Effect of exercise intensity and volume on persistence of insulin sensitivity during training cessation

Bajpeyi, Sudip; Tanner, Charles J.; Slentz, Cris A.; Duscha, Brian D.; McCartney, Jennifer S.; Hickner, Robert C.; Kraus, William E.; Houmard, Joseph A.

doi:10.1152/japplphysiol.91262.2008

Cited by 122 publications

(101 citation statements)

References 30 publications

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“…Previous studies in humans and rodents have reported increased insulin sensitivity after either higher-intensity or longer-duration acute exercise protocols than used in the present study (3,8,15,19,23,34,43,44,54). The exercise intensity achieved in the present study by sheep in the intensive exercise test (30 min, 8% slope, 4 -4.4 km/h) is probably ϳ50 -60% of V O 2max , based on studies in pregnant sheep (26).…”

Section: Discussionsupporting

confidence: 47%

Acute exercise increases insulin sensitivity in adult sheep: a new preclinical model

McConell

Kaur

Falcão-Tebas

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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In healthy humans and rodents, chronic and acute exercise improves subsequent insulin sensitivity of skeletal muscle. A large animal species with similar metabolic responses to exercise would permit longitudinal studies, including repeated biopsies of muscle and other tissues not possible in rodents, and enable study of interactions with insulin-resistant physiological states not feasible in humans. Therefore, we examined whether acute exercise increases insulin sensitivity in adult sheep. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp (HEC) in mature female sheep (n ϭ 7). Sheep were familiarized to treadmill walking and then performed an acute exercise bout (30 min, 8% slope, up to 4.4 km/h). A second HEC was conducted ϳ18 h after the acute exercise. Musculus semimembranosus biopsies were obtained before and after each HEC. Glucose infusion rate during the HEC increased 40% (P ϭ 0.003) and insulin sensitivity (glucose infusion rate/plasma insulin concentration) increased 32% (P ϭ 0.028) after acute exercise. Activation of proximal insulin signaling in skeletal muscle after the HEC, measured as Ser 473 phosphorylation of Akt, increased approximately five-fold in response to insulin (P Ͻ 0.001) and was unaltered by acute exercise performed 18 h earlier. PGC1␣ and GLUT4 protein, glycogen content and citrate synthase activity in skeletal muscle did not change in response to insulin or exercise. In conclusion, improved insulin sensitivity and unchanged proximal insulin signaling on the day after acute exercise in sheep are consistent with responses in humans and rodents, suggesting that the sheep is an appropriate large-animal model in which to study responses to exercise. exercise; insulin sensitivity; muscle; sheep REGULAR EXERCISE TRAINING increases insulin-stimulated whole body and skeletal muscle glucose uptake in humans, in healthy individuals as well as in those who have Type 2 diabetes (T2D) or are obese or aged (reviewed by Refs. 14, 31, 45). Increased expression of hexokinase 2, some insulin signaling proteins and GLUT4, and greater insulin-induced vasodilation are implicated as mechanisms for enhanced insulin-stimulated glucose uptake after training (14,31,45). Exercise training probably acts mainly at distal sites to increase glucose uptake, with the balance of evidence, suggesting that proximal insulin signaling is not upregulated (14, 38). Importantly, a single bout of exercise also increases the insulin sensitivity of glucose uptake during the following 4 -48 h in healthy humans (34,46,52,54,55). Similar effects have been demonstrated in rodents, where an acute exercise bout increases in vitro insulin-stimulated glucose uptake in mouse muscle 85 min after exercise (18) and in rat muscle collected 3-16 h after a single bout of exercise (8,15,19,43,44). Available evidence from studies in humans and rodents suggests that acute exercise, like exercise training, increases insulin sensitivity without changes in proximal insulin signaling (reviewed in Ref. 31).A large animal model with...

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Section: Discussionsupporting

confidence: 47%

Acute exercise increases insulin sensitivity in adult sheep: a new preclinical model

McConell

Kaur

Falcão-Tebas

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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“…However, evidence is accumulating that differences exist in the individual response to exercise training. On average, approximately 15-20% of people failed to improve their glucose tolerance and insulin sensitivity after exercise training interventions (7); this nonresponse is not restricted to a specific type of exercise (endurance or resistance training or combinations), although differences are reported (8)(9)(10)(11).…”

Section: Tgf-b Contributes To Impaired Exercise Response By Suppressimentioning

confidence: 99%

TGF-β Contributes to Impaired Exercise Response by Suppression of Mitochondrial Key Regulators in Skeletal Muscle

et al. 2016

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A substantial number of people at risk of developing type 2 diabetes could not improve insulin sensitivity by physical training intervention. We studied the mechanisms of this impaired exercise response in 20 middle-aged individuals at high risk of developing type 2 diabetes who performed 8 weeks of controlled cycling and walking training at 80% individual Vo2 peak. Participants identified as nonresponders in insulin sensitivity (based on the Matsuda index) did not differ in preintervention parameters compared with high responders. The failure to increase insulin sensitivity after training correlates with impaired upregulation of mitochondrial fuel oxidation genes in skeletal muscle, and with the suppression of the upstream regulators PGC1α and AMPKα2. The muscle transcriptomes of the nonresponders are further characterized by the activation of transforming growth factor (TGF)-β and TGF-β target genes, which is associated with increases in inflammatory and macrophage markers. TGF-β1 as inhibitor of mitochondrial regulators and insulin signaling is validated in human skeletal muscle cells. Activated TGF-β1 signaling downregulates the abundance of PGC1α, AMPKα2, the mitochondrial transcription factor TFAM, and mitochondrial enzymes. Thus, the data suggest that increased TGF-β activity in skeletal muscle can attenuate the improvement of mitochondrial fuel oxidation after training and contribute to the failure to increase insulin sensitivity.

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“…Several studies have indicated that training-related improvements in insulin action are retained after 10 days without physical activity in master athletes (Rogers et al 1990), and after 15 days of inactivity in overweight/obese subjects (Bajpeyi et al 2009). However, to our knowledge, there is no other information concerning the retention characteristics of insulin action after various exercise prescriptions in T2DM.…”

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confidence: 99%

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confidence: 99%

“…Higher volumes of exercise (i.e., more weekly sessions) may induce more changes in the skeletal muscle mitochondrial content compared with lower-volume exercise regimens of the same intensity (65-85% V 4 O 2peak ) 15 days after training cessation (Bajpeyi et al 2009). However, there is a debate about the magnitude of exerciseinduced changes in skeletal muscle mitochondrial content as a function of exercise intensity (40-55% vs. 65-85% O 2peak ) so this deduction should be treated with caution (Bajpeyi et al 2009). Because the mechanisms that govern insulin action are multifactorial and complex (Goodyear and Kahn 1998;Hawley 2004), further studies are needed to explain differences in retention of training-induced improvements in insulin action in exercise regimens of different intensities.…”

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confidence: 99%

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Duration of Exercise as a Key Determinant of Improvement in Insulin Sensitivity in Type 2 Diabetes Patients

Zhang

Guo

et al. 2012

Tohoku J. Exp. Med.

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Exercise duration and intensity are important parameters in exercise prescription and play a major role in improving insulin sensitivity (including transient and persistent improvement effects following cessation of training) in patients with type 2 diabetes mellitus (T2DM). However, whether duration or intensity of exercise is the more important factor has yet to be established. Therefore, we aimed to determine whether exercise prescriptions differing in duration and intensity differ in their ability to aid T2DM patients to retain insulin sensitivity following the conclusion of a period of training. Sedentary T2DM patients (age 51.2 ± 1.3 years) were assigned to either a low-intensity (50% V 4 O 2peak , n = 27) or a high-intensity exercise group (75% V 4 O 2peak , n = 28), and followed a 12-week exercise program of 5 sessions/week and 240 kcal/session. Insulin sensitivity (oral glucose tolerance test, ISI) was measured when subjects were sedentary and at 16-24 h and 15 days after the final training bout. The low-intensity group spent more training time to training per exercise session than the high-intensity group (56.1 ± 3.0 min/session vs. 34.3 ± 2.4 min/ session) (P < 0.01), but the total amount of energy expended was the same. ISI was increased in both groups 16-24 h after the final training session, but only the low-intensity group still had elevated ISI 15 days after the cessation of training. These findings suggest that in T2DM patients, the persistent traininginduced improvements in insulin sensitivity may be more dependent on exercise duration than exercise intensity in regimens with the same level of energy expenditure.

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Effect of exercise intensity and volume on persistence of insulin sensitivity during training cessation

Cited by 122 publications

References 30 publications

Acute exercise increases insulin sensitivity in adult sheep: a new preclinical model

Acute exercise increases insulin sensitivity in adult sheep: a new preclinical model

TGF-β Contributes to Impaired Exercise Response by Suppression of Mitochondrial Key Regulators in Skeletal Muscle

Duration of Exercise as a Key Determinant of Improvement in Insulin Sensitivity in Type 2 Diabetes Patients

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