Calf muscle oxygen saturation and the effects of supervised exercise training for intermittent claudication

Objective: The mechanisms underlying the symptomatic improvement witnessed as a result of exercise training in intermittent claudication remain unclear. There is no reproducible evidence to support increased limb blood flow resulting from neovascularization. Changes in oxygenation of active muscles as a result of blood redistribution are hypothesized but unproven. This study sought evidence of improved gastrocnemius oxygenation resulting from exercise training. Methods: The study recruited 42 individuals with claudication. After an initial control period of exercise advice, participants undertook a 3-month supervised exercise program. Spatially resolved near-infrared spectroscopy monitored calf muscle oxygen saturation (StO(2)) during exercise and after a period of cuff-induced ischemia. Comparison was made with 14 individuals undergoing angioplasty for calf claudication. Clinical outcomes of claudication distance and maximum walking distance were measured by treadmill assessment. Results: Significant increases occurred in mean [interquartile range] claudication disease (57 [38-78] to 119 [97-142] meters; P = .01) and maximum walking distance (124 [102-147] to 241 [193-265] meters; P = .02) after supervised exercise but not after the control period. No change occurred in resting StO(2) at any interval. Angioplasty (27% [21-34] to 19% [13-29]; P = .02) but not exercise training (26% [21-32] vs 23% [20-31]; P > .20) resulted in a reduced StO(2) desaturation in response to submaximal exercise and an increased hyperemic hemoglobin oxygen recovery rate after ischemia (0.48 [0.39-0.55] to 0.63 [0.52-0.69] s(-1); P = .01). However supervised exercise reduced the StO(2) recovery half-time by 17% (82 [64-101] to 68 [55-89] seconds; P = .02). Conclusions: Supervised exercise training is not associated with increased gastrocnemius muscle oxygenation during exercise or increased hyperemic hemoglobin flow after a model of ischemia. This suggests that the symptomatic improvement witnessed is not the result of increased oxygen delivery to the active muscle. The enhanced recovery after exercise training therefore reflects a combination of enhanced metabolic economy and increased oxidative capacity, suggesting that exercise training helps reverse an acquired metabolic myopathy. (J Vasc Surg 2012;56:470-5.)