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Pulmonary rehabilitation programs in Australia generally meet the broad recommendations for practice in terms of components, program length, assessment and exercise training. The prescription of exercise training intensity is an area requiring deeper exploration.

OBJECTIVE -To investigate sprint-training effects on muscle metabolism during exercise in subjects with (type 1 diabetic group) and without (control group) type 1 diabetes.RESEARCH DESIGN AND METHODS -Eight subjects with type 1 diabetes and seven control subjects, matched for age, BMI, and maximum oxygen uptake (V O 2peak ), undertook 7 weeks of sprint training. Pretraining, subjects cycled to exhaustion at 130% V O 2peak . Posttraining subjects performed an identical test. Vastus lateralis biopsies at rest and immediately after exercise were assayed for metabolites, high-energy phosphates, and enzymes. Arterialized venous blood drawn at rest and after exercise was analyzed for lactate and [H ϩ ]. Respiratory measures were obtained on separate days during identical tests and during submaximal tests before and after training.RESULTS -Pretraining, maximal resting activities of hexokinase, citrate synthase, and pyruvate dehydrogenase did not differ between groups. Muscle lactate accumulation with exercise was higher in type 1 diabetic than nondiabetic subjects and corresponded to indexes of glycemia (A1C, fasting plasma glucose); however, glycogenolytic and glycolytic rates were similar. Posttraining, at rest, hexokinase activity increased in type 1 diabetic subjects; in both groups, citrate synthase activity increased and pyruvate dehydrogenase activity decreased; during submaximal exercise, fat oxidation was higher; and during intense exercise, peak ventilation and carbon dioxide output, plasma lactate and [H ϩ ], muscle lactate, glycogenolytic and glycolytic rates, and ATP degradation were lower in both groups.CONCLUSIONS -High-intensity exercise training was well tolerated, reduced metabolic destabilization (of lactate, H ϩ , glycogenolysis/glycolysis, and ATP) during intense exercise, and enhanced muscle oxidative metabolism in young adults with type 1 diabetes. The latter may have clinically important health benefits. Diabetes Care 31:2097-2102, 2008R epeated bouts of brief, highintensity exercise are characterized not only by marked metabolic and ionic destabilization in exercising muscle but also by progressively increasing aerobic ATP generation, such that by just the third 30-s bout, 63% of ATP is generated oxidatively (1). It is therefore not entirely surprising that high-intensity (sprint) exercise training results in oxidative adaptations in muscle. These adaptations include reduced glycogenolysis and lower accumulation of muscle lactate and hydrogen ions during high-intensity matchedwork exercise (2); increased activity of oxidative enzymes such as citrate synthase (3-5), cytochrome c oxidase (6), and ␤-hydroxyacyl-CoA dehydrogenase (␤-HAD) (4); reduced ATP degradation during intense exercise (2,5,7); and increased peak oxygen consumption (V O 2peak ) (2-5,8).The only study (9) to examine muscle metabolism during exercise in patients with type 1 diabetes (compared with control subjects) reported lower muscle oxidative capacity and higher glycolytic flux and acidosis. No studies have directly investiga...

Traditionally, manual hyperinflation has been performed using "rapid release" to promote a fast peak expiratory flow rate (PEFR) but rapid release has not been described. In addition, it has been demonstrated that different resuscitation circuits provide varying degrees of resistance to expiratory flow and it is known that a variety of circuits are used in Australia for manual hyperinflation. The aim of this study was to document current practice, the effect of rapid release, controlling inspiration, different volumes and circuit type on flow rates, and the inspiratory to expiratory flow rate (I:E) ratio during manual hyperinflation. Using a test lung model, 15 physiotherapists performed 11 trials using the Air Viva 2, a Mapleson-C and a Mapleson-F circuit, both with and without rapid release, and delivering two volumes. The order of the trials was randomised. Rapid release produced a faster PEFR irrespective of circuit type or volume delivered. The effect of rapid release, and the absolute PEFR, was less for the Air Viva 2 compared with the Mapleson circuits. Expiratory flow rate was faster for the larger volume. The theoretically optimal I:E ratio to move secretions was achieved delivering the lower target volume with the Mapleson circuits and using rapid release.