Exercise training (EX) imposes stress on skeletal muscle, resulting in improved mitochondrial respiratory capacity and fat oxidation. Heat, which is one of the stresses of exercise, has been previously shown to increase mitochondrial respiration in human skeletal muscle. Still, it is unknown how the effects of localized heat therapy (HEAT) compare to the effects of EX, or if HEAT improves fat oxidation capacity. Therefore, the objective of this study was to determine the extent to which 6 weeks of HEAT improve mitochondrial function compared to EX. We hypothesized that HEAT would increase mitochondrial respiratory capacity, fatty acid oxidation and citrate synthase (CS) activity, but to a lesser extent than EX. Subjects were randomized into three groups: HEAT (n=11), EX (n=8), and a sham control group (CON, n=12). Subjects in the HEAT group were exposed to 2 hrs/day, 3 days/wk of short‐wave diathermy, which raised internal muscle temperature by 3.2 ± 0.33° C, while CON subjects experienced no change in muscle temperature during sham diathermy sessions. EX consisted of single‐leg extension exercise on a modified cycle ergometer for 45 min/day, 3 days/week, and resulted in a 1.8 ± 0.42° C increase in muscle temperature. Muscle biopsies were performed at baseline, and after 3 and 6 weeks of intervention. Small muscle fiber bundles (2‐4 mg wet wt.) were permeabilized, and mitochondrial respiration was assessed using high‐resolution respirometry (Oroboros O2k, Innsbruck, Austria). CS and 3‐hydroxyacyl‐CoA dehydrogenase (HAD) activity assays were performed in duplicate on supernatant from homogenized muscle samples. At 6 weeks, EX resulted in 27.9 ± 8.7% and 33.2 ± 11.7% increases in maximal coupled and uncoupled respiration, respectively, which were significantly different from baseline (p<0.05). At 6 weeks, HEAT resulted in 24.8 ± 6.2% and 24.5 ± 6.2% increases in maximal coupled and uncoupled respiration, respectively, which were significantly different from baseline (p<0.05), but not different from EX. Fatty acid oxidation was improved only in EX subjects after 6 weeks (29.5 ± 6.8%), compared to baseline (p<0.05), with no change in HEAT or CON subjects. CS activity increased in EX subjects (25.9 ± 10.5 µmol·min‐1·mg protein‐1 or 19.0 ± 7.4%) compared to all others (p<0.05), but no changes were observed in HEAT or CON subjects. Furthermore, no change in HAD activity occurred in any group. These results suggest that HEAT improves mitochondrial respiratory capacity to a similar extent as EX but does not result in other EX‐induced adaptations like increased fat oxidation and CS activity. Still, HEAT‐induced improvements in respiratory capacity may have therapeutic potential in the context of skeletal muscle disease or disuse, and further investigation is warranted.
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