Abstract
Introduction Assessments of dynamic changes in recovery respiratory kinetics following resistance exercise can provide information on the control and regulation of O2 transport and utilization. An important parameter in this context is the arterio-venous difference in O2concentration (avDO2). The avDO2 measured by respiratory oxygen uptake (V’O2) and cardiac output (CO) may be used as an indicator of the synchronization of muscle perfusion and muscular O2 demands. Moreover, the delay between offset in exercise and changes in the avDO2 can be used as an indicator of transport delays between muscle and lungs. Methods Thirteen healthy male subjects aged 26.9±3.1 years, performed a 20-repetition isokinetic (combined, concentric and eccentric) arm or leg exercise protocol at 60 deg/s, 150 deg/s, and 240 deg/s, in randomized order. Recovery (150 seconds) breath-by-breath V’O2 and beat-to-beat CO by impedance cardiography were recorded to determine post-exercise avDO2. Statistical analysis for the peaks of avDO2 (see below) were analyzed for amplitude and maximum time via a two-way (factors: ‘limb’ × ‘speed’) ANOVA for repeated measurements. Results The first peak was identified in 76 of 78 cases. Amplitudes of the first peak (mL/L) ranged from 186 (SD 52) at 60 deg/s to 174 (SD 32) at 240 deg/s for the arms; 174 (SD 32) at 60 deg/s to 179 (SD 42) for the leg exercise. Time to attain the first peak ranged from 7.2s at 60 deg/s to 6.8s at 240 deg/s for the arms; 8.2s at 60 deg/s to 5.6s at 240 deg/s for the legs. There were no significant between factors differences for the first amplitude of the avDO2 curves. These first peaks were significantly influenced (P=0.032) by muscle mass (i.e. arm versus leg) involved. A second avDO2 peak was identified in 45 of 78 cases. Since there was no systematic pattern of distribution of these second wavef orms across the testing conditions, no further analyses were conducted. Discussion It can be assumed that the restriction of muscle blood flow during sets of concentric-eccentric contractions inhibits aerobic metabolism at the end of this phase. At the onset of recovery, the first avDO2 wave is caused by the arrival of O2 desaturated blood from the muscle to the lungs. This delay results from the occlusion of venous volume and blood flow within the active musculature. Therefore, the second avDO2 ‘wave represents this imbalance in perfusion during recovery. This delay between the offset in exercise and changes in the avDO2 can be used to gauge transport delays between the muscular and pulmonary sites.
References Cunningham D, St Croix,C, Paterson D., Özyener F, Whipp B.( 2000). Exp. Physiol. 85, 339-347.
Haseler L, Hogan M, Richardson R. (1999). J. Appl. Physiol. 86, 2013-2018.
Lai N, Nasca M, Silva M, Silva F, Whipp B, Cabrera M. (2008). Appl. Physiol. Nutr. Metab. 33, 107-117. Linnarsson D. (1974). Acta Physiol. Scand. 415, 4-68.
References Cunningham D, St Croix,C, Paterson D., Özyener F, Whipp B.( 2000). Exp. Physiol. 85, 339-347.
Haseler L, Hogan M, Richardson R. (1999). J. Appl. Physiol. 86, 2013-2018.
Lai N, Nasca M, Silva M, Silva F, Whipp B, Cabrera M. (2008). Appl. Physiol. Nutr. Metab. 33, 107-117. Linnarsson D. (1974). Acta Physiol. Scand. 415, 4-68.
Originalsprache | Englisch |
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Titel | Book of abstracts. 18th annual ECSS Congress of the European College of Sport Science |
Erscheinungsdatum | 2013 |
ISBN (elektronisch) | 978-84-695-7786-8 |
Publikationsstatus | Veröffentlicht - 2013 |
Veranstaltung | Annual Congress of the European College of Sport Science - Barcelona, Spanien Dauer: 26.06.2013 → 29.06.2013 Konferenznummer: 18 |