Journal of Applied Physiology AJP: Heart and Circulatory Physiology
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J Appl Physiol 105: 755-756, 2008; doi:10.1152/japplphysiol.90336.2008c
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POINT-COUNTERPOINT

Rebuttal from Drs. Aliverti and Macklem

We do not dispute the fact that dynamic hyperinflation and skeletal muscle myopathy are important factors limiting exercise in COPD. We suggest, however, that in the natural history of the disease an insufficient energy supply to respiratory and skeletal muscles to meet demand is the primary limiting factor occurring before dynamic hyperinflation and myopathy. The elegant study by Ofir et al. (4) on exercise performance in GOLD stage 1 patients with COPD supports our hypothesis. Although on average these patients hyperinflated during exercise, this evidently did not limit exercise as the inspiratory reserve volume (IRV) at peak exercise (Wmax) was 0.69 liters (±0.31 SD) compared to an IRV in a well-matched control group of 0.70 liters (±0.37 SD). Furthermore, the decrease in inspiratory capacity (IC) at Wmax had a large standard deviation (mean decrease in IC: –0.54 liters (±0.34 SD); with the 95% confidence limits of ±2 SD, some patients must have increased IC at Wmax or else the data were not normally distributed.

Disuse muscle atrophy was also an unlikely cause of limitation because the patients exercised as much during daily activities as controls.

On the other hand the exercise work rate at the ventilatory threshold, a parameter closely related to the anaerobic threshold when energy supplies are no longer adequate to meet demand, was significantly lower in COPD at 79 ± 13 W compared with 91 ± 32 W in the controls. Furthermore the minute ventilation per unit of oxygen consumption (VE/VO2) at the ventilatory threshold was increased in COPD 32.0 ± 5.2 vs. 27.7 ± 3.6 in controls.. The work and O2 cost of breathing (VO2resp) must also have been increased in the patients (2) due to the increased VE, frequency dependence of lung compliance (3), presumed expiratory flow-limitation causing dynamic hyperinflation, and the threshold load resulting from dynamic hyperinflation. Because the VO2/work rate was normal, but VO2resp increased, the delivery of O2 to working skeletal muscles must have been decreased and this would account for the early onset of metabolic acidosis due to competition between respiratory and skeletal muscles for the available energy supplies (1, 5). Indeed 81% of the COPD patients stopped exercise because of leg symptoms either alone or combined with dyspnea. Thus the low ventilatory threshold, the increased VO2resp, the normal VO2/work rate, and predominance of leg symptoms all indicate an early onset of an imbalance between energy supplies and demands to working skeletal and respiratory muscles that limited exercise in GOLD stage 1 COPD patients.

REFERENCES

  1. Harms CA, Babcock MA, McClaran SR, Pegelow DF, Nickele GA, Nelson WB, Dempsey JA. Respiratory muscle work compromises leg blood flow during maximal exercise. J Appl Physiol 82: 1573–1583, 1997.[Abstract/Free Full Text]
  2. Levison H, Cherniack RM. Ventilatory cost of exercise in chronic obstructive pulmonary disease. J Appl Physiol 25: 21–27, 1968.[Free Full Text]
  3. Mead J, Lindgren I, Gaensler EA. The mechanical properties of the lungs in emphysema. J Clin Invest 34: 1005–1016, 1955.[CrossRef][Web of Science][Medline]
  4. Ofir D, Laveneziana P, Webb KA, Lam YM, O'Donnell DE. Mechanisms of dyspnea during cycle exercise in symptomatic patients with GOLD stage I COPD. Am J Respir Crit Care Med 177: 622–629, 2008.[Abstract/Free Full Text]
  5. Roussos C, Macklem PT. The respiratory muscles. N Engl J Med 307: 786–797, 1982.[Web of Science][Medline]



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S. H. Loring, M. Garcia-Jacques, and A. Malhotra
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J Appl Physiol, July 1, 2009; 107(1): 309 - 314.
[Abstract] [Full Text] [PDF]

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