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LETTERS TO THE EDITOR
Exercise Physiology Laboratory
Department of Integrative Biology
University of California
Berkeley, CA 94720-3140
e-mail: gbrooks{at}berkeley.edu
The following is the abstract of the article discussed in the subsequent letter:
The aim of this study was to determine whether the decreased muscle and blood lactate during exercise with hyperoxia (60% inspired O2) vs. room air is due to decreased muscle glycogenolysis, leading to decreased pyruvate and lactate production and efflux. We measured pyruvate oxidation via PDH, muscle pyruvate and lactate accumulation, and lactate and pyruvate efflux to estimate total pyruvate and lactate production during exercise. We hypothesized that 60% O2 would decrease muscle glycogenolysis, resulting in decreased pyruvate and lactate contents, leading to decreased muscle pyruvate and lactate release with no change in PDH activity. Seven active male subjects cycled for 40 min at 70% 
O2 peak on two occasions when breathing 21 or 60% O2. Arterial and femoral venous blood samples and blood flow measurements were obtained throughout exercise, and muscle biopsies were taken at rest and after 10, 20, and 40 min of exercise. Hyperoxia had no effect on leg O2 delivery, O2 uptake, or RQ during exercise. Muscle glycogenolysis was reduced by 16% with hyperoxia (267 ± 19 vs. 317 ± 21 mmol/kg dry wt), translating into a significant, 15% reduction in total pyruvate production over the 40-min exercise period. Decreased pyruvate production during hyperoxia had no effect on PDH activity (pyruvate oxidation) but significantly decreased lactate accumulation (60%: 22.6 ± 6.4 vs. 21%: 31.3 ± 8.7 mmol/kg dry wt), lactate efflux, and total lactate production over 40 min of cycling. Decreased glycogenolysis in hyperoxia was related to an 
44% lower epinephrine concentration and an attenuated accumulation of potent phosphorylase activators ADPf and AMPf during exercise. Greater phosphorylation potential during hyperoxia was related to a significantly diminished rate of PCr utilization. The tighter metabolic match between pyruvate production and oxidation resulted in a decrease in total lactate production and efflux over 40 min of exercise during hyperoxia.
Pyruvate metabolism in working human skeletal muscle
To the editor:
We consider studies of muscle energy substrate metabolism, particularly with regard to the partitioning of fuels exchanged across a tissue bed and those utilized within it, to be important. Consequently, we continually look forward to seeing the contributions of others to the body of knowledge. There are few data sets describing pyruvate exchange across working muscle beds, and reports that do exist are from studies of varying designs and provide differing results (1, 3, 4). Therefore, any contribution to this literature should be important in that it ought to help form a model regarding carbohydrate metabolism in working muscle. Regrettably, the recent paper of Stellingwerff et al. (5) is an exception because, in their unjustified portrayal of our findings (3), the authors demonstrated inability to grasp essential physiological concepts and objectively interpret the literature.
Stellingwerff et al. failed to recognize that, in important ways, their results corroborated ours. For instance, we (3) and they (5) both showed that pyruvate net release by the working limb during exercise may be far greater than previously shown (1, 4) and that femoral venous pyruvate concentration is much larger than arterial pyruvate concentration during sustained exercise. However, the authors did not focus on those findings, but rather they appear to have been most concerned with the ratio of pyruvate net release to lactate net release. Strangely, the authors likened their results to those of Lundgren et al. (4), who showed net pyruvate uptake (not release) during 2.5 min of foot pedal ergometry, and to those of Ahlborg and Felig (1), who showed an order of magnitude less pyruvate net release than we or Stellingwerff et al. showed. Nonetheless, Stellingwerff et al. asserted that our findings (3) "are erroneous and at odds with the majority of published results." According to them, this "majority of published results" seems to consist of two reports of different experimental designs, opposite results, and data discrepant from their own.
Stellingwerff et al. (5) were careless in reading our paper. In our report (3) we measured blood pyruvate by two methods, and we were explicit in stating that the metabolite exchange data were determined on a single leg and extrapolated to both legs during cycling exercise. In contrast, Stellingwerff et al. neither referenced the method of blood pyruvate determination nor gave sufficient information to know whether data were representative of one or both exercising legs. Yet they reported difficulty in understanding our paper (3) because they could not find our lactate concentration and lactate net release data. Stellingwerff et al. wrote, "The differences in pyruvate vs. lactate releases between the present study and Henderson et al. are not readily apparent and are difficult to ascertain, because the former study does not report arterial or venous lactate concentration or lactate efflux data but only reports lactate to pyruvate ratios." However, in contrast to their portrayal of our report, in Henderson et al. (3), we did reiterate lactate net release data from our previous findings in Fig. 8, and we did reference our companion paper (2) containing the original lactate concentration and turnover data.
To justify a perceived discrepancy between their pyruvate and lactate net release data (5) and ours (3), Stellingwerff et al. stated, "The most likely explanation was that the [3-13C]lactate tracer that was used to make some of their essential calculations has been proposed to overestimate lactate production and removal." Remarkably, the reference for that statement comes from an unsubstantiated 1987 letter to the editor. The interpretation by Stellingwerff et al. in this respect is most fanciful because physiologists know that tracer data are not used to calculate metabolite net exchange. Moreover, and more egregiously irrelevant and incorrect, Stellingwerff et al. attributed perceived differences between their and our data sets to isotopic exchange reactions and tracer dilution within the TCA cycle. Again, this is all very confusing because net release rates do not involve the use of tracer data; net tissue exchange is the product of blood flow and (a-v) concentration difference. Hence, the only conclusion possible is that Stellingwerff et al. understood neither their calculations nor ours. Although we would have hoped that the work of Stellingwerff et al. would add to a growing understanding of pyruvate metabolism in working muscle, their report is tainted by their misinterpretation of the literature and methods used to measure metabolite kinetics.
REFERENCES
This article has been cited by other articles:
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  T. Stellingwerff, G. J. F. Heigenhauser, and L. L. Spriet Reply to letter "Pyruvate metabolism in working human skeletal muscle" by Henderson et al. Am J Physiol Endocrinol Metab, April 1, 2007; 292(4): E1238 - E1239. [Full Text] [PDF]
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