Heat acclimation during low-intensity exercise increases ˙VO2maxV̇O2max<math><msub><mover><mi>V</mi><mo>̇</mo></mover><mrow><msub><mi>O</mi><mn>2</mn></msub><mi>max</mi></mrow></msub></math> and Hsp72, but not markers of mitochondrial biogenesis and oxidative phosphorylation, in skeletal tissue

New findings: What is the central question of this study? Heat acclimation increases tolerance to exercise performed in the heat and may improve maximal oxygen uptake (VO2 max) and performance in temperate environments. However, it is unknown if HA affects the expression of proteins related to mitochondrial biogenesis and oxidative capacity in skeletal muscle. What is the main finding and its importance? We showed that heat acclimation increased VO2 max in a temperate environment but did not change markers of mitochondrial biogenesis and oxidative phosphorylation in the skeletal muscle. Heat acclimation (HA) increases tolerance to exercise performed in the heat and may improve maximal oxygen uptake ( ˙VO2maxV̇O2max&lt;math&gt;&lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt;&lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt;&lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt;&lt;mi&gt;max&lt;/mi&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/math&gt; ) in temperate environments. However, it is unknown if HA affects the expression of proteins related to mitochondrial biogenesis and oxidative capacity in skeletal muscle. The purpose of this study was to investigate the effect of HA on skeletal muscle markers of mitochondrial biogenesis and oxidative phosphorylation in recreationally trained adults. Thirteen (7 males and 6 females) individuals underwent 10 days of HA. Participants performed two 45 min bouts of exercise (walking at 30-40% maximal velocity at 3% grade) with 10 min rest per session in a hot environment (∼42°C and 30-50% relative humidity). ˙VO2maxV̇O2max&lt;math&gt;&lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt;&lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt;&lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt;&lt;mi&gt;max&lt;/mi&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/math&gt; , ventilatory thresholds (VT), and protein expression of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), mitochondrial transcription factor A (TFAM), calcium/calmodulin-dependent protein kinase (CaMK), electron transport chain (ETC) complexes I-IV, and heat shock protein 72 (Hsp72) in skeletal muscle were measured pre- and post-HA. Comparing day 1 to day 10, HA was confirmed by lower resting core temperature (Tcore ) (P = 0.026), final Tcore (P &lt; 0.0001), mean heart rate (HR) (P = 0.002), final HR (P = 0.003), mean ratings of perceived exertion (RPE) (P = 0.026) and final RPE (P = 0.028). Pre- to post-HA ˙VO2maxV̇O2max&lt;math&gt;&lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt;&lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt;&lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt;&lt;mi&gt;max&lt;/mi&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/math&gt; (P = 0.045) increased but VT1 (P = 0.263) and VT2 (P = 0.239) were unchanged. Hsp72 (P = 0.007) increased, but skeletal muscle protein expression (PGC-1α, P = 0.119; TFAM, P = 0.763; CaMK, P = 0.19; ETC I, P = 0.629; ETC II, P = 0.724; ETC III, P = 0.206; ETC IV, P = 0.496) were not affected with HA. HA during low-intensity exercise increased ˙VO2maxV̇O2max&lt;math&gt;&lt;msub&gt;&lt;mover&gt;&lt;mi&gt;V&lt;/mi&gt;&lt;mo&gt;̇&lt;/mo&gt;&lt;/mover&gt;&lt;mrow&gt;&lt;msub&gt;&lt;mi&gt;O&lt;/mi&gt;&lt;mn&gt;2&lt;/mn&gt;&lt;/msub&gt;&lt;mi&gt;max&lt;/mi&gt;&lt;/mrow&gt;&lt;/msub&gt;&lt;/math&gt; in a temperate environment and Hsp72 but it did not affect markers of mitochondrial biogenesis and oxidative phosphorylation in the skeletal muscle.