High-intensity Swimming Research Articles

The ergogenic effect of beta-alanine combined with sodium bicarbonate on high-intensity swimming performance

We investigated the effect of beta-alanine (BA) alone (study A) and in combination with sodium bicarbonate (SB) (study B) on 100- and 200-m swimming performance. In study A, 16 swimmers were assigned to receive either BA (3.2 g·day(-1) for 1 week and 6.4 g·day(-1) for 4 weeks) or placebo (PL; dextrose). At baseline and after 5 weeks of supplementation, 100- and 200-m races were completed. In study B, 14 were assigned to receive either BA (3.2 g·day(-1) for 1 week and 6.4 g·day(-1) for 3 weeks) or PL. Time trials were performed once before and twice after supplementation (with PL and SB), in a crossover fashion, providing 4 conditions: PL-PL, PL-SB, BA-PL, and BA-SB. In study A, BA supplementation improved 100- and 200-m time-trial performance by 2.1% (p = 0.029) and 2.0% (p = 0.0008), respectively. In study B, 200-m time-trial performance improved in all conditions, compared with presupplementation, except the PL-PL condition (PL-SB, +2.3%; BA-PL, +1.5%; BA-SB, +2.13% (p < 0.05)). BA-SB was not different from BA-PL (p = 0.21), but the probability of a positive effect was 78.5%. In the 100-m time-trial, only a within-group effect for SB was observed in the PL-SB (p = 0.022) and BA-SB (p = 0.051) conditions. However, 6 of 7 athletes swam faster after BA supplementation. The probability of BA having a positive effect was 65.2%; when SB was added to BA, the probability was 71.8%. BA and SB supplementation improved 100- and 200-m swimming performance. The coingestion of BA and SB induced a further nonsignificant improvement in performance.

Declines in swimming performance with age: a longitudinal study of Masters swimming champions

IntroductionBecause of its many participants and thorough records, competitive Masters swimming offers a rich data source for determining the rate of physical decline associated with aging in physically fit individuals. The decline in performance among national champion swimmers, both men and women and in short and long swims, is linear, at about 0.6% per year up to age 70–75, after which it accelerates in quadratic fashion. These conclusions are based primarily on cross-sectional studies, and little is known about individual performance declines with aging. Herein we present performance profiles of 19 male and 26 female national and international champion Masters swimmers, ages 25 to 96 years, participating in competitions for an average of 23 years.Methods and resultsSwimmers’ longitudinal data were compared with the fastest times of world record holders across ages 35–100 years by two regression methods. Neither method proved to accurately model this data set: compared with the rates of decline estimated from the world record data, which represent the best recorded times at given ages, there was bias toward shallower rates of performance decline in the longitudinal data, likely owing to a practice effect in some swimmers as they began their Masters programs. In swimmers’ later years, once maximum performance had been achieved, individual profiles followed the decline represented in the world records, and a few swimmers became the world record holders. In some instances, the individual profiles indicated performance better than the world record data; these swimmers achieved their times after the world record data were collected in 2005–2006.ConclusionDeclining physiological functional capacity occurs with advancing age, and this is reflected in the performance decrements of aging Masters swimmers. Individual swimmers show different performance trajectories with aging, declines being mitigated by practice, which improves both physiological capacity and swimming technique, particularly in the early years of participation. The longitudinal data of this study indicate that individuals can participate in high-intensity swimming over several decades, competitively improving over those decades until, in some instances, they become world record holders for their age groups.

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.

Individual profiles of spatio-temporal coordination in high intensity swimming

The aim of the present study was to examine the inter-subject variability in inter-arm coordination during front crawl swimming at high intensity. Ten male competitive swimmers swam 200m front crawl at race pace. Two above water and four underwater cameras videotaped the test and APAS was used to assess the 3D anatomical points position and to calculate, afterwards, the angular position, velocity and the continuous relative phase, which was used to analyze upper limbs coupling during two arm stroke cycles for each 50m lap of the 200m front crawl event. The kinematics of the two arm stroke cycles was filtered and normalized to the total cycle duration. A significant decrease, caused by fatigue, was observed in the biomechanical and coordinative (temporal) parameters. The topography of the mean continuous relative phase curve showed a higher inter-subject variability between two groups (63.1° vs. 76.0°; p<.05), suggesting that several profiles of inter-limb coordination exist. Two clusters arose from the coordination profiling, which mainly stemmed from organismic constraints (i.e., the swimmer’s technique).

Estimating the energy contribution during single and repeated sprint swimming

The extent to which aerobic processes contribute to energy supply during short duration sprint swimming is not known. Therefore, the energy contribution to a maximal 30 s fully tethered swim (FTS), and repeated 4 × 30 s high intensity semi-tethered swimming bouts (STS) with 30 s of passive rest at 95% of the 30 s FTS intensity was estimated in eight elite male swimmers. Blood lactate concentration and pH after the 4 × 30 s test were 12.1 ± 3.6 mmol/L and 7.2 ± 0.1, respectively. Accumulated oxygen demand was estimated to be 50.9 ± 9.6 mL/kg and 48.3 ± 8.4, 47.2 ± 8.5, 47.4 ± 8.3, and 45.6 ± 6.8 mL/kg for the 30 s FTS and 4 × 30 s bouts, respectively. Accumulated oxygen uptake was 16.6 ± 3.6 for the 30 s FTS and progressively increased during the 4 × 30 s bouts 12.2 ± 2.1, 21.6 ± 2.5, 22.8 ± 1.8, and 23.5 ± 2.0 mL/kg (P < 0.01). The estimated aerobic contribution therefore was 33 ± 8% for the 30 s FTS and 25 ± 4, 47 ± 9, 49 ± 8, 52 ± 9% for bouts 1-4 during the 4 × 30 s STS test (P < 0.01). The results underline the importance of aerobic energy contribution during single and repeated high intensity swimming, which should be considered when prescribing swimming training sets of this nature.

Lactate Threshold and Performance Adaptations to 4 Weeks of Training in Untrained Swimmers: Volume Vs. Intensity

The purpose of this study was to investigate the impact of 4 weeks of high-intensity vs. high-volume swim training on lactate threshold (LT) characteristics and performance. Thirteen untrained swimmers with a mean age of 19.0 ± 0.5 undertook an incremental swimming test before and after 4 weeks of training for the determination of LT. Performance was evaluated by a 50-m maximum freestyle test. The swimmers were assigned to 1 of each of 2 training groups. The high-intensity group (n = 6) focused on sprint training (SP) and swam a total of 1,808 ± 210 m. The high-volume group (n = 7) followed the same program as the SP group but swam an additional 1,100 m (38% more) of endurance swimming (SP + End). A training effect was evident in both groups as seen by the similar improvements in sprint performance of the 50-m maximum time (p < 0.01), peak velocity increases and the lower value of lactate at the individual LTs (p < 0.01). Lactate threshold velocity improved only in the SP + End group from 1.20 ± 0.12 m·s(-1) pretraining to 1.32 ± 0.12 m·s(-1) posttraining (p = 0.77, effect size = 1, p < 0.01), expressed by the rightward shifts of the individual lactate-velocity curves, indicating an improvement in the aerobic capacity. Peak lactate and lactate concentrations at LT did not significantly change. In conclusion, this study was able to demonstrate that 4 weeks of either high-intensity or high-volume training was able to demonstrate similar improvements in swimming performance. In the case of lack of significant changes in lactate profiling in response to high-intensity training, we could suggest a dissociation between the 2.

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.

Ergogenic effect of hyperoxic recovery in elite swimmers performing high‐intensity intervals

This investigation tested the hypothesis that breathing oxygen-enriched air (F(i)O(2) =1.00) during recovery enhances peak (P(peak)) and mean power (P(mean)) output during repeated high-intensity exercise. Twelve elite male swimmers (21 ± 3 years, 192.1 ± 5.9 cm, 79.1 ± 8.2 kg) inhaled either hyperoxic (HOX) or normoxic (NOX) air during 6-min recovery periods between five repetitions of high-intensity bench swimming, each involving 40 maximal armstrokes. Oxygen partial pressure (pO(2)) and saturation (SO(2)), [H(+)], pH, base excess and blood lactate concentration were measured before and after all intervals. The production of the reactive oxygen species (ROS) hydrogen peroxide was measured before, directly after and 15 min after the test. P(peak) and P(mean) with HOX recovery were significantly higher than with NOX throughout the third, fourth and fifth intervals (P<0.001-0.04). With HOX, electromyography activity was lower during the third, fourth and fifth intervals than during the first (P=0.05-0.001), with no such changes in NOX (P=0.99). There were no differences in blood lactate, pH, [H(+)] or base excess and ROS production at any time point with either HOX or NOX recovery. These findings demonstrate that the P(peak) and P(mean) of elite swimmers performing high-intensity intervals can be improved by exposure to oxygen-enriched air during recovery.

Game Activity and Blood Lactate in Men's Elite Water-Polo Players

The purpose of this study was to examine game demands during highly competitive men's water-polo games after the introduction of the new Federation International Natation Association (FINA) rules. Participants of this study were 77 outfield international level men's water-polo players (age 25.9 ± 4.5 years, height 188 ± 4.5 cm, body mass 93 ± 10.9 kg). Game earlobe blood lactate, speed, and distance covered (semiautomatic image recognition system) were measured during 6 highly competitive matches (FINA International Tournament). In the game, players covered 1,613 ± 150 m (n = 68). This corresponds to a mean coverage rate of 54 ± 5.8 m·min (n = 68). At speeds faster than 1.4 m·s⁻¹ (high-intensity swimming), players covered 44% of the total distance. A significant decrease in coverage rate was detected during the final stage of the game. Mean blood-lactate concentration was 7.7 ± 1.0 mmol·L⁻¹ (range 2.2-14.3). Center Defenders (1,816 ± 496 m) covered significantly (p < 0.05) more distance swimming compared to Field (1,676 ± 348 m) and Center-Forward (1,317 ± 281 m) players. Mean match blood-lactate concentrations for Center Forwards, Center Defenders, and Field Players were 11.2 ± 1.0 (3-14.3), 6.7 ± 0.9 (1.4-8), and 5.3 ± 0.9 mmol·L⁻¹ (2.2-11.9), respectively. This study confirmed the high-intensity nature of male elite level water polo showing remarkable role-dependent game demands. As a result, strength and conditioning interventions should be individualized and mainly address intermittent high-intensity endurance and anaerobic fitness.

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.

Influence of Different Breathing Frequencies on the Severity of Inspiratory Muscle Fatigue Induced by High-Intensity Front Crawl Swimming

The aim of the present study was to assess the influence of 2 different breathing frequencies on the magnitude of inspiratory muscle fatigue after high-intensity front crawl swimming. The influence of different breathing frequencies on postexercise blood lactate ([La]) and heart rate (HR) was also examined. Ten collegiate swimmers performed 2 x 200-m front crawl swims at 90% of race pace with the following breathing frequencies: 1) 1 breath every second stroke (B2), and 2) 1 breath every fourth stroke (B4). Maximal inspiratory pressure (PImax) was measured at the mouth from residual volume before (baseline) and after swimming, in a standing position. The HR and [La] were assessed at rest and immediately at the cessation of swimming. The PImax decreased by 21% after B4 and by 11% after B2 compared with baseline (p < 0.05). The [La] was lower by 15% after B4 than after B2 (p < 0.05). The HR was not significantly different between B2 and B4. These data suggest that there is significant global inspiratory muscle fatigue after high-intensity swimming. Inspiratory muscle fatigue is, however, greater when breathing frequency is reduced during high-intensity front crawl swimming. Respiratory muscle training should be used to improve respiratory muscle strength and endurance in swimmers.

상대적 수영운동 강도가 흰쥐 갈색지방조직의 UCP-1과 UCP-3 mRNA 발현, 혈중 인슐린 및 혈당에 미치는 효과

본 연구에서는 F344계 흰쥐를 대상으로 8주간 저강도 운동군과 고강도 운동군으로 나누어 수영운동을 실시하여, 갈색지방조직 내 UCP-1과 UCP-3mRNA 발현을 관찰하고 혈당 및 인슐린 수준이 어떠한 변화를 나타내는지 알아보았다. 그 결과 저강도 수영을 실시한 그룹이 대조군과 고강도 운동그룹보다 갈색지방조직 내 UCP-1과 UCP-3 mRNA 발현이 증가되는 것을 관찰하였으며, 고강도 수영군에서 대조군 보다 인슐린 수준이 낮게 나타났으나 혈당에서는 유의한차가 나타나지 않았다. 하지만 저강도 수영군에서 대조군보다 혈당 및 인슐린 수준이 유의하게 감소하는 것을 관찰하였다. 이러한 결과는 저강도 수영운동이 갈색지방조직 내 UCP-1과 UCP-3mRNA 발현을 증가시키고, 당대사를 활성화하여 인슐린민감도를 개선시킬 수 있음을 보여주는 결과이다. The purpose of this study was to investigate the UCP-1, UCP-3 mRNA expression in brown adipose tissue with glycometabolism according to intensity and duration of swimming in rat. F344 rat were randomly divided into three groups (n=10 in each group): control (CON), low-intensity swimming (LIS) groups, and high-intensity swimming (HIS) groups. Animals in the LIS group were forced to swim in swimming pool for 30min once a day for 8 consecutive weeks with a light intensity. In the HIS group, the rats repeated fifteen 20-s swimming bouts with a weight equivalent to 10% of body weight for 8weeks, respectively. The present result demonstrated that in LIS group, serum insulin and glucose levels significantly decreased in LIS group compared to CON. Brown adipose tissue UCP-1 and UCP-3mRNA expression was significantly increase in LIS group compared to CON and HIS groups. From those results, it can be suggested that low-intensity swimming may improve glycometablism control by up-regulating UCP-1 and UCP-3mRNA expression.

Relationships between stroke parameters and critical swimming speed in a sprint interval training set

The aim of this study was to determine whether a relationship exists between stroke parameters and critical swimming speed (which is defined as the speed that can theoretically be maintained without exhaustion). Stroke parameters (stroke rate and length) and velocity were recorded for each 25-m length during a controlled sprint interval training set in which participants swam one of the four competitive strokes at a range of intensities below, at, and above critical speed. Eleven participants (8 females, 3 males; age 17.9 ± 0.9 years) completed a progressive (descending) set of 8 × 100 m repetitions in a 25-m pool according to target times that ranged in intensity from 65% to 100% of the swimmer's best time (the intensity for each repetition increased by 5% throughout the set). The data showed that participants reached critical speed on the fourth repetition and that substantial and unpredictable changes in stroke parameters occurred once critical speed had been reached. Specifically, post-critical speed stroke rate and stroke length were significantly (P < 0.01) greater and less, respectively, than the pre-critical speed values, and these changes occurred in an abrupt and non-linear manner. Overall, the findings suggest that critical speed represents a transition point between two different sets of stroke parameter relationships – one for low-intensity aerobic swimming and one for high-intensity anaerobic swimming.

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.

Left ventricular function in physiologic and pathologic hypertrophy in Sprague–Dawley rats

Objective The aim of this study was to design a high intensity swimming training and two-kidney, one-clip (2K1C) hypertension protocol in Sprague–Dawley (SD) rats and to use current echocardiography techniques to examine the differential diagnosis between physiological and pathological left ventricular hypertrophy. Methods One group of SD rats performed swimming training at high intensive swimming training (HIGH) for eight weeks. In animals of the other arm of the study, a 2KIC hypertension was created and maintained for eight weeks. Results After eight weeks, all rats were studied by standard and tissue Doppler echocardiography. The heart weight/body weight ratio (HW/BW) of 2K1C and HIGH rats increased by 16% and 42%, respectively. Echocardiography showed increased septal and posterior wall thickness in both the 2K1C and HIGH rats. Left ventricular increased by 35 and 41% respectively. Left ventricular diameters, stroke volumes, cardiac output, and ejection fractions were unchanged in either group. Mitral inflow showed a decrease in late-wave velocity, thus increasing the E/A ratio in HIGH rats. However, mitral inflow showed an increase in late-wave velocity, thus decreasing the E/A ratio in 2K1C rats. There was a significant increase in Ea and early diastolic (Em)/late diastolic (Am) in HIGH rats in basal septum and lateral mitral valve annulus. And there was a significant increase in Am, which led to a significant decrease of Em/Am in 2K1C rats. No significant change occurred in pulmonary vein systolic velocity and diastolic velocity, in either of the three animal groups. However, there was significant increase in atrial reversal velocity in HIGH rats. Conclusions Doppler echocardiographic parameters of LV diastolic function can be of diagnostic importance for discrimination between pathologic and physiologic LV hypertrophy.

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.

Volume vs. Intensity in the Training of Competitive Swimmers

The present study aimed at comparing a high-volume, low-intensity vs. low-volume, high-intensity swim training. In a randomized cross-over design, 10 competitive swimmers performed two different 4-week training periods, each followed by an identical taper week. One training period was characterized by a high-training volume (HVT) whereas high-intensity training was prevalent during the other program (HIT). Before, after two and four weeks and after the taper week subjects performed psychometric and performance testing: profile of mood states (POMS), incremental swimming test (determination of individual anaerobic threshold, IAT), 100 m and 400 m. A small significant increase in IAT was observed after taper periods compared to pre-training (+ 0.01 m/s; p = 0.01). Maximal 100-m and 400-m times were not significantly affected by training. The POMS subscore of "vigor" decreased slightly after both training periods (p = 0.06). None of the investigated parameters showed a significant interaction between test-time and training type (p > 0.13). Nearly all (83 %) subjects swam personal best times during the 3 months after each training cycle. It is concluded that, for a period of 4 weeks, high-training volumes have no advantage compared to high-intensity training of lower volume.

Circulating regulatory T‐cells: Acute exercise response in elite swimmers

Several authors have found higher rates of allergy and asthma (AA) among elite endurance athletes. The purpose of this study was to characterize the pattern of Regulatory T‐cells (Tregs) and FoxP3+ Tregs at baseline (Pre) and at the end of high‐intensity swim exercise (EE). On the weekend after their last high school swim meet, 22 elite swimmers (12 males, mean age=15.4 years, AA group=12) participated in a swim study. Spirometry was measure before and 10–15 minutes post EE and blood collected Pre and EE. Neither Pre nor EE blood lactate, FEV1, heart rate, or lymphocyte subsets (% of cells or absolute counts, #s) differed between the groups (control vs AA). Controls had lower CD4+CD25+FoxP3 dim cells (% of lymphs) than the AA group (p&lt;0.05), though absolute cell counts did not differ. As shown on Figure 1, the AA group had higher percentages and absolute FoxP3+ cell counts (n.s.) at both Pre and EE. Absolute cell counts increased in both groups during exercise however, the percentages of FoxP3+ cells decreased from Pre to EE. An ancillary finding of this study was that the baseline levels of Tregs and FoxP3+ cells in the elite swimmers appeared to be substantially lower than values previously reported for non‐endurance athletes. This study was funded by USA Swimming and NIH P01 HD048721.

Proteomic adaptation to chronic high intensity swimming training in the rat heart

Cardiac hypertrophy induced by exercise is associated with less cardiac fibrosis and better systolic and diastolic function, suggesting that the adaptive mechanisms may exist in exercise-induced hypertrophy. To identify molecular mechanisms by which exercise training stimulates this favorable phenotype, a proteomic approach was employed to detect rat cardiac proteins that were differentially expressed or modified after exercise training. Sixteen male Sprague–Dawley rats were divided into trained (T) and control(C). T rats underwent eight weeks of swimming training seven days/week, using a high intensity protocol. Hearts were used to generate 2-D electrophoretic proteome maps. Training significantly altered 23 protein spot intensities ( P < 0.05), including proteins associated with the mitochondria oxidative metabolism, such as prohibitin, malate dehydrogenase, short-chain acyl-CoA dehydrogenase, triosephosphate isomerase, electron transfer flavoprotein subunit beta, ndufa10 protein, ATP synthase subunit alpha and isocitrate dehydrogenase [NAD] subunit. Additionally, Prohibitin was increased in the exercise-induced hearts. Cytoskeletal, signal pathway, stress and oxidative proteins also increased within T groups. These results strongly support the notion that the observed changes in the expression of energy metabolism proteins resulted in a potential increase in the capacity to synthesise ATP, probably via mitochondrial oxidative metabolism. The observed changes in the expression of these metabolic and structural proteins induced by training may beneficially influence heart metabolism, stress response and signalling paths, and therefore improve the overall cardiac function.