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Exercising Muscles (exercising + muscle)
Selected AbstractsCardiovascular function in the heat-stressed humanACTA PHYSIOLOGICA, Issue 4 2010C. G. Crandall Abstract Heat stress, whether passive (i.e. exposure to elevated environmental temperatures) or via exercise, results in pronounced cardiovascular adjustments that are necessary for adequate temperature regulation as well as perfusion of the exercising muscle, heart and brain. The available data suggest that generally during passive heat stress baroreflex control of heart rate and sympathetic nerve activity are unchanged, while baroreflex control of systemic vascular resistance may be impaired perhaps due to attenuated vasoconstrictor responsiveness of the cutaneous circulation. Heat stress improves left ventricular systolic function, evidenced by increased cardiac contractility, thereby maintaining stroke volume despite large reductions in ventricular filling pressures. Heat stress-induced reductions in cerebral perfusion likely contribute to the recognized effect of this thermal condition in reducing orthostatic tolerance, although the mechanism(s) by which this occurs is not completely understood. The combination of intense whole-body exercise and environmental heat stress or dehydration-induced hyperthermia results in significant cardiovascular strain prior to exhaustion, which is characterized by reductions in cardiac output, stroke volume, arterial pressure and blood flow to the brain, skin and exercising muscle. These alterations in cardiovascular function and regulation late in heat stress/dehydration exercise might involve the interplay of both local and central reflexes, the contribution of which is presently unresolved. [source] Muscle fractal vascular branching pattern and microvascular perfusion heterogeneity in endurance-trained and untrained menTHE JOURNAL OF PHYSIOLOGY, Issue 2 2003Kari K. Kalliokoski Less heterogeneous skeletal muscle perfusion has recently been reported in endurance-trained compared to untrained men at macrovascular level. The causes of this difference in perfusion heterogeneity are unknown as is whether the same difference is observed in microvasculature. We hypothesised that the difference could be caused by changes in muscle vascular branching pattern. Perfusion was measured in resting and exercising muscle in 14 endurance-trained and seven untrained men using [15O]water and positron emission tomography. Fractal dimension (D) of perfusion distribution was calculated as a measure of fractal characteristics of muscle vascular branching pattern. Perfusion heterogeneity in microvascular units (1 mm3 samples) was estimated using the measured heterogeneity in voxels of positron emission tomography (PET) images (relative dispersion, RD =s.d./mean) and corresponding D values. D was similar between the groups (exercising muscle 1.11 ± 0.07 and 1.14 ± 0.06, resting muscle 1.12 ± 0.06 and 1.14 ± 0.03, trained and untrained, respectively). Trained men had lower perfusion (151 ± 44 vs. 218 ± 87 ml min,1 kg,1, P < 0.05) and macrovascular perfusion heterogeneity (relative dispersion 21 ± 5 vs. 25 ± 5 %, P < 0.05) in exercising muscle than untrained men. Furthermore, estimated perfusion heterogeneity in microvascular units in exercising muscle was also lower in trained men (33 ± 7 vs.48 ± 19 %, P < 0.05). These results show that fractal vascular branching pattern is similar in endurance-trained and untrained men but perfusion is less heterogeneous at both the macro- and the microvascular level in endurance-trained men. Thus, changes in fractal branching pattern do not explain the differences in perfusion heterogeneity between endurance-trained and untrained men. [source] Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exerciseJOURNAL OF INTERNAL MEDICINE, Issue 3 2005Y. JAMMES Abstract. Objectives., Because the muscle response to incremental exercise is not well documented in patients suffering from chronic fatigue syndrome (CFS), we combined electrophysiological (compound-evoked muscle action potential, M wave), and biochemical (lactic acid production, oxidative stress) measurements to assess any muscle dysfunction in response to a routine cycling exercise. Design., This case,control study compared 15 CFS patients to a gender-, age- and weight-matched control group (n = 11) of healthy subjects. Interventions., All subjects performed an incre-mental cycling exercise continued until exhaustion. Main outcome measures., We measured the oxygen uptake (Vo2), heart rate (HR), systemic blood pressure, percutaneous O2 saturation (SpO2), M-wave recording from vastus lateralis, and venous blood sampling allowing measurements of pH (pHv), PO2 (PvO2), lactic acid (LA), and three markers of the oxidative stress (thiobarbituric acid-reactive substances, TBARS, reduced glutathione, GSH, and ascorbic acid, RAA). Results., Compared with control, in CFS patients (i) the slope of Vo2 versus work load relationship did not differ from control subjects and there was a tendency for an accentuated PvO2 fall at the same exercise intensity, indicating an increased oxygen uptake by the exercising muscles; (ii) the HR and blood pressure responses to exercise did not vary; (iii) the anaerobic pathways were not accentuated; (iv) the exercise-induced oxidative stress was enhanced with early changes in TBARS and RAA and enhanced maximal RAA consumption; and (v) the M-wave duration markedly increased during the recovery period. Conclusions., The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress together with marked alterations of the muscle membrane excitability. These two objective signs of muscle dysfunction are sufficient to explain muscle pain and postexertional malaise reported by our patients. [source] Capillary Hemodynamics and Oxygen Pressures in the Aging MicrocirculationMICROCIRCULATION, Issue 4 2006DAVID C. POOLE ABSTRACT Healthy aging acts to redistribute blood flow (Q,) and thus O2 delivery (Q,O2) among and within the exercising muscles such that Q,O2 to highly oxidative muscle fibers may be compromised. Within the microcirculation of old muscles capillary hemodynamics are altered and the matching of Q,O2 to oxidative requirements (V,O2) is impaired such that at exercise onset the microvascular O2 pressure falls below that seen in their younger counterparts. This is important because the microvascular O2 pressure denotes the sole driving force for blood-myocyte O2 transfer and any compromise may slow V,O2 kinetics and reduce exercise tolerance. This review considers the microcirculatory evidence for a reduced perfusive (Q,O2) and diffusive O2 flux within aged muscle and highlights the pressing need for intravital microscopy studies of the muscle microcirculation during exercise. [source] The cardiovascular challenge of exercising in the heatTHE JOURNAL OF PHYSIOLOGY, Issue 1 2008José González-Alonso Exercise in the heat can pose a severe challenge to human cardiovascular control, and thus the provision of oxygen to exercising muscles and vital organs, because of enhanced thermoregulatory demand for skin blood flow coupled with dehydration and hyperthermia. Cardiovascular strain, typified by reductions in cardiac output, skin and locomotor muscle blood flow and systemic and muscle oxygen delivery accompanies marked dehydration and hyperthermia during prolonged and intense exercise characteristic of many summer Olympic events. This review focuses on how the cardiovascular system is regulated when exercising in the heat and how restrictions in locomotor skeletal muscle and/or skin perfusion might limit athletic performance in hot environments. [source] | |||||||||||||