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Objectives This study aimed to analyze the daily heart rate variability (HRV) in well-trained female cyclists during the 2017 Tour de France circuit and to relate it to the load and perceived exertion response. Methods Ten female cyclists volunteered to participate in the study. HRV was recorded with a portable heart rate monitor each morning at rest in supine (7 min.) and upright (7 min.) positions, as well as throughout each day’s stage. Pre-Tour baseline HRV recordings were made, as well as during the four weeks following completion of the Tour. Exercise daily load was assessed using the training impulse score (TRIMPS). Post-exercise rate of perceived exertion (RPE) was assessed daily using the Borg CR-10 scale. Results The results show a HRV imbalance, increase of sympathetic and decrease of vagal activities respectively, along the event that correlated with rate of perceived exertion (r = 0.46), training impulse score (r = 0.60), and kilometers (r = 046). The greatest change in HRV balance was observed the days after the greatest relative physical load. Mean heart rate and heart rate variability values returned to their baseline values one week after completion of the event. Conclusions Despite incomplete recovery from day-to-day, fatigue is not summative or augmented with each successive stage and its physical load. Just one week is sufficient to restore baseline values. Heart rate and HRV can be used as a tool to strategically plan the effort of female cyclists that participate in multi-stage events.

BackgroundInformations about the effects of intense exercise training on diabetes-induced myocardial dysfunctions are lacking. We have examined the effects of intense exercise training on the cardiac function of diabetic rats, especially focusing on the Langendorff β-adrenergic responsiveness and on the β-adrenoceptors protein expression.MethodsControl or Streptozotocin induced-diabetic male Wistar rats were randomly assigned to sedentary or trained groups. The training program consisted of 8 weeks running on a treadmill (10° incline, up to 25 m/min, 60 min/day) and was considered to be intense for diabetic rats.ResultsThis intense exercise training amplified the in vivo diabetes-induced bradycardia. It had no effect on Langendorff basal cardiac contraction and relaxation performances in control and diabetic rats. In diabetic rats, it accentuated the Langendorff reduced responsiveness to β-adrenergic stimulation. It did not blunt the diabetes-induced decrease of β1-adrenoceptors protein expression, displayed a significant decrease in the β2-adrenoceptors protein expression and normalized the β3-adrenoceptors protein expression.ConclusionsIntense exercise training accentuated the decrease in the myocardial responsiveness to β-adrenergic stimulation induced by diabetes. This defect stems principally from the β2-adrenoceptors protein expression reduction. Thus, these results demonstrate that intense exercise training induces specific effects on the β-adrenergic system in diabetes.

BackgroundThe aim of this study was to examine the effects of intense physical training on vascular function in streptozotocin-diabetic rats. We focused on the endothelium-dependent relaxation (EDR) induced by acetylcholine (ACh) and stable ADP adenosine-5′- O – (2-thiodiphosphate) (ADPβS).MethodsControl or diabetic male Wistar rats (n=44) were randomly assigned to sedentary or trained groups. The training program consisted in a regular period of running on a treadmill during 8 weeks (10° incline and up to 25 m/min, 60 min/day). The reactivity of isolated thoracic aorta rings of healthy, diabetic and/or trained has been tested.ResultsACh and ADPβS-induced EDR were observed in phenylephrine (PE) pre-contracted vessels. As compared to sedentary control group, diabetic rats showed an increase in PE-induced contraction and a decrease in ACh and ADPβS-induced EDR (p<0.05). Moreover, there were no increase in ACh and ADPβS-induced EDR in diabetic rats. N-Nitro-L-Arginine Methyl Ester inhibited the nitric oxide synthase in diabetic and control rats, thereby resulting in a strong inhibition of the EDR induced by ACh and ADPβS (10-6 M).ConclusionDiabetes induced an endothelium dysfunction. Nevertheless, our intense physical training was not effective to restore the aorta endothelial function.