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J Appl Physiol 83: 2167-2168, 1997;
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Vol. 83, Issue 6, 2167-2168, December 1997


LETTERS TO THE EDITOR
Letters to the Editor

ABSTRACT
LETTER
REFERENCES
REPLY
REFERENCES


ABSTRACT

The following is the abstract of the article discussed in the subsequent letter:

Batterham, Alan M., Keith Tolfrey, and Keith P. George. Nevill's explanation of Kleiber's 0.75 mass exponent: an artifact of collinearity problems in least squares models? J. Appl. Physiol. 82(2): 693-697, 1997.---Intraspecific allometric modeling (Y = a · massb, where Y is the physiological dependent variable and a is the proportionality coefficient) of peak oxygen uptake (VO2peak) has frequently revealed a mass exponent (b) greater than that predicted from dimensionality theory, approximating Kleiber's 3/4 exponent for basal metabolic rate. Nevill (J. Appl. Physiol. 77: 2870-2873, 1994) proposed an explanation and a method that restores the inflated exponent to the anticipated 2/3. In human subjects, the method involves the addition of "stature" as a continuous predictor variable in a multiple log-linear regression model: ln Y = ln a + c · ln stature + b · ln mass + ln epsilon , where c is the general body size exponent and epsilon  is the error term. It is likely that serious collinearity confounds may adversely affect the reliability and validity of the model. The aim of this study was to critically examine Nevill's method in modeling VO2peak in prepubertal, teenage, and adult men. A mean exponent of 0.81 (95% confidence interval, 0.65-0.97) was found when scaling by mass alone. Nevill's method reduced the mean mass exponent to 0.67 (95% confidence interval, 0.44-0.9). However, variance inflation factors and tolerance for the log-transformed stature and mass variables exceeded published criteria for severe collinearity. Principal components analysis also diagnosed severe collinearity in two principal components, with condition indexes >30 and variance decomposition proportions exceeding 50% for two regression coefficients. The derived exponents may thus be numerically inaccurate and unstable. In conclusion, the restoration of the mean mass exponent to the anticipated 2/3 may be a fortuitous statistical artifact.


LETTER

Collinearity: A Function of the Sample Size, Range, and Similarity of Observations

To the Editor: I wish to express my surprise that the Journal of Applied Physiology decided to publish the paper by Batterham et al. (2) entitled "Nevill's explanation of Kleiber's 0.75 mass exponent: an artifact of collinearity problems in least squares models?". Based on a sample size of n = 75 (prepubertal, teenage, and adult males), the authors examined how peak oxygen uptake (VO2; 1 min) might be scaled for differences in body size. Although the study confirms the work of Nevill (8) that an inflated mass exponent occurs (0.81) if mass alone is used to scale peak VO2, the authors are concerned that by including stature in addition to mass as a second covariate, the result may lead to collinearity.

The authors' concerns are unfounded. There are numerous examples in the literature when both height and weight have been used to predict various dependent variables, e.g., body fat (1, 5, 7), blood pressure (6, 9), and the dependent variable of interest, peak VO2 (3, 8, 10, and unpublished observations of Nevill and Holder). In all these papers, the contributions of height and weight were both significant, and no collinearity was reported. For example, when blood pressure was used as the dependent variable (see Refs. 6, 9), the contributions from both height and weight provided highly significant exponents (P < 0.0001) but with opposite signs, i.e., predicting a stature-adjusted weight index (approximately the body mass index ratio) as a measure of "overweight."

There also exists overwhelming evidence that both height and weight are necessary when predicting peak VO2, i.e., taller subjects have significantly greater peak VO2, having already controlled for differences in body weight (3, 8, 10, and unpublished observations of Nevill and Holder). The sample sizes used in these studies were as follows; Baxter Jones et al. (3), n = 453 young elite athletes (231 men and 222 women); Welsman et al. (10), n = 156 school children (73 boys and 83 girls), and Nevill and Holder (unpublished observations), n = 1,732 adults, age 16 yr and over (852 men and 880 women). The strength of collinearity observed in Batterham et al. (2) (sample size n = 75) may be a function of the sample size and the range and similarity of observations (4), a problem more evident in Batterham et al. (2) than in the studies of Baxter-Jones et al. (3), Nevill (8), Welsman et al. (10), and Nevill and Holder (unpublished observations).

Nevill (8) suggested that the significant contribution of height in addition to body weight might be explained by a disproportionate increase in muscle mass with body size. However, based on the unpublished findings of Nevill and Holder, an alternative explanation now becomes apparent. The best model to predict maximal VO2 incorporated a significant contribution from forced vital capacity (FVC; also known to be predominately stature related) as well as body mass, whereas the height term became redundant, no longer making a significant contribution to the regression model. Clearly, on the basis of these findings, the apparent advantage of being taller would appear to be more accurately explained by the subjects' greater FVC. In effect, the significant contribution of the height term, found in the earlier studies (3, 8, 10), would appear to have been inadvertently providing an estimate of the subjects' FVC. This was an unexpected result, although not entirely surprising. Taking the analogy with the motor car engine, we would expect a greater performance (maximum speed and power output) from an engine with a greater cubic capacity, so perhaps we might also expect a greater maximum VO2 from a subject with a greater (forced) vital capacity.


REFERENCES

1. Abdel-Malek, A. K., D. Mukherjee, and A. F. Roche. A method of constructing an index of obesity. Human Biol. 57: 415-430, 1985[Medline].
2. Batterham, A. M., K. Tolfrey, and K. P. George. Nevill's explanation of Kleiber's 0.75 mass exponent: an artifact of collinearity problems in least squares models? J. Appl. Physiol. 82: 693-697, 1997[Abstract/Free Full Text].
3. Baxter-Jones, A., H. Goldstein, and P. Helms. The development of aerobic power in young athletes. J. Appl. Physiol. 75: 1160-1167, 1993[Abstract/Free Full Text].
4. Belsley, D. A., E. Kuh, and R. E. Welsch. Regression Diagnostic: Identifying Influential Data and Sources of Collinearity. New York: Wiley, 1980.
5. Benn, R. T. Some mathematical properties of weight-for-height indices used as measures of adiposity. Br. J. Prev. Soc. Med. 25: 42-50, 1971[Medline].
6. Fentem, P. H., A. M. Nevill, and R. H. Holder. Physical activity and arterial blood pressure. Med. Sci. Sport Exerc. 28: 112S, 1996.
7. Garrow, J. S., and J. Webster. Quetelet's index (W/H2) as a measure of fatness. Int. J. Obes. 9: 147-153, 1985[Medline].
8. Nevill, A. M. The need to scale for differences in body size and mass: an explanation of Kleiber's 0.75 mass exponent. J. Appl Physiol. 77: 2870-2873, 1994[Abstract/Free Full Text].
9. Nevill, A. M., R. L. Holder, P. H. Fentem, M. Rayson, T. Marshall, C. B. Cooke, and W. Tuxworth. Modelling the associations of BMI, physical activity and diet with arterial blood pressure; some results from the Allied Dunbar national fitness survey. Ann. Human Biol. 24: 229-247, 1997[Medline].
10. Welsman, J. R., N. Armstrong, A. M. Nevill, E. M. Winter, and B. J. Kirby. Scaling peak VO2 for differences in body size. Med. Sci. Sports Exerc. 28: 259-265, 1996[Medline].

0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society




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