Aerobic exercise capacity in normal adolescents and those with type 1 diabetes mellitus

Komatsu, William Ricardo; Gabbay, Mônica Andrade Lima; Castro, Maria da Graça Tanori de; Saraiva, Gabriela Luporini; Chacra, Antônio Roberto; Neto, Turíbio Leite de Barros; Dib, Sérgio Atala

doi:10.1111/j.1399-543x.2005.00120.x

Cited by 106 publications

(114 citation statements)

References 22 publications

(20 reference statements)

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“…The decreased exercise capacity of Akita mice observed in this study is supported by previous work in rodent models of T1D (26,27) as well as in human subjects with T1D (28)(29)(30)(31). Although the precise cause for this diminished capacity remains controversial, a number of factors are thought to contribute to this decline (30,31).…”

Section: Discussionsupporting

confidence: 87%

“…Fibers were fixed immediately after isolation (referred to as Control fibers) or placed in culture dishes with plating media (10% normal horse serum, 0.5% chick embryo extract in DMEM) overnight (18 h; referred to as Activated fibers). For all single-fiber experiments, the minimum and maximum number of fibers analyzed is provided in a range (i.e., [25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40] and is derived from at least three mice per experimental group.…”

Section: Single Muscle Fiber Isolationmentioning

confidence: 99%

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Decreased Satellite Cell Number and Function in Humans and Mice With Type 1 Diabetes Is the Result of Altered Notch Signaling

et al. 2016

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Type 1 diabetes (T1D) negatively influences skeletal muscle health; however, its effect on muscle satellite cells (SCs) remains largely unknown. SCs from samples from rodents (Akita) and human subjects with T1D were examined to discern differences in SC density and functionality compared with samples from their respective control subjects. Examination of the Notch pathway was undertaken to investigate its role in changes to SC functionality. Compared with controls, Akita mice demonstrated increased muscle damage after eccentric exercise along with a decline in SC density and myogenic capacity. Quantification of components of the Notch signaling pathway revealed a persistent activation of Notch signaling in Akita SCs, which could be reversed with the Notch inhibitor DAPT. Similar to Akita samples, skeletal muscle from human subjects with T1D displayed a significant reduction in SC content, and the Notch ligand, DLL1, was significantly increased compared with control subjects, supporting the dysregulated Notch pathway observed in Akita muscles. These data indicate that persistent activation in Notch signaling impairs SC functionality in the T1D muscle, resulting in a decline in SC content. Given the vital role played by the SC in muscle growth and maintenance, these findings suggest that impairments in SC capacities play a primary role in the skeletal muscle myopathy that characterizes T1D.

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Section: Discussionsupporting

confidence: 87%

Section: Single Muscle Fiber Isolationmentioning

confidence: 99%

Decreased Satellite Cell Number and Function in Humans and Mice With Type 1 Diabetes Is the Result of Altered Notch Signaling

et al. 2016

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“…Many studies have noted pulmonary gas transfer limitations in subjects with type 1 diabetes who are of average or belowaverage fitness at rest (Benbassat et al 2001;Britton 1988;Cooper et al 1990;Fuso et al 1996;Innocenti et al 1994;Ramirez et al 1991;Sandler et al 1986;Strojek et al 1992;Villa et al 2004;Weir et al 1988) and in type 1 diabetic subjects who are of average fitness during exercise (Hsia and Raskin 2005;Komatsu et al 2005;Ljubic et al 1998;Niranjan et al 1997). However, the exact mechanism for this gas diffusion limitation, reductions in D M or decrements in V C has not been elucidated.…”

mentioning

confidence: 94%

Glycemic control influences lung membrane diffusion and oxygen saturation in exercise-trained subjects with type 1 diabetes

et al. 2010

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Lung diffusing capacity (DLCO) is influenced by alveolar-capillary membrane conductance (D (M)) and pulmonary capillary blood volume (V (C)), both of which can be impaired in sedentary type 1 diabetes mellitus (T1DM) subjects due to hyperglycemia. We sought to determine if T1DM, and glycemic control, affected DLNO, DLCO, D (M), V (C) and SaO(2) during maximal exercise in aerobically fit T1DM subjects. We recruited 12 T1DM subjects and 18 non-diabetic subjects measuring DLNO, DLCO, D (M), and V (C) along with SaO(2) and cardiac output (Q) at peak exercise. The T1DM subjects had significantly lower DLCO/Q and D (M)/Q with no difference in Q, DLNO, DLCO, D (M), or V (C) (DLCO/Q = 2.1 ± 0.4 vs. 1.7 ± 0.3, D (M)/Q = 2.8 ± 0.6 vs. 2.4 ± 0.5, non-diabetic and T1DM, p < 0.05). In addition, when considering all subjects there was a relationship between DLCO/Q and SaO(2) at peak exercise (r = 0.46, p = 0.01). Within the T1DM group, the optimal glycemic control group (HbA1c <7%, n = 6) had higher DLNO, DLCO, and D (M)/Q than the poor glycemic control subjects (HbA1c ≥ 7%, n = 6) at peak exercise (DLCO = 38.3 ± 8.0 vs. 28.5 ± 6.9 ml/min/mmHg, DLNO = 120.3 ± 24.3 vs. 89.1 ± 21.0 ml/min/mmHg, D (M)/Q = 3.8 ± 0.8 vs. 2.7 ± 0.2, optimal vs. poor control, p < 0.05). There was a negative correlation between HbA1c with DLCO, D (M) and D (M)/Q at peak exercise (DLCO: r = -0.70, p = 0.01; D (M): r = -0.70, p = 0.01; D (M)/Q: r = -0.68, p = 0.02). These results demonstrate that there is a reduction in lung diffusing capacity in aerobically fit athletes with T1DM at peak exercise, but suggests that maintaining near-normoglycemia potentially averts lung diffusion impairments.

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“…Various authors have demonstrated that, during the incremental exercise test, type 1 diabetic patients have a peak of oxygen uptake (VO2-peak), which is lower than in healthy controls [82,83]. The VO2-peak indicates the maximum amount of oxygen that can be used by an individual during a physical activity involving large muscle groups.…”

Section: Cardiopulmonary Exercise Testmentioning

confidence: 99%

The Diabetic Lung - A New Target Organ?

Pitocco

Fuso²,

Conte³

et al. 2012

Rev Diabet Stud

146

112

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■ AbstractSeveral abnormalities of the respiratory function have been reported in patients with type 1 and type 2 diabetes. These abnormalities concern lung volume, pulmonary diffusing capacity, control of ventilation, bronchomotor tone, and neuroadrenergic bronchial innervation. Many hypotheses have emerged, and characteristic histological changes have been described in the "diabetic lung", which could explain this abnormal respiratory function. Given the specific abnormalities in diabetic patients, the lung could thus be considered as a target organ in diabetes. Although the practical implications of these functional changes are mild, the presence of an associated acute or chronic pulmonary and/or cardiac disease could determine severe respiratory derangements in diabetic patients. Another clinical consequence of the pulmonary involvement in diabetes is the accelerated decline in respiratory function. The rate of decline in respiratory function in diabetics has been found to be two-to-three times faster than in normal non-smoking subjects, as reported in longitudinal studies. This finding, together with the presence of anatomical and biological changes similar to those described in the aging lung, indicates that the "diabetic lung" could even be considered a model of accelerated aging. This review describes and analyses the current insight into the relationship of diabetes and lung disease, and suggests intensifying research into the lung as a possible target organ in diabetes.

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Aerobic exercise capacity in normal adolescents and those with type 1 diabetes mellitus

Cited by 106 publications

References 22 publications

Decreased Satellite Cell Number and Function in Humans and Mice With Type 1 Diabetes Is the Result of Altered Notch Signaling

Decreased Satellite Cell Number and Function in Humans and Mice With Type 1 Diabetes Is the Result of Altered Notch Signaling

Glycemic control influences lung membrane diffusion and oxygen saturation in exercise-trained subjects with type 1 diabetes

The Diabetic Lung - A New Target Organ?

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