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Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals
Open accessAbstract
AIMS/HYPOTHESIS: We previously showed that type 2 diabetic patients are characterised by compromised intrinsic mitochondrial function. Here, we examined if exercise training could increase intrinsic mitochondrial function in diabetic patients compared with control individuals. METHODS: Fifteen male type 2 diabetic patients and 14 male control individuals matched for age, BMI and VO(2max) enrolled in a 12 week exercise intervention programme. Ex vivo mitochondrial function was assessed by high-resolution respirometry in permeabilised muscle fibres from vastus lateralis muscle. Before and after training, insulin-stimulated glucose disposal was examined during a hyperinsulinaemic-euglycaemic clamp. RESULTS: Diabetic patients had intrinsically lower ADP-stimulated state 3 respiration and lower carbonyl cyanide 4-(trifluoro-methoxy)phenylhydrazone (FCCP)-induced maximal oxidative respiration, both on glutamate and on glutamate and succinate, and in the presence of palmitoyl-carnitine (p < 0.05). After training, diabetic patients and control individuals showed increased state 3 respiration on the previously mentioned substrates (p < 0.05); however, an increase in FCCP-induced maximal oxidative respiration was observed only in diabetic patients (p < 0.05). The increase in mitochondrial respiration was accompanied by a 30% increase in mitochondrial content upon training (p < 0.01). After adjustment for mitochondrial density, state 3 and FCCP-induced maximal oxidative respiration were similar between groups after training. Improvements in mitochondrial respiration were paralleled by improvements in insulin-stimulated glucose disposal in diabetic patients, with a tendency for this in control individuals. CONCLUSIONS/INTERPRETATION: We confirmed lower intrinsic mitochondrial function in diabetic patients compared with control individuals. Diabetic patients increased their mitochondrial content to the same extent as control individuals and had similar intrinsic mitochondrial function, which occurred parallel with improved insulin sensitivity.
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TL;DR
In a 12-week supervised combined endurance and resistance training programme, men with type 2 diabetes and matched control individuals both increased skeletal muscle mitochondrial content and ex vivo mitochondrial respiration, with diabetic patients improving insulin-stimulated glucose disposal but not restoring it to control levels. The training-induced improvement in mitochondrial respiration was largely explained by increased mitochondrial density, and intrinsic mitochondrial function became similar between groups after training.
Key findings
- Before training, diabetic patients had lower intrinsic mitochondrial function than controls: lower ADP-stimulated state 3 respiration on glutamate (MG3 17.2 ± 1.4 vs 22.5 ± 2.0 pmol mg−1 s−1, p < 0.05) and glutamate + succinate (MGS3 28.1 ± 2.0 vs 33.8 ± 2.0 pmol mg−1 s−1, p = 0.05), and lower FCCP-induced maximal respiration on glutamate + succinate (41.2 ± 2.8 vs 53.3 ± 3.1 pmol mg−1 s−1, p < 0.05) and with palmitoyl-carnitine (44.8 ± 3.1 vs 55.8 ± 3.1 pmol mg−1 s−1, p < 0.05); differences largely remained after normalisation to mtDNA copy number.
- Training increased mitochondrial content by about 30%: mtDNA copy number rose from 2.0 ± 0.14 × 10⁶ to 2.7 ± 0.14 × 10⁶ AU in diabetic patients and from 1.8 ± 0.12 × 10⁶ to 2.7 ± 0.13 × 10⁶ AU in controls (both p < 0.01).
- Training increased state 3 respiration in both groups (diabetic patients: MG3 +34%, MGS3 +33%, p < 0.01; controls: MG3 +26%, p < 0.05, MGS3 +28%, p < 0.01), but FCCP-induced maximal respiration increased only in diabetic patients (e.g. +33% on glutamate + succinate and +27% with palmitoyl-carnitine, p < 0.05). After adjustment for mitochondrial density, state 3 and FCCP-induced maximal respiration were similar between groups after training.
- Insulin-stimulated glucose disposal (ΔRd) was lower in diabetic patients before training (8.1 ± 1.4 vs 16.0 ± 2.3 μmol kg−1 min−1, p < 0.01), increased in diabetic patients to 12.0 ± 1.9 μmol kg−1 min−1 (p < 0.05), showed a tendency to increase in controls (18.2 ± 2.5 μmol kg−1 min−1, p = 0.09), and remained lower in diabetic patients after training (p < 0.05). No correlations were found between ex vivo mitochondrial function and insulin-stimulated glucose disposal.
Methods
- Fifteen male type 2 diabetic patients and 14 male normoglycaemic control individuals, matched for age, BMI and maximal aerobic capacity, completed a 12-week supervised combined endurance and resistance exercise training programme. Diabetic patients had well-controlled type 2 diabetes (HbA1c 7.1 ± 0.2%) and were on metformin only or metformin plus sulfonylurea.
- Ex vivo mitochondrial function was measured by high-resolution respirometry in permeabilised vastus lateralis muscle fibres using multiple substrate combinations (glutamate, succinate, palmitoyl-carnitine, FCCP, oligomycin); mtDNA copy number was used as a marker of mitochondrial density. Insulin sensitivity was assessed with a 3 h hyperinsulinaemic–euglycaemic clamp combined with [6,6-²H₂]glucose infusion.
- Data are means ± SE; between-group differences were tested with independent Student’s t tests, and within-group training effects with repeated-measures ANOVA; significance was set at p < 0.05.
Limitations
- Stated: the study cannot determine whether the training-induced increase in mitochondrial content and oxidative function is responsible for improved insulin sensitivity; no correlation was found between changes in insulin sensitivity and mitochondrial function, suggesting they may be parallel rather than causally related.
- Stated: substrate competition may differ between the ex vivo condition, where substrates were provided in excess, and the in vivo situation; it could not be deduced whether CPT1 or other substrate transporters are altered by training. The exact meaning of the finding that controls did not enhance FCCP-driven maximal respiratory capacity after training cannot be deduced from this study.
- Evident from the text: the sample was small and included only men, limiting generalisability; one control individual was a non-responder for insulin sensitivity, and the figure legend reports 17 control individuals while the Methods report 14, indicating a possible inconsistency in reporting.
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Claims the paper makes
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Diabetic patients increased their mitochondrial content to the same extent as control individuals and had similar intrinsic mitochondrial function, which occurred parallel with improved insulin sensitivity.”
- Also stated in: § Discussion · plain
“Importantly, type 2 diabetic patients had similar intrinsic mitochondrial function compared with control individuals, paralleled by an improvement, but not restoration, of insulin sensitivity.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Abstract > Conclusions/interpretation
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
- Also stated in: § Discussion · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Mitochondrial density measured as mtDNA copy number was not different between diabetic patients and control individuals before training (2.0 ± 0.14 × 106 vs 1.8 ± 0.12 × 106 AU).”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Mitochondrial density
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“After training, mtDNA copy number was not significantly different between control individuals and diabetic patients.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Mitochondrial density
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Also, state 4 respiration and maximal respiratory capacity (FCCP-driven state u) levels increased by 28% (p < 0.01) and 33% (p < 0.01), respectively.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Ex vivo mitochondrial respirometry: effect of training
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The insulin-stimulated change in R a (ΔR a) was significant lower in type 2 diabetic patients compared with control individuals (ΔR a 9.1 ± 1.3 vs 18.6 ± 2.8 μmol kg−1 min−1; p < 0.05).”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Insulin-mediated glucose disposal
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Rests on an assumption: The 1-week discontinuation of glucose-lowering medication before testing is sufficient to eliminate medication effects on mitochondrial function and insulin sensitivity.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Before and after training, no correlations were found between ex vivo mitochondrial function and insulin-stimulated glucose disposal. Also, when ex vivo mitochondrial function was normalised for mitochondrial content, no correlations with markers of insulin sensitivity were found.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Ex vivo mitochondrial respirometry: effect of training
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Rests on an assumption: The 1-week discontinuation of glucose-lowering medication before testing is sufficient to eliminate medication effects on mitochondrial function and insulin sensitivity.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“After training, insulin-mediated glucose disposal in type 2 diabetic patients remained significantly lower compared with control individuals (p < 0.05).”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Insulin-mediated glucose disposal
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Rests on an assumption: The 1-week discontinuation of glucose-lowering medication before testing is sufficient to eliminate medication effects on mitochondrial function and insulin sensitivity.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“O4 respiration on MGS3 increased by 32% (p < 0.01) after training; however, FCCP-driven maximal respiratory capacity in the presence of glutamate and succinate was similar before and after training.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Ex vivo mitochondrial respirometry: effect of training
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When palmitoyl-carnitine was added as a substrate, state 3 respiration on a combination of palmitoyl-carnitine, glutamate and succinate (MPGS3) tended to be lower in diabetic patients compared with control individuals (31.2 ± 2.1 vs 39.1 ± 3.9 pmol mg−1 s−1; p = 0.08).”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Ex vivo mitochondrial respirometry before training
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Diabetic patients had intrinsically lower ADP-stimulated state 3 respiration and lower carbonyl cyanide 4-(trifluoro-methoxy)phenylhydrazone (FCCP)-induced maximal oxidative respiration, both on glutamate and on glutamate and succinate, and in the presence of palmitoyl-carnitine (p < 0.05).”
- Also stated in: § Ex vivo mitochondrial respirometry before training · plain
“Maximal respiratory capacity (FCCP-driven state u) in the presence of glutamate and succinate was significantly lower in diabetic patients compared with control individuals (41.2 ± 2.8 vs 53.3 ± 3.1 pmol mg−1 s−1; p < 0.05).”
- Also stated in: § Ex vivo mitochondrial respirometry before training · plain
“The maximal respiratory capacity (FCCP-driven state u) in the presence of palmitoyl-carnitine, glutamate and succinate was significantly lower in diabetic patients compared with control individuals (44.8 ± 3.1 vs 55.8 ± 3.1 pmol mg−1 s−1; p < 0.05).”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Abstract > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Ex vivo mitochondrial respirometry before training · plain
- It may state two separate claims as one. 9
- The quote only partly states this claim. 1
- Probably not a substantial claim. 2
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The ΔR a upon exercise training increased to 12.3 ± 1.5 (p < 0.05) in diabetic patients and to 21.2 ± 3.0 μmol kg−1 min−1 (p < 0.05) in control individuals, with ΔR a remaining significantly lower in diabetic patients compared with control individuals.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Insulin-mediated glucose disposal
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The 1-week discontinuation of glucose-lowering medication before testing is sufficient to eliminate medication effects on mitochondrial function and insulin sensitivity.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and increased significantly after exercise training in diabetic patients to 12.0 ± 1.9 μmol kg−1 min−1 (p < 0.05) with a tendency for increase in control individuals (ΔR d 18.2 ± 2.5 μmol kg−1 min−1; p = 0.09).”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Insulin-mediated glucose disposal
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The 1-week discontinuation of glucose-lowering medication before testing is sufficient to eliminate medication effects on mitochondrial function and insulin sensitivity.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Diabetic patients had intrinsically lower ADP-stimulated state 3 respiration and lower carbonyl cyanide 4-(trifluoro-methoxy)phenylhydrazone (FCCP)-induced maximal oxidative respiration, both on glutamate and on glutamate and succinate, and in the presence of palmitoyl-carnitine (p < 0.05).”
- Also stated in: § Ex vivo mitochondrial respirometry before training · plain
“State 3 respiration on MG3 and on MGS3 was significantly lower in diabetic patients compared with control individuals (MG3: 17.2 ± 1.4 vs 22.5 ± 2.0 pmol mg−1 s−1, p < 0.05 and MGS3: 28.1 ± 2.0 vs 33.8 ± 2.0 pmol mg−1 s−1, p = 0.05).”
- Also stated in: § Discussion · plain
“In agreement with earlier results [5], we showed a ∼25% lower state 3 respiration and a ∼31% lower FCCP-induced maximal oxidative capacity in type 2 diabetic patients compared with control individuals, even when normalised to mitochondrial content.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Abstract > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Ex vivo mitochondrial respirometry before training · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Similarly, upon the addition of palmitoyl-carnitine, MPG3 increased upon exercise training by 38% (p < 0.01), MPGS3 by 34% (p < 0.01) and O4 upon MPGS3 increased by 17% (p < 0.05).”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Ex vivo mitochondrial respirometry: effect of training
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The increase in mitochondrial respiration was accompanied by a 30% increase in mitochondrial content upon training (p < 0.01).”
- Also stated in: § Mitochondrial density · plain
“After training, mtDNA copy number increased significantly to 2.7 ± 0.14 × 106 AU in diabetic patients (p < 0.01) and to 2.7 ± 0.13 × 106 AU (p < 0.01) in control individuals.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Abstract > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe quote only partly states this claim.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
- Also stated in: § Mitochondrial density · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“After training, diabetic patients and control individuals showed increased state 3 respiration on the previously mentioned substrates (p < 0.05); however, an increase in FCCP-induced maximal oxidative respiration was observed only in diabetic patients (p < 0.05).”
- Also stated in: § Ex vivo mitochondrial respirometry: effect of training · plain
“Also, state 4 respiration and maximal respiratory capacity (FCCP-driven state u) levels increased by 28% (p < 0.01) and 33% (p < 0.01), respectively.”
- Also stated in: § Ex vivo mitochondrial respirometry: effect of training · plain
“O4 respiration on MGS3 increased by 32% (p < 0.01) after training; however, FCCP-driven maximal respiratory capacity in the presence of glutamate and succinate was similar before and after training.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Abstract > Results
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
- Also stated in: § Ex vivo mitochondrial respirometry: effect of training · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Improvements in mitochondrial respiration were paralleled by improvements in insulin-stimulated glucose disposal in diabetic patients, with a tendency for this in control individuals.”
- Also stated in: § Discussion · plain
“These improvements were paralleled by improved insulin-stimulated glucose disposal in type 2 diabetic patients and control individuals.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Abstract > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The 1-week discontinuation of glucose-lowering medication before testing is sufficient to eliminate medication effects on mitochondrial function and insulin sensitivity.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
- Also stated in: § Discussion · plain
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All substrates were added in excess to ensure that respiratory measurements were not limited by substrate availability influencing oxygen flux.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, when respiration values were normalised to mtDNA copy number, significant differences reported for all states before and after training in diabetic patients no longer persisted (Fig. 2a,b), illustrating that the major part of the improvement in mitochondrial function was because of an increase in mitochondrial content.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Ex vivo mitochondrial respirometry: effect of training
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Again, as in diabetic patients, the increase in mitochondrial respiration (with or without the addition of palmitoyl-carnitine) upon training was mainly accounted for by an increase in mitochondrial density, as no significant increase in intrinsic mitochondrial respiration was observed after adjustment for mtDNA copy number upon exercise training (Fig. 2a,b).”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Results > Ex vivo mitochondrial respirometry: effect of training
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The final exercise bout of the training programme was performed at least 2 days before the clamp.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Methods > Hyperinsulinaemic–euglycaemic clamp
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Remarkably, in control individuals only, exercise training did not enhance FCCP-driven maximal respiratory capacity, as occurred in type 2 diabetic patients. As a result of the increase in mitochondrial content, FCCP-driven maximal respiratory capacity per mitochondrion was actually lower after training.”
§ Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals > Discussion
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
The paper relies on this without support.
The 1-week discontinuation of glucose-lowering medication before testing is sufficient to eliminate medication effects on mitochondrial function and insulin sensitivity.
“Glucose-lowering medication was continued throughout the study except for the week preceding the actual tests and sampling of the biopsy.”
“Diabetic patients discontinued their glucose-lowering medication 1 week prior to the clamp, but restarted the use of medication after the test days.”
The paper relies on this without support.
The final exercise bout at least 2 days before the clamp is sufficient to avoid acute exercise effects on mitochondrial function and insulin sensitivity.
“The final exercise bout of the training programme was performed at least 2 days before the clamp.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“In humans, physical exercise increases total mitochondrial mass and uncoupling in skeletal muscular cells [192].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [192]
In the citing paper
“In patients with T2DM, walking and ergometer cycling exercise increased mitochondrial muscle respiration and mitochondrial content and density, as well as the activity of oxidative enzymes214,215.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [215]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Figure 1 lists more controls than were enrolled
MinorThe paper says 14 control individuals were included, but the Figure 1 caption says it shows 17 control individuals.
“In this study, 15 male type 2 diabetic patients and 14 normoglycaemic control individuals were included”
“Figure: Fig. 1 Intrinsic mitochondrial respiration ([pmol mg−1 s−1]/[mtDNA copy number × 106]) in 17 control individuals (white bars) vs 15 diabetic patients (black bars) before training.”
Citations
Cites
Glucose clamp technique: a method for quantifying insulin secretion and resistance.
DeFronzo, R. A., Tobin, J. D., & Andres, R. (1979) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1979.237.3.e214 · Cited by 7,425
Dysfunction of Mitochondria in Human Skeletal Muscle in Type 2 Diabetes
Kelley, D. E., He, J., Menshikova, E. V., & Ritov, V. B. (2002) · Diabetes · doi:10.2337/diabetes.51.10.2944 · Cited by 2,321
Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes
Petersen, K. F., Dufour, S., Befroy, D., Garcia, R., & Shulman, G. I. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa031314 · Cited by 2,193
Mitochondrial dysfunction and type 2 diabetes
Lowell, B. B., & Shulman, G. I. (2005) · Science · doi:10.1126/science.1104343 · Cited by 2,070
Diet, muscle glycogen and physical performance.
Bergström, J., Hermansen, L., Hultman, E., & Saltin, B. (1967) · Acta Physiologica Scandinavica · doi:10.1111/j.1748-1716.1967.tb03720.x · Cited by 1,740 · cited 1×
“lidocaine) according the technique of Bergstrom et al. [ 18 ].”
MethodMitochondrial respiration is decreased in skeletal muscle of patients with type 2 diabetes
Mogensen, M., Sahlin, K., Fernström, M., Glintborg, D., Vind, B. F., Beck-Nielsen, H., & Højlund, K. (2007) · Diabetes · doi:10.2337/db06-0981 · Cited by 573
Effective exercise modality to reduce insulin resistance in women with type 2 diabetes
Cuff, D. J., Meneilly, G. S., Martin, A., Ignaszewski, A., Tildesley, H. D., & Frohlich, J. J. (2003) · Diabetes Care · doi:10.2337/diacare.26.11.2977 · Cited by 545
Patients with type 2 diabetes have normal mitochondrial function in skeletal muscle
Boushel, R., Gnaiger, E., Schjerling, P., Skovbro, M., Kraunsøe, R., & Dela, F. (2007) · Diabetologia · doi:10.1007/s00125-007-0594-3 · Cited by 519
Veksler, V., Kuznetsov, A. V., Sharov, V. G., Kapelko, V. I., & Saks, V. A. (1987) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/0005-2728(87)90174-5 · Cited by 371
Phielix, E., Schrauwen-Hinderling, V. B., Mensink, M., Lenaers, E., Meex, R., Hoeks, J., Kooi, M. E., Moonen-Kornips, E., Sels, J.-P., Hesselink, M. K. C., et al. (2008) · Diabetes · doi:10.2337/db08-0391 · Cited by 359
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From host genome to the gut microbiome: an Indian lens on the global diabetes genomics landscape
Arjun, S., & Mohan, V. (2025) · Proceedings of the Indian National Science Academy · doi:10.1007/s43538-025-00565-1
“Physically active men, for instance, have been shown to exhibit significantly lower postprandial blood glucose, serum creatinine, BMI, and waist circumference compared to those with insufficient PA (Phielix et al. 2010; Verma et al. 2025).”
Tajane, T., Chandrakar, M., Ambulkar, P. S., Waghmare, P. J., Taksande, B., & Waghmare, J. E. (2025) · Human Gene · doi:10.1016/j.humgen.2025.201520
Inankur, A., O'Hare, D., Arevalo, E., Dursus-Élisée, R., Schwartz, L. P., & Sterling, S. R. (2026) · Nutrients · doi:10.3390/nu18111683
“Exercise programs carried out over one to 12 weeks have been shown to increase insulin sensitivity, likely due to improved mitochondrial function [53,54].”
Li, Z., Liu, C., & Liu, Y. (2026) · Endocrine · doi:10.1007/s12020-026-04775-5
“These benefits are thought to arise from several physiological adaptations, such as increased expression of glucose transporter type 4 (GLUT4) [9], enhanced mitochondrial function [10], improved insulin sensitivity [11], and greater fat oxidation [12].”
Metadata
- Authors
- Phielix, E., Meex, R., Moonen-Kornips, E., Hesselink, M. K. C., & Schrauwen, P.
- Affiliations
- Maastricht University Medical Centre (NL)
- Corresponding author
- Schrauwen, P.
- Venue
- Diabetologia
- Published
- 2010-04-27
- Volume
- 53
- Issue
- 8
- Pages
- 1714-1721
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- PMC
- PMC2892060
- OpenAlex
- W1966012125
- Cited by
- 206
- References
- 22
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 16 · 2023: 23 · 2022: 12 · 2021: 15 · 2020: 13 · 2019: 6 · 2018: 8 · 2017: 23 · 2016: 12 · 2015: 10 · 2014: 11 · 2013: 12 · 2012: 14
- FWCI
- 5.60
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Diabetologia (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (publishedVersion, cc-by-nc)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Funders
- Diabetes Fonds (2004.00.059)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Keywords
- type 2 diabetes, exercise training, mitochondrial function, mitochondrial content, skeletal muscle, vastus lateralis, insulin-stimulated glucose disposal, insulin sensitivity, oxidative respiration, state 3 respiration, palmitoylcarnitine, mitochondrial density
- MeSH terms
- Analysis of Variance, Blood Glucose, Diabetes Mellitus, Type 2, Humans, Insulin, Insulin Resistance, Male, Middle Aged, Mitochondria, Oxygen Consumption, Glucose Clamp Technique, Exercise, Muscle, Skeletal
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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