|
 
 |
| ORIGINAL ARTICLE |
|
| Year : 2017 | Volume
: 8
| Issue : 1 | Page : 19-23 |
|
Relation of peak expiratory flow rate to body mass index in young adults
Sunil Kumar Jena, Meena Mirdha, Purnima Meher, Akshaya Kumar Misra
Department of Physiology, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Odisha, India
| Date of Web Publication | 2-Feb-2017 |
Correspondence Address:
Sunil Kumar Jena
Department of Physiology, Veer Surendra Sai Institute of Medical Sciences and Research, Burla - 768 017, Odisha
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0975-9727.199369
Background: Peak expiratory flow rate (PEFR) is a measure of airflow in bronchial tree and it provides idea of bronchial tone. It is affected by age, sex, height, body weight, and other physical activity. There is evidence that obesity has a link to bronchial hyperresponsiveness. Thus, we proposed this study to find out the relation between PEFR and body mass index (BMI). Materials and Methods: In this study, 56 male and 49 female young subjects (total = 105) were recruited. As sex is a definite factor for variation in PEFR, subjects were classified into normal (BMI = 18–24.99 kg/m2), over weight (BMI = 25–29.99 kg/m2), and obese (BMI = 30–34.99 kg/m2) separately for both male and female. After written consent, PEFR of each subject was recorded between 7 and 8 am. Then, data analysis was done by one-way ANOVA, Pearson correlation, and regression analysis. Results: In male subjects, the mean difference of PEFR of normal, over weight, and obese subjects were 498 L/min, 488 L/min, and 391 L/min, respectively, which is statistically significant (P = 0.000). In female subjects, the mean difference of PEFR of normal, over weight, and obese subjects were 377 L/min, 348 L/min, and 325 L/min, respectively, which is statistically significant (P = 0.002). Pearson correlation showed negative correlation between BMI and PEFR both in male (r = −0.512) and in female (r = −0.539). Conclusion: This study concluded that PEFR declines with increase in BMI, and there is negative correlation between BMI and PEFR. Keywords: Body mass index, bronchial tone, peak expiratory flow rate
How to cite this article:
Jena SK, Mirdha M, Meher P, Misra AK. Relation of peak expiratory flow rate to body mass index in young adults. Muller J Med Sci Res 2017;8:19-23 |
How to cite this URL:
Jena SK, Mirdha M, Meher P, Misra AK. Relation of peak expiratory flow rate to body mass index in young adults. Muller J Med Sci Res [serial online] 2017 [cited 2023 Jun 4];8:19-23. Available from: https://www.mjmsr.net/text.asp?2017/8/1/19/199369 |
| Introduction | |  |
The peak expiratory flow rate (PEFR) is defined as the maximum or peak flow rate that is attained during a forceful expiratory effort after taking a deep inspiration. It is expressed in liters per minute. It measures airflow through the bronchial tree and provide an idea about bronchial tone. Pulmonary functions are usually determined by respiratory muscle strength, compliance of the thoracic cavity, airway resistance, and elastic recoil of the lungs.[1] It is well known that pulmonary functions may vary according to the physical characteristics including age, height, and body weight.[2] For demonstrating the bronchial tone, different expiratory flow rates are employed. PEFR is one such parameter that can be easily measured by a peak flow meter and is a convenient tool to measure lung functions in a field study.[3] It is considered as a good indicator of bronchial hyperresponsiveness and does not require body temperature pressure saturated correction.[4] The PEFR values are also affected by various other factors, such as sex, body surface area, obesity, physical activity, posture, environment, and racial differences.[5],[6],[7] The average PEFR of healthy young Indian males and females is around 500 and 350 L/min, respectively.[8] Obesity has been linked with impaired pulmonary function and airway hyperresponsiveness.[9],[10] Different studies of PEFR have been done with respect to age, sex, height, and weight, but fewer studies have done with body mass index (BMI). Thus, this study was proposed to observe the change in PEFR with respect to BMI and find the relationship between BMI and PEFR.
| Materials and Methods | | |
This study was conducted in the Department of Physiology, Veer Surendra Sai Institute of Medical Sciences and Research, Burla, Sambalpur, Odisha, India. The study was carried out from March 2015 to February 2016 after getting ethical approval from Veer Surendra Sai Institutional Research and Ethics Committee. This was a comparative study in which healthy young adults were recruited as the subjects. Total 105 subjects were selected which included 56 male and 49 female. All subjects were between ages 18 and 24 years. For selection of subject, general health checkup as well as different systemic examinations were done. Only healthy and nonsmoker young adults were selected for this study. Persons having any systemic disease, pulmonary disease, and smoking history were excluded from study.
After review of different literatures, we found that there is strong evidence of sex variation of PEFR. Thus, we classified all subjects into male and female categories to analyze data separately for both sex. After the selection of subjects, they were explained properly about the purpose and output of the study. Written consent was taken from each subject before doing the experimental procedures. Basic demographic data such as age and sex was recorded. Weight of the subjects was recorded by weighing machine (VIRGO Model no 9811 B). Height was measured by measuring tape. For calculation of BMI, height and weight was used (BMI = weight in kg/height in m 2). Subjects were classified into three groups according to their BMI separately for male and female, i.e., normal (BMI = 18–24.99 kg/m 2), over weight (BMI = 25–29.99 kg/m 2), and obese (BMI = 30–34.99 kg/m 2).
The PEFR was recorded by Mini Wright Peak Flow meter (Soulgenie portable peak flow meter). Before recording the PEFR, first, the subjects were trained about the recording procedure of PEFR. For accuracy of methodology, training was essential because PEFR is a subjective method, proper training, and cooperation of subjects was highly valuable. After proper training, recording of PEFR was done for each subject between 7 and 8 am. Each subject was instructed to stand erect and hold the instrument in horizontal position. Precaution was taken to avoid the obstruction of the pointer by fingers while moving in the slot. They were instructed to take a deep breath, put the mouthpiece of the peak flow meter inside mouth between the upper and lower jaw, and expel the air forcefully in one blow. Like this at a time, each subject was asked to perform the test 3 times, and the highest PEFR value was recorded for data analysis.
Statistical analysis was done for both male and female separately. One-way ANOVA was used to compare the mean PEFR in different BMI. Pearson correlation and Linear Regression Analysis were used to find out the relationship between PEFR and BMI. P < 0.05 was considered to be statistically significant. Microsoft excel and word was used for designing the tables.
| Results | | |
In this study, the researchers focused to establish the relation between BMI and PEFR. The result was analyzed separately for both male and female as sex is an established factor for variation in PEFR. [Table 1] depicts the mean and standard deviation (SD) of different parameters in male and female subjects. The mean height of male was 168.4 cm and female was 156.4 cm. The mean weight of male was 66.5 kg and female was 58.1 kg. The mean BMI of male was 23.4 kg/m 2 and female was 24.2 kg/m 2. Mean PEFR in male was 469 L/min and female was 365 L/min.
[Table 2] depicts the variation in PEFR in different BMI. The data were analyzed by one-way ANOVA test separately for both male and female. In male subjects, the mean and SD of PEFR of normal, over weight, and obese subjects were 498 ± 52 L/min, 488 ± 50 L/min, and 391 ± 48 L/min, respectively. This variation in PEFR between different group of subjects was found statistically significant (P = 0.000). Detail study with post hoc analysis as shown in [Table 3] found that difference in PEFR between normal and overweight subjects was not statistically significant (P = 0.541), difference in PEFR between normal and overweight subjects was statistically significant (P = 0.000), and difference in PEFR between overweight and obese subjects was statistically significant (P = 0.000). In female subjects, the mean and SD of PEFR of normal, over weight, and obese subjects were 377 ± 37 L/min, 348 ± 39 L/min, and 325 ± 12 L/min, respectively. This variation in PEFR between different group of subjects was found statistically significant (P = 0.002). Detail study with post hoc analysis as shown in [Table 3] found that difference in PEFR between normal and overweight subjects was statistically significant (P = 0.043), difference in PEFR between normal and overweight subjects was statistically significant (P = 0.000), difference in PEFR between overweight and obese subjects was not statistically significant (P = 0.215).
[Table 4] shows the correlation between BMI and PEFR in male and female. In this study, we found negative correlation between MBI and PEFR both in male and female. In male subjects, the Pearson correlation coefficient (r) was −0.512 (P = 0.000), and in female subjects, the Pearson correlation coefficient (r) was − 0.539 (P = 0.000).
[Table 5] depicts the linear regression analysis between BMI and PEFR. It shows that BMI affects PEFR in male and female both. In male, R is 0.512, R2 is 0.262, and adjusted R2 is 0.249. Thus, BMI as an independent predictor predicts only 24.9% of variability, which is statistically significant (P = 0.000). Unstandardized coefficient B is − 6.46 suggested that each unit increase in BMI lead to 6.64 unit decrease in PEFR. In female, R is 0.539, R2 is 0.291, and adjusted R2 is 0.276. Thus, BMI as an independent predictor predicts only 27.6% of variability which is statistically significant (P = 0.000). Unstandardized coefficient B is −5.30 suggested that each unit increase in BMI lead to 5.30 unit decrease in PEFR.
| Discussion | | |
The principal factor that affects PEFR is airway diameter primarily under the control of bronchial tone. Other factors that affect PEFR are the strength of expiratory muscles and elastic recoil of lungs.[11] There is a relationship between height, weight, chest circumferences with PEFR. PEFR is an important diagnostic and prognostic tool of lung functions which predicts variations in airflow. Our aim was to establish whether BMI can be considered as a predictor of PEFR. The major findings that we found in this study were (1) statistically significant difference in PEFR between normal (BMI = 18–24.99 kg/m 2), over weight (BMI = 25–29.99 kg/m 2), and obese individuals (BMI = 30–34.99 kg/m 2) (2) negative correlation between BMI and PEFR.
In this study, we found that BMI independently affects PEFR both in male female subjects of younger age group. Similar study was done by different researchers, and they found BMI and PEFR was negatively correlated in elderly (>40 years) age group persons.[12],[13],[14],[15] In our study, we found similar result in younger (<30 years) age group subjects.
In the study conducted by Chinn et al. on young adults found evidence of linearity in relation of slope to BMI.[4] The “Slope” declined with increasing BMI in males, that is, bronchial hyperresponsiveness increased. Similar result was found in this study. In the study conducted by Carey et al. on obese healthy subjects suggests that both total respiratory resistance and airway resistance increased significantly with the level of obesity, disclosing a statistically significant linear relationship between airway conduction and functional residual capacity (FRC).[16] In younger age group, i.e., <30 years of age PEFR shows some statistically significant declining trend with higher BMI. It could be explained through several possible mechanisms such as mechanical effects on the diaphragm and fat deposition between the muscles and the ribs that can lead to increase in the metabolic demands and work load of breathing.[14]
In the obese patient, the tidal volume (TV) and FRC are decreased due to changes in elastic properties of the chest wall.[17],[18] Retractile forces of the lung parenchyma on the airways are reduced at low lung volume. At low FRC, the airway smooth muscle may be unloaded with a paradoxical increased shortness in response to normal parasympathetic tone or to other bronchial-constricting agents.[19] Thus, it has been hypothesized that in obese patients, breathing at low TV does not allow the normal stretching of airway smooth muscle during breathing, which causes the detachment of actin – myosin crossbridge of the airway smooth muscle. The bigger the TV, the greater the ensuing bronchial dilation.[20] This fact, known as “deep inhalation effect,” allows restoration of the dilation of the airways in normal conditions. This protective effect is reduced in obese individuals in comparison to lean subjects.[21],[22] Therefore, the net result of airway narrowing occurs in obese subjects. Other mechanical factors may involve is due to the repeated chronic small airway closure observed in many obese subjects breathing at low TV. Repeated opening and closing of peripheral airways may determine the rupture of alveolar attachments to bronchioles that lead to exacerbation of the airway narrowing.[23] It has been well established that obesity is also characterized by low-grade systemic inflammation that spills over into the blood of a series of mediators, known as adipokines, which induce an inflammatory activated state in organs distant to adipose tissue. Adipokines include interleukin-6, tumor necrosis factor-α, eotaxin, vascular endothelial growth factor, and monocyte chemotactic protein that have been associated with asthma and may have a role in the common state of inflammation.[17] These inflammatory mediators may involve in airway narrowing, leading to decrease in PEFR.
In this study, we found low PEFR in both over weight and obese subjects in comparison to normal subjects. This signified that with increase in BMI, there was decrease in PEFR. Previous studies shown low PEFR in obese subjects, but in this study, we found low PEFR both in over weight and obese subjects both in male and female. This evidence may be correlated with more chance of asthma attack in over weight and obese subjects, i.e., in higher BMI.
| Conclusion | | |
This study concludes that with increase BMI, the PEFR decreases which signifies that there is bronchoconstriction due to various mechanisms as discussed above. Thus, in subjects of high BMI the chance of bronchial asthma is more. Therefore, we advised and counseled the subjects regarding the adverse effect of high BMI and to practice regular weight loss by regular exercise and suitable diet pattern to live free of asthma.
Acknowledgments
It is the pleasure to acknowledge the subjects involved in this study without whom the study was not accomplished. We are very much thankful to students Ankita Pal and Tusharkanti Sahoo for their cooperation toward this work.
Financial Support and Sponsorship
Nil.
Conflicts of Interest
There are no conflicts of interest.
| References | | |
| 1. | Cotes JE. Lung Function Assessment and Application in Medicine. 3 rd ed. Oxford: Blackwell Scientific Publications; 1975. p. 281-7.  |
| 2. | Polgar G, Weng TR. The functional development of the respiratory system. Am Rev Respir Dis 1979;170:625-95. |
| 3. | Wright BM, McKerrow CB. Maximum forced expiratory flow rate as a measure of ventilatory capacity: With a description of a new portable instrument for measuring it. Br Med J 1959;2:1041-6. |
| 4. | Chinn S, Jarvis D, Burney P; European Community Respiratory Health Survey. Relation of bronchial responsiveness to body mass index in the ECRHS. European Community Respiratory Health Survey. Thora×2002;57:1028-33. |
| 5. | Benjaponpitak S, Direkwattanachai C, Kraisarin C, Sasisakulporn C. Peak expiratory flow rate values of students in Bangkok. J Med Assoc Thai 1999;82 Suppl 1:S137-43. |
| 6. | Srinivas P, Chia YC, Poi PJ, Ebrahim S. Peak expiratory flow rate in elderly Malaysians. Med J Malaysia 1999;54:11-21. |
| 7. | Raju PS, Prasad KV, Ramana YV, Murthy KJ. Pulmonary function tests in Indian girls – Prediction equations. Indian J Pediatr 2004;71:893-7. |
| 8. | Dikshit MB, Raje S, Agrawal MJ. Lung functions with spirometry: An Indian perspective – I. Peak expiratory flow rates. Indian J Physiol Pharmacol 2005;49:8-18. |
| 9. | Gibson GJ. Obesity, respiratory function and breathlessness. Thorax 2000;55 Suppl 1:S41-4. |
| 10. | Rubinstein I, Zamel N, DuBarry L, Hoffstein V. Airflow limitation in morbidly obese, nonsmoking men. Ann Intern Med 1990;112:828-32. |
| 11. | Sahebjami H. Dyspnea in obese healthy men. Chest 1998;114:1373-7. |
| 12. | Mahajan KK, Mahajan SK, Maini BK, Srivastava SC. Peak expiratory flow rate and its prediction formulae in Haryanvis. Indian J Physiol Pharmacol 1984;28:319-25. |
| 13. | Jepegnanam V, Amritharaj G, Damodarasamy S, Madhusudanrao V. Peak expiratory flow rate in random healthy population of Coimbatore. Ind J Physiol Pharmacol 1996;40:127-33. |
| 14. | Saxena Y, Purwar B, Upmanyu R. Adiposity: Determinant of peak expiratory flow rate in young Indian adults male. Indian J Chest Dis Allied Sci 2011;53:29-33. |
| 15. | Paul J, Price K, Arthur N, Macstephen AO. Correlation between body mass index and peak expiratory flow rate of an indigenous Nigerian population in the Niger delta region. Res J Recent Sci 2013;2:28-32. |
| 16. | Carey IM, Cook DG, Strachan DP. The effects of adiposity and weight change on forced expiratory volume decline in a longitudinal study of adults. Int J Obes Relat Metab Disord 1999;23:979-85. |
| 17. | Shore SA. Obesity and asthma: Possible mechanisms. J Allergy Clin Immunol 2008;121:1087-93. |
| 18. | Naimark A, Cherniack RM. Compliance of the respiratory system and its components in health and obesity. J Appl Physiol 1960;15:377-82. |
| 19. | Shore SA, Johnston RA. Obesity and asthma. Pharmacol Ther 2006;110:83-102. |
| 20. | Gump A, Haughney L, Fredberg J. Relaxation of activated airway smooth muscle: Relative potency of isoproterenol vs. tidal stretch. J Appl Physiol 2001;90:2306-10. |
| 21. | Boulet LP, Turcotte H, Boulet G, Simard B, Robichaud P. Deep inspiration avoidance and airway response to methacholine: Influence of body mass index. Can Respir J 2005;12:371-6. |
| 22. | Crimi E, Pellegrino R, Milanese M, Brusasco V. Deep breaths, methacholine, and airway narrowing in healthy and mild asthmatic subjects. J Appl Physiol 2002;93:1384-90. |
| 23. | Milic-Emili J, Torchio R, D'Angelo E. Closing volume: A reappraisal. J Appl Physiol 2007;99:567-83. |
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]
|
Search Pubmed for