Abstract

The effect of added respiratory work on leg muscle oxygenation during constant-load cycle ergometry was examined in six healthy adults. Exercise was initiated from a baseline of 20 W and increased to a power output corresponding to 90% of the estimated lactate threshold (moderate exercise) and to a power output yielding a tolerance limit of 11.8 min (+/- 1.4, S.D.) (heavy exercise). Ventilation and pulmonary gas exchange were measured breath-by-breath. Profiles of leg muscle oxygenation were determined throughout the protocol using near-infrared (NIR) spectroscopy (Hamamatsu NIRO 500) with optodes aligned midway along the vastus lateralis of the dominant leg. Four conditions were tested: (i) control (Con) where the subjects breathed spontaneously throughout, (ii) controlled breathing (Con Br) where breathing frequency and tidal volume were matched to the Con profile, (iii) increased work of breathing (Resist Br) in which a resistance of 7 cmH2O l(-1) s(-1) was inserted into the mouthpiece assembly, and (iv) partial leg blood flow occlusion (Leg Occl), where muscle perfusion was reduced by inflating a pressure cuff (approximately 90 mmHg) around the upper right thigh. During Resist Br and Leg Occl, subjects controlled their breathing pattern to reproduce the ventilatory profile of Con. An approximately 3 min period with respiratory resistance or pressure cuff was introduced approximately 4 min after exercise onset. NIR spectroscopy data for reduced haemoglobin-myoglobin (delta[Hb]) were extracted from the continuous display at specific times prior to, during and after removal of the resistance or pressure cuff. While the delta[Hb] increased during moderate- and heavy-intensity exercise, there was no additional increase in delta[Hb] with Resist Br. In contrast, delta[Hb] increased further with Leg Occl, reflecting increased muscle O2 extraction during the period of reduced muscle blood flow. In conclusion, increasing the work of breathing did not increase leg muscle deoxygenation during heavy exercise. Assuming that leg muscle O2 consumption did not decrease, this implies that leg blood flow was not reduced consequent to a redistribution of flow away from the working leg muscle.

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