Perceived training intensity and performance changes quantification in judo.

The objective of this study was to determine the methods of quantification for training and performance, which would be the most appropriate for modeling the responses to long-term training in cadet and junior judo athletes. For this, 10 young male judo athletes (15.9 ± 1.3 years, 64.9 ± 10.3 kg, and 170.8 ± 5.4 cm) competing at a regional/state level volunteered to take part in this study. Data were collected during a 2-year training period (i.e., 702 days) from January 2011 to December 2012. Their mean training volume was 6.52 ± 0.43 hours per week during the preparatory periods and 4.75 ± 0.49 hours per week during the competitive periods. They followed a training program prescribed by the same coach. The training load (TL) was quantified through the session rating of perceived exertion (RPE) and expressed in arbitrary unit (a.u.). Performance was quantified from 5 parameters and divided into 2 categories: performance in competition and performance in training. The evaluation of performance in competition was based on the number of points per level. Performance in training was assessed through 4 different tests. A physical test battery consisting of a standing long jump, 2 judo-specific tests that were the maximal number of dynamic chin-up holding the judogi, and the Special Judo Fitness Test was used. System modeling for describing training adaptations consisted of mathematically relating the TL of the training sessions (system input) to the change in performance (system output). The quality of the fit between TL and performance was similar, whether the TL was computed directly from RPE (R = 0.55 ± 0.18) or from the session RPE (R = 0.56 ± 0.18) and was significant in 8 athletes over 10, excluding the standing jump from the computation of the TL, leading to a simplest method. Thus, this study represents a first attempt to model TL effects on judo-specific performance and has shown that the best relationships between amounts of training and changes in performance were obtained when training amounts were quantified simply from RPE.

Autophagy is essential to support skeletal muscle plasticity in response to endurance exercise.

Physical exercise is a stress that can substantially modulate cellular signaling mechanisms to promote morphological and metabolic adaptations. Skeletal muscle protein and organelle turnover is dependent on two major cellular pathways: Forkhead box class O proteins (FOXO) transcription factors that regulate two main proteolytic systems, the ubiquitin-proteasome, and the autophagy-lysosome systems, including mitochondrial autophagy, and the MTORC1 signaling associated with protein translation and autophagy inhibition. In recent years, it has been well documented that both acute and chronic endurance exercise can affect the autophagy pathway. Importantly, substantial efforts have been made to better understand discrepancies in the literature on its modulation during exercise. A single bout of endurance exercise increases autophagic flux when the duration is long enough, and this response is dependent on nutritional status, since autophagic flux markers and mRNA coding for actors involved in mitophagy are more abundant in the fasted state. In contrast, strength and resistance exercises preferentially raise ubiquitin-proteasome system activity and involve several protein synthesis factors, such as the recently characterized DAGK for mechanistic target of rapamycin activation. In this review, we discuss recent progress on the impact of acute and chronic exercise on cell component turnover systems, with particular focus on autophagy, which until now has been relatively overlooked in skeletal muscle. We especially highlight the most recent studies on the factors that can impact its modulation, including the mode of exercise and the nutritional status, and also discuss the current limitations in the literature to encourage further works on this topic.

Autophagy and protein turnover signaling in slow-twitch muscle during exercise.

PURPOSE: The aim of this study was to characterize skeletal muscle protein breakdown and mitochondrial dynamics markers at different points of endurance exercise. METHODS: Mice run at 10 m·min(-1) during 1 h, and running speed was increased by 0.5 m·min(-1) every minute during 40 min and then by 1 m·min(-1) until exhaustion. Animals were killed by cervical dislocation at 30, 60, 90, and 120 min; at time to exhaustion (Te); and at 3 and 24 h during recovery. The soleus and the deep red regions of the quadriceps muscles were pooled. RESULTS: AMPK phosphorylation (Thr172) increased from 30 min to Te, and FoxO3a phosphorylation (Thr32 and Ser253) decreased from 120 min to 3 h after exercise. FoxO3a-dependent E3 ligases Mul1 and MuRF1 proteins increased from 30 min to Te and at Te and 3 h after exercise, respectively, whereas MAFbx/atrogin-1 protein expression did not change significantly. The autophagic markers LC3B-II increased at 120 min and Te, and p62 significantly decreased at Te. The AMPK-dependent phosphorylation of Ulk1 at Ser317 and Ser555 increased from 60 min to Te and at 30 and 60 min, respectively. Akt (Ser473), MTOR (Ser2448), and 4E-BP1 (Thr37/46) phosphorylation decreased from 90 min to Te, and the MTOR-dependent phosphorylation of Ulk1 (Ser757) decreased from 120 min to Te. Ser616 phosphorylation of the mitochondrial fission marker DRP1 increased from 60 min to Te, but protein expression of the fusion markers mitofusin-2, a substrate of Mul1, and OPA1 did not significantly change. CONCLUSIONS: These results fit with a regulation of protein breakdown triggered by FoxO3a and Ulk1 pathways after AMPK activation and Akt/MTOR inhibition. Furthermore, our data suggest that mitochondrial fission is quickly increased, and mitochondrial fusion is unchanged during exercise.

FoxO transcription factors: their roles in the maintenance of skeletal muscle homeostasis.

Forkhead box class O family member proteins (FoxOs) are highly conserved transcription factors with important roles in cellular homeostasis. The four FoxO members in humans, FoxO1, FoxO3, FoxO4, and FoxO6, are all expressed in skeletal muscle, but the first three members are the most studied in muscle. In this review, we detail the multiple modes of FoxO regulation and discuss the central role of these proteins in the control of skeletal muscle plasticity. FoxO1 and FoxO3 are key factors of muscle energy homeostasis through the control of glycolytic and lipolytic flux, and mitochondrial metabolism. They are also key regulators of protein breakdown, as they modulate the activity of several actors in the ubiquitin­proteasome and autophagy­lysosomal proteolytic pathways, including mitochondrial autophagy, also called mitophagy. FoxO proteins have also been implicated in the regulation of the cell cycle, apoptosis, and muscle regeneration. Depending of their activation level, FoxO proteins can exhibit ambivalent functions. For example, a basal level of FoxO factors is necessary for cellular homeostasis and these proteins are required for adaptation to exercise. However, exacerbated activation may occur in the course of several diseases, resulting in metabolic disorders and atrophy. A better understanding of the precise functions of these transcriptions factors should thus lead to the development of new therapeutic approaches to prevent or limit the muscle wasting that prevails in numerous pathological states, such as immobilization, denervated conditions, neuromuscular disease, aging, AIDS, cancer, and diabetes.

Modelling training response in elite female gymnasts and optimal strategies of overload training and taper.

The aim of the study is the modelling of training responses with a variable dose-response model in a sport discipline that requires highly complex coordination. We propose a method to optimise the training programme plan using the potential maximal performance gain associated with overload and tapering periods. Data from five female elite gymnasts were collected over a 3-month training period. The relationship between training amounts and performance was then assessed with a non-linear model. The optimal magnitude of training load reduction and its duration were investigated with and without an overload period using simulation procedures based on individual responses to training. The correlation between actual and modelled performances was significant (R² = 0.81 ± 0.02, P < 0.01). The standard error was 2.7%. Simulations revealed that taper preceded by an overload period allows a higher performance to be achieved compared to an absence of overload period (106.3 ± 0.3% vs. 105.1 ± 0.3%). With respect to the pre-taper load, the model predicts that optimal load reductions during taper were 48.4 ± 0.7% and 42.5 ± 1.0% for overloading and non-overloading strategies, respectively. Moreover, optimal durations of the taper period were 34 ± 0.5 days and 22 ± 0.5 days for overloading and non-overloading strategies, respectively. In conclusion, the study showed that the variable dose-response model describes precisely the training response in gymnasts.

The role of AMP-activated protein kinase in the coordination of skeletal muscle turnover and energy homeostasis.

The AMP-activated protein kinase (AMPK) is a serine/threonine protein kinase that acts as a sensor of cellular energy status switch regulating several systems including glucose and lipid metabolism. Recently, AMPK has been implicated in the control of skeletal muscle mass by decreasing mTORC1 activity and increasing protein degradation through regulation of ubiquitin-proteasome and autophagy pathways. In this review, we give an overview of the central role of AMPK in the control of skeletal muscle plasticity. We detail particularly its implication in the control of the hypertrophic and atrophic signaling pathways. In the light of these cumulative and attractive results, AMPK appears as a key player in regulating muscle homeostasis and the modulation of its activity may constitute a therapeutic potential in treating muscle wasting syndromes in humans.

Influence of a conservative sleep management strategy during a solo Pacific Ocean crossing on anxiety and perceived fatigue: a case study.

The aim of this case study was to determine whether a sailor's deliberate choice of a conservative strategy to manage sleep deprivation would allow him to cross the Pacific Ocean and to minimize his state of anxiety and perceived fatigue. The participant, who had more than 10 years' sailing experience in severe conditions, was tested on a small catamaran without any living quarters during a solo Pacific Ocean crossing. Estimations of sleep hours, state anxiety, and perceived fatigue were self-reported by the sailor on a daily basis using a specific questionnaire. The most important finding is that the sailor's deliberate sleep strategy, 5.4 h sleep per day (24% less than on-shore), was enough to keep his anxiety and perceived fatigue within acceptable limits and enabled him to achieve his goal, which was the first crossing of the Pacific Ocean on a catamaran of less than 6 m. In conclusion, our results suggest that the sailor observed in the present case study was able to minimize anxiety and perceived fatigue with adequate sleep to optimize his performance, security, and to achieve his goal.

Effects of hypoxic interval training on cycling performance.

PURPOSE: The aim of this study was to test the hypothesis that intermittent hypoxic interval training improves sea level cycling performance more than equivalent training in hypoxia or normoxia. METHODS: Thirty-three well-trained cyclists and triathletes (25.9 +/- 2.7 yr, VO(2max) 66.1 +/- 6.1 mL.min(-1).kg(-1)) were divided into three groups: intermittent hypoxic (IHT, N = 11, P(I)O(2) of 100 mm Hg), intermittent hypoxic interval training (IHIT, N = 11) and normoxia (Nor, N = 11, P(I)O(2) of 160 mm Hg) and completed a 7-wk training program, consisting of two high-intensity (100 or 90% relative peak power output) interval training sessions each week. Each interval training session was performed in a laboratory on the subject's own bicycle, in normoxic or hypoxic conditions for the Nor and the IHT group, respectively. The IHIT group performed warm-up and cool-down plus recovery from each interval in hypoxic conditions. In contrast to IHT, interval exercise bouts were performed in normoxic conditions. RESULTS: Mean power output during a 10-min cycle time trial improved after the first 4 wk of training by 5.2 +/- 3.9, 3.7 +/- 5.9, and 5.0 +/- 3.4% for IHIT, IHT, and Nor, respectively, without significant differences between groups. Moreover, mean power output did not show any significant improvement in the following 3 wk in any group. VO(2max) (L.min(-1)) increased only in IHIT during the training period (8.7 +/- 9.1%; P < 0.05). No changes in cycling efficiency or in hematological variables (P > 0.05) were observed. CONCLUSION: Four weeks of interval training induced an improvement in endurance performance. However, short-term exposure to hypoxia (approximately 114 min.wk(-1)) did not elicit a greater increase in performance or any hematological modifications.

Evaluation of a theoretical model to quantify the sources of metabolic cost in walking.

OBJECTIVE: To evaluate the validity of a theoretical model of walking in which the oxygen uptake (V(O2)) is described as a function of speed by an equation in the form y = ax + b, with constant a representing the metabolic cost for performing the walking movement, and constant b representing the sum of the metabolic costs for basal metabolism and maintaining balance and posture. DESIGN: Repeated-measures analysis of variance was used to analyze our theoretical model. In a human exercise research laboratory, 12 healthy male subjects walked on a level treadmill at speeds of 0.39-1.83 m/sec under a control condition, while wearing "instability" shoes with peripheral vision obstructed, and with 2-kg weights around each wrist. Total transported mass was the same under each condition through the carriage of 4 kg in a back pack during the control and instability conditions. Outcome was determined by equations describing (V(O2)) as a function of speed and by kinematics of the center of mass. RESULTS: The constant b was higher (P < 0.01) for the instability condition than the other conditions, but constant a did not differ among the conditions. However, external work was greatest (P < 0.05) for the instability condition. CONCLUSIONS: Because the kinematic data demonstrate that the instability condition increased the metabolic cost for performing the walking movement compared with the control condition, and there was no difference among conditions in constant a, the theoretical model seems invalid.

Assessment of wheelchair drag resistance using a coasting deceleration technique.

OBJECTIVE: To apply a recently developed coasting deceleration method to measure rolling and aerodynamic resistances opposing wheelchair propulsion on a variety of different wheelchairs and wheel combinations and on two different ground surfaces. DESIGN: For each condition, 20-25 trials were performed across a speed range of approximately 70-300 m/min. The least-squares method was then used to arrive at values for the coefficient of rolling resistance (CR) and effective frontal area of the wheelchair and occupant. RESULTS: Wheelchair rolling resistance was found to be velocity dependent under some circumstances. CR values on linoleum differed among folding lightweight wheelchairs and when compared with a rigid ultralight and racing wheelchair. Changing rear wheels and tires on one wheelchair resulted in a 14% difference in CR. Carpet increased CR values by an average of 0.0118 over the values determined on linoleum. As expected, effective frontal area of the wheelchair and occupant values were lower for the racer than for the folding lightweight wheelchair. CONCLUSIONS: Wheelchair rolling resistance is not always independent of velocity, and CR on linoleum can vary among wheelchairs by as much as seven-fold, and carpet can more than double CR.