Acute local heating increases rat skeletal muscle oxygenation partially via nitric oxide-dependent mechanisms

Accumulating evidence indicates that acute local heating elevates skeletal muscle oxygen delivery via peripheral hemodynamic mechanisms. However, the effects of acute local heating on interstitial oxygen pressures (PO 2 is; the sole driving force for O 2 flux into the myocyte), and the potential contribution of nitric oxide (NO) bioavailability, remain unknown. Purpose: To determine the effects of acute local heating, with and without NO synthase (NOS) inhibition, on skeletal muscle PO 2 is in healthy rats. We hypothesized that, while core temperature (Tc) was maintained using external cooling, graded local heating would progressively elevate resting muscle PO 2 is without altering central hemodynamics, and that this response would be significantly attenuated by NOS inhibition. Methods: Spinotrapezius muscle PO 2 is was determined via phosphorescence quenching in 20 male Sprague-Dawley rats under NG-nitro-L-arginine methyl ester (L-NAME, non-selective NOS inhibition; n=10) or Krebs-Henseleit bicarbonate-buffered superfusion (control, CON; n=10). Progressive muscle heating was achieved using infrared light in 20-min increments (40, 41 and 42°C; 60 min total), while Tc was maintained with a water-perfused cooling pad. Following the heating protocol, sodium nitroprusside (SNP; 300 µM) was superfused locally to assess the viability of the preparation. Mean arterial pressure (MAP) and heart rate (HR) were assessed throughout experimental procedures via the caudal (tail) artery. Results: Acute local heating did not affect MAP or HR (p>0.05 for both) during either CON or L-NAME superfusion conditions. Muscle heating progressively increased PO 2 is from baseline (15.6±0.4) to 40°C (35.5±1.2), 41°C (40.4±1.2) and 42°C (42.7±1.6 mmHg; p< 0.05 for all) during CON in the setting of unchanged Tc (36.9±0.4, 36.9±0.3, 36.9±0.4, and 37.1±0.4°C, respectively; p>0.05 for all). NOS inhibition with L-NAME attenuated the increase in muscle PO 2 is with acute heating from baseline (12.8±0.3) to 40°C (21.8±0.4), 41°C (28.5±0.4), and 42°C (30.8±0.6 mmHg; p< 0.05 for all) with Tc maintained (37.1±0.2, 36.9±0.3, 37.0±0.4, 36.9±0.5°C, respectively; p>0.05 for all). Overall, NOS inhibition attenuated the heating-induced increase in PO 2 is by ~36% (Δ+28.3 mmHg in CON vs. Δ+18.1 mmHg with L-NAME at 42°C; p< 0.05), indicating a substantial NO-dependent component of the response. There were no differences in Tc between CON and L-NAME at any time point (p>0.05 for all). SNP increased muscle PO 2 is during both CON (18.3±4.1 vs. 36.1±10.5; p< 0.05) and L-NAME (15.0±5.1 vs. 39.1±15.3 mmHg; p< 0.05) conditions. Conclusions: Acute local heating elevates skeletal muscle PO 2 is (and thus blood-myocyte O 2 diffusion) at maintained Tc, independent of changes in MAP and HR. NOS inhibition significantly attenuates this response, indicating a partial NO dependence. These results support a role for local heating as a targeted strategy to enhance skeletal muscle oxygenation. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.