L’ischémie d’exercice caractérisée par l’incapacité du système circulatoire de faire face à l’augmentation des besoins en substrats énergétiques et en oxygène nécessaire à dégrader ces substrats. La claudication à la marche est une cause majeure de limitation fonctionnelle.Il existe de nombres techniques d'évaluation de la macrocirculation et de la microcirculation permettant d'évaluer la réponse endothéliale dépendante(iontophorèse, test au garrot, modification de température locale) avec un enregistrement laser Doppler ou Speckle.Si les techniques ultrasonores permettent d’explorer la présence de lésions, elles rendent mal compte de la collatéralité. Ces techniques peu applicables à l’exercice et nécessitent d’être améliorées pour être applicables à l’effort. L’ischémie artérielle, entraîne une souffrance cellulaire avec métabolisme anaérobie, réversible à l’arrêt de l’exercice. En cas de développement de circulation collatérale suffisante, l’ischémie est alors incomplète, la souffrance des tissus est modérée et réversible rapidement. La recherche de pathologie artérielle au reposa été largement étudiée, nous nous intéressons dans nos études à la pathologie artérielle à l’effort, mais aussi aux phénomènes physiopathologiques susceptibles d’interférer avec la fonctionnalité musculaire (hypoxémie induite par l’exercice). La mesure de la pression partielle transcutanée en oxygène (TcpO2) à l’exercice permet d’estimer en cours de l’exercice l’importance de l’ischémie, segment de membre par segment de membre,de façon bilatérale et continue. Par cette nouvelle technique nous tentons d’explorer la physiopathologie de l’ischémie vasculaire à l’exercice. / Exercise ischemia is characterized by the inability of the circulatory system to fulfil the increased need forenergy substrates and the oxygen needed for substrates’ metabolism. Claudication is a major cause of functional limitation. There are several methods for assessing macrocirculation (mainly ultrasound imaging) and microcirculation (iontophoresis, tourniquet test, local temperature modification with Laser or Speckle recording. If ultrasound techniques can explore the occurrence of lesions is not optimal to evaluate the hemodynamic consequences because pressure measurements do not necessarily correlate with flow impairment. Laser techniques are not appropriate during exercise tests and need to be improved to be applicable. During exercise the severity of arterial ischemia depends on collateral circulation. Further ischemia is reversible at the end of exercise. Although research of restingarterial ischemia has been extensively studied few isknown in arterial ischemia during exercise, but al soin other physiopathological dysfunctions that may interfere with muscle function (exercise-inducedhypoxemia). The measurement of the transcutaneous oxygen partial pressure (TcpO2) during exercise estimates during exercise the importance of ischemia, limb segment by limbsegment, bilaterally and continuously. With this new technique we try to investigate the Physiopathology of vascular ischemia during exercise.

Current knowledge indicates that nonthermal muscle metaboreflex activity plays a critical role in the modulation of skin vasodilation and sweating. However, the mechanisms of control have primarily been studied during isometric handgrip exercise in which muscle metaboreceptor activation is induced by a brief post-exercise ischemia of the upper limb. While the reflex increase in mean arterial pressure associated with this period of ischemia is consistent with the activation of muscle metaboreceptors, the change in baroreflex activity may in itself modulate the response. Thus, we sought to understand how these nonthermal stimuli interact in modulating the control of skin perfusion and sweating under conditions of elevated hyperthermia. Furthermore, we examined the mechanisms responsible for the maintenance of arterial blood pressure under varying levels of heat stress during isometric handgrip exercise. Our study findings indicate that the parallel activation of muscle metaboreceptors and baroreceptors during post-exercise ischemia causes divergent influences on the control of skin blood flow and sweating; and these nonthermal stimuli are dependent on the level of hyperthermia. Moreover, we report that heat stress reduces the increase in arterial blood pressure during isometric handgrip exercise and this attenuation is attributed to a blunted increase in peripheral resistance, since cardiac output increased to similar levels for all heat stress conditions. These results provide important insight and understanding into the role of muscle metabo- and baroreflex activity on the control of skin blood flow and sweating; along with further knowledge into the cardiovascular mechanisms responsible for the regulation of arterial blood pressure during hyperthermia.

Current knowledge indicates that nonthermal muscle metaboreflex activity plays a critical role in the modulation of skin vasodilation and sweating. However, the mechanisms of control have primarily been studied during isometric handgrip exercise in which muscle metaboreceptor activation is induced by a brief post-exercise ischemia of the upper limb. While the reflex increase in mean arterial pressure associated with this period of ischemia is consistent with the activation of muscle metaboreceptors, the change in baroreflex activity may in itself modulate the response. Thus, we sought to understand how these nonthermal stimuli interact in modulating the control of skin perfusion and sweating under conditions of elevated hyperthermia. Furthermore, we examined the mechanisms responsible for the maintenance of arterial blood pressure under varying levels of heat stress during isometric handgrip exercise. Our study findings indicate that the parallel activation of muscle metaboreceptors and baroreceptors during post-exercise ischemia causes divergent influences on the control of skin blood flow and sweating; and these nonthermal stimuli are dependent on the level of hyperthermia. Moreover, we report that heat stress reduces the increase in arterial blood pressure during isometric handgrip exercise and this attenuation is attributed to a blunted increase in peripheral resistance, since cardiac output increased to similar levels for all heat stress conditions. These results provide important insight and understanding into the role of muscle metabo- and baroreflex activity on the control of skin blood flow and sweating; along with further knowledge into the cardiovascular mechanisms responsible for the regulation of arterial blood pressure during hyperthermia.

Current knowledge indicates that nonthermal muscle metaboreflex activity plays a critical role in the modulation of skin vasodilation and sweating. However, the mechanisms of control have primarily been studied during isometric handgrip exercise in which muscle metaboreceptor activation is induced by a brief post-exercise ischemia of the upper limb. While the reflex increase in mean arterial pressure associated with this period of ischemia is consistent with the activation of muscle metaboreceptors, the change in baroreflex activity may in itself modulate the response. Thus, we sought to understand how these nonthermal stimuli interact in modulating the control of skin perfusion and sweating under conditions of elevated hyperthermia. Furthermore, we examined the mechanisms responsible for the maintenance of arterial blood pressure under varying levels of heat stress during isometric handgrip exercise. Our study findings indicate that the parallel activation of muscle metaboreceptors and baroreceptors during post-exercise ischemia causes divergent influences on the control of skin blood flow and sweating; and these nonthermal stimuli are dependent on the level of hyperthermia. Moreover, we report that heat stress reduces the increase in arterial blood pressure during isometric handgrip exercise and this attenuation is attributed to a blunted increase in peripheral resistance, since cardiac output increased to similar levels for all heat stress conditions. These results provide important insight and understanding into the role of muscle metabo- and baroreflex activity on the control of skin blood flow and sweating; along with further knowledge into the cardiovascular mechanisms responsible for the regulation of arterial blood pressure during hyperthermia.

Current knowledge indicates that nonthermal muscle metaboreflex activity plays a critical role in the modulation of skin vasodilation and sweating. However, the mechanisms of control have primarily been studied during isometric handgrip exercise in which muscle metaboreceptor activation is induced by a brief post-exercise ischemia of the upper limb. While the reflex increase in mean arterial pressure associated with this period of ischemia is consistent with the activation of muscle metaboreceptors, the change in baroreflex activity may in itself modulate the response. Thus, we sought to understand how these nonthermal stimuli interact in modulating the control of skin perfusion and sweating under conditions of elevated hyperthermia. Furthermore, we examined the mechanisms responsible for the maintenance of arterial blood pressure under varying levels of heat stress during isometric handgrip exercise. Our study findings indicate that the parallel activation of muscle metaboreceptors and baroreceptors during post-exercise ischemia causes divergent influences on the control of skin blood flow and sweating; and these nonthermal stimuli are dependent on the level of hyperthermia. Moreover, we report that heat stress reduces the increase in arterial blood pressure during isometric handgrip exercise and this attenuation is attributed to a blunted increase in peripheral resistance, since cardiac output increased to similar levels for all heat stress conditions. These results provide important insight and understanding into the role of muscle metabo- and baroreflex activity on the control of skin blood flow and sweating; along with further knowledge into the cardiovascular mechanisms responsible for the regulation of arterial blood pressure during hyperthermia.

Distortion to hemodynamic, ischemic and metabolic stimuli during low load resistance exercise with blood flow restriction (BFR) may influence regional vascular adaptation. This thesis investigated the acute response and chronic adaptations of the peripheral vasculature to low load resistance exercise with BFR. The methodology utilised Doppler ultrasound, strain gauge plethysmography and muscle biopsy for insightful measures of the vasculature at different regions of the arterial tree. Short term (4-6 weeks) localised low load (30-40% 1RM) resistance exercise with BFR increased brachial (3.1%) and popliteal (3.3%) artery maximal diameter (in response to ischemic exercise), forearm (29%) and calf (24%) post-occlusive blood flow, and calf filtration capacity (14%). These findings indicate potential vascular remodelling at the conduit (chapters 3, 4) resistance (chapter 4) and capillary (chapter 4) level of the vascular tree. Regional, rather than systemic, factors are responsible for these adaptations as evidenced by an absent response in the contralateral control limb. Transient improvements in popliteal artery FMD% occurred at week 2 before increased maximal diameter at week 6, suggesting functional changes precede structural remodelling (chapter 4). Maximal brachial artery diameter and forearm post-occlusive blood flow returned to baseline values after a 2 week detraining period, signifying rapid structural normalisation after stimulus removal (chapter 3). Enhanced capillarity, despite low training loads, could be explained by augmentation of VEGF (~7 fold), PGC-1α (~6 fold) and eNOS (~5 fold) mRNA, and upregulation VEGFR-2 (~5 fold) and HIF-1α (~2.5 fold) mRNA with BFR (chapter 5). This indicates a targeted angiogenic response potentially mediated through enhanced metabolic, ischemic and shear stress stimuli. Large between subject variability in the level of BFR was observed during upper and lower limb cuff inflation protocols. Adipose tissue thickness and mean arterial pressure were the largest independent determinants of upper and lower limb BFR, respectively (Chapter 6). In conclusion, this thesis demonstrates that low load resistance exercise with BFR induces adaptation in the conduit, resistance and capillary vessels. The mediators of this response are likely to be the hemodynamic and chemical signals elicited by repeated bouts of BFR resistance exercise, although confirmation of these mechanisms is required. The functional significance of these adaptations is unknown and warrants further investigation.