# ROLE OF 02 TRANSPORT IN DETERMINING V02 MAX OF MUSCLE > **NIH NIH R01** · UNIVERSITY OF FLORIDA · 1990 · $78,845 ## Abstract This project addresses the general question of whether, in whole body exercise, maximal O2 uptake (V02max) really represents a specific limitation of O2 availability in the working muscle or whether some other factor intervenes. This question arises from observations that show whole body VO2max is elevated during exercise by hyperoxia and increased red cell concentration and decreased by modest hypoxia, while efforts to show parallel changes in working muscle VO2max have failed to show the expected response. However, these measurements are difficult to make in intact exercising animals, and studies using muscles in situ with isolated circulation have not achieved the highest VO2 the muscles can reach. This project will use the gastrocnemius- plantaris muscles of anesthetized dogs and cats with circulations isolated in situ. Two tetanic contraction modes will be used: 1) a 25 minute progessive format to VO2max, a model of progressive exercise, and 2) a 4 minute repetitive format, a model of a 4 minute maximal test. Each of the variables of O2 supply to the muscles, O2 tension (PaO2), O2 content (CaO2) and blood flow (Q) will be varied by 1) increasing or deceasing the fractions of O2 in inspired gas to values above and below room air (at sea level); 2) changing red cell mass by transfusing packed red cells or dextran for blood exchange and 3) changing flow. The specific aims are 1) to ascertain whether muscle VO2max in the progressive contractions is changed by whole body hyperoxia and hypoxia; 2) to determine if muscle V02max in the repetitive contractions is changed by whole body hyperoxia adn hypoxia; 3) to ascertain whether V02max of the muscles in both contraction types is changed by local hyperoxia and hypoxia produced by a small gas exchanger in the arterial supply of the muscles; 4) to see whether reperfusion of the muscle with its own venous blood with P02 restored to normoxic levels changes V02; 5) to establish whether muscles of the cat with a different fiber type composition respond the same as the main test muscle of the dog; and 6) to determine the O2 saturation of mitochondial cytochrome oxidase during contractions under the hyperoxic and hypoxic conditions. In addition to V02, CO2 output (Vco2), lactate output (L), muscle (lactate)/(pyruvate) and plasma epinephrine and norepinephrine will be measured. The results will show 1) whether whole body and local hyperoxia and hypoxia produce the same changes in Vo2max and whether a circulating factor is involved; 2) whether fatigue is a factor in the longer contraction format; 3) whether muscles of differing fiber types respond similarily; 4) whether metabolite washout is a factor and 5) when cytochrome oxidase becomes significantly desaturated. This last is the crucial measurement in determining the presence of specific O2 limitation of Vo2. ## Key facts - **NIH application ID:** 3159410 - **Project number:** 5R01AR039378-03 - **Recipient organization:** UNIVERSITY OF FLORIDA - **SAM.gov UEI:** NNFQH1JAPEP3 - **Principal Investigator:** WENDELL N STAINSBY - **Activity code:** R01 (R01, R21, SBIR, etc.) - **Funding institute:** NIH - **Fiscal year:** 1990 - **Award amount:** $78,845 - **Award type:** 5 - **Project period:** 1988-04-01 → 1992-03-31 ## Primary source NIH RePORTER: https://reporter.nih.gov/project-details/3159410 ## Citation > US National Institutes of Health, RePORTER application 3159410, ROLE OF 02 TRANSPORT IN DETERMINING V02 MAX OF MUSCLE (5R01AR039378-03). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3159410. Licensed CC0. --- *[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*