Effect of circuit weight training (CWT) on functional capacity and vascular function in non-insulin-dependent diabetes (NIDDM)

Abstract

Exercise training programs are often recommended for patients with NtDDM to improve physical conditioning and glycaemic control. We investigated the effect of a program of combined aerobic and resistance exercise on measures of functional capacity, strength, body composition and vascular function. After familiarisation sessions, 16 patients (53+_2 years, 89±4kg; mean±SE) undertook a randomised, cross-over design study of 8 weeks of supervised CWT. VO 2 peak, sum of 7 maximal voluntary contractions and the sum of 8 skinfolds were assessed at entry, cross-over and 16 weeks. Vascular function was determined by forearm strain-gauge plethysmography and by high-resolution ultrasound. V02 peak significantly increased as a result of CWT {23.1_+1.2 v 24.8_+1.4ml/kg/mm; P<0.05, paired t-test) as did exercise test duration (12.6+1.2 v 14.8+1.3 rain; P<0.01) and muscular strength (396___29 v 456_+30kg; P<0.01). Skinfolds significantly decreased (149_+11 v 141_+10mm; P<0.05), whilst body weight was unchanged. Glycated haemoglobin decreased from 8.5 + 0.4 to 7.9_+0.3 (P<0.05). The forearm blood flow ratio responses to three incremental doses of acetylcholine significantly increased after exercise training (P<0.05) as did flow mediated dilation to hyperaemia (P<0.01). A CWT program improved objective measures of functional capacity and muscular strength in patients with NIDDM. Endothelium-dependent vasodilation was enhanced, indicating that clinically relevant exercise training programs may reverse the endothelial dysfunction which is associated with this disease. In summary, we have developed a specific RIA for 17K GH, the levels of which are increased in acromegaly, and change in parallel with 22K GH with pharmacologic manipulation of pituitary GH release. 17K levels are reduced, but not undetectable in GH deficiency and are unaffected by exogenous administration of 22k GH. We conclude that 17K GH is derived from the pituitary as well as extrapituitary sources, but is not generated from exogenously administered recombinant 22K GH. The presence of an extrapituitary source of 17K may limit its utility as a marker for GH doping.