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Biomedical subjects

Ronald J Sigal

Publications and source records attributed to Ronald J Sigal.

11 recordsLinked to original sources

Stroke associated with diabetes among Canadians: sex and age differences.

OBJECTIVE: To determine the age and sex variations in the relationship between diabetes and stroke. METHODS: This analysis was based on data from 61,327 Canadians > or =45 years of age who participated in the Canadian Community Health Survey in 2000-2001. Logistic regression analysis was conducted to evaluate the association between diabetes and stroke, and effect modification by age and sex. RESULTS: The association between diabetes and stroke was stronger in the 45- to 64-year age group than the > or =65 year age group in men but not in women. The increased risk of stroke associated with diabetes was much stronger in men (adjusted OR = 3.86, 95% CI = 2.44-6.13) than in women (adjusted OR = 1.63, 95% CI = 0.88-2.99), and this difference was only observed in the younger age group. The results were similar after further adjustment for hypertension and heart disease. CONCLUSIONS: There is a stronger association between stroke and diabetes in men than in women 45-64 years of age, suggesting men are more susceptible to stroke than women when they have diabetes.

Age Distribution↗

Postexercise hypotension causes a prolonged perturbation in esophageal and active muscle temperature recovery.

We examined the effect of two levels of exercise-induced hypotension on esophageal (Tes) and active and nonactive muscle temperatures during and following exercise. Seven males performed an incremental isotonic test on a Kin-Com isokinetic apparatus to determine their peak oxygen consumption during bilateral knee extensions (VO2sp). This was followed on separate days by 15-min of isolated bilateral knee extensions at moderate (60% VO2sp) (MEI) and high (80% VO2sp) (HEI) exercise intensities, followed by 90 min of recovery. Muscle temperature was measured with an intramuscular probe inserted in the left vastus medialis (Tvm) and triceps brachii (Ttb) muscles under ultrasound guidance. The deepest sensor (tip) was located approximately 10 mm from the femur and deep femoral artery and from the superior ulnar collateral artery and humerus for the Tvm and Ttb, respectively. Additional sensors were located 15 and 30 mm from the tip with an additional sensor located at 45 mm for the Tvm measurements only. Following exercise, mean arterial pressure (MAP) remained significantly below preexercise rest for the initial 60 min of recovery after MEI and for the duration of the postexercise recovery period after HEI (P< or =0.05). After HEI, significantly greater elevations from preexercise rest were recorded for Tes and all muscle temperatures paralleled a greater decrease in MAP compared with MEI (P< or =0.05). By the end of 90-min postexercise recovery, MAP, Tes, and all muscle temperatures remained significantly greater after HEI than MEI. Furthermore, a significantly shallower muscle temperature profile across Tvm, relative to preexercise rest, was observed at the end of exercise for both HEI and MEI (P< or=0.05), and for 30 min of recovery for MEI and throughout 90 min of recovery for HEI. No significant differences in muscle temperature profile were observed for Ttb. Thus we conclude that the increase in the postexercise hypotensive response, induced by exercise of increasing intensity, was paralleled by an increase in the magnitude and recovery time of the postexercise esophageal and active muscle temperatures.

Adult↗

Factors associated with physical activity in Canadian adults with diabetes.

INTRODUCTION: The purpose of this study was to identify key demographic and health factors associated with physical activity (PA) participation in adults with type 1 or type 2 diabetes. METHODS: Participants were adults > or = 18 yr of age living in the province of Alberta, Canada who were previously diagnosed with type 1 (N = 697) or type 2 (N = 1614) diabetes. Individuals were recruited from the Canadian Diabetes Association (Alberta) registry and through a random digit-dialing protocol. Multiple and logistic regression models were employed to identify demographic and health factors related to PA levels, of which many to date have not been examined in this population. Analyses were conducted separately for type 1 and type 2 groups. RESULTS: Of those with type 1 and type 2 diabetes, 63.7 and 71.9%, respectively, were not achieving recommended PA levels. For those with type 1, higher PA levels were associated with a younger age, being single, higher income, lower level of perceived disability, and not smoking. For the type 2 group, a younger age, male gender, higher education, higher income, lower body mass index, and lower level of perceived disability were associated with higher PA levels. CONCLUSIONS: Many of our results for both diabetes types are consistent with findings from other limited research in this domain. Contrary to previous research, however, a significant negative relationship was reported between body mass index and PA for the type 2 group. In addition, perceived disability was negatively associated with PA, which, to date, has not been reported in the literature with type 2 individuals. Research and practice related to physical activity promotion for this population should take into account specific demographic and health factors associated with PA.

Alberta↗

Effect of exercise intensity on the postexercise sweating threshold.

The hypothesis that the magnitude of the postexercise onset threshold for sweating is increased by the intensity of exercise was tested in eight subjects. Esophageal temperature was monitored as an index of core temperature while sweat rate was measured by using a ventilated capsule placed on the upper back. Subjects remained seated resting for 15 min (no exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption (V(o2 peak)) followed by a 20-min seated recovery. Subjects then donned a liquid-conditioned suit used to regulate mean skin temperature. The suit was first perfused with 20 degrees C water to control and stabilize skin and core temperature before whole body heating. Subsequently, the skin was heated ( approximately 4.0 degrees C/h) until sweating occurred. Exercise resulted in an increase in the onset threshold for sweating of 0.11 +/- 0.02, 0.23 +/- 0.01, and 0.33 +/- 0.02 degrees C above that measured for the no-exercise resting values (P < 0.05) for the 55, 70, and 85% of V(o2 peak) exercise conditions, respectively. We did note that there was a greater postexercise hypotension as a function of exercise intensity as measured at the end of the 20-min exercise recovery. Thus it is plausible that the increase in postexercise threshold may be related to postexercise hypotension. It is concluded that the sweating response during upright recovery is significantly modified by exercise intensity and may likely be influenced by the nonthermal baroreceptor reflex adjustments postexercise.

Anaerobic Threshold↗

Cutaneous active vasodilation in humans during passive heating postexercise.

The hypothesis that exercise causes an increase in the postexercise esophageal temperature threshold for onset of cutaneous vasodilation through an alteration of active vasodilator activity was tested in nine subjects. Increases in forearm skin blood flow and arterial blood pressure were measured and used to calculate cutaneous vascular conductance at two superficial forearm sites: one with intact alpha-adrenergic vasoconstrictor activity (untreated) and one infused with bretylium tosylate (bretylium treated). Subjects remained seated resting for 15 min (no-exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption followed by 20 min of seated recovery. A liquid-conditioned suit was used to increase mean skin temperature ( approximately 4.0 degrees C/h), while local forearm temperature was clamped at 34 degrees C, until cutaneous vasodilation. No differences in the postexercise threshold for cutaneous vasodilation between untreated and bretylium-treated sites were observed for either the no-exercise or exercise trials. Exercise resulted in an increase in the postexercise threshold for cutaneous vasodilation of 0.19 +/- 0.01, 0.39 +/- 0.02, and 0.53 +/- 0.02 degrees C above those of the no-exercise resting values for the untreated site (P < 0.05). Similarly, there was an increase of 0.20 +/- 0.01, 0.37 +/- 0.02, and 0.53 +/- 0.02 degrees C for the treated site for the 55, 70, and 85% exercise trials, respectively (P < 0.05). It is concluded that reflex activity associated with the postexercise increase in the onset threshold for cutaneous vasodilation is more likely mediated through an alteration of active vasodilator activity rather than through adrenergic vasoconstrictor activity.

Adrenergic Agents↗