One of the most popular topics today is the implementation of the “glycemic index” into our diets, which refers to the rise in glucose levels after a meal. Diets today such as nutrisystem base their entire diet on the “glycemic advantage” claiming that low GI carbs are good, while sugars, etc. are what causes fat gain.
Probably the only debate of whether or not we should have high GI carbs post workout has been this very issue – fat gain and decreased insulin sensitivity. Because there is no denying it is optimal for performance, glycogen replenishment, and protein balance.
Surprisingly, despite all of the hoopla over the miracle that is low GI carbs, I have failed to find substantial evidence supporting these claims.
Now before you glycemic index disciples flog me (!) please read on first! As I was once a disciple myself, but am now questioning my convictions. [img]/forum/images/graemlins/tongue.gif[/img]
To begin, here is the position off American Diabetes Association (2008) for diabetes nutritional interventions, in relation to sugar consumption,
“There is no evidence to support prescribing diets such as "no concentrated sweets" or "no sugar added." (E) “
“Meal plans such as no concentrated sweets, no sugar added, low sugar, and liberal diabetic diet also are no longer appropriate. These diets do not reflect current diabetes nutrition recommendations and unnecessarily restrict sucrose.”
“There is not sufficient, consistent information to conclude that low–glycemic load diets reduce the risk for diabetes. Nevertheless, low–glycemic index foods that are rich in fiber and other important nutrients are to be encouraged. (E) “
“There is debate as to the potential role of low–glycemic index and –glycemic load diets in prevention of type 2 diabetes. Although some studies have demonstrated an association between glycemic load and risk for diabetes, other studies have been unable to confirm this relationship, and a recent report showed no association of glycemic index/glycemic load with insulin sensitivity (39).
Thus, there is not sufficient, consistent information to conclude that low–glycemic load diets reduce risk for diabetes. Prospective randomized clinical trials will be necessary to resolve this issue. Nevertheless, low–glycemic index foods that are rich in fiber and other important nutrients are to be encouraged. A 2004 American Diabetes Association statement reviewed this issue in depth (40), and issues related to the role of glycemic index and glycemic load in diabetes management are addressed in more detail in the CARBOHYDRATE section of this document.”
Now lets discuss some of this research. Basically, most of the evidence in support of low GI foods are correlational studies in large cohorts. For example, McKeown et al. (2004) investigated the relationship between carbohydrate-related dietary factors, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort (2,834 subjects), which is a longitudinal community-based study on cardiovascular disease using the offspring of participants of the Framingham Heart Study Cohort. Altogether, participants consuming high glycemic carbohydrates were 40% more likely to have metabolic syndrome than participants consuming low glycemic carbohydrates. For those of you that do not know, Metabolic Syndrome is a cluster of metabolic abnormalities that increases the risk of cardiovascular disease, diabetes, and other disorders. However, other correlation studies were not consistent with McKeown (see Lau et al., 2005)
There has been few type “A” studies on this subject. Intervention studies in animals has shown a strong correlation with high fructose and sucrose diets to insulin resistance (Storlien et al., 2000); however, these studies are either hypercaloric or contain unrealistic sugar contents (i.e. 70-80% of total calories).
Neil et al. (2006) performed one of the rare type A studies on the effects of carbohydrate composition on insulin resistance. They investigated the effects of two eucaloric, identical fiber content, low vs. high sucrose diets (25 vs. 10%, respectively, of total energy intake) in 13 healthy subjects aged 33 (± 3 years; BMI 26.6 ± 0.9 kg/m2), in a randomized crossover design with sequential 6-week dietary interventions separated by a 4-week washout. Results showed no differences between conditions in insulin sensitivity, glycemic profiles, or measures of vascular compliance. Suggesting that carbohydrate composition has little effect on insulin resistance syndrome when fiber and calories are controlled for.
What research does support is that:
1.) Low fiber diets
2.) Hypercaloric diets
Do increase insulin resistance.
When you control for these factors, the correlation between high GI foods and metabolic abnormalities disappears.
Now, I don’t think I can make extreme recommendations on this like consuming all of your carbs from sugar – research does NOT support this. But based on this, I think it is silly to fuss over 1 or 2 high GI carbohydrates centered around your workout routines to optimize performance. And really, I am not sure how much we should fuss over having moderate GI carbs, or even higher, as long as we have a lot of fiber in our diet (10 g per 1000 calories). But I can’t say for sure…
Here is a direct study that examined the effects of post workout sugar consumption on body comp and performance.
This study by Bird (2006) showed that after 12 weeks of resistance training twice weekly, consuming CHO+ EAA post exercise increased muscle mass to a greater extent, lowered protein degredation, raised insulin and lowered cortisol to a greater extent than CHO or EAA's alone. With no differences in body fat gain observed.
1: Eur J Appl Physiol. 2006 May;97(2):225-38. Epub 2006 Mar 24.
Independent and combined effects of liquid carbohydrate/essential amino acid ingestion on hormonal and muscular adaptations following resistance training in untrained men.
Bird SP, Tarpenning KM, Marino FE.
School of Human Movement Studies, Charles Sturt University, Allen House 2.13, Bathurst, NSW, Australia. firstname.lastname@example.org
This investigation examined chronic alteration of the acute hormonal response associated with liquid carbohydrate (CHO) and/or essential amino acid (EAA) ingestion on hormonal and muscular adaptations following resistance training. Thirty-two untrained young men performed 12 weeks of resistance training twice a week, consuming ~675 ml of either, a 6% CHO solution, 6 g EAA mixture, combined CHO + EAA supplement or placebo (PLA). Blood samples were obtained pre- and post-exercise (week 0, 4, 8, and 12), for determination of glucose, insulin, and cortisol. 3-Methylhistidine excretion and muscle fibre cross-sectional area (fCSA) were determined pre- and post-training. Post-exercise cortisol increased (P<0.05) during each training phase for PLA. No change was displayed by EAA; CHO and CHO + EAA demonstrated post-exercise decreases (P<0.05). All groups displayed reduced pre-exercise cortisol at week 12 compared to week 0 (P<0.05). Post-exercise insulin concentrations showed no change for PLA; increases were observed for the treatment groups (P<0.05), which remained greater for CHO and CHO + EAA (P<0.001) than PLA. EAA and CHO ingestion attenuated 3-methylhistidine excretion 48 h following the exercise bout. CHO + EAA resulted in a 26% decrease (P<0.01), while PLA displayed a 52% increase (P<0.01). fCSA increased across groups for type I, IIa, and IIb fibres (P<0.05), with CHO + EAA displaying the greatest gains in fCSA relative to PLA (P<0.05). These data indicate that CHO + EAA ingestion enhances muscle anabolism following resistance training to a greater extent than either CHO or EAA consumed independently. The synergistic effect of CHO + EAA ingestion maximises the anabolic response presumably by attenuating the post-exercise rise in protein degradation.
What are your guys thoughts?
1. American Heart Associate. (2004). Metabolic syndrome statistics. http://www.nlm.nih.gov/cgi/medlineplus/l...FS15META4%2Epdf
2. Carroll, S., and M., Dudfield. (2004). What is the relationship between exercise and metabolic abnormalities? A review of the metabolic syndrome. Sports Medicine. 34 (6): 371-418.
3. Fukagawa NK, Anderson JW, Hageman G, Young VR, Minaker KL. (1990). High-carbohydrate, high-fiber diets increase peripheral insulin sensitivity in healthy young and old adults. Am J Clin Nutr 52:524–528.
4. Hodge AM, Montgomery J, Dowse GK, Mavo B, Watt T, Zimmet PZ. (1996). A case-control study of diet in newly diagnosed NIDDM in the Wanigela people of Papua New Guinea. Diabetes Care 19:457–462.
5. Howard BV, Wylie-Rosett J. (2002). Sugar and cardiovascular disease: a statement for healthcare professionals from the committee on nutrition of the council on nutrition, physical activity, and metabolism of the American Heart Association. Circulation 106:523–527.
6. Lau, CathrinE, Kristine Færch, Charlotte Glümer, Inge Tetens, Oluf Pedersen, Bendix Carstensen, Torben Jørgensen, and Knut Borch-Johnsen (2005). Dietary Glycemic Index, Glycemic Load, Fiber, Simple Sugars, and Insulin Resistance. Diabetes Care 28:1397-1403.
7. Marshall JA, Bessesen DH, Hamman RF. (1997). High saturated fat and low starch and fibre are associated with hyperinsulinaemia in a non-diabetic population: the San Luis Valley Diabetes study. Diabetologia 40:430–438.
8. McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PWF, Jacques PF. (2004). Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort. Diabetes Care 27:538–546.
9. Neil R., A. Black1, Michelle Spence2, Ross O. McMahon1, Geraldine J. Cuskelly2, Cieran N. Ennis1, David R. McCance1, Ian S. Young2, Patrick M. Bell1, and Steven J. Hunter. (2006). Effect of Eucaloric High- and Low-Sucrose Diets With Identical Macronutrient Profile on Insulin Resistance and Vascular Risk. Diabetes 55:3566-3572.
10. Storlien LH, Higgins JA, Thomas TC, Brown MA, Wang HQ, Huang XF, Else PL. (2000). Diet composition and insulin action in animal models. Br J Nutr 83 (Suppl. 1):S85–S90.
11. World Health Organization. Diet, Nutrition and the Prevention of Chronic Diseases: Report of a Joint WHO/FAO Expert Consultation. Geneva, World Health Org., 2002 (Tech. Rep. Ser., no. 916).