International Journal of Medical and Pharmaceutical Research
2026, Volume-7, Issue 1 : 861-865
Original Article
Peak VO₂ During Bicycle Ergometry Is Reduced Even in Early Diabetics
 ,
 ,
 ,
Received
Dec. 22, 2025
Accepted
Jan. 13, 2026
Published
Jan. 23, 2026
Abstract

Background: Type 2 diabetes mellitus (T2DM) is associated with early cardiovascular and metabolic alterations that may precede overt complications. Peak oxygen uptake (Peak VO₂) is a key indicator of aerobic capacity and cardiovascular fitness.

Objective: To assess Peak VO₂ during bicycle ergometry in early diagnosed T2DM patients and compare it with healthy controls. And also to assess the correlation between peak VO2 and duration of diabetes

Material and Methodology: The Cardiopulonary Exercise Testing was performed on a USA based GASSYS3 BIOPAC gas analyzer machine on 64 diabetic and 64 healthy subjects. Oxygen consumption (VO2), CO2 production (VCO2), Respiratory exchange ratio (RER) and Minute ventilation (VE) were recorded both at rest and after performing symptom limited CPET on the bicycle ergometer.

Result: Peak VO2 was found to be significantly (p<0.01) reduced while RER was found to be significantly (p=0.01) increased in early diabetics. However, VO2 at rest, was not significantly different among the groups (p >0.05). Peak VO2 also showed a significantly negative correlation with duration of diabetes. (p<0.01; r = -0.34)

Conclusion: Peak VO₂ is reduced even in the early stages of T2DM, indicating early impairment of aerobic capacity. Bicycle ergometry is a useful non-invasive tool for early functional assessment in diabetic patients

Keywords
INTRODUCTION

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease characterized by hyperglycemia resulting from insulin resistance and relative insulin deficiency.(1,2) Globally, T2DM prevalence is rising, affecting younger adults and increasing the burden of cardiovascular disease, particularly in developing countries like India(3). While the long-term complications of diabetes are well recognized, growing evidence suggests that cardiovascular and metabolic dysfunction begins early in the course of the disease(4,5).

 

Peak oxygen uptake (Peak VO₂) reflects the integrated response of the cardiovascular, pulmonary, and muscular systems during exercise(6,7) and is considered the gold standard measure of aerobic fitness(8). Reduced Peak VO₂ is associated with increased cardiovascular risk and mortality.(9)

 

Exercise testing using bicycle ergometry is a safe and reproducible method to evaluate exercise capacity(10). Previous studies predominantly focused on long-standing diabetes or patients with complications. There is limited data evaluating VO₂ peak in early-stage diabetes (<5 years duration). Identifying reduced functional capacity early could guide preventive strategies, including tailored aerobic exercise programs and lifestyle interventions.

 

This study aimed to assess VO₂ peak during bicycle ergometry in early diabetics and compare it with healthy controls to determine early impairment in aerobic capacity. And also aimed to assess the correlation between peak VO2 and duration of diabetes.

 

MATERIALS AND METHODS

This cross-sectional study was conducted in the Department of Physiology, G. R. Medical College, Gwalior. A total of 128 subjects were enrolled, including 64 patients with type 2 diabetes mellitus of less than five years’ duration and 64 age- and sex-matched healthy controls. Diabetic subjects were recruited from the Medicine Outpatient Department of Jaya Arogya Hospital, Gwalior.

 

The study group comprised patients aged 30–60 years with type 2 diabetes mellitus and no history of cardiovascular disease. The control group included healthy individuals without any chronic illness. Exclusion criteria were refusal to participate, body mass index (BMI) >30 kg/m², resting blood pressure >140/90 mmHg, abnormal electrocardiographic findings, history of cardiovascular, respiratory, hepatic, or renal disease, and presence of endocrine disorders other than diabetes mellitus.

 

A detailed medical history was obtained from all participants, followed by general physical examination and anthropometric measurements. Written informed consent was obtained prior to participation

 

Cardiopulmonary exercise testing (CPET) was performed using a GASSYS3 BIOPAC gas analyzer. After application of a tight-fitting face mask, resting oxygen consumption (VO₂), carbon dioxide production (VCO₂), respiratory exchange ratio (RER), and minute ventilation (VE) were recorded. Participants performed a 2-minute warm-up on a cycle ergometer, followed by rest until heart rate returned to baseline.

 

Submaximal, symptom-limited CPET was conducted using a constant work-rate protocol as described by Mezzani et al(11). Exercise was continued until approximately 75% of age-predicted maximum heart rate was achieved or till volitional fatigue.

 

Heart rate and blood pressure were recorded at rest and immediately after exercise. Peak VO₂, peak VCO₂, peak RER, and VE were documented.

 

OBSERVATION TABLES

Table 1: Anthropometric Parameters of Diabetic and Healthy Group

S. No.

Parameters

Diabetics Group

HealthyGroup

p-value

1

Age (years)

44.61±7.243

43.70±7.206

0.4793

2

Height (cm)

165± 6.08

164±4.34

0.3551

3

Weight (Kg)

67.92±6.84

66.17±5.851

0.1227

4

BMI (kg/m2)

24.91±1.707

24.54±1.670

0.2162

 

*=p<0.05 = Statistically Significant**=p<0.01 = Statistically Highly Significant

***=p<0.001 = Statistically Very Highly Significant

 

Table 2: Comparison of investigations between Diabetic Group and Healthy Group

S.No.

Parameters

Diabetics Group

HealthyGroup

p-value

1.

Triglyceride (mg/dl)

137±23.1

130±52.0

0.380

2.

Cholesterol (mg/dl)

146±21.0

142±29.0

0.4818

3.

FBS (mg/dl)

118.4 ± 16.75

83.89±9.71

<0.001***

4.

RBS (mg/dl)

154±20.8

119±19.0

<0.001***

 

Table 3: Comparison of haemodynamic parameters of Diabetic Group & Healthy Group at rest

S.No.

Parameters

Diabetics Group

HealthyGroup

p-value

1

SBP (mm Hg)

126.9±6.872

125±4.605

0.0671

2

DBP (mm Hg)

81.2 ±3.98

80.9 ±4.66

0.7141

3

Mean BP (mm Hg)

96.4 ± 3.57

95.6 ±3.72

0.2040

4

Pulse rate/min

73.38 ±5.86

74.34 ±8.16

0.4423

 

Table 4: Comparison of haemodynamic parameters of Diabetic and Healthy group at end of exercise

S.No.

Parameters

Diabetics Group

Healthy Group

p-value

1

SBP mm Hg

153 ±7.87

151 ±6.29

0.076

2

DBP mm Hg

84.00 ± 4.00

83.44 ± 4.238

0.4415

3

Mean BP mm Hg

107.3±3.60

106.4±3.57

0.067

4

Pulse rate/min

116 ± 5.25

118±8.54

0.1219

 

 

5: Comparison of Cardiopulmonary Exercise Test Parameters between Diabetics and Healthy groups at rest

S.No.

Parameters

Diabetics Group

Healthy Group

p-value

1.

VO2(ml/kg/min)

3.66 ±0.610

3.59 ±0.599

0.56

2.

VCO2(l/min)

0.2831±0.058

0.2736±0.051

0.2864

3.

RER

0.874±0.081

0.876±0.083

0.91

4.

VE (l/min)

6.40±2.33

5.85±1.68

0.1239

 

Table 6: Comparison of Cardiopulmonary Exercise Test Parameters between Diabetics and Healthy groups at end of exercise

S.No.

Parameters

Diabetics Group

Healthy Group

p-value

1.

VO2(ml/kg/min)

15.3± 2.92

18.1±2.52

<0.0001

2.

VCO2(l/min)

1.405±0.2436

1.461±0.1897

0.1512

3.

RER

1.262±0.0633

1.230±0.0787

0.0126*

4.

VE (L/min)

37.86 ± 8.388

37.23 ± 6.544

0.6379

 

Table7: Correlation of Cardiopulmonary exercise test with Duration of Diabetes Mellitus

S.No.

Parameter

p-value

Pearson r

01

VO2 peak (ml/kg/min)

0.0058*

-0.3414

02

VCO2 (L/min)

0.2497

-0.1460

03

RER

0.8077

-0.0310

04

VE (L/min)

0.9349

0.0104

*- signifies significant difference having p-value<0.05.

 

Statistical Analysis

Data were expressed as mean ± standard deviation. Student’s unpaired t-test was used for comparison between groups. A p-value <0.05 was considered statistically significant.

 

RESULTS

Anthropometric measurements and hemodynamic parameters at rest were comparable between the two groups (p>0.05). Even early(less than 5 years) diabetic subjects demonstrated significantly lower Peak VO₂ values, along with reduced exercise duration and early onset of fatigue.

 

DISCUSSION

This study evaluated cardiovascular fitness in normotensive patients with early type 2 diabetes mellitus using cardiopulmonary exercise testing (CPET) and compared the findings with healthy controls. Anthropometric parameters were comparable between the two groups, thereby minimizing the potential confounding effects of body composition on exercise capacity. As expected, fasting and random blood glucose levels were significantly higher in diabetic subjects, reflecting suboptimal glycemic control, while lipid profiles did not differ significantly between groups. Similar observations have been reported by DeFronzo and Ferrannini et al(12), who highlighted that metabolic abnormalities often precede overt cardiovascular manifestations in early diabetes.

 

Resting systolic and diastolic blood pressure, mean arterial pressure, and heart rate were comparable between diabetic and control subjects, confirming preserved resting hemodynamic status and normotension. Post-exercise increases in hemodynamic parameters were observed in both groups without significant intergroup differences. These findings are consistent with earlier studies by Regensteiner et al.  (13)and Fang et al.(14), who demonstrated preserved resting cardiovascular function in patients with early type 2 diabetes prior to the onset of overt cardiovascular disease.

 

Resting oxygen consumption (VO₂) did not differ significantly between groups, suggesting similar basal metabolic requirements. However, peak oxygen consumption (VO₂ peak) was significantly lower in diabetic subjects, indicating impaired cardiorespiratory fitness. VO₂ peak is a well-established indicator of aerobic capacity and cardiovascular health, and its reduction reflects early limitations in oxygen delivery and utilization. Similar reductions in VO₂ peak among patients with type 2 diabetes have been consistently reported by Regensteiner et al. (1) and Baldi and Snowling et al(15).

 

Several mechanisms may underlie the observed reduction in VO₂ peak. Chronic hyperglycemia contributes to endothelial dysfunction, impaired nitric oxide–mediated vasodilation, and microvascular remodeling, resulting in reduced skeletal muscle perfusion during exercise (Hamburg et al.,(16); Ceriello et al(17). In addition, mitochondrial dysfunction, decreased oxidative enzyme activity, and reduced skeletal muscle oxidative capacity have been demonstrated in patients with type 2 diabetes Kelley et al.,(18); Phielix and Mensink et al, (19). The accumulation of advanced glycation end products further compromises vascular compliance and oxygen diffusion Brownlee et al, (20).

 

The present findings align with previous investigations suggesting that diminished aerobic capacity may represent an early marker of subclinical cardiovascular dysfunction in type 2 diabetes. Studies by Poole et al.(21) and Ratchford et al. (22)have shown that impaired cardiac output, reduced peripheral oxygen extraction, and a diminished arteriovenous oxygen difference contribute to reduced exercise tolerance in diabetic individuals.

 

Peak respiratory exchange ratio (RER) was significantly higher in diabetic subjects, indicating an increased reliance on anaerobic metabolism during maximal exercise. This finding suggests reduced metabolic flexibility and an early shift toward glycolytic pathways. Impaired mitochondrial oxidative phosphorylation, altered substrate utilization, and suboptimal blood flow distribution to exercising muscles may account for this response Mogensen et al.,(23); Schrauwen and Hesselink et al, (24).

 

A significant negative correlation between diabetes duration and VO₂ peak was observed, indicating a progressive decline in cardiovascular fitness with increasing disease duration. Prolonged exposure to hyperglycemia promotes cumulative oxidative stress, endothelial injury, inflammation, and microvascular damage, which collectively impair cardiovascular and metabolic function (Laakso et al, (25); Stratton et al., (26)). These findings support earlier evidence linking longer duration of diabetes with increased cardiovascular risk and reduced functional capacity.

 

CONCLUSION

In conclusion, normotensive patients with early type 2 diabetes demonstrate significantly reduced aerobic capacity despite preserved resting hemodynamics and comparable anthropometric characteristics. CPET emerges as a sensitive tool for detecting early impairments in cardiovascular fitness in this population. Early identification of reduced VO₂ peak may facilitate timely lifestyle and therapeutic interventions aimed at improving glycemic control and cardiorespiratory fitness, thereby reducing future cardiovascular risk.

 

 

REFERENCES

  1. Regensteiner JG. Type 2 diabetes mellitus and cardiovascular exercise performance. Rev Endocr Metab Disord. 2004 Aug;5(3):269–76.
  2. Kanaley JA, Colberg SR, Corcoran MH, Malin SK, Rodriguez NR, Crespo CJ, et al. Exercise/Physical Activity in Individuals with Type 2 Diabetes: A Consensus Statement from the American College of Sports Medicine. Med Sci Sports Exerc. 2022 Feb 1;54(2):353–68.
  3. Tabish SA. Is Diabetes Becoming the Biggest Epidemic of the Twenty-first Century? Int J Health Sci. 2007 July;1(2):V–VIII.
  4. Anjana RM, Unnikrishnan R, Deepa M, Pradeepa R, Tandon N, Das AK, et al. Metabolic non-communicable disease health report of India: the ICMR-INDIAB national cross-sectional study (ICMR-INDIAB-17). Lancet Diabetes Endocrinol. 2023 July;11(7):474–89.
  5. Alvin C. Powers, Kevin D. Niswender, Carmella Evans-Molina.Diabetes Mellitus: Diagnosis, Classification, and Pathophysiology | Harrison’s Principles of Internal Medicine, 21e; chapter 403: 3094-3103 - Google Search [Internet]. [cited 2026 Jan 13].
  6. Green S, Egaña M, Baldi JC, Lamberts R, Regensteiner JG. Cardiovascular Control during Exercise in Type 2 Diabetes Mellitus. J Diabetes Res. 2015;2015:654204.
  7. Malhotra R, Bakken K, D’Elia E, Lewis GD. Cardiopulmonary Exercise Testing in Heart Failure. JACC Heart Fail. 2016 Aug;4(8):607–16.
  8. Gonzales TI, Westgate K, Strain T, Hollidge S, Jeon J, Christensen DL, et al. Cardiorespiratory fitness assessment using risk-stratified exercise testing and dose-response relationships with disease outcomes. Sci Rep. 2021 July 28;11(1):15315.
  9. Seyoum B, Estacio RO, Berhanu P, Schrier RW. Exercise capacity is a predictor of cardiovascular events in patients with type 2 diabetes mellitus. Diab Vasc Dis Res. 2006 Dec;3(3):197–201.
  10. Eckstein ML, Farinha JB, McCarthy O, West DJ, Yardley JE, Bally L, et al. Differences in Physiological Responses to Cardiopulmonary Exercise Testing in Adults With and Without Type 1 Diabetes: A Pooled Analysis. Diabetes Care. 2021 Jan;44(1):240–7.
  11. Mezzani A. Cardiopulmonary Exercise Testing: Basics of Methodology and Measurements. Ann Am Thorac Soc. 2017 July;14(Supplement_1):S3–11.
  12. DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin North Am. 2004 July;88(4):787–835, ix.
  13. Regensteiner JG, Sippel J, McFarling ET, Wolfel EE, Hiatt WR. Effects of non-insulin-dependent diabetes on oxygen consumption during treadmill exercise. Med Sci Sports Exerc. 1995 June;27(6):875–81.
  14. Fang ZY, Prins JB, Marwick TH. Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications. Endocr Rev. 2004 Aug;25(4):543–67.
  15. Baldi JC, Snowling N. Resistance training improves glycaemic control in obese type 2 diabetic men. Int J Sports Med. 2003 Aug;24(6):419–23.
  16. Hamburg NM, McMackin CJ, Huang AL, Shenouda SM, Widlansky ME, Schulz E, et al. Physical inactivity rapidly induces insulin resistance and microvascular dysfunction in healthy volunteers. Arterioscler Thromb Vasc Biol. 2007 Dec;27(12):2650–6.
  17. Ceriello A. Oxidative Stress and Diabetes-Associated Complications. Endocr Pract. 2006 Jan 1;12:60–2.
  18. Kelley DE, He J, Menshikova EV, Ritov VB. Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes. Diabetes. 2002 Oct;51(10):2944–50.
  19. Phielix E, Mensink M. Type 2 diabetes mellitus and skeletal muscle metabolic function. Physiol Behav. 2008 May 23;94(2):252–8.
  20. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001 Dec 13;414(6865):813–20.
  21. Poole DC, Hirai DM, Copp SW, Musch TI. Muscle oxygen transport and utilization in heart failure: implications for exercise (in)tolerance. Am J Physiol Heart Circ Physiol. 2012 Mar 1;302(5):H1050-1063.
  22. 12. Ratchford SM, Kargl J, Healey CM, et al. Vascular dysfunction and reduced aerobic capacity in individuals with type 2 diabetes. J Appl Physiol. 2016;121(2):527–35. - Google Search [Internet]. [cited 2026 Jan 15].
  23. Mogensen M, Sahlin K, Fernström M, Glintborg D, Vind BF, Beck-Nielsen H, et al. Mitochondrial respiration is decreased in skeletal muscle of patients with type 2 diabetes. Diabetes. 2007 June;56(6):1592–9.
  24. Schrauwen P, Hesselink MKC. Oxidative capacity, lipotoxicity, and mitochondrial damage in type 2 diabetes. Diabetes. 2004 June;53(6):1412–7.
  25. Laakso M. Cardiovascular disease in type 2 diabetes: challenge for treatment and prevention. J Intern Med. 2001 Mar;249(3):225–35.
  26. Stratton IM, Adler AI, Neil HA, Matthews DR, Manley SE, Cull CA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ. 2000 Aug 12;321(7258):405–12.

 

Recommended Articles
Research Article Open Access
Study of prevalence of haemoglobin subtypes/variants in the ethnic population of Manipur
2026, Volume-7, Issue 1 : 2497-2500
Research Article Open Access
Prevalence of Rifampicin resistance detected by TrueNat assay in suspected pulmonary cases in a teritiary care hospital, Kurnool
2026, Volume-7, Issue 1 : 2492-2496
Research Article Open Access
Comparative Analgesic Efficacy of Intrathecal Fentanyl versus Intrathecal Midazolam as Adjuvants to Hyperbaric Bupivacaine for Elective Caesarean Section: A Randomized Double-Blinded Clinical Trial
2026, Volume-7, Issue 1 : 2477-2484
Research Article Open Access
Cancer Pattern at a Tertiary Care hospital in Pir Panjal (Rajouri & Poonch) region of Jammu and Kashmir
2026, Volume-7, Issue 1 : 2485-2491
International Journal of Medical and Pharmaceutical Research journal thumbnail
Volume-7, Issue 1
Citations
68 Views
69 Downloads
Share this article
License
Copyright (c) International Journal of Medical and Pharmaceutical Research
Creative Commons Attribution License Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
All papers should be submitted electronically. All submitted manuscripts must be original work that is not under submission at another journal or under consideration for publication in another form, such as a monograph or chapter of a book. Authors of submitted papers are obligated not to submit their paper for publication elsewhere until an editorial decision is rendered on their submission. Further, authors of accepted papers are prohibited from publishing the results in other publications that appear before the paper is published in the Journal unless they receive approval for doing so from the Editor-In-Chief.
IJMPR open access articles are licensed under a Creative Commons Attribution-ShareAlike 4.0 International License. This license lets the audience to give appropriate credit, provide a link to the license, and indicate if changes were made and if they remix, transform, or build upon the material, they must distribute contributions under the same license as the original.
Logo
International Journal of Medical and Pharmaceutical Research
About Us
The International Journal of Medical and Pharmaceutical Research (IJMPR) is an EMBASE (Elsevier)–indexed, open-access journal for high-quality medical, pharmaceutical, and clinical research.
Follow Us
facebook twitter linkedin mendeley research-gate
© Copyright | International Journal of Medical and Pharmaceutical Research | All Rights Reserved