Moderate-Intensity Exercise and High-Intensity Interval Training Affect Insulin Sensitivity Similarly in Obese Adults

Abstract

<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Objective</jats:title> <jats:p>We compared the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on insulin sensitivity and other important metabolic adaptations in adults with obesity.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>Thirty-one inactive adults with obesity (age: 31 ± 6 years; body mass index: 33 ± 3 kg/m2) completed 12 weeks (4 sessions/week) of either HIIT (10 × 1-minute at 90%HRmax, 1-minute active recovery; n = 16) or MICT (45 minutes at 70%HRmax; n = 15). To assess the direct effects of exercise independent of weight/fat loss, participants were required to maintain body mass.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Training increased peak oxygen uptake by ~10% in both HIIT and MICT (P &amp;lt; 0.0001), and body weight/fat mass were unchanged. Peripheral insulin sensitivity (hyperinsulinemic-euglycemic clamp) was ~20% greater the day after the final exercise session compared to pretraining (P &amp;lt; 0.01), with no difference between HIIT and MICT. When trained participants abstained from exercise for 4 days, insulin sensitivity returned to pretraining levels in both groups. HIIT and MICT also induced similar increases in abundance of many skeletal muscle proteins involved in mitochondrial respiration and lipid and carbohydrate metabolism. Training-induced alterations in muscle lipid profile were also similar between groups.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion</jats:title> <jats:p>Despite large differences in training intensity and exercise time, 12 weeks of HIIT and MICT induce similar acute improvements in peripheral insulin sensitivity the day after exercise, and similar longer term metabolic adaptations in skeletal muscle in adults with obesity. These findings support the notion that the insulin-sensitizing effects of both HIIT and MICT are mediated by factors stemming from the most recent exercise session(s) rather than adaptations that accrue with training.</jats:p> </jats:sec>

Mechanisms underlying the metabolic actions of testosterone in humans: A narrative review

“…18,19 A few weeks of exercise can enhance insulin sensitivity by 20% in previously sedentary obese adults, independent of weight loss. 20,21 However, the main effect of exercise on glucose uptake in the working skeletal muscle is insulin-independent and is partly mediated via AMPK. 22 An interesting aspect to consider is that testosterone treatment may improve fatigue and physical * Testosterone ) n i m / g k / g m ( e t a r n o i s u f n i e s o c u l G 0 2 4 6 8 10 baseline 3 weeks 24 weeks Placebo F I G U R E 1 Insulin sensitivity, expressed as glucose infusion rate during hyperinsulinaemic euglycaemic clamps, after treatment with intramuscular testosterone or saline (placebo) for 24 weeks in men with hypogonadism and type 2 diabetes.…”

Exercise training decreases whole‐body and tissue iron storage in adults with obesity

“…Our finding that the abundance of myoglobin in skeletal muscle was unaffected by exercise training is in accordance with previous findings in humans (Jacobs et al, 1987;Svedenhag et al, 1983) and indicates that the reduction in skeletal muscle iron storage was not driven by myoglobin expansion. We previously reported that HIIT and MICT increased the abundance of mitochondrial respiratory proteins to a similar extent (Ryan et al, 2020b); several of the mitochondrial respiratory complexes contain functional iron, and it is likely that the decrease in muscle iron storage supports both local (i.e., skeletal muscle) and systemic iron homeostasis. Given that excess iron accumulation in skeletal muscle has been linked with increased oxidative stress and consequent cellular dysfunction (Liang et al, 2019;Reardon & Allen, 2009), training-mediated lowering of muscle iron storage might be beneficial for individuals with obesity and elevated muscle iron stores.…”

Are Alterations in Skeletal Muscle Mitochondria a Cause or Consequence of Insulin Resistance?

“…However, the lack of improvement in blood glucose in that study may have been due to insufficient exercise frequency [16,17]. Exercise-induced improvements in insulin resistance were recently shown to disappear after four non-exercise days [63], while other studies have reported a much slower decline in mitochondrial content [49]. This suggests that although exercise training is able to improve insulin resistance and increase muscle mitochondrial content, exercise-induced improvements in insulin resistance may be related to acute effects rather than longer-term changes such as alterations in mitochondrial content.…”