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.