Training Effects (T1–T2)
There was no significant main effect of training (P = 0.724) or condition (P = 0.072) on fasting glucose concentration (Table 2). There was also no significant main effect of training (P = 0.434) or condition (P = 0.292) on fasting insulin concentration (Table 2). There was also no main effect of training (P = 0.814) or condition (P = 0.925) on glucose AUC (Fig. 3A). There was, however, a trend for a main effect of training to decrease insulin AUC (P = 0.054) and a trend (P =0.052) for a main effect of condition, with FIR tending to have a greater insulin AUC (Fig. 3B). There was also a significant interaction of condition × time (P = 0.050), that is, with training, FIR reduced insulin AUC to a greater extent than C. There were neither significant effects of training (P = 0.496) nor condition (P = 0.464) on HOMA-IR (Table 2).
No significant main effects of training on the proportion of MHC I (P = 0.153), MHC IIA (P = 0.144), or MHC IIX (P = 0.369) were observed (Fig. 2). There were also no main condition effects on MHC isoform distribution after training (P > 0.050). There was a negative correlation between OGTT glucose AUC and MHC I content after training, that is, the greater the glucose AUC, the lower the proportion of MHC I (R 2 = 0.268, P = 0.040). There was a positive correlation between fasting blood insulin concentration and MHC IIA content after training (P = 0.046), that is, the greater the fasting blood insulin concentration, the greater the amount of MHC IIA (R 2 =0.254). Glucose AUC after training was also positively correlated with MHC IIX content (R 2 = 0.264, P = 0.041).
Anthropometric measures did not change in response to training (P > 0.05), except for thigh girth, which increased by 1.2 cm (P ≤ 0.001, Table 2). There were no differences between FIR and C in anthropometric measures in response to training.
There was a significant main effect of training to increase vertical distance jumped (P = 0.001); however, there was no significant (P = 0.342) main effect of condition (Table 2). There was a significant (P = 0.005) main effect of training to improve peak power, with no significant (P = 0.182) main effect of condition (Table 2). There was a significant main effect of training on 3RM with increases in the leg press, leg extension, leg curl, and squat exercises (all P ≤ 0.001, Fig. 1). No significant main effects of condition on leg press, leg extension, leg curl, or squat exercises were observed (P = 0.458, P = 0.125, P = 0.154, and P = 0.192, respectively; Fig. 1)
Detraining Effects (T2–T3)
The mean duration of detraining until retesting was 9.2 wk (64.5 d; range, 61–67 d). All participants returned to similar baseline physical activity levels as before the beginning of the study, determined by physical activity records (P = 0.140).
There were no significant main effects of detraining or condition on fasting glucose concentration (P = 0.240 and P = 0.236, respectively; Table 2). There were also no significant main effects of detraining or condition on fasting insulin concentration (P = 0.877 and P = 0.163, respectively; Table 2). There were also no significant main effects of detraining or condition on glucose AUC (P = 0.817 and P = 0.940, respectively, Fig. 3A). However, there were significant main effects of detraining and condition on insulin AUC (P = 0.031 and P = 0.018, respectively; Fig. 3B). There was also a significant condition × time interaction (P = 0.023), that is, insulin AUC increased in FIR but not in C as a result of detraining (Fig. 3B). There were no significant main effects of detraining or condition on HOMA-IR (P = 0.900 and P = 0.232, respectively; Table 2).
There were no significant main effects of detraining on MHC I or MHC IIA isoform distributions (P = 0.213 and P = 0.100, respectively); however, there was a significant main effect of detraining to increase percentage MHC IIX (P = 0.026, Fig. 2). There were no significant main effects of condition on MHC I (P = 0.854), MHC IIA (P = 0.310), or MHC IIX (P = 0.535) proportions. An inverse correlation between fasting blood glucose concentration and MHC IIX was observed at T3, that is, the greater the fasting blood glucose concentration, the less the MHC IIX content after detraining (R 2 = 0.345, P = 0.027).
There were no differences in anthropometric measures between FIR and C as a result of detraining (Table 1). The body mass, percentage body fat, or thigh girth did not change with detraining (P = 0.359, P = 0.075, and P = 0.078, respectively). There was a trend to increase waist/hip ratio with detraining (P = 0.052).
There was no significant main effect of detraining on vertical distance jumped (P = 0.594), nor was there a significant main effect of condition (P = 0.342) (Table 2). There was also no main effect of detraining on peak power (P = 0.334), with no significant main effect of condition (P = 0.174) (Table 2). There was a significant main effect of detraining to decrease 3RM in the leg press (P = 0.002), leg extension (P < 0.001), leg curl (P < 0.001), and squat exercises (P = 0.001, Fig. 1). No significant main effects of condition for leg press, leg extension, leg curl, or squat exercises were observed (P = 0.481, P = 0.159, P = 0.168, and P = 0.227, respectively).
A key finding of the current study is a rise in insulin AUC when abstaining from resistance training, after a period of training, in those with a familial link to T2DM, despite continuation of other activities. It also appears that resistance training elicits a greater, and metabolically significant, response in reducing insulin AUC in those with a familial link to T2DM compared with those without this link. Confirming our hypotheses, these findings demonstrate that individuals with parents of T2DM may be more responsive to this exercise mode and may be more metabolically sensitive to detraining than C. This highlights the effect of a resistance exercise intervention and importance of maintenance, particularly in individuals who may have a genetic predisposition to T2DM.
A reduction in insulin AUC without altered glucose response has been observed by others (13,23). In those studies, a 75- to 100-g OGTT was used to assess changes in insulin response before and after a period of 8–10 wk of resistance training in type 2 diabetic participants (13) and healthy individuals (23). Insulin AUC decreased by 10% in those with T2DM (13), 18.9% in healthy individuals (23). In the current study, the mean reduction in insulin AUC as a result of training just failed to reach significance (P = 0.054). The time of sampling, 72 h after exercise, was selected to avoid the acute effects of the last exercise bout. This interval may explain the lack of a significant change in insulin AUC with training, relative to other studies in which sampling was conducted 48 h after exercise (13,23). Although we were looking for chronic rather than acute effects of exercise, when designing this type of study, one may want to consider the timing of the measurement with respect to how frequently the individuals in question typically train and alter sampling time accordingly. The apparent decrease in training effect on insulin response with increasing time since the last exercise bout indicates that the frequency of exercise is important and suggests that to optimize the training response, exercise may need to be conducted at least every other day.
The majority of studies in which comparable measures (i.e., an OGTT) were taken have had detraining periods (returning to normal activities of daily living) of 15 d or less (6,17,22,26) and consisted of the removal of the training (training cessation) (6,17,22) or bed rest (26), with the exception of Andersen et al. (3) who used a detraining period (training cessation) of 90 d. Despite no changes in HOMA-IR with detraining, a significant difference between our two groups in the insulin response to an oral glucose load was observed. This difference in insulin response was evident despite no differences in percentage body fat, thigh girth (indicating muscle mass), or waist/hip ratio. It can therefore be concluded that cessation of resistance training of this length is sufficient to increase the insulin response to glucose ingestion in those who have a familial link to T2DM, even with continuation of other forms of physical activity.
Although no baseline differences in glucose or insulin measures were observed, it is plausible that the differential response of insulin to a glucose load with training and detraining may be related to initial differences in insulin responsiveness but, because of low statistical power, were not detected. Nevertheless, the observed differences in insulin AUC in those with a familial link to type 2 diabetes indicate that this group may be particularly advantaged by undertaking a resistance training regimen and particularly disadvantaged if the training stimulus is removed.
Our results contrast with an earlier finding of an increased number of Type IIB fibers in the offspring of those with T2DM (24). It has been observed in rodents that Type II fiber proportion increases when exposed to insulin (18); therefore, it is likely that among our FIR participants, the metabolic environment for this transition was not sufficient to elicit differences in MHC IIX at baseline; this is supported by no observable large differences between groups in baseline fasting insulin or glucose.
With resistance training, we expected an increase in MHC IIA with a corresponding decrease in MHC IIX; however, this was not observed. This is in contrast with results from the resistance training literature in those without T2DM (1,2,4,27). It is possible that in our participants, prior alternative training had already resulted in this shift or that the duration of the training period was not long enough to result in these changes. Typically, these changes are observed after 12 wk of training (35–45 sessions) (2), although some have seen directional changes at 8 wk (8). The high individual variability and low power would also have prevented detection of small changes.
Typically, if a period of detraining occurs after training, MHC IIX expression is increased (2,4). In the current study, this increase in IIX was observed with detraining, despite no change in the opposite direction previously with training. It may also have been that we missed a possible change in fiber type to more IIA in between when the training ended and at the end of detraining. It is unknown what happened in between these two time points, and adaptation to the training may still have been taking place into recovery. Most of our subjects admitted to having muscle soreness from a previous session when showing up for each subsequent training. This supports the idea that adaptation may not have fully occurred until the early part of the detraining period. The fact that our subjects trained three times per week (in contrast to most other studies in which subjects trained twice per week) may explain the soreness and possible delayed adaptation.
The effect of “downtime” on fiber type adaptations, and particularly MHC IIX overshoot, has ramifications, particularly for the training athlete, and may be positive or negative depending on whether the sport is endurance or strength/speed based.
GLUT-4 expression is less in fast (Type II) muscle fibers than that in slow (Type I) fibers (15). Therefore, Type II fibers have a reduced capacity to take up glucose than Type I fibers. This may account for the positive correlation observed between fasting blood insulin and MHC IIA content after training and the negative correlation between glucose AUC and MCH1 content.
Nine weeks of resistance training improved strength and power in both groups.
We can confirm that the physical activity completed during detraining was not different from baseline, which is also confirmed by the decrease in strength in all 3RM tests. However, despite decreases in strength, participants were able to maintain power after 9 wk of detraining. Maintenance of power in this circumstance could have resulted from increased proportion of MHC IIX fibers observed as a result of detraining.
This study was limited by small numbers, particularly of FIR for which there were strict criteria. Another limitation is the lack of a control group, making it difficult to ascertain if there was a seasonal effect. Furthermore, training intervention studies of this duration are notoriously difficult in terms of recruitment as well as maintenance. That all except one participant completed the intervention is positive; unfortunately, the one who dropped out was FIR.
Because of the small numbers and large variability, the lack of significance, particularly for fasting insulin and HOMA-IR, may be related to low power. On the basis of n = 6 (FIR), the power to detect a training effect in fasting insulin was 0.07, and for n = 10 (C), the power was 0.10, with α = 0.05 and mean SD of 25.9. Even if we had increased to n = 20, the power would only have been 0.16. For HOMA-IR for n = 6, a power of 0.07 was obtained, and for n = 10, a power of 0.09 was obtained, with α = 0.05 and mean SD of 0.88.
Thus, increasing subject numbers may not have altered the result to a trend for a significant difference, unless variability within each group changed. The control group had similar baseline variability as FIR, including some subjects who were beyond the clinical cut-offs for fasting insulin and HOMA-IR. It appears that fasting values, and the calculated indices derived from them, do not have the sensitivity that dynamic responses to a glucose load do.
In summary, this is the first study to measure metabolic adaptations, along with MHC isoform distributions, in young adult individuals (with and without a familial link to T2DM) before and after 9 wk of resistance training and 9 wk of detraining. Insulin AUC decreased considerably with training, and increased in response to detraining, in those with a possible genetic link to T2DM. Clinically, this highlights the positive effect a resistance training program may have and the quick return to pretraining state when training is discontinued. A moderate level of resistance training may play a role in the prevention of T2DM, particularly in those individuals who have a familial link and may be more at risk of developing T2DM.
Funding for insulin and glucose analyses was provided by the Sports Nutrition and Exercise Metabolism Research Group Discretionary Fund, Department of Human Nutrition, Otago University.
We are very appreciative of the dedication of our participants during training and testing. We acknowledge the assistance of Margaret Waldron (University of Otago, New Zealand) with cannulations, Dr. David Gerrard (University of Otago, New Zealand) for assisting with muscle biopsy sampling, and Brian Niven for statistical analysis advice.
No conflict of interest is declared for KL Schofield, NJ Rehrer, TL Perry, A Ross, JL Andersen, and H Osborne.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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Keywords:©2012The American College of Sports Medicine
STRENGTH TRAINING; OGTT; POWER; MHC