Robin Candau

Effects of concurrent endurance and strength training on running economy and VO 2 kinetics

PURPOSE It has been suggested that endurance training influences the running economy (CR) and the oxygen uptake (.VO(2)) kinetics in heavy exercise by accelerating the primary phase and attenuating the .VO(2) slow component. However, the effects of heavy weight training (HWT) in combination with endurance training remain unclear. The purpose of this study was to examine the influence of a concurrent HWT+endurance training on CR and the .VO(2) kinetics in endurance athletes. METHODS Fifteen triathletes were assigned to endurance+strength (ES) or endurance-only (E) training for 14 wk. The training program was similar, except ES performed two HWT sessions a week. Before and after the training period, the subjects performed 1) an incremental field running test for determination of .VO(2max) and the velocity associated (V(.VO2max)), the second ventilatory threshold (VT(2)); 2) a 3000-m run at constant velocity, calculated to require 25% of the difference between .VO(2max) and VT(2), to determine CR and the characteristics of the VO(2) kinetics; 3) maximal hopping tests to determine maximal mechanical power and lower-limb stiffness; 4) maximal concentric lower-limb strength measurements. RESULTS After the training period, maximal strength were increased (P < 0.01) in ES but remained unchanged in E. Hopping power decreased in E (P < 0.05). After training, economy (P < 0.05) and hopping power (P < 0.001) were greater in ES than in E. .VO(2max), leg hopping stiffness and the .VO(2) kinetics were not significantly affected by training either in ES or E. CONCLUSION Additional HWT led to improved maximal strength and running economy with no significant effects on the .VO(2) kinetics pattern in heavy exercise.

AMPK promotes skeletal muscle autophagy through activation of forkhead FoxO3a and interaction with Ulk1.

In skeletal muscle, protein levels are determined by relative rates of protein synthesis and breakdown. The balance between synthesis and degradation of intracellular components determines the overall muscle fiber size. AMP‐activated protein kinase (AMPK), a sensor of cellular energy status, was recently shown to increase myofibrillar protein degradation through the expression of MAFbx and MuRF1. In the present study, the effect of AMPK activation by AICAR on autophagy was investigated in muscle cells. Our results show that FoxO3a transcription factor activation by AMPK induces the expression of the autophagy‐related proteins LC3B‐II, Gabarapl1, and Beclin1 in primary mouse skeletal muscle myotubes and in the Tibialis anterior (TA) muscle. Time course studies reveal that AMPK activation by AICAR leads to a transient nuclear relocalization of FoxO3a followed by an increase of its cytosolic level. Moreover, AMPK activation leads to the inhibition of mTORC1 and its subsequent dissociation of Ulk1, Atg13, and FIP200 complex. Interestingly, we identify Ulk1 as a new interacting partner of AMPK in muscle cells and we show that Ulk1 is associated with AMPK under normal conditions and dissociates from AMPK during autophagy process. Moreover, we find that AMPK phosphorylates FoxO3a and Ulk1. In conclusion, our data show that AMPK activation stimulates autophagy in skeletal muscle cells through its effects on the transcriptional function of FoxO3a and takes part in the initiation of autophagosome formation by interacting with Ulk1. Here, we present new evidences that AMPK plays a crucial role in the fine tuning of protein expression programs that control skeletal muscle mass. J. Cell. Biochem. 113: 695–710, 2012.

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 ubiquitin–proteasome and autophagy–lysosomal 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.

Aerodynamic drag in field cycling with special reference to the Obree's position

In cycling at race speeds, 90% of total resistance opposing motion, R T(N) T depends on aerodynamic drag of air, which is directly proportional to the effective frontal area, AC d(m2). R T was measured on a cyclist, in an open velodrome, in order to evaluate AC d in four different positions on a traditional bicycle: upright d position (UP), dropped position (DP), aero position (AP) and Obrees position (OP : the hands in support under the chest, the forearms tucked on the arms, the trunk tilted forward). R T was determined at different constant speeds, Vc(m s−1) with a special device (Max One), which allows the measurement of the external mechanical power P ext(W) in real conditions of cycling locomotion ext (R T = P ext Vc−1). Experiments were carried out in order to test the validity and the reproducibility of P ext provided by the measurement device. P ext was measured twice in the same experimental conditions (exercise on a treadmill against slopes varying from 1 to 14%) and no significant difference ...

Poling forces during roller skiing: effects of technique and speed

PURPOSE Although it has been reported that the majority of propulsive forces are generated through the poles with ski skating, no study has systematically examined poling forces among different skating techniques. The objective of the present study was to examine poling forces and timing during roller skiing on a 2.1% uphill. METHODS Nine highly skilled cross-country skiers roller skied at three paced speeds and maximal speed using the V1 skate (V1), V2-alternate (V2A), V2 skate (V2), and double pole (DP) techniques while poling forces and timing were measured with piezoelectric transducers. RESULTS Peak force (PF) values with the skating techniques were significantly lower than with DP and ranged from 18.9 +/- 3.1% of body weight (BW) to 31.5 +/- 5.6% BW across the speeds of the study. Average force over the entire cycle (ACF) increased with speed with DP, V2A and V1 (P < 0.01) but not with V2. PF and ACF were higher (P < 0.01) with V2 than V1 and V2A. Poling time was longer (P < 0.01) with V2A compared with V1 and V2. CONCLUSIONS The results of this study suggest that 1) the use of the upper body is greater with V2 than with other skating techniques while there is a relatively greater reliance on the lower body for generation of the additional propulsive forces required to increase velocity, and (2) poling forces do not appear to be as effectively applied with V2 as with V2A.

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.

Level ground and uphill cycling efficiency in seated and standing positions.

PURPOSE This study was designed to examine the effects of cycling position (seated or standing) during level-ground and uphill cycling on gross external efficiency (GE) and economy (EC). METHODS Eight well-trained cyclists performed in a randomized order five trials of 6-min duration at 75% of peak power output either on a velodrome or during the ascent of a hill in seated or standing position. GE and EC were calculated by using the mechanical power output that was measured by crankset (SRM) and energy consumption by a portable gas analyzer (Cosmed K4b(2)). In addition, each subject performed three 30-s maximal sprints on a laboratory-based cycle ergometer or in the field either in seated or standing position. RESULTS GE and EC were, respectively, 22.4 +/- 1.5% (CV = 5.6%) and 4.69 +/- 0.33 kJ x L(-1) (CV = 5.7%) and were not different between level seated, uphill seated, or uphill standing conditions. Heart rate was significantly ( < 0.05) higher in standing position. In the uphill cycling trials, minute ventilation was higher ( < 0.05) in standing than in seated position. The average 30-s power output was higher ( < 0.01) in standing (803 +/- 103 W) than in seated position (635 +/- 123 W) or on the stationary ergometer (603 +/- 81 W). CONCLUSION Gradient or body position appears to have a negligible effect on external efficiency in field-based high-intensity cycling exercise. Greater short-term power can be produced in standing position, presumably due to a greater force developed per revolution. However, the technical features of the standing position may be one of the most determining factors affecting the metabolic responses.

Myostatin up-regulation is associated with the skeletal muscle response to hypoxic stimuli

Myostatin and hypoxia signalling pathways are able to induce skeletal muscle atrophy, but whether a relationship between these two pathways exists is currently unknown. Here, we tested the hypothesis that a potential mechanism for hypoxia effect on skeletal muscle may be through regulation of myostatin. We reported an induction of myostatin expression in muscles of rats exposed to chronic hypoxia. Interestingly, we also demonstrated increased skeletal muscle myostatin protein expression in skeletal muscle of hypoxemic patients with severe chronic obstructive pulmonary disease (COPD). Parallel studies in human skeletal muscle cell cultures showed that induction of myostatin expression in myotubes treated with hypoxia-mimicking agent such as cobalt chloride (CoCl(2)) is associated with myotube atrophy. Furthermore, we demonstrated that inhibition of myostatin by means of genetic deletion of myostatin or treatment with blocking antimyostatin antibodies inhibits the CoCl(2)-induced atrophy in muscle cells. Finally, addition of recombinant myostatin restored the CoCl(2)-induced atrophy in myostatin deficient myotubes. These results strongly suggest that myostatin can play an essential role in the adaptation of skeletal muscle to hypoxic environment.

Early Activation of Rat Skeletal Muscle IL-6/STAT1/STAT3 Dependent Gene Expression in Resistance Exercise Linked to Hypertrophy

Cytokine interleukin-6 (IL-6) is an essential regulator of satellite cell-mediated hypertrophic muscle growth through the transcription factor signal transducer and activator of transcription 3 (STAT3). The importance of this pathway linked to the modulation of myogenic regulatory factors expression in rat skeletal muscle undergoing hypertrophy following resistance exercise, has not been investigated. In this study, the phosphorylation and nuclear localization of STAT3, together with IL-6/STAT3-responsive gene expression, were measured after both a single bout of resistance exercise and 10 weeks of training. Flexor Digitorum Profundus muscle samples from Wistar rats were obtained 2 and 6 hours after a single bout of resistance exercise and 72 h after the last bout of either 2, 4, or 10 weeks of resistance training. We observed an increase in IL-6 and SOCS3 mRNAs concomitant with phosphorylation of STAT1 and STAT3 after 2 and 6 hours of a single bout of exercise (p<0.05). STAT3-dependent early responsive genes such as CyclinD1 and cMyc were also upregulated whereas MyoD and Myf5 mRNAs were downregulated (p<0.05). BrdU-positive satellite cells increased at 2 and 6 hours after exercise (p<0.05). Muscle fiber hypertrophy reached up to 100% after 10 weeks of training and the mRNA expression of Myf5, c-Myc and Cyclin-D1 decreased, whereas IL-6 mRNA remained upregulated. We conclude that the IL-6/STAT1/STAT3 signaling pathway and its responsive genes after a single bout of resistance exercise are an important event regulating the SC pool and behavior involved in muscle hypertrophy after ten weeks of training in rat skeletal muscle.

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.