High-intensity Swimming Exercise Research Articles

Papaya Leaf Ethanol Extract Lowers Malondialdehyde Levels, Increases Superoxide Dismutase Levels, and Increases Leydig Cell Count in Male Rats Given High-Intensity Swimming Exercise

Physical activity is any body movement that occurs due to skeletal muscle contractions that require energy expenditure. Overtraining can trigger oxidative stress due to chronic systemic hypoxia, cause an increase in systemic inflammatory response and multiorgan damage, and accelerate the aging process. The aging process is influenced by many factors, one of which is high-intensity swimming exercise which triggers the emergence of free radicals and leads to systemic oxidative stress. High-intensity swimming exercise is associated with an increase in Reactive Oxygen Species (ROS). The Papaya plant is famous for its therapeutic and nutritional properties. Papaya leaves contain secondary metabolites from papaya leaf extract including tannins, saponins, flavonoids, phenolics, and alkaloids. Papaya leaf extract has strong medicinal properties as an antibacterial, antiviral, antitumor, and antioxidant. This research is an experimental study with a post-test-only control group design. The sample in this study were male white rats (Rattus norvegicus) with an age range of 3-4 months with an average body weight range of 180-200 grams. As many as 36 rats were divided into 2 treatment groups. Treatment group 1 (P1) rats were given high-intensity swimming exercise treatment and aquabidest. Treatment group 2 (P2) rats were given high-intensity swimming exercise treatment and papaya leaf extract 60mg / 200g BB orally. Each treatment was carried out for 21 days. The data obtained will be analyzed using an independent sample T-test. The results of this study obtained: (1) the average MDA levels showed that the P1 group (1.02±0.064) was higher than the P2 group (0.86±0.44) with a value of p<0.001; (2) the average SOD level in the P2 group (2.72±0.437) was higher than P1 (1.46±0.288) with p<0.001; (3) the average number of Leydig cells in the P1 group (13.0±5.05) was lower than in the P2 group (30.0±5.05) with p<0.001. This study concluded that papaya leaf ethanol extract in rats was able to reduce MDA levels, increase SOD levels and increase the number of Leydig cells in male rats given high-intensity swimming exercise.

Pterostilbene Attenuates High-Intensity Swimming Exercise-Induced Glucose Absorption Dysfunction Associated with the Inhibition of NLRP3 Inflammasome-Induced IECs Pyroptosis

The study investigated the effect of pterostilbene (PTE) on intestinal glucose absorption and its underlying mechanisms in high-intensity swimming exercise (HISE)-treated mice. Male C57BL/6 mice were treated with PTE for 4 weeks and performed high-intensity swimming training in the last week. Intestinal epithelial cells (IECs) were pretreated with 0.5 and 1.0 μM PTE for 24 h before being incubated in hypoxia/reoxygenation condition. Intestinal glucose absorption was detected by using an oral glucose tolerance test and d-xylose absorption assay, and the levels of factors related to mitochondrial function and pyroptosis were measured via western blot analyses, cell mito stress test, and quantitative real-time polymerase chain reaction. In vivo and in vitro, the results showed that PTE attenuated HISE-induced intestinal glucose absorption dysfunction and pyroptosis in mice intestine. Moreover, PTE inhibited NLRP3 inflammasome and the mitochondrial homeostasis as well as the ROS accumulation in IEC in vitro. Additionally, knockdown of SIRT3, a major regulator of mitochondria function, by siRNA or inhibiting its activity by 3-TYP abolished the effects of PTE on pyroptosis, mitochondrial homeostasis, and ROS generation of IEC in vitro. Our results revealed that PTE could alleviate HISE-induced intestinal glucose absorption dysfunction associated with the inhibition of NLRP3 inflammasome-induced IECs pyroptosis.

High-intensity swimming alleviates nociception and neuroinflammation in a mouse model of chronic post-ischemia pain by activating the resolvin E1-chemerin receptor 23 axis in the spinal cord.

Physical exercise effectively alleviates chronic pain associated with complex regional pain syndrome type-I. However, the mechanism of exercise-induced analgesia has not been clarified. Recent studies have shown that the specialized pro-resolving lipid mediator resolvin E1 promotes relief of pathologic pain by binding to chemerin receptor 23 in the nervous system. However, whether the resolvin E1-chemerin receptor 23 axis is involved in exercise-induced analgesia in complex regional pain syndrome type-I has not been demonstrated. In the present study, a mouse model of chronic post-ischemia pain was established to mimic complex regional pain syndrome type-I and subjected to an intervention involving swimming at different intensities. Chronic pain was reduced only in mice that engaged in high-intensity swimming. The resolvin E1-chemerin receptor 23 axis was clearly downregulated in the spinal cord of mice with chronic pain, while high-intensity swimming restored expression of resolvin E1 and chemerin receptor 23. Finally, shRNA-mediated silencing of chemerin receptor 23 in the spinal cord reversed the analgesic effect of high-intensity swimming exercise on chronic post-ischemic pain and the anti-inflammatory polarization of microglia in the dorsal horn of the spinal cord. These findings suggest that high-intensity swimming can decrease chronic pain via the endogenous resolvin E1-chemerin receptor 23 axis in the spinal cord.

High-intensity swimming exercise reduces inflammatory pain in mice by activation of the endocannabinoid system.

As exercise intervention solely for pain reduction is relatively new, the available research still leaves an incomplete picture of responsible mechanisms and pathways. Nonetheless, evidence indicates that exercise-induced analgesia involves activation of the endocannabinoid (eCB) system. The present study investigated the role of the eCB system on the antihyperalgesic effect of high-intensity swimming exercise (HISE) in an animal model of peripheral persistent inflammation. Male Swiss mice were allocated to non-exercised and exercised groups and subjected to subcutaneous intraplantar injection (i.pl.) of a single dose of complete Freund's adjuvant (CFA) to induce inflammatory pain. Cumulative HISE was performed once a day, and mechanical hyperalgesia and edema were evaluated 0.5hour after HISE for seven consecutive days. To investigate the role of the eCB system on the antihyperalgesic effect of HISE, non-exercised and exercised mice received intraperitoneal (ip), intrathecal (i.t.) or i.pl. injections of vehicle, AM281 (a CB1 cannabinoid receptor antagonist) or AM630 (a CB2 cannabinoid receptor antagonist) from the 3rd to 5th day after CFA injection. Mechanical hyperalgesia was evaluated 0.5hour after HISE. In addition, the effect of the fatty acid amide hydrolase [FAAH] inhibitor or monoacylglycerol lipase [MAGL] inhibitor on the antihyperalgesic action of HISE was investigated. HISE reduced mechanical hyperalgesia with effects prevented by AM281 or AM630 pretreatment in all delivery routes tested. The inhibition of FAAH and MAGL prolonged the antihyperalgesic effect of HISE. These data demonstrate evidence for the role of the eCB system upon exercise-induced analgesia in a murine model of inflammatory pain.

Low-Intensity Running and High-Intensity Swimming Exercises Differentially Improve Energy Metabolism in Mice With Mild Spinal Muscular Atrophy

Spinal Muscular Atrophy (SMA), an autosomal recessive neurodegenerative disease characterized by the loss of spinal-cord motor-neurons, is caused by mutations on Survival-of-Motor Neuron (SMN)-1 gene. The expression of SMN2, a SMN1 gene copy, partially compensates for SMN1 disruption due to exon-7 excision in 90% of transcripts subsequently explaining the strong clinical heterogeneity. Several alterations in energy metabolism, like glucose intolerance and hyperlipidemia, have been reported in SMA at both systemic and cellular level, prompting questions about the potential role of energy homeostasis and/or production involvement in disease progression. In this context, we have recently reported the tolerance of mild SMA-like mice (SmnΔ7/Δ7; huSMN2+/+) to 10 months of low-intensity running or high-intensity swimming exercise programs, respectively involving aerobic and a mix aerobic/anaerobic muscular metabolic pathways. Here, we investigated whether those exercise-induced benefits were associated with an improvement in metabolic status in mild SMA-like mice. We showed that untrained SMA-like mice exhibited a dysregulation of lipid metabolism with an enhancement of lipogenesis and adipocyte deposits when compared to control mice. Moreover, they displayed a high oxygen consumption and energy expenditure through β-oxidation increase yet for the same levels of spontaneous activity. Interestingly, both exercises significantly improved lipid metabolism and glucose homeostasis in SMA-like mice, and enhanced oxygen consumption efficiency with the maintenance of a high oxygen consumption for higher levels of spontaneous activity. Surprisingly, more significant effects were obtained with the high-intensity swimming protocol with the maintenance of high lipid oxidation. Finally, when combining electron microscopy, respiratory chain complexes expression and enzymatic activity measurements in muscle mitochondria, we found that (1) a muscle-specific decreased in enzymatic activity of respiratory chain I, II, and IV complexes for equal amount of mitochondria and complexes expression and (2) a significant decline in mitochondrial maximal oxygen consumption, were reduced by both exercise programs. Most of the beneficial effects were obtained with the high-intensity swimming protocol. Taking together, our data support the hypothesis that active physical exercise, including high-intensity protocols, induces metabolic adaptations at both systemic and cellular levels, providing further evidence for its use in association with SMN-overexpressing therapies, in the long-term care of SMA patients.

Effects of High-Fat Diet on eHSP72 and Extra-to-Intracellular HSP70 Levels in Mice Submitted to Exercise under Exposure to Fine Particulate Matter.

Obesity, air pollution, and exercise induce alterations in the heat shock response (HSR), in both intracellular 70 kDa heat shock proteins (iHSP70) and the plasmatic extracellular form (eHSP72). Extra-to-intracellular HSP70 ratio (H-index = eHSP70/iHSP70 ratio) represents a candidate biomarker of subclinical health status. This study investigated the effects of moderate- and high-intensity exercise in the HSR and oxidative stress parameters, in obese mice exposed to fine particulate matter (PM2.5). Thirty-day-old male isogenic B6129F2/J mice were maintained for 16 weeks on standard chow or high-fat diet (HFD). Then, mice were exposed to either saline or 50 μg of PM2.5 by intranasal instillation and subsequently maintained at rest or subjected to moderate- or high-intensity swimming exercise. HFD mice exhibited high adiposity and glucose intolerance at week 16th. HFD mice submitted to moderate- or high-intensity exercise were not able to complete the exercise session and showed lower levels of eHSP70 and H-index, when compared to controls. PM2.5 exposure modified the glycaemic response to exercise and modified hematological responses in HFD mice. Our study suggests that obesity is a critical health condition for exercise prescription under PM2.5 exposure.

Does Sodium Citrate Cause the Same Ergogenic Effect As Sodium Bicarbonate on Swimming Performance?

The aim of this study was to investigate the effect of ingesting sodium bicarbonate (SB) and sodium citrate (SC) on 400 m high-intensity swimming performance and blood responses. Six nationally ranked male swimmers (20.7 ± 2.1 yrs; 184 ± 6 cm; 79.9 ± 3.9 kg; 10.6 ± 1% body fat) participated in a double blinded, placebo controlled crossover trial. Ninety minutes after consuming SB (0.3 g·kg-1), SC (0.3 g·kg-1) or a placebo (PL) participants completed a single 400-m freestyle maximal test on three consecutive days. The order of the supplementation was randomized. Capillary blood samples were collected on 4 occasions: at rest (baseline), 60 min post-ingestion, immediately post-trial and 15 min post-trial. Blood pH, HCO3- concentration and base excess (BE) were determined. Blood pH, HCO3-, BE were significantly elevated from before loading to the pre-test (60 min post-ingestion) (p < 0.05) after SB ingestion, but not after SC ingestion (p > 0.05). Performance times were improved by 0.6% (p > 0.05) after supplementation of SB over PL in 5 out of 6 participants (responders). In contrast, ingestion of SC decreased performance by 0.2% (p > 0.05). No side effects were observed in either trial. Delayed blood response was observed after SC ingestion compared to SB and this provided no or modest ergogenic effect, respectively, for single bout high-intensity swimming exercise. Monitoring the magnitude of the time-to-peak level rise in alkalosis may be recommended in order to individualize the loading time accordingly before commencement of exercise.

Influence of excessive exercise on immunity, metabolism, and gut microbial diversity in an overtraining mice model.

The purpose of this study was to evaluate the negative influence of excessive exercise on immunity, substance and energy metabolism as well as gut microbiota in mice. Firstly, an overtraining model of Male Kunming mice was established by high-intensity swimming exercise for 4weeks. Then, a series of evaluation indicators, including the routine blood analysis, immune organ coefficient, digestive enzymes, and aquaporins expression levels of small intestine and colon tissue, histological examinations of liver, spleen, small intestine, and colon, were determined based on this model. Furthermore, 16S rRNA gene sequencing was also employed to measure the microbial composition in gut. The results found that immune parameters, substance and energy metabolism of all mice was altered and disturbed after high-intensity swimming for 4weeks, led to an atrophy of thymus and spleen as well as abnormal structural changes in liver when compared to non-swimming mice. Besides, excessive swimming mice had lower microbial diversity compared to non-swimming mice. However, there was no significant difference in gut microbial taxa between the two groups. The data indicated that excessive exercise exhibits negative impacts on immunity, substance and energy metabolism as well as gut microbial diversity.

The Differential Impact Of High-Intensity Swimming Exercise and Inflammatory Bowel Disease On IL-1b, TNF-a, and COX-2 Gene Expression in the Small Intestine and Colon in Mice

Background and Objective&#x0D; We aimed to examine the impact of high-intensity swimming exercise and inflammatory bowel disease (IBD) on IL-1β, TNF-α, and COX-2 gene expression in the small intestine and colon of mice.&#x0D; Material and Methods&#x0D; Forty male C57BL/6 mice were divided into 4 groups: the control group (CON), swimming exercise group (EX), 50% ethanol (EtoH) control group (50%EtoH CON), and 2,4,6-trinitrobenzene sulfonic acid group (TNBS). The EX group performed 4 weeks of exercise. Intrarectal TNBS injection induced IBD in the TNBS group; the 50%EtoH CON group received control injections. Reverse transcription and real-time polymerase chain reaction were used to examine IL-1β, TNF-α, and COX-2 mRNA expression in the small intestine and colon.&#x0D; Results&#x0D; IL-1β, TNF-α, and COX-2 mRNA expression was significantly increased in the EX group compared to that in the CON group (p’s&lt;0.05). IL-1β and COX-2 mRNA expression was significantly increased in the TNBS group compared to that in the 50%EtoH CON group (p’s&lt;0.05).&#x0D; Conclusion&#x0D; Thus, inflammatory cytokine IL-1β and COX-2 expression in the small intestine and colon was increased in both high-intensity swimming exercise and IBD models. However, TNF-α was increased only in the swimming exercise model. Further research is required to confirm these observations and establish swimming exercise regimes appropriate for patients with IBD.

High-Intensity Swimming Exercise Decreases Glutamate-Induced Nociception by Activation of G-Protein-Coupled Receptors Inhibiting Phosphorylated Protein Kinase A.

Several studies in humans have reported that improved pain control is associated with exercise in a variety of painful conditions, including osteoarthritis, fibromyalgia, and neuropathic pain. Despite the growing amount of experimental data on physical exercise and nociception, the precise mechanisms through which high-intensity exercise reduces pain remain elusive. Since the glutamatergic system plays a major role in pain transmission, we firstly analyzed if physical exercise could be able to decrease glutamate-induced nociception through G-protein-coupled receptor (G-PCR) activation. The second purpose of this study was to examine the effect of exercising upon phosphorylation of protein kinase A (PKA) isoforms induced by intraplantar (i.pl.) glutamate injection in mice. Our results demonstrate that high-intensity swimming exercise decreases nociception induced by glutamate and that i.pl. or intrathecal injections of cannabinoid, opioid, and adenosine receptor antagonists, AM281, naloxone, and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX), respectively, prevent this effect. Furthermore, the peripheral A1 and opioid receptors, but not CB1, are also involved in exercise's effect. We also verified that glutamate injection increases levels of phosphorylated PKA (p-PKA). High-intensity swimming exercise significantly prevented p-PKA increase. The current data show the direct involvement of the glutamatergic system on the hyponociceptive effect of high-intensity swimming exercise as well as demonstrate that physical exercise can activate multiple intracellular pathways through G-PCR activation, which share the same endogenous mechanism, i.e., inhibition of p-PKA.

Abstract 169: Elucidating the role of GRK5 in Physiological Hypertrophy

Cardiac function is dynamically regulated by various G protein-coupled receptors (GPCRs). GPCR kinases (GRKs) are important in cardiac GPCR regulation through phosphorylation and desensitization of these receptors. GRK2 and GRK5 are the predominant GRKs in the heart, and the most widely characterized as they are both up-regulated in the failing heart. Prior studies from our Lab have determined that GRK5 plays a crucial role in pathological cardiac hypertrophy. Another type of hypertrophy termed, “physiological hypertrophy” occurs with exercise training and is defined as an enlargement in cardiac myocyte size leading to favorable cardiac adaptations. At present, it is unclear if GRK5 is a regulator of physiological hypertrophy in addition to its role in maladaptive hypertrophy. We hypothesize that GRK5 will not regulate physiological hypertrophy such that mice with cardiac-specific overexpression of GRK5 (TgGRK5) will yield a similar post-exercise cardiac physiological hypertrophic response as that of control wild-type (WT) mice. To test this hypothesis, TgGRK5 and WT mice were exposed to a 21 day high-intensity swimming exercise protocol. For each line, sham mice, which did not swim served as appropriate controls. At the conclusion of this protocol, mice were sacrificed and heart weight (HW), body weight (BW), and tibia length (TL) measured. TgGRK5 and WT mice both exhibited a characteristic 10-15% increase in HW/BW and HW/TL ratios, which are standard measures of cardiac hypertrophy. In addition, hearts were sectioned and H&amp;E stained to evaluate myocyte size. Both TgGRK5 and WT mice exhibited a significant increase in myocyte size. Cardiac function was evaluated via echocardiography both prior to and after exercise training, and no changes were observed between TgGRK5 and WT mice after training. These data were re-affirmed in H9C2 cells and neonatal rat ventricular myocytes overexpressing either GFP or GRK5, which exhibited similar increases in cell size and AKT phosphorylation after IGF-1 treatment, a physiological hypertrophy stimulus. Taken together, these data suggest that physiological hypertrophy is similar in both control and TgGRK5 mice, confirming that GRK5 is solely a regulator of pathological cardiac hypertrophy.

High-Intensity Swimming Exercise Increases Dust Mite Extract and 1-Chloro-2,4-Dinitrobenzene-Derived Atopic Dermatitis in BALB/c Mice

The aim of this study was to investigate the effect of high-intensity swimming exercise (HISE) on atopic dermatitis (AD). For the study, we established an AD model in BALB/c mice by repeated local exposure of house dust mite extract (Dermatophagoides farinae extract, DFE) and 1-chloro-2,4-dinitrobenzene (CDNB) to the ears. After HISE for 4weeks, epidermal thickness, mast cell infiltration, serum immunoglobulin E (IgE), and histamine were measured. In addition, the gene expression of interleukin (IL)-5 and IL-31 in the ears was assayed. HISE increased DFE/CDNB-induced AD symptoms based on ear thickness, histopathological analysis, and serum IgE level. Moreover, HISE exercise stimulated mast cell infiltration into the ear, elevation of serum histamine, and DFE/CDNB-induced expression of IL-5 and IL-31 in the ears in the AD model. Taken together, our results indicate the possibility that HISE-induced stress gives rise to AD symptoms through the stimulation of IgE level by increasing IL-5 and IL-31 production.

Effects of endurance and high-intensity swimming exercise on the redox status of adolescent male and female swimmers

Throughout adolescence, swimmers begin to carry out demanding endurance and high-intensity training sets, the effect of which on redox status is largely unknown. The aim of the present study was to investigate the effects of 2000-m continuous swimming and 6 × 50-m maximal swimming on the redox status of adolescent swimmers. Fifteen male and 15 female swimmers, aged 14–18 years, provided blood samples before, immediately after, 1 h after, and 24 h after each exercise for the determination of redox status parameters. Oxidative damage was short-lived and manifest as increases in 8-hydroxy-2΄-deoxyguanosine (8-OHdG) 1 h after high-intensity exercise (39%, P < 0.001) and in malondialdehyde immediately after both exercises (65%, P < 0.001). Alterations in antioxidant parameters were sustained during recovery: reduced glutathione decreased 24 h post-exercise (11%, P = 0.001), uric acid increased gradually after high-intensity exercise (29%, P < 0.001) and bilirubin peaked 24 h post-exercise (29%, P < 0.001). Males had higher 8-OHdG (49%, P = 0.001) and uric acid (29%, P < 0.001) concentrations than females. However, females showed higher values of malondialdehyde than males immediately post-exercise (30%, P = 0.039), despite lower pre-exercise values. In conclusion, both endurance and high-intensity exercise perturbed the redox balance without inducing prolonged oxidative damage in trained adolescent male and female swimmers. These swimming training trials were not found to be detrimental to the redox homeostasis of adolescents.

흰쥐 좌골신경 압좌손상 후 수영운동의 부하에 따른 근육 회복

PURPOSE: The aim of this study was to compare the effects of different loading swimming exercises on muscle recovery after sciatic nerve crush injury in rats. METHODS: For this study, thirty-one Sprague-Dawley male rats were randomly divided into five groups. There were the negative control group (NCG, n=5), the positive control group (PCG, n=7), the low intensity swimming exercise group (LISEG, n=7), the moderate intensity swimming exercise group (MISEG, n=7) and the high intensity swimming exercise group (HISEG, n=5). Each rat was weighed to determine the lead weight to be attached to the base of its tail. Subsequently, the PCG, the LISEG, the MISEG and the HISEG were underwent standard unilateral sciatic nerve crush. The LISEG (no load), the MISEG (lead weight equivalent to 2% average body mass) and the HISEG (lead weight equivalent to 4% average body mass) were received the 10 minute swimming exercise in a day for 10 days. The NCG and PCG were not received with any therapeutic intervention. The diameter of the calf muscle and the level of serum lactate dehydrogenase (LDH) were measured to detect the effects of the swimming exercise. RESULT: The maximum diameter of the calf muscles was significantly increased after seventh swimming exercise in the LISEG, the MISEG and the HISEG compared with the PCG (p<0.05). However, there was no statistically significant difference between the LISEG, the MISEG and the HISEG. Also, the level of the serum LDH was significantly decreased in the LISEG, the MISEG and the HISEG compared with the PCG (p<0.05). CONCLUSION: Taken together, these results suggest that swimming exercise could accelerate muscle recovery processes after crush injury, but the different intensity of the swimming exercise does not affect healing processes.

High-intensity swimming exercise reduces neuropathic pain in an animal model of complex regional pain syndrome type I: Evidence for a role of the adenosinergic system

This study investigated the involvement of the adenosinergic system in antiallodynia induced by exercise in an animal model of complex regional pain syndrome type I (CRPS-I). Furthermore, we analyzed the role of the opioid receptors on exercise-induced analgesia. Ischemia/reperfusion (IR) mice, nonexercised and exercised, received intraperitoneal injections of caffeine (10mg/kg, a non selective adenosine receptor antagonist), 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (0.1mg/kg, a selective adenosine A1 receptor antagonist), ZM241385 (3mg/kg, a selective adenosine A2A receptor antagonist), adenosine deaminase inhibitor erythro-9-(2-hydroxy-3nonyl) adenine [(EHNA), 5mg/kg, an adenosine deaminase inhibitor] or naloxone (1mg/kg, a nonselective opioid receptor antagonist). The results showed that high-intensity swimming exercise reduced mechanical allodynia in an animal model of CRPS-I in mice. The antiallodynic effect caused by exercise was reversed by pretreatment with caffeine, naloxone, DPCPX but it was not modified by ZM241385 treatment. In addition, treatment with EHNA, which suppresses the breakdown of adenosine to inosine, enhanced the pain-relieving effects of the high-intensity swimming exercise. This is the first report demonstrating that repeated sessions of high-intensity swimming exercise attenuate mechanical allodynia in an animal model of CRPS-I and that the mechanism involves endogenous adenosine and adenosine A1 receptors. This study supports the use of high-intensity exercise as an adjunct therapy for CRPS-I treatment.

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.

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.