High-intensity Intermittent Swimming Research Articles

Effect of Eight Weeks of High-Intensity Intermittent Swimming Training on the Biochemical Factors of Lipid Metabolism and Hippocampal Memory Function of Male Rats with Non-Alcoholic Steatohepatitis (NASH)

Introduction: The molecular mechanisms of the improvement of exercise on memory are in the aura of ambiguity.Therefore, the aim of this research was studying the effect of eight weeks of high-intensity intermittent swimming training (HIIST) on the biochemical factors of lipid metabolism and hippocampal memory function of male rats with non-alcoholic steatohepatitis (NASH).
 Methods: The present study was experimental. 40 male Sprague-Dawley rats were divided into two groups: healthy (n=20) and high-fat HFD (n=20) groups. Rats in the HFD group were fed a high-fat diet for eight weeks with the aim of inducing NASH. After proving the disease in HFD group rats, the remaining rats were randomly divided into four groups: healthy-sedentary (n=9), healthy-swimming (n=9), sedentary disease (n=9) and diseased-swimming (n=9). The exercise groups performed eight weeks of HIIST (three sessions/week, each session lasting 30 minutes). At the end, FNDC5 protein was evaluated by western blot method and brain hippocampal irisin and serum FFA by ELISA method. Memory performance was measured by the water Maz-Morris behavioral test. One-way ANOVA test was used to determine the difference between groups, and Bonferroni's post hoc test was used to determine the difference between two groups (p<0.05).
 Results: The findings showed that there was a significant difference in the FNDC5 protein and irisin of the brain hippocampus and serum FFA and in memory function variables between the groups (p<0.05).
 Conclusion: HIIST in NASH model can activate lipid metabolism in the hippocampus of the brain and improve memory function. However, more research is needed in this field.

Effect of High-intensity Intermittent Swimming Training on peroxisome proliferator-activated receptors-αand Liver Enzymes in Non-alcoholic Steatohepatitis Male Rats

Introduction: Accumulation of fat in the liver tissue is known as the most important cause of non-alcoholic steatohepatitis, which is associated with a decrease in the protein of hepatic peroxisome proliferator-activated receptors (PPAR-α). This study aimed to investigate the effect of eight weeks of high-intensity interval training (HIST) on PPAR-α and liver enzymes in high-fat diet-induced non-alcoholic steatohepatitis rats.
 Methods: The current research was semi-experimental. 40 Spraguedauli male rats (age: 6 to 8 weeks and weight: 230 ± 20 grams) were selected and divided into two equal groups, healthy and high-fat diet (HFD). The HFD group was subjected to gavage for eight weeks with the aim of inducing the disease. Rats were divided into four groups: control-healthy (n=9), healthy-swimming (n=9), control- disease (n=9) and disease -swimming (n=9). The training groups performed HIST for eight weeks (three sessions per week, each session lasting 30 minutes). In the end, liver PPAR-α was measured by western blot analysis; and ALT, AST and GGT enzymes in serum level were measured by photometric method. One-way analysis of variance and Bonferroni's post hoc test were used to analyze the data. Significant level (P≥0.05) and all statistical methods were performed using SPSS16 software.
 Results: HIST controlled the weight gain caused by HFD and there was a significant decrease in serum ALT and AST in the healthy-swimming and sick-swimming groups compared to the control-patient group and a significant decrease in serum GGT in the healthy-swimming group compared to the control-patient (P≤0.001) and patient-swimming (P≤0.044) were observed. A significant increase in hepatic PPAR-α was observed in healthy-swimming patients compared to the control-patients (P≤0.002).
 Conclusion: HIST can control body weight and reduce liver enzymes. However, more research is needed to obtain definitive results.

Effects of Thiamin Restriction on Exercise-Associated Glycogen Metabolism and AMPK Activation Level in Skeletal Muscle

This study aimed to investigate the direct influence of a decrease in the cellular thiamin level, before the onset of anorexia (one of the symptoms of thiamin deficiency) on glycogen metabolism and the AMP-activated protein kinase (AMPK) activation levels in skeletal muscle at rest and in response to exercise. Male Wistar rats were classified as the control diet (CON) group or the thiamin-deficient diet (TD) group and consumed the assigned diets for 1 week. Skeletal muscles were taken from the rats at rest, those that underwent low-intensity swimming (LIS), or high-intensity intermittent swimming (HIS) conducted immediately before dissection. There were no significant differences in food intake, locomotive activity, or body weight between groups, but thiamin pyrophosphate in the skeletal muscles of the TD group was significantly lower than that of the CON group. Muscle glycogen and lactate levels in the blood and muscle were equivalent between groups at rest and in response to exercise. The mitochondrial content was equal between groups, and AMPK in the skeletal muscles of TD rats was normally activated by LIS and HIS. In conclusion, with a lowered cellular thiamin level, the exercise-associated glycogen metabolism and AMPK activation level in skeletal muscle were normally regulated.

Genome-wide identification of brain miRNAs in response to high-intensity intermittent swimming training in Rattus norvegicus by deep sequencing

BackgroundPhysical exercise can improve brain function by altering brain gene expression. The expression mechanisms underlying the brain’s response to exercise still remain unknown. miRNAs as vital regulators of gene expression may be involved in regulation of brain genes in response to exercise. However, as yet, very little is known about exercise-responsive miRNAs in brain.ResultsWe constructed two comparative small RNA libraries of rat brain from a high-intensity intermittent swimming training (HIST) group and a normal control (NC) group. Using deep sequencing and bioinformatics analysis, we identified 2109 (1700 from HIST, 1691 from NC) known and 55 (50 from HIST, 28 from NC) novel candidate miRNAs. Among them, 34 miRNAs were identified as significantly differentially expressed in response to HIST, 16 were up-regulated and 18 were down-regulated. The results showed that all members of mir-200 family were strongly up-regulated, implying mir-200 family may play very important roles in HIST response mechanisms of rat brain. A total of 955 potential target genes of these 34 exercise-responsive miRNAs were identified from rat genes. Most of them are directly involved in the development and regulatory function of brain or nerve. Many acknowledged exercise-responsive brain genes such as Bdnf, Igf-1, Vgf, Ngf c-Fos, and Ntf3 etc. could be targeted by exercise-responsive miRNAs. Moreover, qRT-PCR and SABC immunohistochemical analysis further confirm the reliability of the expression of miRNAs and their targets.ConclusionsThis study demonstrated that physical exercise could induce differential expression of rat brain miRNAs and 34 exercise-responsive miRNAs were identified in rat brain. Our results suggested that exercise-responsive miRNAs could play important roles in regulating gene expression of rat brain in response to exercise.

PO-297 Effects of different exercise patterns on TWEAK and its signal in rat skeletal muscle

Objective To study the effects of different exercise patterns on TWEAK and its downstream NF-kB/ MuRF1 in rat skeletal muscle, and to explore the relationship between TWEAK and skeletal muscle metabolism by different exercise interventions.
 Methods Thirty-two male Sprague-Dawley rats aged 12 weeks were randomly divided into 4 groups: quiet group, high-intensity intermittent swimming group, medium-intensity continuous swimming group, and ladder-moving group, with 8 rats in each group. The exercise group adopted high-intensity intermittent swimming training, medium-intensity continuous swimming training, and ladder training, and trained for 5 days per week for 8 weeks. The right gastrocnemius muscle of the rat was taken the next day after the last training. The expression of TWEAK, NF-KB, MuRF1 proteins was detected by Western Blot.
 Results 1. The gastrocnemius muscle mass index exercise group was higher than the quiet group. 2. Compared with the quiet group, the expression of TWEAK in the exercise group was reduced, and the reduction in the ladder exercise group was more significant. 3. Compared with the quiet group, the expression of NF-KB and MURF1 was decreased in the exercise group, and the reduction in the ladder exercise group was more significant.
 Conclusions TWEAK may be involved in skeletal muscle catabolism. All three exercise patterns can alleviate skeletal muscle atrophy in rats, and the effect of ladder movement is more significant.

A Mechanism Underlying Preventive Effect of High-Intensity Training on Colon Cancer.

We examined effects of high-intensity training on chemically induced aberrant crypt foci (ACF) in rat colon. We also investigated mechanisms that may underlie the results obtained, with a focus on secreted protein acidic and rich in cysteine (SPARC), which has been proposed as an exercise-related factor of colon cancer prevention. After an administration of 1,2-dimethylhydrazine, F344 rats executed high-intensity intermittent swimming training (HIIST) (twelve 20-s swimming with a weight [16% body weight] with 10-s pauses between the bouts) 5 d·wk for 4 wk. The acute and chronic effects of the HIIST on SPARC were evaluated in rats. We evaluated the in vitro and in vivo effects of 5' AMP-activated protein kinase (AMPK) activator on SPARC in rat serum and epitrochlearis muscle. In human subjects, we determined serum SPARC after exhaustive bicycling consisting of six to seven bouts of exercise at 170% V˙O2max with 10-s rests between the bouts (high-intensity intermittent bicycling [HIIB]). The SPARC mRNA in human vastus lateralis was measured before and after the HIIB for 4 d·wk for 6 wk (HIIB-training [HIIBT]). The numbers of ACF were lower in the HIIST (47 ± 22) compared with the control (122 ± 47) rats (P < 0.05). SPARC in epitrochlearis and serum after HIIS of the trained rat was higher than that in the control resting rats. In vitro and vivo AMPK stimulation increased mRNA and SPARC protein in rat epitrochlearis, respectively. The human serum SPARC after the HIIB was elevated. SPARC mRNA in human muscle was elevated after the HIIBT. The results demonstrated that HIIST inhibits 1,2-dimethylhydrazine-induced colon ACF development. This effect may be explained by SPARC induction by the exercise intensity-related factor AMPK, potentially explaining the preventive effects of high-intensity intermittent exercise training against colon cancer.

Effects of high-intensity swimming training on the bones of ovariectomized rats.

[Purpose]This study was performed to assess the effects of high-intensity intermittent swimming training(HIT) on bone in ovariectomized rats.[Methods]Six-week-old female Sprague-Dawley rats were randomly assigned to either sham operation or bilateral ovariectomy. After surgery, they were divided into the following four groups: 1) sham-operated sedentary (S), 2) sham-operated exercise training (SE), 3) OVX sedentary (O), 4) OVX exercise training (OE) 5) OVX given 17β-estradiol (OE2) and 6) OVX exercise training and given 17β-estradiol (OEE). SE, OE and OEE rats were used extremely high-intensity swim exercise. The rats repeated fourteen 20-s swimming bouts with a weight equivalent to 14, 15, and 16% of body weight for the first 5, the next 9, and the last 5 days, respectively. Between exercise bouts, a 10-s pause was allowed. HIT was originally designed as an exercise method; a method that very quickly induces an increase in the maximum oxygen intake (Tabata I et al., 1996). OEE and OE2 rats were subcutaneously injected ethanol with 25μg/kg body weight 17β-estradiol 3 times per week.[Results]Bone strength, bone mineral density and trabecular bone parameters were measured after a 8-weeks experimental period. Bone strength was significantly higher in the SE, OE, OE2 and OEE group compared with the O group. BV/TV was significant increase in the SE, OE groups compared with the O group. BMD showed no difference in the OE group compared with the O group.[Conclusion]This study demonstrate some beneficial effects of postmenopausal osteoporosis of high-intensity intermittent swimming training on bone structure and strength.

Low-volume high-intensity swim training is superior to high-volume low-intensity training in relation to insulin sensitivity and glucose control in inactive middle-aged women.

We tested the hypothesis that low-volume high-intensity swimming has a larger impact on insulin sensitivity and glucose control than high-volume low-intensity swimming in inactive premenopausal women with mild hypertension. Sixty-two untrained premenopausal women were randomised to an inactive control (n=20; CON), a high-intensity low-volume (n=21; HIT) or a low-intensity high-volume (n=21; LIT) training group. During the 15-week intervention period, HIT performed 3 weekly 6-10×30-s all-out swimming intervals (average heart rate (HR)=86±3% HRmax) interspersed by 2-min recovery periods and LIT swam continuously for 1h at low intensity (average HR=73±3% HRmax). Fasting blood samples were takenand an oral glucose tolerance test (OGTT) was conducted pre- and post-intervention. After HIT, resting plasma [insulin] was lowered (17±34%; P<0.05) but remained similar after LIT and CON. Following HIT, 60-min OGTT plasma [insulin] and [glucose] was lowered (24±30% and 10±16%; P<0.05) but remained similar after LIT and CON. Total area under the curve for plasma [glucose] was lower (P<0.05) after HIT than LIT (660±141 vs. 860±325mmolminL(-1)). Insulin sensitivity (HOMA-IR) had increased (P<0.05) by 22±34% after HIT, with no significant change after LIT or CON, respectively. Plasma soluble intracellular cell adhesion molecule 1 was lowered (P<0.05) by 4±8 and 3±9% after HIT and CON, respectively, while plasma soluble vascular cell adhesion molecule 1 had decreased (P<0.05) by 8±23% after HIT only. These findings suggest that low-volume high-intensity intermittent swimming is an effective and time-efficient training strategy for improving insulin sensitivity, glucose control and biomarkers of vascular function in inactive, middle-aged mildly hypertensive women.

Effects of soccer vs swim training on bone formation in sedentary middle-aged women.

The present study examined the effects of 15 weeks of soccer training and two different swimming training protocols on bone turnover in sedentary middle-aged women. Eighty-three premenopausal mildly hypertensive women [age: 45 ± 6 (± SD) years, height: 165 ± 6 cm, weight: 80.0 ± 14.1 kg, body fat: 42.6 ± 5.7 %, systolic blood pressure/diastolic blood pressure: 138 ± 6/85 ± 3 mmHg] were randomized into soccer training (SOC, n = 21), high-intensity intermittent swimming (HS, n = 21), moderate-intensity swimming (MS, n = 21) intervention groups, and a control group (C, n = 20). The training groups completed three sessions per week for 15 weeks. DXA scans were performed and resting blood samples were drawn pre- and post-intervention. In SOC, plasma osteocalcin, procollagen type I N propeptide and C-terminal telopeptide increased (P < 0.05) by 37 ± 15, 52 ± 23 and 42 ± 18 %, respectively, with no changes in MS, HS and C. The intervention-induced increase in SOC was larger (P < 0.05) than in MS, HS and C. In SOC, leg BMC increased (P < 0.05) by 3.1 ± 4.5 %, with a larger increase in SOC than in C. Femoral shaft and trochanter bone mineral density (BMD) increased (P < 0.05) by 1.7 ± 1.9 and 2.4 ± 2.9 %, respectively, in SOC, with a greater (P < 0.05) change in SOC than in MS and C, whereas total body and total leg BMD did not change in any of the groups. In conclusion, 15 weeks of soccer training with sedentary middle-aged women caused marked increases in bone turnover markers, with concomitant increases in leg bone mass. No changes in bone formation and resorption markers were seen after prolonged submaximal or high-intensity intermittent swimming training. Thus, soccer training appears to provide a powerful osteogenic stimulus in middle-aged women.

High-intensity intermittent swimming improves cardiovascular health status for women with mild hypertension.

To test the hypothesis that high-intensity swim training improves cardiovascular health status in sedentary premenopausal women with mild hypertension, sixty-two women were randomized into high-intensity (n = 21; HIT), moderate-intensity (n = 21; MOD), and control groups (n = 20; CON). HIT performed 6–10 × 30 s all-out swimming interspersed by 2 min recovery and MOD swam continuously for 1 h at moderate intensity for a 15-week period completing in total 44 ± 1 and 43 ± 1 sessions, respectively. In CON, all measured variables were similar before and after the intervention period. Systolic BP decreased (P < 0.05) by 6 ± 1 and 4 ± 1 mmHg in HIT and MOD; respectively. Resting heart rate declined (P < 0.05) by 5 ± 1 bpm both in HIT and MOD, fat mass decreased (P < 0.05) by 1.1 ± 0.2 and 2.2 ± 0.3 kg, respectively, while the blood lipid profile was unaltered. In HIT and MOD, performance improved (P < 0.05) for a maximal 10 min swim (13 ± 3% and 22 ± 3%), interval swimming (23 ± 3% and 8 ± 3%), and Yo-Yo IE1 running performance (58 ± 5% and 45 ± 4%). In conclusion, high-intensity intermittent swimming is an effective training strategy to improve cardiovascular health and physical performance in sedentary women with mild hypertension. Adaptations are similar with high- and moderate-intensity training, despite markedly less total time spent and distance covered in the high-intensity group.

Vitamin C supplementation does not alter high-intensity endurance training-induced mitochondrial biogenesis in rat epitrochlearis muscle

The purpose of this study was to investigate whether vitamin C supplementation prevents high-intensity intermittent endurance training-induced mitochondrial biogenesis in the skeletal muscle. Male Wistar-strain rats were assigned to one of five groups: a control group, training group, small dose vitamin C supplemented training group, middle dose vitamin C supplemented training group, and large dose vitamin C supplemented training group. The rats of the trained groups were subjected to intense intermittent swimming training. The vitamin C supplemented groups were administrated vitamin C for the pretraining and training periods. High-intensity intermittent swimming training without vitamin C supplementation significantly increased peroxisome proliferator-activated receptor-γ coactivator-1α protein content and citrate synthase activity in the epitrochlearis muscle. The vitamin C supplementation did not alter the training-induced increase of these regardless of the dose of vitamin C supplementation. The results demonstrate that vitamin C supplementation does not prevent high-intensity intermittent training-induced mitochondrial biogenesis in the skeletal muscle.

Possible involvement of AMPK in acute exercise-induced expression of monocarboxylate transporters MCT1 and MCT4 mRNA in fast-twitch skeletal muscle

ObjectiveThe regulatory mechanisms responsible for acute exercise-induced expression of monocarboxylate transporters MCT1 and MCT4 mRNA in skeletal muscle remain unclear. 5′-adenosine-activated protein kinase (AMPK) is a key signaling molecule that regulates gene expression at the mRNA level. We examined whether AMPK activation is involved in acute exercise-induced expression of MCT1 and MCT4 mRNA in fast-twitch muscle. Materials/MethodsMale Sprague–Dawley rats were subjected to an acute bout of either 5min high-intensity intermittent swimming (HIS) or 6-h low-intensity prolonged swimming (LIS). The effects of acute exercise on the phosphorylation of AMPK (p-AMPK), calcium/calmodulin pendent kinase II (p-CaMKII), p38 mitogen-activated protein kinase (p-p38MAPK), and MCTs mRNA were analyzed in vivo. To observe the direct effects of AMPK activation on MCTs mRNA, the effects of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), caffeine, and dantrolene were analyzed in vitro using an isolated muscle incubation model. ResultsThe p-AMPK increased in response to both HIS and LIS, although the p-CaMKII and p-p38MAPK were increased only following HIS. Irrespective of exercise intensity, MCT1 and MCT4 mRNA was also transiently upregulated by both HIS and LIS. Direct exposure of the epitrochlearis muscle to 0.5mmol/L AICAR or 1mmol/L caffeine, which activated p-AMPK increased both MCT1 and MCT4 mRNA levels. When pAMPK was inhibited by dantrolene, neither MCT1 nor MCT4 mRNA was increased. ConclusionThese results suggest that acute exercise-induced increases in MCT1 and MCT4 mRNA expression may be possibly mediated by AMPK activation, at least in part in fast-twitch muscle.

Effect of AMPK activation on acute exercise‐induced monocarboxylate transporter (MCT) 1 and MCT4 mRNA expression in skeletal muscle

We examined the mechanism on acute exercise‐induced MCT1 and MCT4 mRNA expression in skeletal muscle. The rats were subjected to a bout of high‐intensity intermittent swimming (HIS) or low‐intensity prolonged swimming exercise (LIS). The HIS rats swam for fifteen 20‐second with a weight equal to 18% of their body weight. The LIS rats swam without load in two 3h sessions separated by 45min of rest. HIS elevated the phosphorylation of 5 fAMP‐activated prtein kinase (pAMPK), calcium/calmodulin‐dependent kinase II (pCaMKII), and p38 mitogen‐activated protein kinase (pMAPK), which are characterized upstream modulators of transcriptional regulation. LIS elevated pAMPK, whereas pCaMKII and pMAPK were not altered. MCT1 and MCT4 mRNA were transiently upregulated by HIS and LIS. Direct exposure of epitrochlearis to 0.5mM 5‐aminoimidazole‐4‐carboxamide‐1‐ƒÀ‐d‐ribonucleoside (AICAR) or 1mM caffeine increased both MCT1 and MCT4 mRNA. When 1mM caffeine‐induced pAMPK was inhibited by dantrolene, neither MCT1 nor MCT4 mRNA was increased. The present findings suggest that, irrespective of exercise intensity, acute exercise may upregulate MCT1 and MCT4 mRNA expression, through AMPK‐mediated pathway in skeletal muscle.

The effect of high-intensity intermittent swimming on post-exercise glycogen supercompensation in rat skeletal muscle

A single bout of prolonged endurance exercise stimulates glucose transport in skeletal muscles, leading to post-exercise muscle glycogen supercompensation if sufficient carbohydrate is provided after the cessation of exercise. Although we recently found that short-term sprint interval exercise also stimulates muscle glucose transport, the effect of this type of exercise on glycogen supercompensation is uncertain. Therefore, we compared the extent of muscle glycogen accumulation in response to carbohydrate feeding following sprint interval exercise with that following endurance exercise. In this study, 16-h-fasted rats underwent a bout of high-intensity intermittent swimming (HIS) as a model of sprint interval exercise or low-intensity prolonged swimming (LIS) as a model of endurance exercise. During HIS, the rats swam for eight 20-s sessions while burdened with a weight equal to 18% of their body weight. The LIS rats swam with no load for 3h. The exercised rats were then refed for 4, 8, 12, or 16h. Glycogen levels were almost depleted in the epitrochlearis muscles of HIS- or LIS-exercised rats immediately after the cessation of exercise. A rapid increase in muscle glycogen levels occurred during 4h of refeeding, and glycogen levels had peaked at the end of 8h of refeeding in each group of exercised refed rats. The peak glycogen levels during refeeding were not different between HIS- and LIS-exercised refed rats. Furthermore, although a large accumulation of muscle glycogen in response to carbohydrate refeeding is known to be associated with decreased insulin responsiveness of glucose transport, and despite the fact that muscle glycogen supercompensation was observed in the muscles of our exercised rats at the end of 4h of refeeding, insulin responsiveness was not decreased in the muscles of either HIS- or LIS-exercised refed rats compared with non-exercised fasted control rats at this time point. These results suggest that sprint interval exercise enhances muscle glycogen supercompensation in response to carbohydrate refeeding as well as prolonged endurance exercise does. Furthermore, in this study, both HIS and LIS exercise prevented insulin resistance of glucose transport in glycogen supercompensated muscle during the early phase of carbohydrate refeeding. This probably led to the enhanced muscle glycogen supercompensation after exercise.

Effects of nonexhaustive bouts of high-intensity intermittent swimming training on GLUT-4 expression in rat skeletal muscle

We previously reported that 14 bouts of exhaustive high-intensity intermittent training [20 s periods of swimming while carrying a weight (14% of body weight), separated by pauses of 10 s] is the highest stimuli in terms of exercise training-induced glucose transporter 4 (GLUT-4) expression in rat epitrochlearis (EPI) muscles. In the present study, we found that the GLUT-4 protein content in the skeletal muscle of male Sprague-Dawley rats (age 5 weeks old; body weight 90-110 g) that underwent intermittent exercise training of 3 and 14 bouts of 20 s swimming for 5 days was increased over age-matched sedentary control rats by 75 and 71%, respectively, 18 h after the last bout of exercise. These results suggest that GLUT-4 content in rat EPI muscle increases dramatically after very short (60 s) and nonexhaustive high-intensity intermittent exercise training.

Effect of acute high-intensity intermittent swimming on post-exercise insulin responsiveness in epitrochlearis muscle of fed rats

Maximally insulin-stimulated glucose uptake in skeletal muscle, ie, insulin responsiveness, is reduced in fed animals as compared with fasted animals; but acute prior endurance exercise improves insulin responsiveness in the muscles of fed rats. The effect of acute prior sprint interval exercise on insulin responsiveness in the muscles of fed animals has not been clarified, and we therefore compared the effect of short high-intensity swimming as a model of sprint interval exercise on insulin responsiveness in the muscles of fed rats with the effect of prolonged low-intensity swimming as a model of endurance exercise. The fed rats were subjected to an acute bout of high-intensity intermittent swimming (HIS) or low-intensity continuous swimming (LIS). The HIS rats swam for eight 20-second periods with a weight equal to 18% of their body weight. The LIS rats swam with no load for 3 hours. HIS increased (P < .05) the phosphorylation of adenosine monophosphate–activated protein kinase (AMPK) Thr172 and that of its downstream target acetyl-CoA carboxylase (ACC) Ser79 12.6- and 3.1-fold, respectively, whereas LIS increased them 3.8- and 1.9-fold, respectively, immediately after exercise compared with rested muscle. HIS and LIS increased the insulin responsiveness of 2-deoxyglucose uptake measured 4 hours after exercise by 39% and 41%, respectively, compared with rested muscles. These results show that very short (160 seconds) HIS exercise with greater AMPK activation increases the responsiveness of glucose uptake to insulin in the muscles of fed rats to a similar level observed after prolonged (3 hours) LIS exercise with lower AMPK activation. Therefore, it is suggested that an acute bout of sprint interval exercise that activates AMPK to a sufficiently high level can increase post-exercise insulin responsiveness on muscle glucose uptake irrespective of very short exercise duration.

An acute bout of high-intensity intermittent swimming induces glycogen supercompensation in rat skeletal muscle

High-intensity intermittent exercise substantially increases muscle glucose transport, which is thought to be the rate-limiting step for glycogen synthesis. In the present study, we compared muscle glycogen supercompensation after high-intensity intermittent exercise with that observed after low-intensity continuous exercise in rats. Four- to five-week-old male Sprague-Dawley rats performed either low-intensity swimming (240 min of swimming exercise with a weight equivalent to 1% of their body mass; LOW) or high-intensity swimming (twenty 30-s swimming bouts with 30 s rest between bouts with a weight equivalent to 16% of their body mass; HIGH) to deplete muscle glycogen. After the glycogen-depleting exercise, rats were given a rodent chow diet plus 5% glucose solution for 6 h or 24 h. Immediately after the two types of exercise, glycogen concentration in rat epitrochlearis muscle was similarly depleted. After the 6-h and 24-h recovery periods, muscle glycogen concentrations in both the HIGH and LOW groups were restored well above the normally fed state. Furthermore, muscle glycogen accumulation in the HIGH group for the 6-h and 24-h recovery periods was not significantly different from that observed in the LOW group. The high-intensity intermittent swimming exercise also induced muscle glycogen supercompensation in well-trained rats that had performed 7 days of endurance swimming training (6 h per day). Our results indicate that high-intensity intermittent exercise as well as low-intensity continuous exercise could induce glycogen supercompensation in rat skeletal muscle.

Effect of high-intensity intermittent swimming on postexercise insulin sensitivity in rat epitrochlearis muscle

A bout of prolonged aerobic exercise can enhance the sensitivity of muscle glucose uptake to insulin, and this may be mediated by activation of 5′-adenosine monophosphate–activated protein kinase (AMPK). The aim of this study was to examine whether high-intensity short-term exercise resulting in a significantly greater increase in the activation of AMPK is more effective in enhancing muscle insulin sensitivity compared with low-intensity prolonged aerobic exercise. We measured insulin sensitivity after high-intensity intermittent swimming (HIS) or low-intensity continuous swimming (LIS) exercise in rat epitrochlearis muscle. During HIS, the rats underwent eight 20-second bouts of swimming with a weight equal to 18% of body weight. The LIS rats swam with no load for 3 hours. High-intensity intermittent swimming increased ( P < .05) 2-deoxyglucose uptake ∼8-fold, whereas LIS increased it ( P < .05) ∼2-fold immediately after exercise compared with rested muscle. This response was associated with an increase ( P < .05) in phosphorylation of AMPK Thr 172 and its downstream target acetyl-coenzyme A carboxylase (ACC) Ser 79 in HIS (13- and 6-fold, respectively) and LIS (2.8- and 2-fold, respectively) immediately after exercise. In contrast, submaximal (30 μU/mL) insulin-stimulated 2-deoxyglucose uptake measured 4 hours after exercise was 73% and 46% higher ( P < .05) in LIS and HIS, respectively, compared with rest. The HIS exercise resulted in a greater activation of AMPK compared with LIS, but insulin sensitivity was higher after LIS compared with HIS. The results suggest that HIS is not more effective in enhancing insulin sensitivity than LIS. Thus, AMPK activation immediately after exercise may not be the only factor that determines the magnitude of the exercise-induced increase in insulin sensitivity in rat epitrochlearis muscle.

EFFECTS OF SHORT-LASTING HIGH-INTENSITY SWIMMING ON PGC-1 PROTEIN EXPRESSION IN RAT EPITROCHLEARIS MUSCLE

PURPOSE We reported that the peroxisome proliferator-activated receptor γ coactivator-1 (PGC-1) mRNA in rat epitrochlearis (EPI) muscle was significantly increased after 18-h incubation with AICAR (a AMPK activator)(BBRC,2002). Since AMPK was shown to be activated in an exercise-intensity dependent manner, in the present investigation, we assessed the effects of short-lasting high-intensity swimming exercise, which is postulated to substantially increase AMPK activity, on PGC-1 protein content in rat EPI muscle, and to compare its effects on PGC-1 protein with that observed after low-intensity prolonged swimming exercise, which is known to increase PGC-1 mRNA. METHOD Male SD rats (5–6 week-old) were randomly assigned to high-intensity swimming exercise (HIS), or low intensity swimming exercise (LIS). Age-matched sedentary rats were used as a control (CON). During HIS, the rats repeated fourteen 20-s swimming with a weight equivalent to 14% of body weight. Between exercise sessions, a 10-s pause was allowed. Rats in the LIS group swam without a load for 6-h in two 3-h sessions, separated by 45-min rest. RESULT PGC-1 protein in rat EPI muscle was significantly increased by 126, 140, and 126% at 2-h, 6-h, and 18-h, respectively, after HIS, compared with that of the CON muscle (p < 0.001). Immediately, 6-h, and 18-h after the LIS, the PGC-1 protein content in the muscle was significantly elevated by 84, 95, and 67%, respectively (p < 0.001). The increment in PGC-1 protein at 6-h after the HIS did not differ from that observed after the LIS at the same time point. Both HIS and LIS induced significant increases (7- and 3-fold higher than that of CON muscle, respectively) in AMPK activity. CONCLUSION The present investigation demonstrated that the PGC-1 protein in rat EPI muscle rapidly increased in response to an acute bouts of swimming exercise. Further, the results showed that extremely high-intensity intermittent swimming exercise lasting only 280 s elevated the PGC-1 protein in rat EPI muscle to a level comparable to that attained after the 6-h low-intensity swimming exercise.

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

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 micromol . 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 micromol 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.