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High-Intensity Training Improves Plasma Glucose and Acid-Base Regulation During Intermittent Maximal Exercise in Type 1 Diabetes

¹ Department of Exercise and Sports Science, University of Sydney, Lidcombe, New South Wales, Australia
² Department of Physiotherapy, University of Sydney, Lidcombe, New South Wales, Australia
³ Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia
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
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{at}usyd.edu.au

Abbreviations: HIE, high-intensity exercise • SID, strong ion difference

	INTRODUCTION

TOP INTRODUCTION RESEARCH DESIGN AND METHODS-- RESULTS-- CONCLUSIONS-- References

 
In individuals without diabetes, high-intensity exercise (HIE) training may reduce (1) the characteristic postexercise rise in plasma glucose with HIE (2–4) and reduces (5,6) the marked acid-base balance perturbations (5–8). In type 1 diabetes, continuous HIE induces sustained hyperglycemia (9,10), while very brief intermittent HIE may reduce hyperglycemia (11). Acid-base disturbances during exercise may be heightened in type 1 diabetes (12–14). Effects of HIE training on glycemia and acid-base balance during intermittent HIE in type 1 diabetes are unknown; thus, despite the potential clinical importance of such exercise, there is no evidence on which to base patient guidelines. The aim of the present study was thus to investigate the effects of HIE training on glycemia and acid-base regulation during intermittent HIE in type 1 diabetes.

	RESEARCH DESIGN AND METHODS—

TOP INTRODUCTION RESEARCH DESIGN AND METHODS-- RESULTS-- CONCLUSIONS-- References

 
Eight subjects with type 1 diabetes (duration of diabetes 7.1 ± 4.0 years) and seven subjects without diabetes (control group), all of whom were healthy and took no medications (other than insulin in type 1 diabetic subjects), consented to participate. The study was approved by the human ethics committees of The University of Sydney and the South Sydney West Area Health Service. Control subjects closely matched those with diabetes for age (type 1 diabetes 25 ± 4 years and control 25 ± 4 years), BMI (25.4 ± 3.2 and 23.8 ± 5.0 kg/m², 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 sodium-potassium ATPase and on plasma potassium during maximal exercise (15).

Testing was conducted after overnight fasting. Type 1 diabetic subjects delayed 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. Arterialised 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 previously described (15). With the exception of lactate, which was analyzed using a standard enzymatic technique (17), plasma ions were analyzed using an automated blood gas analyzer (Corning 865; Chiron Diagnostics). The plasma strong ion difference (SID) was calculated: SID (mmol/) = ([potassium] + [sodium]) – ([lactate] + [chloride]). Data were analyzed with repeated-measures ANOVA (SPSS version 10.0 for Windows). When significance was detected, pairwise comparison between means was performed by a contrast technique. Significance was accepted at P < 0.05. Results are reported as means ± SD.

	RESULTS—

TOP INTRODUCTION RESEARCH DESIGN AND METHODS-- RESULTS-- CONCLUSIONS-- References

 
Exercise training did not alter A1C in type 1 diabetic subjects (preexercise 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 significantly thereafter. After training, [PG] was markedly attenuated in both groups (P = 0.001) (Fig. 1A). Insulin did not differ between groups at rest or after training, 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) (Figs. 1C and D) were markedly attenuated after training (P < 0.001), with no group differences. After training, bicarbonate fell less (P < 0.001) (Fig. 1E) in both groups. Bicarbonate was greater (P < 0.05) and chloride lesser (P < 0.01) in type 1 diabetic subjects than control subjects across all times and both days, but both were within the normal range. PO₂ did not differ between days or groups. After training, PCO₂ returned more rapidly toward resting values during recovery (P < 0.01), with no group differences. PCO₂ was greater across both days and all times in type 1 diabetic subjects than in control subjects (P < 0.01); however, resting values were within the normal range.

View larger version (45K): [in this window] [in a new window]   Figure 1— Effects of intermittent maximal exercise (hatched bars) before and after intense intermittent exercise training in the type 1 diabetic (T1D) group and in the control (CON) group on the change () in plasma glucose concentration (A), plasma strong ion difference (B), plasma hydrogen ion concentration (C), plasma lactate concentration (D), and plasma bicarbonate concentration (E). Data are means ± SE. A: *P < 0.001, main effect of time; P = 0.001, main effect of training status, pre- > posttraining; P < 0.001, training status-by-time interaction, pre- > posttraining; P < 0.001, time-by-group interaction, type 1 diabetic > control subjects; and ¶P < 0.001, type 1 diabetic > control subjects. B: *P < 0.001, main effect of time; P = 0.001, main effect of training status, post- > pretraining; P < 0.01, training status-by-time interaction, post- > pretraining; and P < 0.05, type 1 diabetic > control subjects. C and D: *P < 0.001, main effect of time; P < 0.001, main effect of training status, pre- > posttraining; and P < 0.001, training status-by-time interaction, pre- > posttraining. E: *P < 0.001, main effect of time; P < 0.001, main effect of training status, post- > pretraining; P < 0.001, training status-by-time interaction, post- > pretraining; and P < 0.05, type 1 diabetic > control subjects.

	CONCLUSIONS—

TOP INTRODUCTION RESEARCH DESIGN AND METHODS-- RESULTS-- CONCLUSIONS-- References

Plasma acid-base status during HIE depends primarily on the SID and PCO₂; reduced SID and increased PCO₂ will increase [H⁺] and reduce bicarbonate (19,20). Less acid-base perturbation after training is consistent with the higher SID, due mainly to less rise in lactate, which is perhaps consequent to greater skeletal muscle oxidative metabolism (5). Plasma PCO₂, SID, and bicarbonate were greater and chloride lesser in type 1 diabetic subjects than in control subjects (though within normal range), while plasma [H⁺] did not differ between groups. The mechanism of greater PCO₂ in type 1 diabetic subjects cannot be determined from this study; however, higher PCO₂ may have induced chloride movement into cells via the chloride/bicarbonate exchange (20). This is consistent with lower plasma chloride and hence greater SID in type 1 diabetic subjects, which likely explains the similar acidosis between groups.

HIE training did not improve A1C (however, this may reflect a type II error) but did improve glycemia and acid-base regulation during intermittent HIE in patients with type 1 diabetes.

	Acknowledgments

 
We are very appreciative of the dedication and efforts of our subjects. We are grateful to Dr. Grace Bryant and Associate Professor Martin Thompson for blood sampling, as well as Kuet Li and Donna Wilks (Garvan Institute of Medical Research) and Nadine Mackay (The University of Sydney) for excellent technical assistance.

	Footnotes

 
Published ahead of print at http://care.diabetesjournals.org on 26 February 2007. DOI: 10.2337/dc06-1790.

A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

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.

Received for publication August 23, 2006. Accepted for publication February 12, 2007.

	References

TOP INTRODUCTION RESEARCH DESIGN AND METHODS-- RESULTS-- CONCLUSIONS-- References

 

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This Article Extract Full Text (PDF) All Versions of this Article: dc06-1790v1 30/5/1269    most recent Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Harmer, A. R. Articles by Flack, J. R. Search for Related Content PubMed PubMed Citation Articles by Harmer, A. R. Articles by Flack, J. R. Social Bookmarking                What's this?