Secondary Logo

Journal Logo

Original Research

Effect of Intensity of Aerobic Training on Insulin Sensitivity/Resistance in Recreationally Active Adults

Grieco, Carmine R.; Swain, David P.; Colberg, Sheri R.; Dowling, Elizabeth A.; Baskette, Kim; Zarrabi, Lida; Gandrakota, Ramya; Kotipalli, Ushasri; Sechrist, Scott R.; Somma, C. Thomas

Author Information
Journal of Strength and Conditioning Research: August 2013 - Volume 27 - Issue 8 - p 2270-2276
doi: 10.1519/JSC.0b013e31827da2f0
  • Free



Insulin resistance (IR) is linked to an increased risk of type 2 diabetes mellitus (T2 DM), greater cardiovascular, and all-cause mortality (6). It has been demonstrated that IR is an independent predictor of cardiovascular mortality (6) and is a significant factor contributing to prediabetes (1). An estimated 35% of the adult U.S. population has prediabetes, putting some 79 million more Americans at a higher risk of developing T2 DM (9).

It has been clearly established that aerobic exercise improves IR; this finding is supported by a wealth of research demonstrating a positive effect of moderate-to-vigorous intensity exercise (3,15,25,27). Consequently, recent guidelines have been established by the American College of Sports Medicine that recommend moderate-to-vigorous intensity (50–80% V[Combining Dot Above]O2R or V[Combining Dot Above]O2reserve) aerobic exercise for improvement of insulin action in individuals with T2 DM, and a preventive measure for those who are prediabetic (4).

However, there is a modicum of evidence suggesting that improvement in insulin effectiveness may be intensity dependent. Several studies have demonstrated that intensity levels ≥70% V[Combining Dot Above]O2R have had a greater impact on insulin action than intensity levels ≤70% V[Combining Dot Above]O2R (8,12,18,29). Importantly though, not all studies have controlled for the total volume of exercise, and it is uncertain whether the observed effect is because of intensity or simply greater energy expenditure.

There are few studies that have investigated the effect of exercise intensity on insulin action while controlling for caloric expenditure. Nevertheless, indirect evidence suggests a potential relationship. For example, studies comparing endurance-trained athletes with age-matched controls have found a positive association between insulin action and V[Combining Dot Above]O2max (14,28), whereas other studies have found a similar relationship among nonathletes (21,26,30). The fact that higher levels of V[Combining Dot Above]O2max are achieved by training at more vigorous exercise intensities suggests an intensity-dependent relationship between insulin action and this fitness measurement.

Although there is some evidence supporting the heightened role of intensity, this concept remains equivocal, and the optimal intensity of aerobic exercise for the maximization of insulin action remains a contentious issue. Few studies have investigated the differential effects of exercise intensities >80% V[Combining Dot Above]O2R while accounting for both exercise volume and energy expenditure. Given the increasing prevalence of diabetes and prediabetes, the differing effects of exercise intensity on IR/sensitivity warrant further investigation. Therefore, the purpose of this study was to compare the differential effects of 3 varying levels of aerobic exercise on insulin effectiveness in young healthy individuals when training protocols were held isocaloric.


Experimental Approach to the Problem

Subjects were matched for age, gender and VO2max, and randomly assigned to one of three exercise groups (moderate, vigorous or maximal intensity) or a non-exercise control group for six weeks. Fasting plasma glucose, insulin, total cholesterol and high density lipoprotein were measured at baseline and following training. Weekly duration and frequency of training varied to ensure equivalent energy expenditure across groups The Homeostasis Model (HOMA) and Quantitative Insulin Sensitivity Check Index (QUICKI) were used to assess changes in insulin effectiveness.


A total of 45 healthy adult subjects (26 women and 19 men; mean age, 22.2 ± 3.9 years) at low risk for cardiovascular disease, according to ACSM guidelines (4), participated in this study. Exclusionary criteria included use of medications that influence heart rate (such as beta blockers), pregnancy, or an irregular menstrual cycle in women, and recently, significant bicycle training (i.e., competitive cyclists or anyone who has engaged in at least 3 hours of cycling per week over the last 3 months). Each subject was informed of potential risks associated with the investigation before providing written informed consent. The study was approved by the local institutional review board.


Height and mass were measured on a Detecto balance scale (Columbia, MD, USA), and body mass index (BMI) was calculated. Body fat was estimated using a 3-site skinfold method (20) with Lange skinfold calipers (Cambridge, MD, USA). Venous blood samples were drawn from an antecubital arm vein the morning after an overnight fast of at least 8 hours. Additionally, participants were required to abstain from exercise for a minimum of 48 hours before each blood draw. Blood analysis included radioimmunoassay of plasma insulin (Siemens Medical Solutions, Los Angeles, CA, USA) and enzymatic analysis of fasting plasma glucose, total cholesterol (TC), and high-density lipoprotein (HDL) (Cholestech, Corp., Hayward, CA, USA). The pretesting and posttesting blood samples for female subjects were drawn during the first half (follicular phase) of the menstrual cycle to minimize the potential effect of hormonal levels on IR. All blood analyses were performed in duplicate to ensure accuracy.

Insulin sensitivity and IR were measured using the quantitative insulin sensitivity check index (QUICKI) (22) and homeostasis model assessment (HOMA) (24), respectively. Both models have demonstrated acceptable correlations (7,22) with the euglycemic hyperinsulinemic clamp method, widely held as the “gold standard” of insulin sensitivity measurement (32). Each method is a mathematical index reflecting fasting glucose and insulin levels in the basal state and represent glucose disposal as a function of insulin concentration. The QUICKI model is the following:

where I0 is fasting plasma insulin (in microunits per milliter) and G0 is fasting plasma glucose (in milligram per deciliter). Subjects were required to abstain from exercising for at least 48 hours before each blood draw. The HOMA model is as follows:

where G0 is fasting plasma glucose (in millimoles per liter), I0 is fasting plasma insulin (in milliunits per liter), and 22.5 is a constant.

On a separate day, each subject completed a maximal incremental exercise test on a cycle ergometer, after the procedures of Gormley et al. (13). Maximal oxygen consumption was calculated as the average of the 3 highest continuous 20-second interval V[Combining Dot Above]O2 measurements. A Polar heart rate monitor (Polar, Kempe, Finland) was used to collect resting and exercise heart rate measurements during maximal testing and during each exercise session. Given that exercise acutely improves insulin action for up to 48 hours (34), the posttesting blood draw was scheduled to occur not <48 hours (and no >72 hours) after the final exercise session. Maximal exercise testing occurred within 1 week of the last exercise session, at a similar time of day as pretraining tests to reduce potential sources of variability.

Exercise Training Protocol

Subjects were matched according to gender and V[Combining Dot Above]O2max and randomly assigned to 1 of 3 exercise groups or to a non-exercising control group. Exercise intensity was varied to ensure equal volume among groups and was defined in aerobic training units, a quantification based up V[Combining Dot Above]O2R (volume = intensity [%V[Combining Dot Above]O2R] × duration [minutes per session] × frequency [sessions per week]). Briefly, the exercise training programs were (a) moderate intensity (MOD), 50% heart rate reserve (HRR); (b) vigorous intensity (VIG), 75% HRR; and (c) maximal-intensity intervals (MAX), 5 minutes at 90–100% HRR/5 minutes at 50% HRR (Table 1). All exercise testing and training were performed on Monark Cycle ergometers (Ergomedic 828E; Varberg, Sweden).

Table 1
Table 1:
Six-week training program.*

Energy expenditure during training was calculated as external work (in joules) on the ergometer as

where R is average resistance (in kilograms), 6 m is the distance the ergometer flywheel traveled per pedal revolution, 60 rpm is the pedal cadence maintained by the subjects, and t is total duration (not including warm-up and cool-down) in minutes of exercise per week.

To account for potential effects of physical activity performed outside of the experimental trials, subjects were asked to keep a detailed daily activity log. All reported physical activity was categorized and assessed using the Compendium of Physical Activities (2). Each activity was assigned an intensity level from the compendium in metabolic equivalents (METs), and 1 MET was subtracted to yield net, not gross, intensity. The MET value was multiplied by the number of hours the activity was performed over the entire 6 weeks to yield MET-hours of energy expenditure. Total MET-hours for each subject from all of his or her activities were summed over the 6-week period.

Statistical Analyses

Six subjects did not meet the requirement of completing at least 90% of training sessions; therefore, only 39 subjects were included in the analysis. Descriptive statistics were compared using analysis of variance (ANOVA). Statistical analyses were performed using PASW 17.0 for Windows (Chicago, IL, USA). A statistical power analysis on previous data demonstrated that an n of 7 would yield a power of ≥0.98 (27). Differences in training variables among groups were analyzed using a 2 × 4 (2 time periods and 4 groups) ANOVA with repeated measures on 1 factor (time), and Tukey post hoc tests. Correlations between V[Combining Dot Above]O2max and both HOMA and QUICKI were assessed at pretest and posttest, as well as the change in V[Combining Dot Above]O2max vs. change in HOMA and QUICKI. Additionally, t-tests for actual vs. prescribed percentage of HRR were performed. Data are presented as mean values ± SD. Significance for all tests was set at p < 0.05.


Four participants withdrew from the study because of scheduling conflicts, another suffered a knee injury during pretesting, and 1 was unable to complete posttesting procedures. Characteristics of remaining subjects (n = 39) are presented in Table 2. There were no significant differences among groups in age, mass, BMI, or body fat at pretesting or posttesting.

Table 2
Table 2:
General subject characteristics and fasting metabolic measurements before and after training.*

External energy expenditure during exercise training arose from 467 ± 200 kJ in week 1 to 1,223 ± 376 kJ in week 3 and remained stable through week 6. There were no significant differences among groups. The MET-hours of outside activity were similar among groups and over time, averaging 17.5 ± 16.0 per week. Baseline V[Combining Dot Above]O2max values were similar among groups. Within groups, however, VIG and MAX exhibited significant increases in maximal oxygen consumption of 15.4 and 14.2% (5.9 and 5.7 ml·min−1·kg−1) over baseline values, respectively (Table 2).

There were no significant differences in insulin sensitivity or IR among groups at baseline or after training in the 3 exercise groups (Table 2). Similarly, fasting plasma glucose, insulin, TC, and HDL were similar among groups at baseline and after training (Table 2). Paradoxically, both QUICKI and HOMA demonstrated significantly improved values in the control group after the training period (p = 0.012 and 0.021, respectively). There were no significant differences of insulin sensitivity or IR attributable to gender between or among groups. Regression correlations of V[Combining Dot Above]O2max against pre- and post-measurements were not significant (data not shown). Additionally, correlational analyses of the delta change in V[Combining Dot Above]O2max compared with change in HOMA and QUICKI were likewise nonsignificant (Figures 1 and 2, respectively).

Figure 1
Figure 1:
Change in V[Combining Dot Above]O2max (ml·min−1·kg−1) vs. change in homeostasis model assessment (HOMA) after a 6-week training protocol.
Figure 2
Figure 2:
Change in V[Combining Dot Above]O2max (ml·min−1·kg−1) vs. change in quantitative insulin sensitivity check index (QUICKI) following a 6-week training protocol.


In the present study, we investigated the relationship among 3 levels of aerobic exercise intensity and both IR and sensitivity in young recreationally active adults, whereas exercise volume and energy expenditure was held constant. Previous research investigating the effect of exercise intensity on insulin effectiveness is equivocal and may be dependent upon the specifics of the methodology used. This investigation did not find a significant relationship between level of intensity and insulin effectiveness. We did, however, confirm previous research that reported that higher intensity exercise (75% HRR and intervals using 90–100% HRR) were more effective than moderate-intensity exercise (50% HRR) at raising V[Combining Dot Above]O2max (13) when volume of work was held constant.

Although aerobic exercise has been shown to improve insulin action in diabetes and prediabetes (11), there is no consensus on the optimal level of exercise intensity for eliciting improvement (16). Although several studies have found an effect of intensity upon insulin action, the literature is inconsistent. It has been suggested, e.g., that improvements in insulin sensitivity require that training exceed a threshold of energy expenditure and, as such, are independent of exercise intensity (23). Another source indicates that exercise duration, independent of energy expenditure, is the critical factor in upregulating the effectiveness of insulin (19). The issue is further clouded by many variables with the potential to affect insulin sensitivity measurements, such as subject population, volumetric control of exercise intervention, and both timing and method of insulin action quantification.

An important factor to consider in the measurement of insulin effectiveness is the timing of analysis. Although insulin is the primary mediator of glucose uptake in the rested state, muscular contractions, independent of insulin, are known to enhance glucose uptake during exercise, and this effect may persist for up to 48 hours (17). Therefore, it is possible that a measurement of insulin sensitivity (or IR) conducted within 48 hours of the last bout of exercise may be impacted by the acute effect of exercise. To isolate a chronic effect, our investigation performed a final blood analysis that occurred >48 hours from the final bout of exercise to localize a training effect and diminish the possibility of an acute effect (testing occurred approximately 60 hours after the final bout of exercise). It is worthwhile to note that some studies demonstrating intensity-related increases in insulin action have conducted their posttraining analysis within this 48-hour window of the final exercise bout (12,18,29).

The present investigation used the HOMA and QUICKI models to quantify changes in insulin action, but the euglycemic hyperinsulinemic clamp technique is widely regarded as the gold standard against which all other methods for assessing insulin sensitivity are measured. Nevertheless, the clamp technique is hampered by several drawbacks, including expense and technical difficulty (32). The HOMA (24) and QUICKI methods (22) are based on a feedback loop created between hepatic glucose output and β-cell insulin secretion in the basal state, providing an estimate of glucose disposal as a function of insulin concentration, which is representative of steady-state metabolism (35). Both methods, therefore, rely upon fasting glucose and insulin values to estimate IR/sensitivity. Although the HOMA and QUICKI models have been previously validated against the euglycemic hyperinsulinemic clamp technique (7,22), they do not enjoy unanimous support as a measurement of insulin action (10,35).

Nevertheless, HOMA has been widely used and is one of the most common measures of IR. However, both HOMA and QUICKI are surrogate measurements of insulin effectiveness, and all previous studies that have found an effect of exercise intensity on insulin action in young healthy populations have used alternate methods. A recent investigation is illustrative of a potentially confounding aspect of HOMA and QUICKI use (5). After 2 weeks of sprint interval training in a young healthy population, insulin sensitivity, as assessed by an oral glucose tolerance test, improved significantly despite no changes in fasting glucose or insulin levels. Such findings could be reflective of the specific population that was used in both the present investigation and by Babraj et al. (5) (young healthy subjects), in whom optimal or near optimal fasting insulin and glucose levels creates a ceiling effect in which improvements are likely undetectable (using HOMA and QUICKI). It is also of significance to note that Babraj et al. (5) performed their insulin sensitivity analysis within 24 hours of the last bout of exercise.

An important strength of the present study is the equalization of exercise volume and energy expenditure across groups. Despite significant differences in intensity level sustained (51.5, 74.7, and 90.5% of HRR for MOD, VIG, and MAX, respectively), no significant differences in energy expended were found nor were there significant differences in energy expended outside the parameters of the study. Several previous studies reporting improvements in insulin sensitivity have used protocols that did not account for differences in energy expenditure across groups (8,18,29) and could potentially account for differences in measures of insulin effectiveness. Without equalization of energy expenditure, it is difficult to pinpoint changes that are attributable to exercise intensity because the amount of glycogen depletion has a direct effect upon insulin-stimulated glucose uptake and subsequent glycogen resynthesis (33).

Why previous studies have demonstrated improvements in insulin effectiveness and the present investigation failed to do so is noteworthy. Previous studies, which have demonstrated significant change attributable to insulin effectiveness, differed in at least 1 significant aspect, such as the method of measuring insulin sensitivity (5,8,12), the timing of insulin analysis (5,29), the subject population (3,12,29,31) or lack of volume, and energy expenditure control of exercise programs (8,18,29).

For example, a recent well-controlled study examined the difference between continuous moderate exercise (70% HRmax) and aerobic interval training (4 minutes at 90% HRmax, 3 minutes at 70% HRmax) in older subjects (approximately 52 years) with metabolic syndrome (31). To equalize energy expenditure, the moderate and interval groups exercise for 47 and 40 minutes, respectively, 3 times per week for 16 weeks. Insulin sensitivity was measured using HOMA at least 4 days after the final exercise bout. In contrast to the present investigation, the authors demonstrated a significant improvement in insulin sensitivity in the high-intensity interval training group. Contrarily, we are not aware of any intensity-related research that has demonstrated significant improvements in insulin action in recreationally active adults using either HOMA or QUICKI.

An acknowledged limitation of this study is the relatively small groups, especially the control group, which experienced an anomalous improvement in insulin effectiveness. This improvement, however, was largely attributable to substantial reductions in fasting insulin values in 2 individuals who displayed uncharacteristically high insulin values pretesting, which subsequently fell to a more representative level posttesting. Similarly, it is possible that the small numbers in the exercise groups were insufficient to reach a level of statistical significance as the likely improvements in young recreationally active adults would be small. Additionally, it should be noted that the present investigation did not control for carbohydrate intake, a factor that may influence insulin action.

In conclusion, we found no effect of intensity of aerobic exercise on insulin sensitivity/resistance in a young recreationally active adult population. Although this investigation failed to support the work of previous investigations, it is noteworthy that no studies, of which the authors are presently aware, have found improvements in insulin action using HOMA and QUICKI in young recreationally active participants. This could be reflective of the blunt nature of the tools used to measure insulin effectiveness (HOMA/QUICKI) or methodological differences among studies, such as subject population, exercise intervention, and both timing and method of insulin sensitivity quantification. Nevertheless, while aerobic exercise is widely regarded as an effective tool for improving insulin sensitivity, there remains controversy regarding the optimal intensity with which to improve insulin action in varying populations. Future research should address these methodological concerns to pinpoint the optimal intensity of aerobic exercise as the prevalence of T2 DM and prediabetes continue to rise at alarming rates.

Practical Applications

Aerobic exercise is considered an important lifestyle tool for maintaining and improving insulin sensitivity (11). Although the present investigation did not support higher exercise intensity for the chronic improvement of insulin effectiveness in a young recreationally active population, it did, however, confirm earlier work demonstrating that higher intensity exercise is more effective at increasing V[Combining Dot Above]O2max than moderate-intensity exercise, even when total work is held constant. This, in itself, demonstrates that exercise intensities ≥75% V[Combining Dot Above]O2R are advantageous as both VIG (75% HRR) and MAX (50/95% HRR) achieved a similar increase in V[Combining Dot Above]O2max.


1. Abdul-Ghani M, Tripathy D, DeFronzo RA. Contributions of β-cell dysfunction and insulin resistance to the pathogenesis of impaired glucose tolerance and impaired fasting glucose. Diabetes Care 29: 1130–1139, 2006.
2. Ainsworth BE, Haskell WL, Whitt MC, Irwin ML, Swartz AM, Strath SJ, O’Brien WL, Bassett DR, Schmitz KH, Emplaincourt PO, Jacobs DR, Leon AS. Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc 32:(9 Suppl): S498–S504, 2000.
3. Al-Mahmood AK, Ismail AA, Rashid FA, Azwany YN, Singh R, Gill G. Effects of therapeutic lifestyle changes on insulin sensitivity of non-obese hyperlipidemic subjects: Preliminary report. J Atheroscler Thromb 14: 122–127, 2007.
4. American College of Sports Medicine. ACSM's Guidelines for Exercise Testing and Prescription (8th ed.). Philadelphia, PA: Lippincott Williams Wilkins 22-30, 234–235, 2010.
5. Babraj JA, Vollaard NBJ, Keast C, Guppy FM, Cottrell G, Timmons JA. Extremely short duration high intensity interval training substantially improves insulin action in young healthy males. BMC Endocr Disord 9: 3, 2009.
6. Barr ELM, Zimmet PZ, Welborn TA, Jolley D, Magliano DJ, Dunstan DW, Cameron AJ, Dwyer T, Taylor HR, Tonkin AM, Wong TY, McNeil J, Shaw JE. Risk of cardiovascular and all-cause mortality in individuals with diabetes mellitus, impaired fasting glucose, and impaired glucose tolerance. Circulation 116: 151–157, 2007.
7. Bonora E, Saggiani F, Targher G, Zenere MB, Alberiche M, Monauni T, Bonadonna RC, Muggeo M. Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity. Diabetes Care 23: 57–63, 2000.
8. Borghouts LB, Backx K, Mensink MF, Keizer HA. Effect of training on insulin sensitivity as evaluated by insulin tolerance test. Eur J Appl Physiol 80: 461–466, 1999.
9. Center for Disease Control and Prevention. National Diabetes Fact Sheet, 2011. Available at: Accessed May 27, 2011.
10. Chang AM, Smith MJ, Bloem CJ, Galecki AT, Halter JB, Supiano MA. Limitations of the homeostasis model assessment to predict insulin resistance and β-cell dysfunction in older people. J Clin Endocrinol Metab 91: 629–634, 2006.
11. Colberg SR, Grieco CR. Exercise in the treatment and prevention of diabetes. Curr Sports Med Rep 8: 169–175, 2009.
12. DiPietro L, Dziura J, Yeckel CW, Neufer PD. Exercise and improved insulin sensitivity in older women: Evidence of the enduring benefits of higher intensity training. J Appl Physiol 100: 142–149, 2005.
13. Gormley SE, Swain DP, Huff R, Spina R, Dowling E, Gandrakota U, Kotipalli R. Effect of intensity of aerobic training on VO2max. Med Sci Sports Exerc 7: 1336–1343, 2008.
14. 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: Effect on blood flow and differential expression of GLUT 4 in skeletal muscles. J Clin Endocrinol Metab 80: 2437–2446, 1995.
15. Hasbum B, Real JT, Sanchez C, Priego MA, Diaz J, Viguer A, Basanta M, Martinez-Valls J, Marin J, Carmena R, Ascaso JF. Effects of a controlled program of moderate physical exercise on insulin sensitivity in nonobese, nondiabetic subjects. Clin J Sports Med 16: 46–50, 2006.
16. Hawley JA, Gibala MJ. Exercise intensity and insulin sensitivity: How low can you go? Diabetologia 52: 1709–1713, 2009.
17. Hawley JA, Lessard SJ. Exercise training-induced improvements in insulin action. Acta Physiol (Oxf) 192: 127–135, 2008.
18. Hayashi Y, Nagasaka S, Takahashi N, Kusaka I, Ishibashi S, Numao S, Lee DJ, Taki Y, Tokuyama K, Tanaka K. A single bout of exercise at higher intensity enhances glucose effectiveness in sedentary men. J Clin Endocrinol Metab 90: 4035–4040, 2005.
19. Houmard JA, Tanner CJ, Slentz CA, Duscha BD, McCartney JS, Kraus WE. Effect of the volume and intensity of exercise training on insulin sensitivity. J Appl Physiol 96: 101–106, 2003.
20. Jackson AS, Pollock ML. Practical assessment of body composition. Phys Sportsmed 13: 76–90, 1985.
21. Kasa-Vubu JZ, Lee CC, Rosenthal A, Singer K, Halter JB. Cardiovascular fitness and exercise as determinants of insulin resistance in postpubertal adolescent females. J Clin Endocrinol Metab 90: 849–854, 2005.
22. Katz A, Nambi SS, Mather K, Baron AD, Follmann DA, Sullivan G, Quon MJ. Quantitative insulin sensitivity check index: A simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab 85: 2402–2410, 2000.
23. Magkos F, Tsekouras Y, Kavouras A, Mittendorfer B, Sidossis LS. Improved insulin sensitivity after a single bout of exercise is curvilinearly related to exercise energy expenditure. Clin Sci 114: 59–64, 2008.
24. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 28:412–419, 1985.
25. Mayer-Davis EJ, D’Agostino R, Karter AJ, Haffner SM, Rewers MJ, Saad M, Bergman RN. Intensity and amount of physical activity in relation to insulin sensitivity. JAMA 279: 669–674, 1998.
26. Østergård T, Andersen JL, Nyholm B, Lund S, Sreekumaran Nair K, Saltin B, Schmitz O. Impact of exercise training on insulin sensitivity, physical fitness, and muscle oxidative capacity in first-degree relatives of type 2 diabetic patients. Am J Physiol Endocrinol Metab 290: E998–E1005, 2006.
27. Potteiger JA, Jacobsen DJ, Donnelly JE, Hill JO. Glucose and insulin responses following 16 months of exercise training in overweight adults: The Midwest exercise trial. Metabolism 52: 1175–1181, 2003.
28. Sato Y, Hayamizu S, Yamamoto C, Ohkuwa Y, Yamanouchi K, Sakamoto N. Improved insulin sensitivity in carbohydrate and lipid metabolism after physical training. Int J Sports Med 7: 307–310, 1986.
29. Segerström AB, Flans F, Eriksson KF, Holmbäck AM, Groop L, Thorsson O, Wollmer P. Impact of exercise intensity and duration on insulin sensitivity in women with T2D. Eur J Intern Med 21: 404–408, 2010.
30. Seibaek M, Vestergaard H, Burchardt H, Sloth C, Torp-Pedersen C, Nielsen SL, Hilderbrandt P, Pedersen O. Insulin resistance and maximal oxygen uptake. Clin Cardiol 26: 515–520, 2003.
31. Tjønna AE, Lee SJ, Rognmo Ø, Stølen T, Bye A, Haram PM, Loennechen JP, Al-Share QY, Skogvoll E, Slørdahl SA, Kemi OJ, Najjar SM, Wisløff U. Aerobic interval training vs. continuous moderate exercise as a treatment for the metabolic syndrome—“A Pilot Study.” Circulation 118: 346–354, 2008.
32. Trout KK, Homko C, Tkacs NC. Methods of measuring insulin sensitivity. Biol Res Nurs 8: 305–318, 2007.
33. Wojtaszewski JFP, Jørgensen SB, Frøsig C, MacDonald C, Birk JB, Richter EA. Insulin signaling: Effects of prior exercise. Acta Physiol Scand 178: 321–328, 2003.
34. Wojtaszewski JFP, Nielsen JN, Richter EA. Exercise effects on muscle insulin signaling and action Invited Review: Effect of acute exercise insulin signaling and action in humans. J Appl Physiol 93: 384–392, 2002.
35. Yeni-Komshian H, Abbasi F, Canantoni M, Reaven GM. Relationship between several surrogate estimates of insulin resistance and quantification of insulin-mediated glucose disposal in 490 healthy nondiabetic volunteers. Diabetes Care 23: 171–175, 2000.

insulin effectiveness; HOMA; interval training; maximal oxygen consumption

Copyright © 2013 by the National Strength & Conditioning Association.