Effects of high-intensity intermittent swimming on glucose transport in rat epitrochlearis muscle

1998 ◽  
Vol 84 (6) ◽  
pp. 1852-1857 ◽  
Author(s):  
Kentaro Kawanaka ◽  
Izumi Tabata ◽  
Ayumi Tanaka ◽  
Mitsuru Higuchi

Recently (K. Kawanaka, I. Tabata, and M. Higuchi. J. Appl. Physiol. 83: 429–433, 1997), we demonstrated that glucose transport activity after repeated 10-s-long in vitro tetani in rat epitrochlearis (Epi) muscle was negatively correlated with the postcontraction muscle glycogen concentration. Therefore, we examined whether high-intensity intermittent swimming, which depletes muscle glycogen to a lower level than that observed after ten 10-s-long in vitro tetani, elicits higher glucose transport than that observed after ten 10-s-long in vitro tetani, which has been regarded as the exercise-induced maximal stimulus for glucose transport. In male rats, 2-deoxy-d-glucose transport rate in Epi muscle after eight bouts of high-intensity intermittent swimming with a weight equal to 18% of body mass (exercise duration: 20 s, rest duration between exercise bouts: 40 s) was higher than that observed after the ten 10-s-long tetani (2.25 ± 0.08 vs. 1.02 ± 0.16 μmol ⋅ ml intracellular water−1 ⋅ 20 min−1). Muscle glycogen concentration in Epi after eight bouts of high-intensity intermittent swimming was significantly lower than that observed after ten 10-s-long in vitro tetani (7.6 ± 0.5 vs. 14.8 ± 1.4 μmol glucose/g muscle). These observations show that the high-intensity intermittent swimming increases glucose transport in rat Epi to a much higher level than that induced by ten 10-s-long in vitro tetani, which has been regarded as the exercise-related maximal stimulus for glucose transport. Furthermore, this finding suggests that the lower muscle glycogen level after high-intensity intermittent swimming than after in vitro tetani may play a role, because there was a significant negative correlation between glucose transport and muscle glycogen concentration in Epi after high-intensity swimming and in vitro tetani.

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Kenya Takahashi ◽  
Yu Kitaoka ◽  
Yutaka Matsunaga ◽  
Hideo Hatta

Objective High-intensity exercise, which increases blood lactate concentration, is known as an effective method to induce mitochondrial biogenesis compared to traditional endurance exercise. In addition, it has been reported that lactate acts as a signaling molecule inducing mitochondrial biogenesis. Therefore, we hypothesized that efficacy of high-intensity exercise is partly induced by lactate. The purpose of this study was to investigate the effects of lactate administration on signaling related to mitochondrial biogenesis. Methods 8-week-old male ICR mice were used in this study. Mice were intraperitoneally administrated phosphate buffered saline (PBS) or 1 g/kg of body weight of sodium lactate. Immediately after the administration, mice were kept sedentary or performed treadmill exercise (20 m/min) for 60 min. Hence, there are the following four groups in this study: the PBS-sedentary, the Lactate-sedentary, the PBS-exercised and the Lactate-exercised. The blood, and the soleus and the plantaris muscles were harvested immediately after the rest or exercise. Nucleus and mitochondria were isolated to assess the localization of p53. Two-way ANOVA (Lactate x Exercise) was performed for statistical analysis. Results We first measured blood substrates and muscle glycogen concentrations. Lactate administration significantly increased blood lactate and plasma free fatty acid concentrations. Exercise significantly decreased glycogen concentration both in the soleus and the plantaris muscles. Furthermore, lactate administration significantly decreased muscle glycogen concentration only in the soleus muscle. To clarify the effects of lactate administration on intramuscular signaling, we assessed kinases related to mitochondrial biogenesis. Main effect of exercise was observed in phosphorylation state of AMPK, ACC, p38 MAPK, and CaMKII in the soleus and the plantaris muscles. There was a trend of negative effect of lactate in CaMKII phosphorylation in the soleus muscle. However, there was no effect of lactate administration on the other kinases. We also investigated phosphorylation and localization of p53. As a result, lactate administration tended to increase p53 phosphorylation in the plantaris muscle. However, p53 was not translocated to nucleus or mitochondria. Conclusions Lactate administration affected plasma FFA concentration and muscle glycogen concentration. However, acute lactate administration did not dramatically change intracellular signaling assessed in this study. 


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Gemma Sanguesa ◽  
Aline Meza ◽  
Anna Alcarraz ◽  
Cira Rubies ◽  
Lluis Mont ◽  
...  

Introduction: There is emerging evidence in men that sustained high-intensity training promotes an adverse cardiovascular remodeling, thereby increasing the risk of atrial fibrillation, ventricular arrhythmias and coronary calcification. Whether men and women are similarly affected by high intensity exercise-induced harm is unclear. Our aim was to study sex differences in a long-term endurance training rat model. Methods: Male and female Wistar rats were subjected to high intensity training for 16 weeks (INT, 60min 60cm/s, male n=20, female n=15). Sedentary rats (SED, male n=20, female n=18) were used as controls. At the end of the training period, rats had an electrocardiogram and echocardiography performed. Vascular fibrosis was assessed in descending aorta, left carotid, and intramyocardial arteries (IMA), right and left atria, and left ventricle (LV) histological samples. mRNA levels of cardiac hypertrophy, fibrosis, oxidative stress and inflammation genes were assessed in LV samples by Real-Time PCR. Results: INT male rats presented lower heart rate (382±9, 340±10, SED vs INT, p<0.01) and a longer QRS duration (18.8±0.6, 22.4±1.1, SED vs INT, p<0.01), while these were not modified in the INT female group. Echocardiography showed eccentric LV hypertrophy in both trained male and female rats. High intensity exercise induced fibrosis in the descending aorta and carotid in both males and females, but IMA were only affected in trained male rats. In the heart, exercise-induced atrial fibrosis similarly occurred in both trained male and female rats. No training-induced fibrosis was evident in the LV of both INT male and female rats. Regarding LV mRNA analysis, INT males showed a reduction of desmin, TTN and N2BA/N2B ratio, whereas INT females exhibited higher desmin mRNA levels and lower αMHC/βMHC ratio. Intense exercise did not increase LV mRNA levels of fibrosis, oxidative stress and inflammation markers neither in males nor in females. In comparison to males, females had lower LV myocardial fibrosis as well as lower fibrosis markers. Conclusions: Male and female rats exhibit qualitatively different cardiovascular remodeling after extreme exercise. Nevertheless, both sexes might develop exercise-induced adverse vascular and cardiac effects.


1997 ◽  
Vol 272 (4) ◽  
pp. E649-E655 ◽  
Author(s):  
J. Jensen ◽  
R. Aslesen ◽  
J. L. Ivy ◽  
O. Brors

The effects of diet-manipulated variations in muscle glycogen concentration and epinephrine on glucose uptake were studied in epitrochlearis muscles from Wistar rats. Both basal and insulin-stimulated glucose uptake [measured with a tracer amount of 2-[1,2-3H(N)]deoxy-D-glucose] inversely correlated with initial glycogen concentration (glycogen concentration vs. basal glucose uptake: Spearman's rho = -0.76, n = 84, P < 0.000001; glycogen concentration vs. insulin-stimulated glucose uptake: Spearman's rho = -0.67, n = 44, P < 0.00001). Two fasting-refeeding procedures were used that resulted in differences in muscle glycogen concentrations, although with similar treatment for the last 48 h before the experiment. In the rats with the lower glycogen concentration, basal as well as insulin-stimulated glucose uptake was elevated. The muscle glycogen concentration had no effect on epinephrine-stimulated glycogenolysis. Epinephrine, however, was found to reduce basal glucose uptake in all groups. These results suggest that 1) the glycogen concentration participates in the regulation of both basal and insulin-stimulated glucose uptake in skeletal muscle, 2) the magnitude of epinephrine-stimulated glycogen breakdown is independent of the glycogen concentration, and 3) epinephrine inhibits basal glucose uptake at all glycogen concentrations.


2005 ◽  
Vol 45 (5) ◽  
pp. 543 ◽  
Author(s):  
R. H. Jacob ◽  
D. W. Pethick ◽  
H. M. Chapman

The aim of this study was to gain an understanding of the distribution of glycogen concentrations and ultimate pH (pHu) in 2 different muscle types for lambs slaughtered under commercial conditions in Western Australia, and to compare muscle glycogen concentrations in lambs on farm and after slaughter. The study included 13 different consignments of prime lambs from a range of commercial scenarios. In each consignment, muscle glycogen concentration was measured in a group of lambs on farm and subsequently after slaughter in 3 different lairage groups. The lairage groups were: slaughter on arrival (no lairage), slaughter after 1 day, and slaughter after 2 days in lairage. Biopsies of M. semimembranosus and the M. semitendinosus were taken from live lambs on farm just before farm curfew before transport and from carcasses immediately after slaughter. There was a significant effect of consignment on muscle glycogen concentration. Muscle glycogen concentrations on farm were lower than 1 g/100 g in 4 consignments for the M. semimembranosus and 11 consignments for the M. semitendinosus. The cause of the differences between consignments was unclear as nutrition, genotype and age class were confounded between consignments. Glycogen concentrations were lower and meat pHu higher for sucker lamb compared with carry-over lamb consignments. However, lambs finished on grain-based feedlot rations had higher muscle glycogen concentrations than lambs finished on pasture and sucker lambs when finished on pastures only. Sucker lambs were only crossbred while carry-over lambs included crossbred and Merino genotypes. When data from different consignments were pooled and the effect of consignment was considered, there were no differences between muscle glycogen concentration measured on farm and muscle glycogen concentration measured after slaughter. However, there were differences between sample times within individual consignments. Glycogen concentration at slaughter was different from glycogen concentration on farm in more consignments for M. semitendinosus than M. semimembranosus, suggesting a difference between consignments for the effect caused by stress. Typically, the M. semimembranosus glycogen concentration at slaughter was lower than on farm in consignments consisting of Merino genotypes that had high muscle glycogen concentrations on farm. In the consignments in which lairage time had an effect on muscle glycogen concentration, the differences were small. In some consignments a difference occurred between lairage times for pHu without any difference occurring for muscle glycogen concentration.


1987 ◽  
Vol 253 (4) ◽  
pp. E331-E335 ◽  
Author(s):  
D. A. Young ◽  
H. Wallberg-Henriksson ◽  
M. D. Sleeper ◽  
J. O. Holloszy

Exercise is associated with an increase in permeability of muscle to glucose that reverses slowly (h) in fasting rats during recovery. Previous studies showed that carbohydrate feeding speeds and carbohydrate restriction slows reversal of the exercise-induced increase in glucose uptake. This study was designed to evaluate the roles of glucose transport, glycogen synthesis, and protein synthesis in the reversal process in rat epitrochlearis muscle. In contrast to recovery in vivo, when muscles were incubated without insulin in vitro, the exercise-induced increase in muscle permeability to sugar reversed rapidly regardless of whether glucose transport or glycogen synthesis occurred. Inhibition of protein synthesis did not prevent the reversal. Addition of 33% rat serum or a low concentration of insulin to the incubation medium markedly slowed reversal in vitro. We conclude that 1) prolonged persistence of the increased permeability of mammalian muscle to glucose after exercise requires a low concentration of insulin, and 2) reversal of the increase in permeability does not require glucose transport, glycogen synthesis, or protein synthesis.


1990 ◽  
Vol 259 (5) ◽  
pp. E685-E691 ◽  
Author(s):  
E. A. Gulve ◽  
G. D. Cartee ◽  
J. R. Zierath ◽  
V. M. Corpus ◽  
J. O. Holloszy

Exercise stimulates insulin-independent glucose transport in skeletal muscle and also increases the sensitivity of the glucose transport process in muscle to insulin. A previous study [D. A. Young, H. Wallberg-Henriksson, M. D. Sleeper, and J. O. Holloszy. Am. J. Physiol. 253 (Endocrinol. Metab. 16): E331–E335, 1987] showed that the exercise-induced increase in glucose transport activity disappears rapidly when rat epitrochlearis muscles are incubated for 3 h in vitro in the absence of insulin and that 7.5 microU/ml insulin in the incubation medium apparently slowed the loss of enhanced sugar transport. We examined whether addition of insulin several hours after exercise increases glucose transport to the same extent as continuous insulin exposure. Addition of 7.5 microU/ml insulin 2.5 h after exercise (when glucose transport has returned to basal levels) increased sugar transport to the same level as that which resulted from continuous insulin exposure. This finding provides evidence for an increase in insulin sensitivity rather than a slowing of reversal of the exercise-induced increase in insulin-independent glucose transport activity. Glucose transport was enhanced only at submaximal, not at maximal, insulin concentrations. Exposure to a high concentration of glucose and a low insulin concentration reduced the exercise-induced increase in insulin-sensitive glucose transport. Incubation with a high concentration of 2-deoxy-D-glucose (2-DG) did not alter the increase in insulin sensitivity, even though a large amount of 2-DG entered the muscle and was phosphorylated.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 74 (6) ◽  
pp. 2998-3005 ◽  
Author(s):  
J. J. Widrick ◽  
D. L. Costill ◽  
W. J. Fink ◽  
M. S. Hickey ◽  
G. K. McConell ◽  
...  

To determine whether the ergogenic benefits of carbohydrate (CHO) feedings are affected by preexercise muscle glycogen levels, eight cyclists performed four self-paced time trials on an isokinetic ergometer over a simulated distance of 70 km. Trials were performed under the following preexercise muscle glycogen and beverage conditions: 1) high glycogen (180.2 +/- 9.7 mmol/kg wet wt) with a CHO beverage (HG-CHO), 2) high glycogen (170.2 +/- 10.4 mmol/kg wet wt) with a non-CHO beverage (HG-NCHO), 3) low glycogen (99.8 +/- 6.0 mmol/kg wet wt) with a CHO beverage (LG-CHO), and 4) low glycogen (109.7 +/- 5.3 mmol/kg wet wt) with a non-CHO beverage (LG-NCHO). The CHO drink (ingested at the onset of exercise and every 10 km thereafter) provided 116 +/- 6 g CHO/trial and prevented the decline in serum glucose observed during both NCHO trials. Performance times ranged from 117.93 +/- 1.44 (HG-CHO) to 122.91 +/- 2.46 min (LG-NCHO). No intertrial differences (P > 0.05) were observed for O2 consumption (75% of maximal O2 consumption), power output (237 W), or self-selected pace (8.44 min/5 km) during the initial 71–79% of exercise. Over the final 14% of the time trial, power output and pace (231 W and 8.62 min/5 km) were similar for the HG-CHO, HG-NCHO, and LG-CHO conditions, but both variables were significantly lower during the LG-NCHO trial (198 W and 9.67 min/5 km, P < 0.05 vs. all other trials).(ABSTRACT TRUNCATED AT 250 WORDS)


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