Hormonal responses to training and its tapering off in competitive swimmers: relationships with performance

During a winter training season, the effects of 12 weeks of intense training and 4 weeks of tapering off (taper) on plasma hormone concentrations and competition performance were investigated in a group of highly trained swimmers (n = 8). Blood samples were collected and the swimmers performed their speciality in competition at weeks 10 (mid-season), 22 (pre-taper) and 26 (post-taper). No statistically significant changes were observed in the concentrations of total testosterone (TT), non-sex hormone binding globulin-boundtestosterone (NSBT), cortisol (C), luteinising hormone, thyroid stimulating hormone, triiodothyronine, thyroxine plasma catecholamines, creatine kinase and ammonia during training and taper. Mid-season NSBT: C ratio and the amount of training were statistically related (r = 0.82,P < 0.05). Competition performance slightly declined during intense training [0.52 (SD 2.51) %, NS] and improved during taper [2.32 (SD 1.69)%,P < 0.01]. Changes in performance during training and taper correlated with changes in ratios TT: C (r = 0.86,P < 0.01andr = 0.81,P < 0.05, respectively) and NSBT: C (r = 0.77,P < 0.05 andr = 0.76,P < 0.05, respectively). In summary, these results showed that the monitored plasma hormones and metabolic indices were unaltered by 12 weeks of intense training and 4 weeks of taper. The TT: C and NSBT: C ratios, however, appeared to be effective markers of the swimmers' performance capacities throughout the training season.     

Detraining: loss of training-induced physiological and performance adaptations. Part I: short term insufficient training stimulus

Detraining is the partial or complete loss of training-induced adaptations, in response to an insufficient training stimulus. Detraining characteristics may be different depending on the duration of training cessation or insufficient training. Short term detraining (less than 4 weeks of insufficient training stimulus) is analysed in part I of this review, whereas part II will deal with long term detraining (more than 4 weeks of insufficient training stimulus). Short term cardiorespiratory detraining is characterised in highly trained athletes by a rapid decline in maximal oxygen uptake (VO2max) and blood volume. Exercise heart rate increases insufficiently to counterbalance the decreased stroke volume, and maximal cardiac output is thus reduced. Ventilatory efficiency and endurance performance are also impaired. These changes are more moderate in recently trained individuals. From a metabolic viewpoint, short term inactivity implies an increased reliance on carbohydrate metabolism during exercise, as shown by a higher exercise respiratory exchange ratio, and lowered lipase activity, GLUT-4 content, glycogen level and lactate threshold. At the muscle level, capillary density and oxidative enzyme activities are reduced. Training-induced changes in fibre cross-sectional area are reversed, but strength performance declines are limited. Hormonal changes include a reduced insulin sensitivity, a possible increase in testosterone and growth hormone levels in strength athletes, and a reversal of short term training-induced adaptations in fluid-electrolyte regulating hormones.     

Detraining: loss of training-induced physiological and performance adaptations. Part II: Long term insufficient training stimulus

This part II discusses detraining following an insufficient training stimulus period longer than 4 weeks, as well as several strategies that may be useful to avoid its negative impact. The maximal oxygen uptake (VO2max) of athletes declines markedly but remains above control values during long term detraining, whereas recently acquired VO2max gains are completely lost. This is partly due to reduced blood volume, cardiac dimensions and ventilatory efficiency, resulting in lower stroke volume and cardiac output, despite increased heart rates. Endurance performance is accordingly impaired. Resting muscle glycogen levels return to baseline, carbohydrate utilisation increases and the lactate threshold is lowered, although it remains above untrained values in the highly trained. At the muscle level, capillarisation, arterial-venous oxygen difference and oxidative enzyme activities decline in athletes and are completely reversed in recently trained individuals, contributing significantly to the long term loss in VO2max. Oxidative fibre proportion is decreased in endurance athletes, whereas it increases in strength athletes, whose fibre areas are significantly reduced. Force production declines slowly, and usually remains above control values for very long periods. All these negative effects can be avoided or limited by reduced training strategies, as long as training intensity is maintained and frequency reduced only moderately. On the other hand, training volume can be markedly reduced. Cross-training may also be effective in maintaining training-induced adaptations. Athletes should use similar-mode exercise, but moderately trained individuals could also benefit from dissimilar-mode cross-training. Finally, the existence of a cross-transfer effect between ipsilateral and contralateral limbs should be considered in order to limit detraining during periods of unilateral immobilisation.     

Exercise intensity and load during mass-start stage races in professional road cycling

PURPOSE: To evaluate exercise intensity and load during mass-start stages in professional road cycling, using competition heart rate (HR) recordings. METHODS: Seventeen world-class cyclists performed an incremental laboratory test during which maximal power output (Wmax), maximal HR (HRmax), onset of blood lactate accumulation (OBLA), lactate threshold (LT), and a HR-power output relationship were assessed. An OBLAZONE (HROBLA +/- 3 beats.min-1) and an LTZONE (HRLT +/- 3 beats.min-1) were described. HR was monitored during 125 flat (< 13 km uphill, < 800-m altitude change; FLAT), 99 semi-mountainous (13-35 km uphill, 800- to 2000-m altitude change; SEMO), and 86 high-mountain (> 35 km uphill, > 2000-m altitude change; HIMO) stages. Each cyclist's competition power output was estimated from competition HR and individual HR-power output relationships. Competition training impulse (TRIMP) values and time spent at "easy," "moderate," and "hard" zones were estimated from HR and race duration. RESULTS: Average %HRmax were 61 +/- 5%, 58 +/- 6%, and 51 +/- 7% in HIMO, SEMO, and FLAT stages, respectively, and estimated average power outputs were 246 +/- 44, 234 +/- 43, and 192 +/- 45 W. Competition HR values relative to HROBLA and HRLT were, respectively, 69 +/- 6, 79 +/- 9% in HIMO; 65 +/- 7, 74 +/- 11% in SEMO; and 57 +/- 8, 65 +/- 10% in FLAT stages. The amount of TRIMP in HIMO, SEMO, and FLAT stages were, respectively, 215 +/- 38, 172 +/- 31, and 156 +/- 31. Percentage time spent in the "moderate" and "hard" zones was highest in HIMO (22 +/- 14, 5 +/- 6%) followed by SEMO (15 +/- 13, 5 +/- 5%) and FLAT (9 +/- 7, 2 +/- 2%) stages. CONCLUSIONS: %HRmax, time distribution around HROBLA and HRLT, TRIMP, and load zones reflected the physiological demands of different mass-start cycling stage categories. The knowledge of these demands could be useful for planning precompetition training strategies.     

Muscular characteristics of detraining in humans

Skeletal muscle is characterized by its ability to dynamically adapt to variable levels of functional demands. During periods of insufficient training stimulus, muscular detraining occurs. This may be characterized by a decreased capillary density, which could take place within 2--3 wk of inactivity. Arterial-venous oxygen difference declines if training stoppage continues beyond 3--8 wk. Rapid and progressive reductions in oxidative enzyme activities bring about a reduced mitochondrial ATP production. The above changes are related to the reduction in VO(2max) observed during long-term training cessation. These muscular characteristics remain above sedentary values in the detrained athlete but usually return to baseline values in recently trained individuals. Glycolytic enzyme activities show nonsystematic changes during periods of training cessation. Fiber distribution remains unchanged during the initial weeks of inactivity, but oxidative fibers may decrease in endurance athletes and increase in strength-trained athletes within 8 wk of training stoppage. Muscle fiber cross-sectional area declines rapidly in strength and sprint athletes, and in recently endurance-trained subjects, whereas it may increase slightly in endurance athletes. Force production declines slowly and in relation to decreased EMG activity. Strength performance in general is readily maintained for up to 4 wk of inactivity, but highly trained athletes' eccentric force and sport-specific power, and recently acquired isokinetic strength, may decline significantly.     

Cardiorespiratory and metabolic characteristics of detraining in humans

Detraining can be defined as the partial or complete loss of training-induced adaptations, in response to an insufficient training stimulus. Detraining is characterized, among other changes, by marked alterations in the cardiorespiratory system and the metabolic patterns during exercise. In highly trained athletes, insufficient training induces a rapid decline in VO2max, but it remains above control values. Exercise heart rate increases insufficiently to counterbalance the decreased stroke volume resulting from a rapid blood volume loss, and maximal cardiac output is thus reduced. Cardiac dimensions are also reduced, as well as ventilatory efficiency. Consequently, endurance performance is also markedly impaired. These changes are more moderate in recently trained subjects in the short-term, but recently acquired VO2max gains are completely lost after training stoppage periods longer than 4 wk. From a metabolic viewpoint, even short-term inactivity implies an increased reliance on carbohydrate metabolism during exercise, as shown by a higher exercise respiratory exchange ratio. This may result from a reduced insulin sensitivity and GLUT-4 transporter protein content, coupled with a lowered muscle lipoprotein lipase activity. These metabolic changes may take place within 10 d of training cessation. Resting muscle glycogen concentration returns to baseline within a few weeks without training, and trained athletes' lactate threshold is also lowered, but still remains above untrained values.     

Nutrition in team sports

Team sports are based on intermittent high-intensity activity patterns, but the exact characteristics vary between and within codes, and from one game to the next. Despite the challenge of predicting exact game demands, performance in team sports is often dependent on nutritional factors. Chronic issues include achieving ideal levels of muscle mass and body fat, and supporting the nutrient needs of the training program. Acute issues, both for training and in games, include strategies that allow the player to be well fuelled and hydrated over the duration of exercise. Each player should develop a plan of consuming fluid and carbohydrate according to the needs of their activity patterns, within the breaks that are provided in their sport. In seasonal fixtures, competition varies from a weekly game in some codes to 2-3 games over a weekend road trip in others, and a tournament fixture usually involves 1-3 days between matches. Recovery between events is a major priority, involving rehydration, refuelling and repair/adaptation activities. Some sports supplements may be of value to the team athlete. Sports drinks, gels and liquid meals may be valuable in allowing nutritional goals to be met, while caffeine, creatine and buffering agents may directly enhance performance.     

Effects of tapering on performance: a meta-analysis

PURPOSE: The purpose of this investigation was to assess the effects of alterations in taper components on performance in competitive athletes, through a meta-analysis. METHODS: Six databases were searched using relevant terms and strategies. Criteria for study inclusion were that participants must be competitive athletes, a tapering intervention must be employed providing details about the procedures used to decrease the training load, use of actual competition or field-based criterion performance, and inclusion of all necessary data to calculate effect sizes. Datasets reported in more than one published study were only included once in the present analyses. Twenty-seven of 182 potential studies met these criteria and were included in the analysis. The dependent variable was performance, and the independent variables were the decrease in training intensity, volume, and frequency, as well as the pattern of the taper and its duration. Pre-post taper standardized mean differences in performance were calculated and weighted according to the within-group heterogeneity to develop an overall effect. RESULTS: The optimal strategy to optimize performance is a tapering intervention of 2-wk duration (overall effect = 0.59 +/- 0.33, P < 0.001), where the training volume is exponentially decreased by 41-60% (overall effect = 0.72 +/- 0.36, P < 0.001), without any modification of either training intensity (overall effect = 0.33 +/- 0.14, P < 0.001) or frequency (overall effect = 0.35 +/- 0.17, P < 0.001). CONCLUSION: A 2-wk taper during which training volume is exponentially reduced by 41-60% seems to be the most efficient strategy to maximize performance gains. This meta-analysis provides a framework that can be useful for athletes, coaches, and sport scientists to optimize their tapering strategy.     

Effectiveness of nanoencapsulated methotrexate against osteosarcoma cells: <Emphasis Type="Italic">in vitro</Emphasis> cytotoxicity under dynamic conditions

Cancer is a leading cause of mortality in the world, with osteosarcoma being one of the most common types among children between 1 and 14 years old. Current treatments including preoperative chemotherapy, surgery and postoperative chemotherapy produce several side effects with limited effectiveness. The use of lipid nanoparticles as biodegradable shells for controlled drug delivery shows promise as a more effective and targeted tumor treatment. However, in vitro validation of these vehicles is limited due to fluid stagnation in current techniques, in which nanoparticles sediment onto the bottom of the wells killing the cells by asphyxiation. In the current series of experiments, results obtained with methotrexate-lipid nanoparticles under dynamic assay conditions are presented as a promising alternative to current free drug based therapies. Effects on the viability of the U-2 OS osteosarcoma cell line of recirculation of cell media, free methotrexate and blank and methotrexate containing lipid nanoparticles in a 11 μM concentration were successfully assessed. In addition, several designs for the microfluidic platform used were simulated using COMSOL-Multiphysics, optimized devices were fabricated using soft-lithography and simulated parameters were experimentally validated. Nanoparticles did not sediment to the bottom of the platform, demonstrating the effectiveness of the proposed system. Moreover, encapsulated methotrexate was the most effective treatment, as after 72 h the cell population was reduced nearly 40% while under free methotrexate circulation the cell population doubled. Overall, these results indicate that methotrexate-lipid nanoparticles are a promising targeted therapy for osteosarcoma treatment.