Abstract
We sought to assess the residual effects (post 72-h training cessation) on fasting plasma glucose (FPG) and fasting insulin (FI) after 12-weeks of high-intensity interval training (HIIT), resistance training (RT), or concurrent training (CT) in women with insulin resistance (IR). We also aimed to determine the training-induced, post-training residual impact of CT. A total of adult 45 women (age 38.5±9.2years) were included in the final analysis and were assigned to a control (CG; n=13, BMI 28.3±3.6kg/m2), HIIT [n=14, BMI 28.6±3.6kg/m2, three sessions/wk., 80–100% of the maximum heart rate (HRmax)], RT [n=8, BMI 29.4±5.5kg/m2, two sessions/wk., 8–10 points of the modified Borg, corresponding to 20 to 50% range of one maximum repetition test (1RM)], or CT group (n=10, BMI 29.1±3.0kg/m2, three sessions/wk., 80–100% of HRmax, and 8–10 Borg, or 20 to 50% range of 1RM, to each HIIT and RT compounds), with the latter including both HIIT and RT regimens. Training interventions lasted 12-weeks. The main outcomes were FPG and FI measured at pre- and 24-h and 72-h post-training (FPG24h, FI24h, and FPG72h, FI72h, respectively). Secondary endpoints were body composition/anthropometry and the adiposity markers waist circumference (WC) and tricípital skinfold (TSF). The residual effects 72-h post-training [delta (∆)] were significantly poorer (all p<0.01) in the CT group (∆FPG72h+6.6mg/dl, η2: 0.76) than in the HIIT (∆FPG72h+1.2mg/dl, η2: 0.07) and RT (∆FPG72h+1.0mg/dl, η2: 0.05) groups. These findings reveal that HIIT reduces FPG and RT reduces FI 24-h post-training; both exercise interventions alone have remarkably better residual effects on FPG and FI (post-72h) than CT in women with insulin resistance.
Highlights
Insulin resistance (IR) is the inability of the insulin hormone to facilitate glucose uptake from peripheral tissues to meet metabolic demands (Abdul-Ghani and DeFronzo, 2010)
The residual effects 72-h post-training [delta (∆)] were significantly poorer in the concurrent training (CT) group (∆FPG72 h + 6.6 mg/dl, η2: 0.76) than in the High-intensity interval training (HIIT) (∆FPG72 h + 1.2 mg/dl, η2: 0.07) and resistance training (RT) (∆FPG72 h + 1.0 mg/dl, η2: 0.05) groups. These findings reveal that HIIT reduces fasting plasma glucose (FPG) and RT reduces fasting insulin (FI) 24-h posttraining; both exercise interventions alone have remarkably better residual effects on FPG and FI than CT in women with insulin resistance
We recently reported beneficial cardiometabolic outcomes in women with hyperglycemia after a 20-week CT intervention, including −4 mg/dl decreases in fasting plasma glucose (FPG), and other physiological adaptations in body composition (−4 cm waist circumference, +400 g increases in lean mass), cardiovascular system (−6/−3 mmHg reduction in systolic/diastolic blood pressure), and plasma lipoproteins (−11 mg/dl LDL-cholesterol reduction) and greater increases in endurance performance (+56 m in the 6-min walking test; Álvarez et al, 2019)
Summary
Insulin resistance (IR) is the inability of the insulin hormone to facilitate glucose uptake from peripheral tissues to meet metabolic demands (Abdul-Ghani and DeFronzo, 2010). The major beneficial metabolic effects of exercise training are associated with structural adaptations (i.e., changes to adipose, skeletal muscle, bone tissue, and vessels), and with residual effects (hours or days post-exercise) in at-risk populations (Andersen and Høstmark, 2007; Short et al, 2012; Burke et al, 2017). It is well known that some training regimens can promote improvements in several cardiometabolic markers (American Diabetes Association, 2017). RT promotes similar glucose control improvements to HIIT (Ross et al, 2021), by increasing skeletal muscle (Brooks et al, 2007) and bone mass (Wood and O’Neill, 2012) in patients with T2DM (Dunstan et al, 2002; Ross et al, 2021). At the level of physiological adaptations from HIIT, RT, and CT, the results are scarce at level of post-exercise cessation, and few studies, and few studies have monitored the residual effects on glucose control markers in IR cohorts (Short et al, 2012)
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