Postmarathon paradox: insulin resistance in the face of glycogen depletion

Abstract

Acute physical exercise enhances insulin sensitivity in healthy subjects. We examined the effect of a 42-km marathon run on insulin sensitivity and lipid oxidation in 19 male runners. In the morning after the marathon run, basal serum free fatty acid concentration was 2.2-fold higher, muscle glycogen content 37% lower (P < 0.01), glycogen synthase fractional activity 56% greater (P < 0.01), and glucose oxidation reduced by 43% (P < 0.01), whereas lipid oxidation was increased by 55% (P < 0.02) compared with the control study. During euglycemic-hyperinsulinemic clamp, whole body glucose disposal was decreased by 12% (P < 0.01) because of a 36% lower glucose oxidation rate (P < 0.05), whereas the rate of lipid oxidation was 10-fold greater (P < 0.02) than in the control study. After the marathon, muscle glycogen content correlated positively with lipid oxidation (r = 0.60, P < 0.05) and maximal aerobic power (Vo2peak; r = 0.61, P < 0.05). Vo2peak correlated positively with basal lipid oxidation (r = 0.57, P < 0.05). In conclusion, 1) after the marathon run, probably because of increased lipid oxidation, the insulin-stimulated glucose disposal is decreased despite muscle glycogen depletion and the activation of glycogen synthase; 2) the contribution of lipid oxidation in energy expenditure is increased in proportion to physical fitness; 3) these adaptations of fuel homeostasis may contribute to the maintenance of physical performance after prolonged exercise.

Metabolic Consequences of Exercise-Induced Muscle Damage

“…None of these findings were present following either the control (no exercise) or concentric exercise interventions. These results indicate that resting muscle glucose uptake is decreased following EIMD, and have been subsequently confirmed by a number of studies [10,16] .…”

“…This initial disruption is followed by degeneration during which the damaged myofibrillar proteins are acted on by proteases. A number of studies have reported the infiltration of immune cells within 2 to 3 days following injury [14,17] , but other researchers have failed to show an immune response [2,10,20] . Regeneration follows with satellite cells becoming centrally located and replacing the damaged myofibrils.…”

“…These findings have led Kirwan and del Aguila (2003) [45] to hypothesise that the decrease in insulin sensitivity in cells during EIMD results from an acute phase response mediated by TNF-, released from inflammatory cells in response to disruptions to cellular integrity. There is evidence to suggest that the inflammatory response does not always occur following EIMD [2,10,20] . TNF- may also be released from adipocytes within the muscle.…”

“…The symptoms of EIMD are common and easily characterised, and include; stiffness and swelling, decreased force of muscular contraction and delayed onset muscular soreness (DOMS) [1] . In addition, EIMD is often characterised by the presence of the intramuscular enzyme creatine kinase (CK) in the blood [2][3][4][5][6][7][8][9][10][11] .…”

“…These include bench stepping [15] , drop jumps [9,11] and downhill running protocols [8'16] . Other research has examined EIMD following exhaustive exercise containing a large number of SSC contractions, such as marathon running [3,5,10,[17][18][19][20] .…”