No abstract

Acute exercise improves insulin sensitivity for hours after the exercise is ceased. The skeleton contributes to glucose metabolism and insulin sensitivity via osteocalcin (OC) in its undercarboxylated (ucOC) form in mice. We tested the hypothesis that insulin sensitivity over the hours after exercise is associated with circulating levels of ucOC. Eleven middle-aged (58.1 AE 2.2 years mean AE SEM), obese (body mass index [BMI] ¼ 33.1 AE 1.4 kg/m 2 ) nondiabetic men completed a euglycemic-hyperinsulinemic clamp at rest (rest-control) and at 60 minutes after exercise (4 Â 4 minutes of cycling at 95% of HR peak ). Insulin sensitivity was determined by glucose infusion rate relative to body mass (GIR, mL/kg/min) as well as GIR per unit of insulin (M-value). Blood samples and five muscle biopsies were obtained; two at the resting-control session, one before and one after clamping, and three in the exercise session, at rest, 60 minutes after exercise, and after the clamp. Exercise increased serum ucOC (6.4 AE 2.1%, p ¼ 0.013) but not total OC (p > 0.05). Blood glucose was $6% lower and insulin sensitivity was $35% higher after exercise compared with control (both p < 0.05). Phosphorylated (P)-AKT (Ak thymoma) was higher after exercise and insulin compared with exercise alone (no insulin) and insulin alone (no exercise, all p < 0.05). In a multiple-linear regression including BMI, age, and aerobic fitness, ucOC was associated with whole-body insulin sensitivity at rest (b ¼ 0.59, p ¼ 0.023) and after exercise (b ¼ 0.66, p ¼ 0.005). Insulin sensitivity, after acute exercise, is associated with circulating levels of ucOC in obese men. Whether ucOC has a direct effect on skeletal muscle insulin sensitivity after exercise is yet to be determined.

The aim of the current study was to examine the influence of exercise intensity on systemic oxidative stress (OS) and endogenous antioxidant capacity. Non-smoking, sedentary healthy adult males (n = 14) participated in two exercise sessions using an electronically braked cycle ergometer. The first session consisted of a graded exercise test to determine maximal power output and oxygen consumption (VO(2max)). One week later, participants undertook 5-min cycling bouts at 40%, 55%, 70%, 85% and 100% of VO(2max), with passive 12-min rest between stages. Measures of systemic OS reactive oxygen metabolites (dROM), biological antioxidant potential (BAP), heart rate (HR), VO(2), blood lactate and rating of perceived exertion were assessed at rest and immediately following each exercise stage. Significant (P<0·05) differences between exercise bouts were examined via repeated measures ANOVA and post hoc pairwise comparisons with Bonferroni correction. Increasing exercise intensity significantly augmented HR (P<0·001), VO(2) (P<0·001), blood lactate (P<0·001) and perceived exertion (P<0·001) with no significant effect on dROM levels compared with resting values. In contrast, increasing exercise intensity resulted in significantly (P<0·01) greater BAP at 70% (2427 ± 106), 85% (2625 ± 121) and 100% (2651 ± 92) of VO(2max) compared with resting levels (2105 ± 57 μmol Fe(2+)/L). The current results indicate that brief, moderate-to-high-intensity exercise significantly elevates endogenous antioxidant defences, possibly to counteract increased levels of exercise-induced reactive oxygen species. Regular moderate-to-high-intensity exercise may protect against chronic OS associated diseases via activation, and subsequent upregulation of the endogenous antioxidant defence system.

Background: Obesity and aging are associated with increased oxidative stress, activation of stress and mitogen activated protein kinases (SAPK), and the development of insulin resistance and metabolic disease. In contrast, acute exercise also increases oxidative stress and SAPK signaling, yet is reported to enhance insulin sensitivity and reduce the risk of metabolic disease. This study explored this paradox by investigating the effect of a single session of high-intensity interval-exercise (HIIE) on redox status, muscle SAPK and insulin protein signaling in eleven middle-aged obese men.Methods: Participants completed a 2 h hyperinsulinaemic-euglycaemic clamp at rest, and 60 min after HIIE (4 × 4 mins at 95% HRpeak; 2 min recovery periods), separated by 1–3 weeks.Results: Irrespective of exercise-induced changes to redox status, insulin stimulation both at rest and after HIIE similarly increased plasma superoxide dismutase activity, plasma catalase activity, and skeletal muscle 4-HNE; and significantly decreased plasma TBARS and hydrogen peroxide. The SAPK signaling pathways of p38 MAPK, NF-κB p65, and JNK, and the distal insulin signaling protein AS160Ser588, were activated with insulin stimulation at rest and to a greater extent with insulin stimulation after a prior bout of HIIE. Higher insulin sensitivity after HIIE was associated with higher insulin-stimulated SOD activity, JNK, p38 MAPK and NF-κB phosphorylation (r = 0.63, r = 0.71, r = 0.72, r = 0.71; p < 0.05, respectively).Conclusion:These findings support a role for redox homeostasis and SAPK signaling in insulin-stimulated glucose uptake which may contribute to the enhancement of insulin sensitivity in obese men 3 h after HIIE.

Low-volume SIE elicited greater post-exercise plasma catalase activity compared to HIIE and CMIE, and greater HO compared to CMIE. Plasma redox status did not, however, adequately reflect skeletal muscle redox-sensitive protein signaling.