High-Intensity Training Improves Plasma Glucose and Acid-Base Regulation During Intermittent Maximal Exercise in Type 1 Diabetes ALISON R. HARMER, PHD 1,2 DONALD J. CHISHOLM, MD 3 MICHAEL J. MCKENNA, PHD 4 NORMAN R. MORRIS, PHD 1 JEANETTE M. THOM, PHD 1 GREG BENNETT, MD 5 JEFF R. FLACK, MD 6 I n individuals without diabetes, high- intensity exercise (HIE) training may reduce (1) the characteristic postexer- cise rise in plasma glucose with HIE (2– 4) and reduces (5,6) the marked acid-base balance perturbations (5– 8). In type 1 di- abetes, continuous HIE induces sustained hyperglycemia (9,10), while very brief in- termittent HIE may reduce hyperglyce- mia (11). Acid-base disturbances during exercise may be heightened in type 1 di- abetes (12–14). Effects of HIE training on glycemia and acid-base balance during in- termittent HIE in type 1 diabetes are un- known; thus, despite the potential clinical importance of such exercise, there is no evidence on which to base patient guide- lines. The aim of the present study was thus to investigate the effects of HIE training on glycemia and acid-base regu- lation during intermittent HIE in type 1 diabetes. RESEARCH DESIGN AND METHODS — Eight subjects with type 1 diabetes (duration of diabetes 7.1  4.0 years) and seven subjects with- out diabetes (control group), all of whom were healthy and took no medications (other than insulin in type 1 diabetic sub- jects), consented to participate. The study was approved by the human ethics com- mittees of The University of Sydney and the South Sydney West Area Health Ser- vice. Control subjects closely matched those with diabetes for age (type 1 diabe- tes 25  4 years and control 25  4 years), BMI (25.4  3.2 and 23.8  5.0 kg/m 2 , respectively), and VO 2peak (42.7  12.2 and 43.7  6.2 ml  kg -1  min -1 ), as detailed in a related study that reported effects of sprint training on muscle sodi- um-potassium ATPase and on plasma po- tassium during maximal exercise (15). Testing was conducted after over- night fasting. Type 1 diabetic subjects de- layed their morning insulin. Subjects completed four 30-s maximal exercise bouts (EB1– 4) (each separated by 4 min rest) on a cycle ergometer. Supervised high-intensity cycling training (5,15,16) was then conducted thrice-weekly for 7 weeks. The number of cycle bouts per training session progressed from 4 in week 1 to 6 in week 2, 8 in week 3, and 10 in weeks 4 –7. After training, EB1– 4 were repeated, with power output set to be identical to the pretraining test. Arteri- alised blood was sampled at rest, before and in the final seconds of EB1– 4, and during recovery. Blood gases, insulin, glucose, and A1C were analyzed as previ- ously described (15). With the exception of lactate, which was analyzed using a standard enzymatic technique (17), plasma ions were analyzed using an auto- mated blood gas analyzer (Corning 865; Chiron Diagnostics). The plasma strong ion difference (SID) was calculated: SID (mmol/) = ([potassium] + [sodium]) - ([lactate] + [chloride]). Data were ana- lyzed with repeated-measures ANOVA (SPSS version 10.0 for Windows). When significance was detected, pairwise com- parison between means was performed by a contrast technique. Significance was ac- cepted at P  0.05. Results are reported as means  SD. RESULTS — Exercise training did not alter A1C in type 1 diabetic subjects (pre- exercise 8.6  0.8%, postexercise 8.1  0.6%; P = 0.09). Resting plasma glucose was higher in type 1 diabetic subjects than in control subjects (13.3  5.3 and 5.0  0.3 mmol/l, respectively; P  0.001), with no change after training. In type 1 diabetes, exercise induced a sustained rise in plasma glucose from rest ([PG]) (Fig. 1A). In control subjects, [PG] peaked at 4 min recovery and did not fall signifi- cantly thereafter. After training, [PG] was markedly attenuated in both groups (P = 0.001) (Fig. 1A). Insulin did not dif- fer between groups at rest or after train- ing, however, fell slightly during exercise in type 1 diabetic subjects, in contrast to the rise in control subjects (P  0.001). Plasma SID fell after EB1 and remained reduced throughout the remainder of the test (P  0.001), mainly due to the rise in plasma lactate, with no group differences. After training, SID was higher (P = 0.001) in both groups (Fig. 1B). SID was greater in type 1 diabetic subjects than control subjects across all times and both days (P  0.05) but was within the normal range. The dramatic rises in plasma [H + ] and lactate during HIE (P  0.001) (Fig. 1C and D) were markedly attenuated after training (P  0.001), with no group dif- ferences. After training, bicarbonate fell ●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●● From the 1 Department of Exercise and Sports Science, University of Sydney, Lidcombe, New South Wales, Australia; the 2 Department of Physiotherapy, University of Sydney, Lidcombe, New South Wales, Australia; the 3 Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia; the 4 School of Human Movement, Recreation, and Performance, Centre for Ageing, Rehabilitation, Exercise and Sport, Victoria University, Melbourne, Victoria, Australia; 5 Sydney Adventist Hospital, Wahroonga, New South Wales, Australia; and the 6 Diabetes Centre, Bankstown-Lidcombe Hospital, Bankstown, New South Wales, Australia. Address correspondence and reprint requests to Alison R. Harmer, PhD, University of Sydney, P.O. Box 170, Lidcombe, NSW, Australia 1825. E-mail: a.harmer@usyd.edu.au. Received for publication 23 August 2006 and accepted in revised form 12 February 2007. Published ahead of print at http://care.diabetesjournals.org on 26 February 2007. DOI: 10.2337/dc06- 1790. Abbreviations: HIE, high-intensity exercise; SID, strong ion difference. A table elsewhere in this issue shows conventional and Syste `me International (SI) units and conversion factors for many substances. © 2007 by the American Diabetes Association. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Clinical Care/Education/Nutrition B R I E F R E P O R T DIABETES CARE, VOLUME 30, NUMBER 5, MAY 2007 1269