ivy JL Goforth HW Jr Damon BM McCauley TR Parsons EC Price TB. Early post exercise muscle glycogen recovery is enhanced with a carbohydrate–protein supplement J Appl Physiol 2002; 93 1337–1344. 

5 Zorzano A, Palacin M, Guma A. Mechanisms regulating GLUT4 glucose transporter expression and glucose transport in skeletal muscle. Acta Physiol Scand. 2005;183(1):43-58. 

6 Morifuji M, Sakai K, Sanbongi C, Sugiura K. Dietary whey protein increases liver and skeletal muscle glycogen levels in exercise-trained rats. Br J Nutr. 2005;93(4):439-45. 

7 Ivy JL, Goforth HW Jr, Damon BM, McCauley TR, Parsons EC, Price TB. Early postexercise muscle glycogen recovery is enhanced with a carbohydrate-protein supplement. J Appl Physiol. 2002;93(4):1337-44. 

8 Carrithers JA, Williamson DL, Gallagher PM, Godard MP, Schulze KE, Trappe SW. Effects of postexercise carbohydrate-protein feedings on muscle glycogen restoration. J Appl Physiol. 2000;88(6):1976-82. 

9 Manninen AH. Hyperinsulinaemia, hyperaminoacidaemia and post-exercise muscle anabolism: the search for the optimal recovery drink. Br J Sports Med. 2006;40(11):900- 5. 

10 Kerksick C, Harvey T, Stout J, Campbell B, Wilborn C, Kreider R, Kalman D, Ziegenfuss T, Lopez H, Landis J, Ivy JL, Antonio J. International Society of Sports Nutrition position stand: nutrient timing. J Int Soc Sports Nutr. 2008 Oct 3;5:17. 

11 Howarth KR, Moreau NA, Phillips SM, Gibala MJ. Coingestion of protein with carbohydrate during recovery from endurance exercise stimulates skeletal muscle protein synthesis in humans. J Appl Physiol. 2009 Apr;106(4):1394-402. Epub 2008 Nov 26. 

12 CarteeGD, Young DA, Sleeper MD, Zierath J, Wallberg-Henriksson H, and Holloszy JO. Prolonged increase in insulin-stimulated glucose transport in muscle after exercise. Am J Physiol Endocrinol Metab 1989;256: E494–E499. 

13 HenriksenEJ. Effects of acute exercise and exercise training on insulin resistance. J Appl Physiol 2002;93:788–796. 

14 Roy BD, Tarnopolsky MA. Influence of differing macronutrient intakes on muscle glycogen resynthesis after resistance exercise. J Appl Physiol. 1998;84(3):890-6. 

15 Ivy JL, Holloszy JO. Persistant increase in glucose uptake by rat skeletal muscle following exercise. Am J Physiol 1981;241:C200-C203. 

16 Ren JM, Semenkovich CF, Gulve EA, Gao J, Holloszy JO. Exercise induces rapid increases in GLUT4 expression, glucose transport capacity, and insulin-stimulated glycogen storage in muscle. J Biol Chem. 1994 20;269(20):14396-401. 

17 Derave W, Lund S, Holman G, Wojtaszewski J, Pedersen O, Richter EA. Contraction- stimulated muscle glucose transport and GLUT-4 surface content are dependent on glycogen content. Am J Physiol Endocrinol Metab 1999;277: E1103–E1110.

18 Kawanaka K, Han D, Nolte LA, Hansen PA, Nakatani A, and Holloszy JO. Decreased insulin-stimulated GLUT-4 translocation in glycogen-supercompensated muscles of exercised rats. Am J Physiol Endocrinol Metab 1999;276: E907–E912. 

19 Knab AM, Shanely RA, Corbin K, Jin F, Sha W, Nieman DC. A 45-Minute Vigorous Exercise Bout Increases Metabolic Rate for 14 Hours. Med Sci Sports Exerc. 2011 Feb 8. [Epub ahead of print] 

20 Heden T, Lox C, Rose P, Reid S, Kirk EP. One-set resistance training elevates energy expenditure for 72 h similar to three sets. Eur J Appl Physiol. 2011 Mar;111(3):477-84. 

21 Cartee GD, Young DA, Sleeper MD, Zierath J, Wallberg-Henriksson H, Holloszy JO. Prolonged increase in insulin-stimulated glucose transport in muscle after exercise. Am J Physiol Endocrinol Metab 1989;256:E494–E499. 

22 Holtz KA, Stephens BR, Sharoff CG, Chipkin SR, Braun B. The effect of carbohydrate availability following exercise on whole-body insulin action. Appl Physiol Nutr Metab. 2008 Oct;33(5):946-56. 

23 Dela F, Larsen JJ, Mikines KJ, Ploug T, Petersen LN, Galbo H 1995 Insulin-stimulated muscle glucose clearance in patients with NIDDM. Effects of one-legged physical training. Diabetes 44:1010-1020. 

24 Hardin DS, Azzarelli B, Edwards J, Wigglesworth J, Maianu L, Brechtel G, Johnson A, Baron A, Garvey WT. Mechanisms of enhanced insulin sensitivity in endurance-trained athletes: effects on blood flow and differential expression of GLUT 4 in skeletal muscles. J Clin Endocrinol Metab 1995; 80:2437-2446. 

25 Clark MG, Wallis MG, Barrett EJ, Vincent MA, Richards SM, Clerk LH, Rattigan S. Blood flow and muscle metabolism: a focus on insulin action. Am J Physiol Endocrinol Metab. 2003;284(2):E241-58. 

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