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.