Abstract
Obesity, sedentary lifestyle and aging are associated with mitochondrial dysfunction and impaired insulin sensitivity. Acute exercise increases insulin sensitivity in skeletal muscle; however, whether mitochondria are involved in these processes remains unclear. The aim of this study was to investigate the effects of insulin stimulation at rest and after acute exercise on skeletal muscle mitochondrial respiratory function (JO2) and hydrogen peroxide emission (JH2O2), and the associations with insulin sensitivity in obese, sedentary men. Nine men (means ± SD: 57 ± 6 years; BMI 33 ± 5 kg.m2) underwent hyperinsulinemic-euglycemic clamps in two separate trials 1–3 weeks apart: one under resting conditions, and another 1 hour after high-intensity exercise (4x4 min cycling at 95% HRpeak). Muscle biopsies were obtained at baseline, and pre/post clamp to measure JO2 with high-resolution respirometry and JH2O2 via Amplex UltraRed from permeabilized fibers. Post-exercise, both JO2 and JH2O2 during ADP stimulated state-3/OXPHOS respiration were lower compared to baseline (P<0.05), but not after subsequent insulin stimulation. JH2O2 was lower post-exercise and after subsequent insulin stimulation compared to insulin stimulation in the rest trial during succinate supported state-4/leak respiration (P<0.05). In contrast, JH2O2 increased during complex-I supported leak respiration with insulin after exercise compared with resting conditions (P<0.05). Resting insulin sensitivity and JH2O2 during complex-I leak respiration were positively correlated (r = 0.77, P<0.05). We conclude that in obese, older and sedentary men, acute exercise modifies skeletal muscle mitochondrial respiration and H2O2 emission responses to hyperinsulinemia in a respiratory state-specific manner, which may have implications for metabolic diseases involving insulin resistance.
Highlights
More than one-third of the adult population worldwide are overweight or obese [1, 2]
The aims of this study were to test the hypothesis that in obese, older and sedentary individuals, mitochondrial respiration and H2O2 emission in permeabilized skeletal muscle fibers would be perturbed in a respiratory state-dependent manner in response to a hyperinsulinemic-euglycemic clamp to a greater extent when preceded by a single session of high intensity interval exercise (HIIE) compared to resting conditions
LEAK respiration: Throughout the SUIT protocol (Fig 2A), there were no significant effects of exercise and/or insulin on JO2 during LEAKCI+electron transfer flavoprotein (ETF) respiration state; in the presence of complex II substrate succinate (LEAKCI+II+ETF), JO2 trended lower in the rest trial after insulin compared to baseline (P = 0.09; Fig 2C)
Summary
More than one-third of the adult population worldwide are overweight or obese [1, 2]. Obesity increases the risk of developing insulin resistance, and this may be exacerbated by aging and sedentary lifestyle [3]. Regular exercise is a primary intervention for the prevention and management of metabolic diseases [4, 5]. The beneficial effects of exercise may occur in part by preventing or alleviating mitochondrial dysfunction which is thought to cause, or at least contribute to these pathophysiologic states [6,7,8]. Even a single bout of exercise increases whole body insulin sensitivity, primarily in skeletal muscle, for up to 48-h post-exercise [9, 10]. Whether skeletal muscle mitochondria are involved in mediating these effects after an acute bout of exercise currently remain unclear
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