Practical internal and external cooling methods do not influence rapid recovery from simulated taekwondo performance.

Background/Objectives: The influence of post-exercise cooling on recovery has gained much attention in the empirical literature, however, data is limited in regards to optimizing recovery from taekwondo performance when combat is repeated in quick succession within the same day. The aim of this study was therefore to compare the effects of external and internal cooling after simulated taekwondo combat upon intestinal temperature (Tint), psychomotor skills (reaction time, response time, movement time), and neuromuscular function (peak torque, average power, time to reach peak torque). Methods: Using a randomized counterbalanced crossover design, 10 well-trained male taekwondo athletes completed four recovery methods on separate occasions: passive recovery (CON), a 5-minute thermoneutral water immersion (35°C) (TWI), a 5-min cold water immersion (15°C) (CWI), and ice slurry ingestion (-1°C) (ICE; consumed every 5 min for 30 min). Heart rate (HR), blood lactate (Blac) concentrations, and Tint were determined at rest, immediately after combat, and at selected intervals during a 90-min recovery period. Neuromuscular functional (measured with isokinetic dynamometer) and psychomotor indices were assessed at baseline and after the recovery period. Results: ICE led to a significantly lower Tint at 30 min (P<0.01) and 45 min (P<0.01) after simulated combat; 15-30 min after cessation of ingesting ice slurry, compared with the CON and TWI conditions, respectively. However, there were no differences in Tint across time points between the other conditions (P>0.05). Psychomotor skills and neuromuscular function indices returned to baseline values after the 90 min recovery period (P>0.05) with no differences observed between conditions (P>0.05). Conclusion: The present findings suggest that internal (ICE) and external (CWI) recovery methods appear to have little impact on physiological and functional indices over the time course required to influence repeated taekwondo combat performance.

Calorie restriction prevents the development of insulin resistance and impaired insulin signaling in skeletal muscle of ovariectomized rats.

Insulin resistance of skeletal muscle glucose transport due to prolonged loss of ovarian function in ovariectomized (OVX) rats is accompanied by other features of the metabolic syndrome and may be confounded by increased calorie consumption. In this study, we investigated the role of calorie consumption in the development of insulin resistance in OVX rats. In addition, we examined the cellular mechanisms underlying skeletal muscle insulin resistance in OVX rats. Female Sprague-Dawley rats were ovariectomized (OVX) or sham-operated (SHAM). OVX rats either had free access to food, pair feeding (PF) with SHAM or received a 35% reduction in food intake (calorie restriction; CR) for 12weeks. Compared with SHAM, ovariectomy induced skeletal muscle insulin resistance, which was associated with decreases (32-70%) in tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-1 (IRS-1), IRS-1 associated p85 subunit of phosphatidylinositol 3-kinase (PI3-kinase), and Akt Ser(473) phosphorylation whereas insulin-stimulated phosphorylation of IRS-1 Ser(307), SAPK/JNK Thr(183)/Tyr(185), and p38 mitogen-activated protein kinase (MAPK) Thr(180)/Tyr(182) was increased (24-62%). PF improved the serum lipid profile but did not restore insulin-stimulated glucose transport, indicating that insulin resistance in OVX rats is a consequence of ovarian hormone deprivation. In contrast, impaired insulin sensitivity and defective insulin signaling were not observed in the skeletal muscle of OVX+CR rats. Therefore, we provide evidence for the first time that CR effectively prevents the development of insulin resistance and impaired insulin signaling in the skeletal muscle of OVX rats.

Contraction regulates site-specific phosphorylation of TBC1D1 in skeletal muscle.

TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) is a Rab-GAP (GTPase-activating protein) that is highly expressed in skeletal muscle, but little is known about TBC1D1 regulation and function. We studied TBC1D1 phosphorylation on three predicted AMPK (AMP-activated protein kinase) phosphorylation sites (Ser231, Ser660 and Ser700) and one predicted Akt phosphorylation site (Thr590) in control mice, AMPKα2 inactive transgenic mice (AMPKα2i TG) and Akt2-knockout mice (Akt2 KO). Muscle contraction significantly increased TBC1D1 phosphorylation on Ser231 and Ser660, tended to increase Ser700 phosphorylation, but had no effect on Thr590. AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside) also increased phosphorylation on Ser231, Ser660 and Ser700, but not Thr590, whereas insulin only increased Thr590 phosphorylation. Basal and contraction-stimulated TBC1D1 Ser231, Ser660 and Ser700 phosphorylation were greatly reduced in AMPKα2i TG mice, although contraction still elicited a small increase in phosphorylation. Akt2 KO mice had blunted insulin-stimulated TBC1D1 Thr590 phosphorylation. Contraction-stimulated TBC1D1 Ser231 and Ser660 phosphorylation were normal in high-fat-fed mice. Glucose uptake in vivo was significantly decreased in tibialis anterior muscles overexpressing TBC1D1 mutated on four predicted AMPK phosphorylation sites. In conclusion, contraction causes site-specific phosphorylation of TBC1D1 in skeletal muscle, and TBC1D1 phosphorylation on AMPK sites regulates contraction-stimulated glucose uptake. AMPK and Akt regulate TBC1D1 phosphorylation, but there must be additional upstream kinases that mediate TBC1D1 phosphorylation in skeletal muscle.

Attenuation of oxidant-induced muscle insulin resistance and p38 MAPK by exercise training.

We have recently shown that direct exposure to an oxidant stress induces resistance to insulin in glucose transport activity in intact rat skeletal muscle. In this study, we evaluated the effectiveness of prior exercise training in attenuating oxidative stress-induced insulin resistance. Male Sprague-Dawley rats either remained sedentary or underwent a treadmill-running regimen for 6 weeks. Isolated soleus muscles were incubated in the absence or presence of hydrogen peroxide (H(2)O(2)) (50-70 microM) with or without insulin for 2 h. In the sedentary animals, H(2)O(2) significantly inhibited insulin action on glucose transport activity and phosphorylation of Akt (Ser(473)), by 28 and 24%, respectively, and substantially activated the phosphorylation levels of p38 MAPK (Thr(180)/Tyr(182)) by 43% and SAPK/JNK (Thr(183)/Tyr(185)) by 111%. Interestingly, the inhibitory effects of H(2)O(2) on insulin-stimulated glucose transport and Akt (Ser(473)) phosphorylation were attenuated by 43 and 75% in exercise-trained muscles. Additionally, the phosphorylation level of p38 MAPK (Thr(180)/Tyr(182)) triggered by oxidative stress was reduced by 59% in the exercise-trained muscle. We have demonstrated for the first time in mammalian skeletal muscle that endurance exercise training can partially protect against glucose transport resistance to insulin induced by oxidative stress, and this benefit of exercise training is at least in part mediated through the insulin signaling pathway and stress-activated signaling elements.

Modulation of insulin resistance in ovariectomized rats by endurance exercise training and estrogen replacement.

Estrogen is known to play a role in fat metabolism, but its role in carbohydrate metabolism remains controversial. We investigated alterations in carbohydrate and fat metabolism after prolonged estrogen deprivation by determining body weight, food intake, visceral fat content, serum lipids, glucose tolerance, and insulin action on glucose transport activity in isolated soleus and extensor digitorum longus muscles. In addition, effects of endurance exercise training with or without estrogen replacement on metabolic alterations occurring under estrogen deficiency were examined. Female Sprague-Dawley rats were ovariectomized (OVX) or sham-operated (SHAM). The OVX rats remained sedentary, received 5 microg of 17beta-estradiol (E(2)), performed exercise training (ET), or underwent both estrogen treatment and exercise training (E(2) + ET) for 12 weeks. Compared with SHAM, OVX animals had greater final body weights, visceral fat content, and serum levels of total and low-density lipoprotein cholesterol (P < .05). Exercise training and E(2) significantly reduced body weights (6% and 25%), visceral fat (37% and 51%), and low-density lipoprotein cholesterol level (19% and 26%). Exercise training alone improved whole-body glucose tolerance (29%), which was enhanced to the greatest extent (51%) in the ET rats that also received E(2). Insulin-stimulated glucose transport activity in OVX group was lower than that in SHAM by 29% to 44% (P < .05). Exercise training and E(2) corrected the diminished insulin action on skeletal muscle glucose transport in OVX animals, which was partly due to elevated glucose transporter-4 protein expression. These findings indicate that 12 weeks of ovariectomy caused metabolic alterations mimicking features of the insulin resistance syndrome. Furthermore, these metabolic disturbances were attenuated by ET or E(2), whereas the beneficial interactive effects of ET and E(2) on these defects were not apparent.