Two hundred and four men with impaired glucose tolerance (borderline diabetes) discovered in a screening examination have been observed for five years and repeated tests of glucose tolerance performed. By pre-determined criteria 27 men 'worsened to diabetes' and this metabolic deterioration was not significantly influenced by treatment with carbohydrate restriction with or without a daily dose of 50 mg phenformin. Of the baseline variables measured prior to treatment allocation only the blood glucose values were significantly predictive of ultimate worsening to diabetes.

The relationship between blood pressure and the blood sugar concentration measured two hours after a 50 g oral glucose load has been examined in two population surveys-the Whitehall and Bedford Surveys. In the Whitehall Survey, which was conducted in men above the age of 40, there was a positive, significant correlation between blood sugar and blood pressure (systolic and diastolic) which was independent of common associations with age, body mass index (BMI) and heart rate. In the Bedford Survey, systolic blood pressures were significantly higher in newly detected diabetics and borderline diabetics, both men and women, than in normoglycaemic controls after adjustment of blood pressures for age and BMI. However, in the stratified random sample of the cooperating Bedford population, only amongst women was the blood sugar significantly and independently correlated with the systolic blood pressure. Evidence is presented and discussed that autonomic, neurohumoral factors may play some part in the pathogenesis of maturity onset diabetes.

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The urinary excretion of albumin was measured in insulin-dependent diabetics under ordinary conditions of life and in response to exercise. Possible mechanisms of exercise induced albuminuria in diabetics were also investigated. Under ordinary conditions of life the insulin-treated diabetics, as a group, had a higher mean urinary albumin excretion than normal controls; however, half of the diabetics had albumin excretion rates within the control range. A given exercise load (600 kpm/min for 20 min) produced an exaggerated albumin excretion in diabetics, particularly evident in the post-exercise period. The elevated urinary albumin excretion was due to an increased transglomerular passage of albumin, not to reduced tubular reabsorption. The increase was not associated with differences in blood pressure or urine flow between controls and diabetics. This exercise test has proved to be a suitable provocation test to unmask abnormalities in the glomerular handling of albumin that might not be recognisable at rest.

Very little is known about the cardiovascular responses of exercising individuals when exposed to carbon monoxide (CO). Sixteen healthy nonsmoking men aged 18-29 years participated in the study. Using a combination of exposures to CO by breathing from a bag or in an environmental chamber, subjects performed a randomized sequence of brief (5 min) multi-level treadmill and hand-crank exercises on different days at less than 2% carboxyhemoglobin (COHb) and after attaining target levels of 5%, 10%, 15%, and 20% COHb. To assess cardiac function changes we employed noninvasive impedance cardiography (ICG) and three-lead electrocardiograms (ECG). The ICG was used to estimate cardiac output, stroke volume, heart rate, cardiac contractility, and time-to-peak ejection time. The ECG was used to assess myocardial irritability and ischemia, and changes in cardiac rhythm. The results showed that the cardiovascular system compensated for the reduced O2-carrying capacity of the blood by augmenting heart rate, cardiac contractility, and cardiac output for both upper-body and lower-body exercise. While this mechanism served well in submaximal exercise, the enhanced cardiovascular response to exercise was not without physiological costs because it began to fail at moderate levels of CO exposure and exercise. We concluded that young, apparently healthy men can perform submaximal upper and lower-body exercise without overt impairment of cardiovascular function after CO exposures attaining 20% COHb.