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Metabolic Responses to Intense Exercise in Lean and Obese Subjects^*

JEAN-FRANÇOIS YALE, LAWRENCE A. LEITER and ERROL B. MARLISS

McGill Nutrition and Food Science Centre Montreal, Quebec, Canada
the Departments of Medicine and Nutritional Sciences, University of Toronto (L.A.L.) Toronto, Ontario, Canada

Address all correspondence and requests for reprints to: Dr. Errol B. Marliss, McGill Nutrition and Food Science Centre, Royal Victoria Hospital, Room H6.90,687 Pine Avenue West, Montreal, Quebec, H3A 1A1 Canada.

Sustained elevations of plasma glucose and insulin concentrations follow intense (80/ maximum oxygen uptake) exercise performed in the postabsorptive state. To provide insights into possible mechanisms and influence of obesity, 8 lean and 12 obese subjects [106 ± 11/ (SD) and 193 ± 31/ of reference table weight, respectively] eating previously isocaloric diets were exercised to exhaustion (7 ± 3 min) on a cycle ergometer, then followed for 60 min of recovery. The obese subjects at rest had slightly increased plasma glucose and insulin and elevated blood glycerol concentrations. Both lean and obese subjects had little or no changes in plasma glucose or insulin during exercise, but the increases during the recovery period were greater and/or sustained longer in the obese. Such results raise the possibility of transient hepatic insulin resistance after exercise and are possibly relevant to restoration of depleted muscle glycogen. Both groups had a marked fall in plasma FFA during exercise; the reduction was sustained in the lean but not in the obese subjects. Blood glycerol increased during the recovery period to higher values in the obese than in the lean subjects. Plasma norepinephrine increased about 4-fold in both groups, returning promptly to preexercise values. In contrast, the exercise-induced increment in plasma epinephrine [values at exhaustion, 933 ± 548 vs. 1970 ± 787 pmol/L; P < 0.005] was markedly attenuated in the obese subjects. Thus, the obese subjects had exercise-induced changes in glucose and inulin metabolism consistent with greater postexercise insulin resistance, despite an impaired plasma epinephrine response to intense exercise.

^* This work was supported in part by grants from the Medical Research Council of Canada (to E.B.M.; MA-5767 and MA-9581).

Present address: Department of Medicine, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada.

Received May 19, 1988.

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