Partial-body cryostimulation does not impact peripheral microvascular responsiveness but reduces muscular metabolic O2 consumption (mVO2) at rest

This study aimed to investigate the effect of partial-body cryostimulation (PBC) on microvascular responsiveness and muscular metabolic O-2 consumption rate (mVO(2)). Twenty healthy young adults (ten males and ten females) underwent a post-occlusive reactive hyperemia (PORH) test at the flexor digitorum superficialis area before and after a 3-min PBC session and a 3-min control session. Using near-infrared spectroscopy, occlusion and reperfusion slopes were calculated: oxyhemoglobin ([HbO(2)]) decrease rate ([HbO(2)] slope 1), deoxyhaemoglobin ([HHb]) increase rate ([HHb] slope 1), [HbO(2)] increase rate ([HbO(2)] slope 2), and [HHb] increase rate ([HHb] slope 2. Using HbO(2) kinetics during the occlusion, mVO(2) was also calculated to characterize myocytes' metabolic O-2 consumption. HbO(2) slope 1 value was lower after PBC than before PBC (0.15 +/- 0.08 vs 0.24 +/- 0.11 s-1; respectively; P < 0.05) in male participants only. A lower [HHb] slope 1 was also observed after PBC compared to before PBC (0.18 +/- 0.10 vs 0.24 +/- 0.16 s 1; P < 0.05) with no interaction for sex categories. m.VO2 was significantly lower after PBC than before (pre values 14.75 +/- 3.94 vs 18.47 +/- 5.73 mu MO(2)Hb.s(-1); respectively; P < 0.01) with no interaction between sex categories. No changes in the calculated slope 2 were observed. These findings suggest that a single session of PBC reduces the muscular metabolic O-2 needs at rest; however, it does not alter the vascular ability to provide O-2 to the myocytes.

Automated summary

This study aimed to investigate the effect of partial-body cryostimulation (PBC) on microvascular responsiveness and muscular metabolic O-2 consumption rate (mVO(2)). The results showed that PBC reduced the oxyhemoglobin decrease rate and deoxyhaemoglobin increase rate, suggesting that PBC can decrease the muscular metabolic O-2 needs at rest without affecting the vascular ability to provide O-2 to the myocytes.