EFFECTS OF INSULIN TREATMENT ON HEART RHYTHM, BODY TEMPERATURE AND PHYSICAL ACTIVITY IN STREPTOZOTOCIN-INDUCED DIABETIC RAT

2006 ◽  
Vol 33 (4) ◽  
pp. 327-331 ◽  
Author(s):  
FC Howarth ◽  
M Jacobson ◽  
M Shafiullah ◽  
E Adeghate
Keyword(s):  
Physical Activity ◽  
Body Temperature ◽  
Insulin Treatment ◽  
Heart Rhythm ◽  
Diabetic Rat

scholarly journals Heart Rate, Body Temperature and Physical Activity Are Variously Affected During Insulin Treatment in Alloxan-Induced Type 1 Diabetic Rat

2011 ◽  
pp. 65-73 ◽  
Author(s):  
F. C. HOWARTH ◽  
M. JACOBSON ◽  
M. SHAFIULLAH ◽  
M. LJUBISAVLJEVIC ◽  
E. ADEGHATE
Keyword(s):  
Physical Activity ◽  
Heart Rate ◽  
Body Temperature ◽  
Insulin Treatment ◽  
Heart Rhythm ◽  
Cardiovascular Complications ◽  
Diabetic Rat ◽  
Qt Intervals

Diabetes mellitus is associated with a variety of cardiovascular complications including impaired cardiac muscle function. The effects of insulin treatment on heart rate, body temperature and physical activity in the alloxan (ALX)-induced diabetic rat were investigated using in vivo biotelemetry techniques. The electrocardiogram, physical activity and body temperature were recorded in vivo with a biotelemetry system for 10 days before ALX treatment, for 20 days following administration of ALX (120 mg/kg) and thereafter, for 15 days whilst rats received daily insulin. Heart rate declined rapidly after administration of ALX. Pre-ALX heart rate was 321±9 beats per minute, falling to 285±12 beats per minute 15-20 days after ALX and recovering to 331±10 beats per minute 5-10 days after commencement of insulin. Heart rate variability declined and PQ, QRS and QT intervals were prolonged after administration of ALX. Physical activity and body temperature declined after administration of ALX. Pre-ALX body temperature was 37.6±0.1 °C, falling to 37.3±0.1 °C 15-20 days after ALX and recovering to 37.8±0.1 °C 5-10 days after commencement insulin. ALX-induced diabetes is associated with disturbances in heart rhythm, physical activity and body temperature that are variously affected during insulin treatment.

scholarly journals Oxidative Stress in Rats After 60 Days of Hypergalactosemia or Hyperglycemia

2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Glutathione Disulfide ◽  
Hepatic Lipid Peroxidation ◽  
Streptozotocin Diabetic Rats

Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosy-lated hemoglobin A1c concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.

scholarly journals Impact of physical activity at different levels in heart rhythm in the long term (IMPAR)

2016 ◽  
Vol 1 (1) ◽  
Author(s):  
Marcio Galindo Kiuchi ◽  
Gustavo Ramalho e Silva ◽  
Luis Marcelo Rodrigues Paz ◽  
Gladyston Luiz Lima Souto ◽  
Shaojie Chen
Keyword(s):  
Physical Activity ◽  
Heart Rhythm ◽  
Different Levels

Heat

2020 ◽  
pp. 1687-1689
Author(s):  
Michael A. Stroud
Keyword(s):  
Physical Activity ◽  
Body Temperature ◽  
Supportive Care ◽  
Physiological Responses ◽  
Heat Stroke ◽  
Heat Exposure ◽  
High Humidity ◽  
Heat Exhaustion ◽  
Clinical Presentations ◽  
Cold Core

Rising body temperature triggers behavioural and physiological responses including reduction in physical activity, alterations of clothing, skin vasodilatation, and sweating. Heat-related illness is relatively common, especially with high humidity or prolonged physical activity. Risk can be reduced by acclimatization with repeated heat exposure, but some individuals seem to be particularly susceptible. Clinical presentations of heat-related illness include (1) ‘heat exhaustion’—the commonest manifestation, with symptoms including nausea, weakness, headache, and thirst. Patients appear dehydrated, complain of being hot, and are flushed and sweaty. Treatment requires rest and fluids, given orally or (in severe cases) intravenously. (2) ‘Heat stroke’ victims often complain of headache, may be drowsy or irritable, and may claim to feel cold. Core temperature is usually 38–41°C, but the patient is shivering with dry, vasoconstricted skin. Treatment requires (a) aggressive rapid cooling; (b) close biochemical monitoring; (c) supportive care for organ failure. There is significant mortality.

scholarly journals Rapidly declining body temperature in a tropical human population

2020 ◽  
Vol 6 (44) ◽  
pp. eabc6599 ◽  
Author(s):  
Michael Gurven ◽  
Thomas S. Kraft ◽  
Sarah Alami ◽  
Juan Copajira Adrian ◽  
Edhitt Cortez Linares ◽  
...  
Keyword(s):  
Physical Activity ◽  
Body Temperature ◽  
Human Population ◽  
Thermal Environment ◽  
The United States ◽  
Antibiotic Usage ◽  
Early 21St Century ◽  
The Past ◽  
Human Body Temperature ◽  
Normal Human

Normal human body temperature (BT) has long been considered to be 37.0°C. Yet, BTs have declined over the past two centuries in the United States, coinciding with reductions in infection and increasing life expectancy. The generality of and reasons behind this phenomenon have not yet been well studied. Here, we show that Bolivian forager-farmers (n = 17,958 observations of 5481 adults age 15+ years) inhabiting a pathogen-rich environment exhibited higher BT when first examined in the early 21st century (~37.0°C). BT subsequently declined by ~0.05°C/year over 16 years of socioeconomic and epidemiological change to ~36.5°C by 2018. As predicted, infections and other lifestyle factors explain variation in BT, but these factors do not account for the temporal declines. Changes in physical activity, body composition, antibiotic usage, and thermal environment are potential causes of the temporal decline.

scholarly journals Recommendations for participation in leisure-time physical activity and competitive sports of patients with arrhythmias and potentially arrhythmogenic conditions. Part 2: ventricular arrhythmias, channelopathies, and implantable defibrillators

EP Europace ◽  
2020 ◽  
Author(s):  
Hein Heidbuchel ◽  
Elena Arbelo ◽  
Flavio D’Ascenzi ◽  
Mats Borjesson ◽  
Serge Boveda ◽  
...  
Keyword(s):  
Physical Activity ◽  
Leisure Time ◽  
Leisure Time Physical Activity ◽  
Heart Rhythm ◽  
Competitive Sports ◽  
Supraventricular Arrhythmias ◽  
Preventive Cardiology ◽  
Structural Problems ◽  
Rhythm Disorder ◽  
Implanted Pacemaker

Abstract This paper belongs to a series of recommendation documents for participation in leisure-time physical activity and competitive sports by the European Association of Preventive Cardiology (EAPC). Together with an accompanying paper on supraventricular arrhythmias, this second text deals specifically with those participants in whom some form of ventricular rhythm disorder is documented, who are diagnosed with an inherited arrhythmogenic condition, and/or who have an implanted pacemaker or cardioverter defibrillator. A companion text on recommendations in athletes with supraventricular arrhythmias is published in the European Journal of Preventive Cardiology. Since both texts focus on arrhythmias, they are the result of a collaboration between EAPC and the European Heart Rhythm Association (EHRA). The documents provide a framework for evaluating eligibility to perform sports, based on three elements, i.e. the prognostic risk of the arrhythmias when performing sports, the symptomatic impact of arrhythmias while performing sports, and the potential progression of underlying structural problems as the result of sports.

Mechanisms of the defect in cardiac myofibrillar function during diabetes

1985 ◽  
Vol 248 (2) ◽  
pp. E170-E175 ◽  
Author(s):  
G. N. Pierce ◽  
N. S. Dhalla
Keyword(s):  
Insulin Treatment ◽  
Diabetic Rat ◽  
Marker Enzyme ◽  
Diabetes Treatment ◽  
Myofibrillar Atpase ◽  
Nitrobenzoic Acid ◽  
Cardiac Membranes ◽  
Gradual Onset ◽  
Rat Hearts

Diabetes was induced in rats by an intravenous injection of streptozotocin (65 mg/kg body wt), and animals were killed 8 wk later. Some animals were maintained in a diabetic state for 6 wk and then given 2 wk of insulin treatment in vivo. Myofibrils were isolated and ATPase activities measured. Mg2+-ATPase and Ca2+-stimulated ATPase activities were depressed in diabetic rat hearts in comparison to control; insulin treatment normalized these activities. The depression in myofibrillar ATPases was of gradual onset as no changes were detected 2 wk after inducing diabetes. Treatment of diabetic animals with thyroid hormone did not restore changes in myofibrillar ATPase activities. Marker enzyme activities did not reveal any detectable contamination by cardiac membranes. Mg2+-ATPase activity of myofibrillar preparations from control and diabetic hearts responded differently to N-ethylmaleimide modification. Furthermore, myofibrillar sulfhydryl reactivity to 5,5'-dithiobis(2-nitrobenzoic acid) was significantly depressed in diabetic preparations in comparison to control and insulin-treated diabetic animals. These results suggest that the defect in myofibrillar ATPase activities in chronic diabetes may be due to some modification of sulfhydryl groups.

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