The perturbations of equilibrium after prolonged exercise were investigated by dynamic posturography on nine well-trained subjects (four athletes and five triathletes). A sensory organization test, where the platform and visual surround were either stable or referenced to the subject's sway with eyes open or closed, was performed before and after a 25-km run (average time 1 h 44 min) by the nine subjects. In addition, the same test was performed on the five triathletes only, before and after ergocycle exercise of identical duration (i.e. ergocycle time = running time). The results showed that the ability to maintain postural stability during conflicting sensory conditions decreased after exercise, with some differences depending on the kind of exercise. Sensory analysis revealed that the subjects made less effective use of vestibular inputs after running than after cycling (P < 0.05). Adaptation to prolonged stimulation of proprioceptive, vestibular and visual inputs had probably occurred in the integrating centres during exercise. This adaptation was maintained during the recovery period and could explain the postexercise balance disorders. Other mechanisms such as impairment of motor efferents or haemodynamic changes should not be excluded.

The purpose of the present study was to check the increase in energy cost of running at the end of a triathlon and a marathon and to link the decrease in energy cost of running with running kinematic parameters. Seven well-trained triathletes performed 3 experimental trials: a 2 h 15 min triathlon (30 min swimming, 60 min cycling and 45 min treadmill running), a 2 h 15 min marathon where the last 45 min (MR) were run at the same speed as the triathlon run (TR) (i.e. 75% of maximal aerobic speed), and a 45 min isolated run (IR) done at the same speed. Oxygen uptake (VO2), minute ventilation (VE), heart rate (HR), respiratory exchange ratio (RER) and kinematic data were recorded during the 3 exercise runs. The results confirm a higher energy cost during MR compared with TR (+ 3.2%; p <0.05) and IR (+ 11.7%; p <0.01). The triathlon and the marathon were associated with greater weight loss (1.6 +/- 0.02 kg; p <0.01) than the isolated run (0.7 +/- 0.2 kg). After cycling, the mean stride length in TR1 was lower during IR1 and increased at the end of TR. The results show that MR led to decrease in stride length compared with IR. After cycling, the triathletes adopted a more forward leaning posture and the trunk gradient was less marked during the marathon. Moreover, the extension of the knee at foot-strike and the maximal knee angle in non-support phase both increased during MR compared with TR and IR. However, it appears that no single kinematic variable can fully explain the decrease in running efficiency: it seems that running economy during a triathlon and a marathon are linked to global alterations of many different parameters.

No abstract

The purpose of this review is to summarise the latest literature on the signalling pathways involved in transcriptional modulations of genes that encode contractile and metabolic proteins in response to endurance exercise. A special attention has been paid to the cooperation between signalling pathways and coordinated expression of protein families that establish myofibre phenotype. Calcium acts as a second messenger in skeletal muscle during exercise, conveying neuromuscular activity into changes in the transcription of specific genes. Three main calcium-triggered regulatory pathways acting through calcineurin, Ca(2+)-calmodulin-dependent protein kinases (CaMK) and Ca(2+)-dependent protein kinase C, transduce alterations in cytosolic calcium concentration to target genes. Calcineurin signalling, the most important of these Ca(2+)-dependent pathways, stimulates the activation of many slow-fibre gene expression, including genes encoding proteins involved in contractile process, Ca(2+) uptake and energy metabolism. It involves the interaction between multiple transcription factors and the collaboration of other Ca(2+)-dependent CaMKs. Although members of mitogen-activated protein kinase (MAPK) pathways are activated during exercise, their integration into other signalling pathways remains largely unknown. The peroxisome proliferator-activated receptor gamma (PPARgamma) coactivator-1alpha (PGC-1alpha) constitutes a pivotal factor of the circuitry which coordinates mitochondrial biogenesis and which couples to the expression of contractile and metabolic genes with prolonged exercise.

The purpose of the present study was to verify the increase in energy cost of running at the end of a triathlon. A group 11 trained male subjects performed a triathlon (15-km swimming, 40-km cycling, 10-km running). At least 1 week later the subjects ran 10-km as a control at the same pace as the triathlon. Oxygen uptake (VO2), ventilation (VE) and heart rate (HR) were measured during both 10-km runs with a portable telemetry system. Blood samples were taken prior to the start of the triathlon and control run, after swimming, cycling, triathlon run and control run. Compared to the control values the results demonstrated that triathlon running elicited a significantly higher (P < 0.005) mean VO2 [51.2 (SEM 0.4) vs 47.8 (SEM 0.4) ml.min-1.kg-1] VE [86 (SEM 4.2) vs 74 (SEM 5.3) l.min-1], and HR [162 (SEM 2) vs 156 (SEM 1.9) beats.min-1)]. The triathlon run induced a greater loss in body mass than the control run [2 (SEM 0.2) vs 0.6 (SEM 0.2) kg], and a greater decrease in plasma volume [14.4% (SEM 1.5) vs 6.7% (SEM 0.9)]. The lactate concentrations observed at the end of both 10-km runs did not differ [2.9 (SEM 0.2) vs 2.5 (SEM 0.2) m.mol.l-1]. Plasma free fatty acids concentrations were higher (P < 0.01) after the triathlon than after the control run [1.53 (SEM 0.2) to 0.51 (SEM 0.07) mmol.l-1]. Plasma creatine kinase concentrations rose under both conditions from 58 (SEM 12) to 112 (SEM 14) UI.l-1 after the triathlon, and from 61 (SEM 7) to 80 (SEM 6) UI.l-1 after the control run. This outdoor study of running economy at the end of an Olympic distance triathlon demonstrated a decrease in running efficiency.

The effects of endurance training on the skeletal muscle of rats have been studied at sea level and simulated high altitude (4,000 m). Male Wistar rats were randomly assigned to one of four groups: exercise at sea level, exercise at simulated high altitude, sedentary at sea level, and sedentary at high altitude (n = 8 in each group). Training consisted of swimming for 1 h/day in water at 36 degrees C for 14 wk. Training and exposure to a high-altitude environment produced a decrease in body weight (P less than 0.001). There was a significant linear correlation between muscle mass and body weight in the animals of all groups (r = 0.89, P less than 0.001). High-altitude training enhanced the percentage of type IIa fibers in the extensor digitorum longus muscle (EDL, P less than 0.05) and deep portions of the plantaris muscle (dPLA, P less than 0.01). High-altitude training also increased the percentage of type IIab fibers in fast-twitch muscles. These muscles showed marked metabolic adaptations: training increased the activity levels of enzymes involved in the citric acid cycle (citrate synthase, CS) and the beta-oxidation of fatty acids (3 hydroxyacyl CoA dehydrogenase, HAD). This increase occurred mainly at high altitude (36 and 31% for HAD in EDL and PLA muscles; 24 and 31% for CS in EDL and PLA muscles). Training increased the activity of enzymes involved in glucose phosphorylation (hexokinase). High-altitude training decreased lactate dehydrogenase activity. Endurance training performed at high altitude and sea level increased the isozyme 1-to-total lactate dehydrogenase activity ratio to the same extent.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this study was to investigate the increase in energy cost of running occurring at the end of a triathlon and a marathon event and to link them to the metabolic and hormonal changes, as well as to variations in stride length. Seven subjects took part in 3 experimental situations: a 2 h 15 min triathlon (30 min swimming, 60 min cycling and 45 min running), a 2 h 15 min marathon (MR) were the last 45 min were run at the same speed as the triathlon run (TR), and a 45 min isolated run (IR) done at triathlon speed. The results show that energy cost during MR was higher than during TR (p < 0.01) (+ 8.9%). Similar observations were made for pulmonary ventilation (+ 7.9%) and heart rate (+ 6.3%). Moreover, the values were significantly greater than the values obtained during the IR. TR and MR lead to greater weight loss (p < 0.01) (2.4 +/- 0.3 kg) than IR (1 +/- 0.2 kg). The triathlon and the marathon produced a large decrease in plasma volume (respectively 19.6 +/- 1.4% and 12.9 +/- 1.1%) compared to IR (2 +/- 0.4%). Plasma renin activity was higher for the triathlon and the marathon than for the IR (p < 0.01). MR produces a significantly greater increase in plasma free fatty acids (F.F.A.) than TR (p < 0.05) and IR (p < 0.01). In addition, the F.F.A. at the end of TR were significantly higher than IR (p < 0.05). At the end of the trial the mean stride lengths for TR and IR were greater (+ 15%) (p < 0.01) than for MR. This study, carried out with subjects running overground, confirms the decrease in running efficiency previously shown at the end of a laboratory triathlon, and demonstrates that this decrease is lower than that occurring during a marathon.

The mitochondrial uncoupling protein of brown adipose tissue (UCP1) was expressed in skeletal muscle and heart of transgenic mice at levels comparable with the amount found in brown adipose tissue mitochondria. These transgenic mice have a lower body weight, and when related to body weight, food intake and energy expenditure are increased. A specific reduction of muscle mass was observed but varied according to the contractile activity of muscles. Heart and soleus muscle are unaffected, indicating that muscles undergoing regular contractions, and therefore with a continuous mitochondrial ATP production, are protected. In contrast, the gastrocnemius and plantaris muscles showed a severely reduced mass and a fast to slow shift in fiber types promoting mainly IIa and IIx fibers at the expense of fastest and glycolytic type IIb fibers. These observations are interpreted as a consequence of the strong potential dependence of the UCP1 protonophoric activity, which ensures a negligible proton leak at the membrane potential observed when mitochondrial ATP production is intense. Therefore UCP1 is not deleterious for an intense mitochondrial ATP production and this explains the tolerance of the heart to a high expression level of UCP1. In muscles at rest, where ATP production is low, the rise in membrane potential enhances UCP1 activity. The proton return through UCP1 mimics the effect of a sustained ATP production, permanently lowering mitochondrial membrane potential. This very likely constitutes the origin of the signal leading to the transition in fiber types at rest. Uncoupling protein 1 (UCP1)1 is expressed exclusively in brown adipose tissue (reviewed in Refs. 1 and 2). Its presence in brown fat mitochondria is responsible for heat production by the mitochondria in brown adipocytes. UCP1 allows return of protons into the matrix without ATP synthesis, and therefore dissipates the proton electrochemical gradient built up after proton pumping by the respiratory complexes. When this gradient reaches high values this makes proton pumping and thus substrate oxidation less easy and therefore slows down respiration. Activity of UCP1 prevents this rise of the proton gradient and therefore allows respiration to occur at a high rate, without phosphorylation of ADP into ATP, and therefore energy is instantaneously released as heat. The essential role of the UCP1 in thermogenesis is illustrated by the cold intolerance of mice whose ucp1 gene has been disrupted (3). Recently, two genes coding for proteins highly homologous to UCP1 have been described (reviewed in Refs. 4 -6). Although there are experimental evidence supporting the hypothesis of an uncoupling activity of these proteins (7,8), their physiological relevance is still incompletely resolved (9 -11). We intended to obtain transgenic mice overexpressing the UCP1 in skeletal muscles, with the aim of examining the effects of the presence of this uncoupling protein on the pattern of myosin expression and metabolic characteristics of locomotor muscles. Two other reports pub...