Home About us Contact
|
Home About us Contact | ||
|
|
||
Min Rest (min + rest)
Selected AbstractsGreater growth hormone and insulin response in women than in men during repeated bouts of sprint exerciseACTA PHYSIOLOGICA, Issue 2 2009M. Esbjörnsson Abstract Aim:, In a previous study, sprint training has been shown to increase muscle cross-sectional area in women but not in men [Eur J Appl Physiol Occup Physiol 74 (1996) 375]. We hypothesized that sprint exercise induces a different hormonal response in women than in men. Such a difference may contribute to explaining the observed gender difference in training response. Method:, Metabolic and hormonal response to three 30-s sprints with 20-min rest between the sprints was studied in 18 physically active men and women. Results:, Accumulation of blood lactate [interaction term gender (g) × time (t): P = 0.022], and plasma ammonia (g × t: P < 0.001) after sprint exercise was greater in men. Serum insulin increased after sprint exercise more so in women than in men (g × t: P = 0.020), while plasma glucose increased in men, but not in women (g × t: P < 0.001). Serum growth hormone (GH) increased in both women and men reaching similar peak levels, but with different time courses. In women the peak serum GH level was observed after sprint 1, whereas in men the peak was observed after sprint 3 (g × t; P < 0.001). Serum testosterone tended to decrease in men and increase in women (g × t: P = 0.065). Serum cortisol increased approx. 10,15% after sprint exercise, independent of gender (time: P = 0.005). Conclusion:, Women elicited a greater response of serum GH and insulin to sprint exercise. This may contribute to explaining the earlier observed muscle hypertrophy in women in response to sprint training. [source] Acute signalling responses to intense endurance training commenced with low or normal muscle glycogenEXPERIMENTAL PHYSIOLOGY, Issue 2 2010Wee Kian Yeo We have previously demonstrated that well-trained subjects who completed a 3 week training programme in which selected high-intensity interval training (HIT) sessions were commenced with low muscle glycogen content increased the maximal activities of several oxidative enzymes that promote endurance adaptations to a greater extent than subjects who began all training sessions with normal glycogen levels. The aim of the present study was to investigate acute skeletal muscle signalling responses to a single bout of HIT commenced with low or normal muscle glycogen stores in an attempt to elucidate potential mechanism(s) that might underlie our previous observations. Six endurance-trained cyclists/triathletes performed a 100 min ride at ,70% peak O2 uptake (AT) on day 1 and HIT (8 × 5 min work bouts at maximal self-selected effort with 1 min rest) 24 h later (HIGH). Another six subjects, matched for fitness and training history, performed AT on day 1 then 1,2 h later, HIT (LOW). Muscle biopsies were taken before and after HIT. Muscle glycogen concentration was higher in HIGH versus LOW before the HIT (390 ± 28 versus 256 ± 67 ,mol (g dry wt),1). After HIT, glycogen levels were reduced in both groups (P < 0.05) but HIGH was elevated compared with LOW (229 ± 29 versus 124 ± 41 ,mol (g dry wt),1; P < 0.05). Phosphorylation of 5,AMP-activated protein kinase (AMPK) increased after HIT, but the magnitude of increase was greater in LOW (P < 0.05). Despite the augmented AMPK response in LOW after HIT, selected downstream AMPK substrates were similar between groups. Phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) was unchanged for both groups before and after the HIT training sessions. We conclude that despite a greater activation AMPK phosphorylation when HIT was commenced with low compared with normal muscle glycogen availability, the localization and phosphorylation state of selected downstream targets of AMPK were similar in response to the two interventions. [source] Computational Network Model Prediction of Hemodynamic Alterations Due to Arteriolar Remodeling in Interval Sprint Trained Skeletal MuscleMICROCIRCULATION, Issue 3 2007Kyle W. Binder ABSTRACT Objectives: Exercise training is known to enhance skeletal muscle blood flow capacity, with high-intensity interval sprint training (IST) primarily affecting muscles with a high proportion of fast twitch glycolytic fibers. The objective of this study was to determine the relative contributions of new arteriole formation and lumenal arteriolar remodeling to enhanced flow capacity and the impact of these adaptations on local microvascular hemodynamics deep within the muscle. Methods: The authors studied arteriolar adaptation in the white/mixed-fiber portion of gastrocnemius muscles of IST (6 bouts of running/day; 2.5 min/bout; 60 m/min speed; 15% grade; 4.5 min rest between bouts; 5 training days/wk; 10 wks total) and sedentary (SED) control rats using whole-muscle Microfil casts. Dimensional and topological data were then used to construct a series of computational hemodynamic network models that incorporated physiological red blood cell distributions and hematocrit and diameter dependent apparent viscosities. Results: In comparison to SED controls, IST elicited a significant increase in arterioles/order in the 3A through 6A generations. Predicted IST and SED flows through the 2A generation agreed closely with in vivo measurements made in a previous study, illustrating the accuracy of the model. IST shifted the bulk of the pressure drop across the network from the 3As to the 4As and 5As, and flow capacity increased from 0.7 mL/min in SED to 1.5 mL/min in IST when a driving pressure of 80 mmHg was applied. Conclusions: The primary adaptation to IST is an increase in arterioles in the 3A through 6A generations, which, in turn, creates an approximate doubling of flow capacity and a deeper penetration of high pressure into the arteriolar network. [source] Glucagon is absorbed from the rectum but does not hasten recovery from hypoglycaemia in patients with type 1 diabetesBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 1 2008David R. Parker WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT , Patients with type 1 diabetes experience recurrent hypoglycaemia and have abnormal glucose counter regulatory responses with a failure to secrete glucagon. It is unknown if rectal glucagon is absorbed and what effect this may have on counter regulation from hypoglycaemia. WHAT THIS STUDY ADDS , A rectal suppository of glucagon results in a rise in plasma glucagon with metabolic effects in normal subjects. Similarly rectal glucagon results in a rise in plasma glucagon in patients with type 1 diabetes, but 1 mg does not improve recovery rates from experimental hypoglycaemia when compared with placebo. , Larger doses of glucagon per rectum may provide pharmacological circulating concentrations with resulting therapeutic benefit during recovery from hypoglycaemia and deserves further study. AIMS A failure to secrete glucagon during hypoglycaemia is near universal in patients with type 1 diabetes 5 years after disease onset and may contribute to delayed counter-regulation during hypoglycaemia. Rectal glucagon delivery may assist glucose recovery following insulin-induced hypoglycaemia in such patients and has not been previously studied. METHODS Six male patients (age 21,38 years) with type 1 diabetes (median duration 10 years) without microvascular complications, were studied supine after an overnight fast on two separate occasions at least 14 days apart. After omission of their usual morning insulin and 45 min rest, hypoglycaemia was induced by an intravenous insulin infusion which was terminated when capillary glucose concentration reached 2.5 mmol l,1. Subjects were randomized to insert a rectal suppository containing 100 mg indomethacin alone (placebo) or 100 mg indomethacin plus 1 mg glucagon at the hypoglycaemic reaction. Serial measurements were made for 120 min. RESULTS In the two groups, mean (SD) plasma glucose concentrations fell to a similar nadir of 1.8 (0.7) mmol l,1 (placebo) and 2.1 (1.2) mmol l,1 (glucagon). Peak plasma glucagon following hypoglycaemia was higher in the glucagon group; 176 (32) ng l,1vs. 99 (22) ng l,1 after placebo (P = 0.006). However, the glucose recovery rate over 120 min after hypoglycaemia did not differ significantly. CONCLUSIONS Our results provide evidence for the absorption of glucagon from the rectum. They also indicate that 1 mg does not constitute a useful mode of therapy to hasten recovery from hypoglycaemia in patients with type 1 diabetes. [source] Cardiac diastolic dysfunction in renal-transplant recipients is associated with increased circulating AdrenomedullinCLINICAL TRANSPLANTATION, Issue 3 2006Bernard Geny Abstract:, Background:, Renal transplantation is an excellent therapeutic alternative for end-stage renal diseases. Nevertheless, the cardiac function is often impaired in renal-transplant patients (RTR) and importantly determines their prognosis. Adrenomedullin (ADM), a peptide involved in cardiovascular homeostasis, is believed to protect both cardiac and renal functions , by increasing local blood flows, attenuating the progression of vascular damage and remodelling and by reducing glomerular injury , and might be involved in renal-transplantation physiopathology. This work was performed to investigate whether an increase in circulating ADM might be related to RTR cardiac function. Methods:, Twenty-nine subjects, 19 RTR and 10 healthy subjects, participated in the study. After 15 min rest in supine position, heart rate and systemic blood pressure were measured together with cyclosporine through levels, creatinine and ADM. Systolic and diastolic cardiac functions were assessed, using Doppler echocardiography. Results:, Subjects were similar concerning age, weight, heart rate and blood pressure. Creatinine and ADM (53.8±6.9 vs. 27.2±4.1 pmol/L, p = 0.02) were significantly increased in RTR (73±10 months after transplantation). Cardiac systolic function was normal, but a reduced mitral E:A ratio was observed in RTR (0.90±0.06 vs. 1.38±0.10, p<0.001), reflecting their impaired left ventricular relaxation. Such a ratio was negatively correlated with ADM (r = ,0.55, p = 0.002). Conclusions:, RTR present with an increased ADM is likely related to cardiac diastolic dysfunction. In view of its protective effect on the cardiovascular system, these data support further studies to better define the role and the therapeutic potential of ADM after renal transplantation. [source] | |||||||||||||