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Forearm Exercise (forearm + exercise)
Selected AbstractsStroke volume decreases during mild dynamic and static exercise in supine humansACTA PHYSIOLOGICA, Issue 2 2009M. Elstad Abstract Aim:, The contributions of cardiac output (CO) and total peripheral resistance to changes in arterial blood pressure are debated and differ between dynamic and static exercise. We studied the role stroke volume (SV) has in mild supine exercise. Methods:, We investigated 10 healthy, supine volunteers by continuous measurement of heart rate (HR), mean arterial blood pressure, SV (ultrasound Doppler) and femoral beat volume (ultrasound Doppler) during both dynamic mild leg exercise and static forearm exercise. This made it possible to study CO, femoral flow (FF) and both total and femoral peripheral resistance beat-by-beat. Results:, During a countdown period immediately prior to exercise, HR and mean arterial pressure increased, while SV decreased. During mild supine exercise, SV decreased by 5,8%, and most of this was explained by increased mean arterial pressure. Dynamic leg exercise doubled femoral beat volume, while static hand grip decreased femoral beat volume by 18%. FF is tightly regulated according to metabolic demand during both dynamic leg exercise and static forearm exercise. Conclusion:, Our three major findings are, firstly, that SV decreases during both dynamic and static mild supine exercise due to an increase in mean arterial pressure. Secondly, femoral beat volume decreases during static hand grip, but FF is unchanged due to the increase in HR. Finally, anticipatory responses to exercise are apparent prior to both dynamic and static exercise. SV changes contribute to CO changes and should be included in studies of central haemodynamics during exercise. [source] Effect of exercise training on endothelium-derived nitric oxide function in humansTHE JOURNAL OF PHYSIOLOGY, Issue 1 2004Daniel J. Green Vascular endothelial function is essential for maintenance of health of the vessel wall and for vasomotor control in both conduit and resistance vessels. These functions are due to the production of numerous autacoids, of which nitric oxide (NO) has been the most widely studied. Exercise training has been shown, in many animal and human studies, to augment endothelial, NO-dependent vasodilatation in both large and small vessels. The extent of the improvement in humans depends upon the muscle mass subjected to training; with forearm exercise, changes are restricted to the forearm vessels while lower body training can induce generalized benefit. Increased NO bioactivity with exercise training has been readily and consistently demonstrated in subjects with cardiovascular disease and risk factors, in whom antecedent endothelial dysfunction exists. These conditions may all be associated with increased oxygen free radicals which impact on NO synthase activity and with which NO reacts; repeated exercise and shear stress stimulation of NO bioactivity redresses this radical imbalance, hence leading to greater potential for autacoid bioavailability. Recent human studies also indicate that exercise training may improve endothelial function by up-regulating eNOS protein expression and phosphorylation. While improvement in NO vasodilator function has been less frequently found in healthy subjects, a higher level of training may lead to improvement. Regarding time course, studies indicate that short-term training increases NO bioactivity, which acts to homeostatically regulate the shear stress associated with exercise. Whilst the increase in NO bioactivity dissipates within weeks of training cessation, studies also indicate that if exercise is maintained, the short-term functional adaptation is succeeded by NO-dependent structural changes, leading to arterial remodelling and structural normalization of shear. Given the strong prognostic links between vascular structure, function and cardiovascular events, the implications of these findings are obvious, yet many unanswered questions remain, not only concerning the mechanisms responsible for NO bioactivity, the nature of the cellular effect and relevance of other autacoids, but also such practical questions as the optimal intensity, modality and volume of exercise training required in different populations. [source] ,-enolase deficiency, a new metabolic myopathy of distal glycolysisANNALS OF NEUROLOGY, Issue 2 2001Giacomo P. Comi MD A severe muscle enolase deficiency, with 5% of residual activity, was detected in a 47-year-old man affected with exercise intolerance and myalgias. No rise of serum lactate was observed with the ischemic forearm exercise. Ultrastructural analysis showed focal sarcoplasmic accumulation of glycogen , particles. The enzyme enolase catalyzes the interconversion of 2-phosphoglycerate and phosphoenolpyruvate. In adult human muscle, over 90% of enolase activity is accounted for by the ,-enolase subunit, the protein product of the ENO3 gene. The ,-enolase protein was dramatically reduced in the muscle of our patient, by both immunohistochemistry and immunoblotting, while ,-enolase was normally represented. The ENO3 gene of our patient carries two heterozygous missense mutations affecting highly conserved amino acid residues: a G467A transition changing a glycine residue at position 156 to aspartate, in close proximity to the catalytic site, and a G1121A transition changing a glycine to glutamate at position 374. These mutations were probably inherited as autosomal recessive traits since the mother was heterozygous for the G467A and a sister was heterozygous for the G1121A transition. Our data suggest that ENO3 mutations result in decreased stability of mutant ,-enolase. Muscle ,-enolase deficiency should be considered in the differential diagnosis of metabolic myopathies due to inherited defects of distal glycolysis. [source] Influence of muscle training on resting blood flow and forearm vessel diameter in patients with chronic renal failure,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 6 2010S. Kumar Background: Blood flow and vessel diameter are predictors of the success of vascular access procedures. This study investigated whether a simple exercise programme could influence these variables. Methods: Twenty-three patients with chronic kidney disease were prescribed a simple exercise programme for one arm only; the investigators were blinded to the patients' choice. All underwent arterial and venous duplex imaging, handgrip strength and blood pressure measurements before and 1 month after the exercise programme. Results: Twelve patients exercised their dominant and 11 their non-dominant arm. In the trained arm, the exercise programme resulted in a significant increase in handgrip strength, by a median (interquartile range) of 4 (0,8) kg (P < 0·001), and in the diameter of the brachial artery (0·2 (0·1,0·3) mm; P < 0·001), radial artery (0·3 (0·2,0·4) mm; P < 0·001), and cephalic vein (0·6 (0·4,1·2) mm in the forearm and 1·1 (0·4,1·2) mm above the elbow; P < 0·001). There was an increase in brachial artery mean velocity (3 (1,7) cm/s; P = 0·009) and peak systolic velocity (8 (1,15) cm/s; P = 0·020), despite a marginally lower systolic blood pressure (,8 (,16 to 0) mmHg; P = 0·007). There was no change in any of these parameters in the non-exercised arm. Conclusion: In patients with chronic kidney disease, forearm exercise increased blood flow and vessel diameters. This may be beneficial before vascular access formation. Copyright © 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] | |||||||||||||