There were no differences between FH and CON in pretraining strength, BMI, or blood glucose or lactate before or after exercise. The hypothesis that both modes of training would illicit the same strength gains was supported; moreover, they also yielded the same FG and lactate responses over time. Therefore, although the fasting blood glucose reductions with HIRT were already significant, data were combined from both modes of training to increase statistical power for glucose and lactate changes. The hypothesis that FG would decrease more in CON than FH was not supported, though fasting blood glucose decreased in CON and FH alike with training (p < 0.01). This is the first study demonstrating that blood glucose concentrations are reduced similarly in FH and CON with HIRFT. In addition, there were no differences in glucose or lactate variables between men and women. This is in agreement with our previous work that detected impaired metabolic flexibility in FH (38), also with no gender differences.
Both modes of training were combined for statistical analysis for glucose and lactate. A high-volume load for strength training was used to increase potential exercise benefits, specifically because previous research indicates that 8 weeks of low-intensity low-volume resistance is not sufficient to decrease metabolic risk factors in T2D (18). In contrast, Bacchi et al. (2) show short-term (3 times per week for 10 weeks) resistance training significantly reduces HbA1c and improves 48-hour glycemic variation as measured by continuous glucose monitoring system. Furthermore, high-intensity interval training has been shown to improve homeostatic model of insulin resistance in individuals with T2D in as little as 2 weeks (40). Our HIRFT protocol involves HIRFT 5 days per week, alternating workouts. Thus, the total number of workouts performed in this study was higher, making the relatively short training interval more effective. Finally, rodent models indicate that a combination of aerobic and resistance training can increase phosphorylated p70S6K, a marker of mTORC1, after only 1 bout of combined training, indicating the activation of pathways leading to muscle synthesis (30). Resistance training is associated with increased strength and increased muscle mass as well as improved whole-body glucose disposal rate (12), which would help explain the reductions of FG and postrecovery lactate in this study. However, we were unable to determine whether glucose disposal occurred because of increased microvascular nutritive flow or increased muscle mass as a result of HIRFT. In this study, strength increased on average 51.2% with training overall. Furthermore, a recent study indicated that similar resistance-type circuit training can decrease metabolic risk factors in young overweight males (9). The increased strength observed in this study suggests that the stimulus used for resistance training was sufficient to elicit a physiologic adaptation of muscle; however, lean muscle mass was not specifically evaluated in this study.
Fasting blood glucose decreased with training. There were no differences in the FG reductions between groups with training. This similar glucose reduction between groups indicates that although the FH population (recruited from the same pool as this study) has impaired metabolic flexibility independent of any glycemic problems (38), their glucoregulatory function seems to adapt to resistance exercise training in a similar fashion as CON. The overall decline in fasting blood glucose concentrations indicates tighter glucoregulatory control after training. This may be because of greater glucose uptake in muscle as previously indicated (12). However, reduced hepatic glucose release cannot be ruled out because we did not measure the glucose source specifically. Therefore, it was not possible to distinguish between glucose appearance and removal rates, and thus we only described what is acutely found in the blood at specific time points. However, postexercise blood glucose decreased more dramatically during passive recovery after training in both groups, indicating greater glucose removal with training. Nonetheless, whether a fasting decrease was from reduced appearance or increased removal, a tighter blood glucose regulation exists after training, further supporting previous studies that this type of training reduces IR (4,9) independent of body mass changes. Recent studies indicate that microvascular IR precedes conduit artery and muscle IR and contributes to the progression of cardiometabolic syndrome (34). If decreased glucose concentration during passive recovery seen after training is due to increased glucose removal, it is possible that training increases nutritive routes of microvascular recruitment, leading to greater myocyte perfusion and glucose uptake. This would not only explain why FG decreased with training but would also help explain the faster postexercise recovery time as indicated by more dramatic 10-minute reductions in both glucose and lactate. More work needs to be performed to examine the effects of resistance training on microvascular recruitment, especially in the FH population.
In this study, there were no changes in fasting lactate; however, sharp increases in lactate in both groups were observed immediately after exercise before and after 7 weeks of training. However, this acute postexercise lactate increase was higher after training than pretraining (9.2 ± 0.7 vs. 11.9 ± 0.8, p = 0.034), indicative of training adaptations (36). In conjunction with increased estimated 1RM, this increased lactate indicates that a greater absolute workload was achieved after 7 weeks of training without increasing the relative workload. This may be because of greater muscle mass with training, though no increases in body weight were noted. Though blood lactate was higher immediately after acute exercise with training, there were no differences in blood lactate after 10 minutes of passive recovery from pre- to posttraining. This indicates a greater rate of lactate removal with training (Figure 3). This greater decrease in blood lactate concentrations may be an indication of higher oxidative enzyme capacity with training, as much lactate is removed by oxidative muscle fibers adjacent to lactate-producing glycolytic fibers and by the liver (5,42).
Although no prescreening testing for metabolic flexibility was performed, FH is at much higher risk of developing T2D (51) and has impaired metabolic flexibility equal to those with T2D during an oral glucose challenge (38). Therefore, we fully expect the FH group in this study to have the same metabolic impairments. This is the first study to demonstrate that HIRFT, including resistance circuits, core, and plyometrics, as well as traditional multiset resistance training with core and plyometrics are equally effective in reducing blood glucose and increasing strength in relatively inactive young adults with and without a family history of T2D equally. Moreover, the inverse correlation between strength gains and reduction in blood glucose in FH suggests that HIRFT could be an effective form of exercise medicine to prevent the development of T2D in this population. Of particular importance in studying the FH population is that they lack many of the confounding factors that are linked with diabetes and prediabetes, yet are predisposed to metabolic impairment (38). Not only does this research directly apply to the FH population but it also helps isolate the earliest detectible challenges in metabolic function that may be responsible for the development of T2D. In addition, it is likely that the short-time commitment for this kind of exercise may lead to better adherence of training over time, resulting in better overall cardiometabolic health. Further research is needed to determine specific mechanisms whereby resistance training alters cardiometabolic health in the FH population.
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