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Sprint training increases muscle oxidative metabolism during high-intensity exercise in patients with type 1 diabetes.

Harmer AR, Chisholm DJ, McKenna MJ, Hunter SK, Ruell PA, Naylor JM, Maxwell LJ, Flack JR - Diabetes Care (2008)

Bottom Line: Posttraining subjects performed an identical test.Pretraining, maximal resting activities of hexokinase, citrate synthase, and pyruvate dehydrogenase did not differ between groups.The latter may have clinically important health benefits.

View Article: PubMed Central - PubMed

Affiliation: 1Discipline of Physiotherapy, University of Sydney, Lidcombe, New South Wales, Australia. a.harmer@usyd.edu.au

ABSTRACT

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 (Vo(2peak)), undertook 7 weeks of sprint training. Pretraining, subjects cycled to exhaustion at 130% Vo(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(+)]. 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(+)], 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(+), 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.

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All data are means ± SE. A and B : Plasma lactate and hydrogen ion concentrations at rest, in the final seconds of exercise (), and during 1 h of recovery in the group with type 1 diabetes (triangles) and the nondiabetic control group (circles), before (white symbols) and after (black symbols) training. A : Plasma lactate concentration: a, main effects of time, P < 0.001; b, training status, P < 0.05; c, training status-by-time interaction, P < 0.05, pre- > posttraining. *P < 0.05; **P < 0.01; ***P < 0.001. There were no significant interaction effects for group: training status-by-group, P = 0.27; time-by-group, P = 0.50; or training status-by-time-by-group, P = 0.75. B: Hydrogen ion concentration: a, main effects of time, P = 0.001; b, training status, P = 0.001; c, training status-by-time interaction, P < 0.05, pre- > posttraining. **P < 0.01; ***P < 0.001. There were no significant interaction effects for training status-by-group, P = 0.28; time-by-group, P = 0.44; or training status-by-time-by-group, P = 0.32. ▵, type 1 diabetes pretraining; ▴, type 1 diabetes posttraining; ○, control pretraining; •, control posttraining. C: Estimated rates of glycogenolysis (total histogram) and glycolysis (hatched bar): both, d, main effect of training status, P < 0.01, pre- > posttraining. D: Citrate synthase activity (maximal in vitro). R, rest; Ex, end-exercise. d, main effect of training status, P < 0.01, post- > pretraining; e, time-by-group interaction, P < 0.05, type 1 diabetes unchanged, control reduced with exercise. T1D, type 1 diabetic group; CON, control group.
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f1: All data are means ± SE. A and B : Plasma lactate and hydrogen ion concentrations at rest, in the final seconds of exercise (), and during 1 h of recovery in the group with type 1 diabetes (triangles) and the nondiabetic control group (circles), before (white symbols) and after (black symbols) training. A : Plasma lactate concentration: a, main effects of time, P < 0.001; b, training status, P < 0.05; c, training status-by-time interaction, P < 0.05, pre- > posttraining. *P < 0.05; **P < 0.01; ***P < 0.001. There were no significant interaction effects for group: training status-by-group, P = 0.27; time-by-group, P = 0.50; or training status-by-time-by-group, P = 0.75. B: Hydrogen ion concentration: a, main effects of time, P = 0.001; b, training status, P = 0.001; c, training status-by-time interaction, P < 0.05, pre- > posttraining. **P < 0.01; ***P < 0.001. There were no significant interaction effects for training status-by-group, P = 0.28; time-by-group, P = 0.44; or training status-by-time-by-group, P = 0.32. ▵, type 1 diabetes pretraining; ▴, type 1 diabetes posttraining; ○, control pretraining; •, control posttraining. C: Estimated rates of glycogenolysis (total histogram) and glycolysis (hatched bar): both, d, main effect of training status, P < 0.01, pre- > posttraining. D: Citrate synthase activity (maximal in vitro). R, rest; Ex, end-exercise. d, main effect of training status, P < 0.01, post- > pretraining; e, time-by-group interaction, P < 0.05, type 1 diabetes unchanged, control reduced with exercise. T1D, type 1 diabetic group; CON, control group.

Mentions: Peak V̇o2 did not differ between the constant-load (3.29 ± 0.21 l/min) and incremental tests (3.24 ± 0.22 l/min; P = 0.56). Pretraining in the constant-load test, the groups did not differ on any respiratory variable (Table 1). Posttraining, during identical exercise, estimated to elicit 125 ± 0.03% of pretraining V̇o2peak (P = 0.06), peak expired ventilation and carbon dioxide output were reduced, with no group differences. Plasma lactate and [H+] were less elevated posttraining, with no group differences (Fig. 1A and B).


Sprint training increases muscle oxidative metabolism during high-intensity exercise in patients with type 1 diabetes.

Harmer AR, Chisholm DJ, McKenna MJ, Hunter SK, Ruell PA, Naylor JM, Maxwell LJ, Flack JR - Diabetes Care (2008)

All data are means ± SE. A and B : Plasma lactate and hydrogen ion concentrations at rest, in the final seconds of exercise (), and during 1 h of recovery in the group with type 1 diabetes (triangles) and the nondiabetic control group (circles), before (white symbols) and after (black symbols) training. A : Plasma lactate concentration: a, main effects of time, P < 0.001; b, training status, P < 0.05; c, training status-by-time interaction, P < 0.05, pre- > posttraining. *P < 0.05; **P < 0.01; ***P < 0.001. There were no significant interaction effects for group: training status-by-group, P = 0.27; time-by-group, P = 0.50; or training status-by-time-by-group, P = 0.75. B: Hydrogen ion concentration: a, main effects of time, P = 0.001; b, training status, P = 0.001; c, training status-by-time interaction, P < 0.05, pre- > posttraining. **P < 0.01; ***P < 0.001. There were no significant interaction effects for training status-by-group, P = 0.28; time-by-group, P = 0.44; or training status-by-time-by-group, P = 0.32. ▵, type 1 diabetes pretraining; ▴, type 1 diabetes posttraining; ○, control pretraining; •, control posttraining. C: Estimated rates of glycogenolysis (total histogram) and glycolysis (hatched bar): both, d, main effect of training status, P < 0.01, pre- > posttraining. D: Citrate synthase activity (maximal in vitro). R, rest; Ex, end-exercise. d, main effect of training status, P < 0.01, post- > pretraining; e, time-by-group interaction, P < 0.05, type 1 diabetes unchanged, control reduced with exercise. T1D, type 1 diabetic group; CON, control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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f1: All data are means ± SE. A and B : Plasma lactate and hydrogen ion concentrations at rest, in the final seconds of exercise (), and during 1 h of recovery in the group with type 1 diabetes (triangles) and the nondiabetic control group (circles), before (white symbols) and after (black symbols) training. A : Plasma lactate concentration: a, main effects of time, P < 0.001; b, training status, P < 0.05; c, training status-by-time interaction, P < 0.05, pre- > posttraining. *P < 0.05; **P < 0.01; ***P < 0.001. There were no significant interaction effects for group: training status-by-group, P = 0.27; time-by-group, P = 0.50; or training status-by-time-by-group, P = 0.75. B: Hydrogen ion concentration: a, main effects of time, P = 0.001; b, training status, P = 0.001; c, training status-by-time interaction, P < 0.05, pre- > posttraining. **P < 0.01; ***P < 0.001. There were no significant interaction effects for training status-by-group, P = 0.28; time-by-group, P = 0.44; or training status-by-time-by-group, P = 0.32. ▵, type 1 diabetes pretraining; ▴, type 1 diabetes posttraining; ○, control pretraining; •, control posttraining. C: Estimated rates of glycogenolysis (total histogram) and glycolysis (hatched bar): both, d, main effect of training status, P < 0.01, pre- > posttraining. D: Citrate synthase activity (maximal in vitro). R, rest; Ex, end-exercise. d, main effect of training status, P < 0.01, post- > pretraining; e, time-by-group interaction, P < 0.05, type 1 diabetes unchanged, control reduced with exercise. T1D, type 1 diabetic group; CON, control group.
Mentions: Peak V̇o2 did not differ between the constant-load (3.29 ± 0.21 l/min) and incremental tests (3.24 ± 0.22 l/min; P = 0.56). Pretraining in the constant-load test, the groups did not differ on any respiratory variable (Table 1). Posttraining, during identical exercise, estimated to elicit 125 ± 0.03% of pretraining V̇o2peak (P = 0.06), peak expired ventilation and carbon dioxide output were reduced, with no group differences. Plasma lactate and [H+] were less elevated posttraining, with no group differences (Fig. 1A and B).

Bottom Line: Posttraining subjects performed an identical test.Pretraining, maximal resting activities of hexokinase, citrate synthase, and pyruvate dehydrogenase did not differ between groups.The latter may have clinically important health benefits.

View Article: PubMed Central - PubMed

Affiliation: 1Discipline of Physiotherapy, University of Sydney, Lidcombe, New South Wales, Australia. a.harmer@usyd.edu.au

ABSTRACT

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 (Vo(2peak)), undertook 7 weeks of sprint training. Pretraining, subjects cycled to exhaustion at 130% Vo(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(+)]. 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(+)], 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(+), 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.

Show MeSH
Related in: MedlinePlus