Natural performance enhancement, muscle hypertrophy and muscle rehabilitation on an expedited timeframe is highly coveted in sports and recreational fitness industries. Some studies have indicated that heat stress can improve upon muscle hypertrophy when used in combination with resistance training (RT), while some have shown no changes. Improvements in performance aspects such as strength, speed and agility in response to long term RT are well established, however the additive effects of heat stress on performance enhancements by RT has only been sparsely investigated. We therefore investigated the effects of full body heat stress applied concurrently during high intensity RT on muscle mass, strength, speed, agility and force in males. A cohort (n=18) of recreationally active, anthropometrically matched males were assigned in to two groups, HEAT (n=8, age= 23.3 ±.3.1, body mass (BM) = 75.6 ± 14.5kg, height = 175.6 ± 8.8 cm) and CON (n=10, age= 21.0 ± 2.7, BM = 76.0 ± 11.3kg, height = 177.2 ± 9.6 cm). Each group undertook an identical, 10 week, full body RT program three days a week with a rest day in between. The control group trained in thermoneutral conditions (23°C, RH 25%), while the HEAT group trained in a climate chamber at 40°C, RH 30%. Strength (1RM leg and bench press via maximal repetition test), speed (5 and 10 m sprint time), agility (T‐test), force (peak force during squat jump and ballistic push up) as well as body composition (DXA scan) were assessed at pre intervention, at week five and post intervention. Core temperature, HEAT (average peak temperature =38.18 ± 0.27 °C) and CON (37.97 ± 0.32 °C), as well as muscle temperature (at a depth of 3.5 cm in the vastus lateralis), HEAT (36.79 ± 1.55 °C) and CON (35.94 ± 1.51 °C) were also measured. Leg press 1 RM increased from pre intervention to post in both CON (50.25 ± 13.99 kg, p<0.05) and HEAT (32.75 ± 5.89 kg, p<0.05) while bench press 1RM showed no improvement. However, the relative strength (1RM divided by total muscle mass) improved only in bench press in both groups from pre intervention to post with CON (0.12 ± 0.009 kg.kg MM‐1, p<0.05) and HEAT (0.06 ± 0.008 kg.kg MM‐1) with relative leg press strength showing no improvement. Agility improved in the HEAT group at five weeks (0.3 s ± 0.16 s, p<0.05), however it was not different from pre intervention at post intervention. Agility did not improve in the CON group. No improvements were observed in 5m or 10m sprint time, or peak force generated in squat jump or ballistic push up in either group. Total upper body muscle mass increased in each group at post intervention, CON (1507.0 g ± 293.1 g, p<0.05), HEAT (806.6 g ± 213.9 g p<0.05) along with total muscle mass, CON (1760.8 g ± 306.4 g p<0.05) and HEAT (971.0 g ± 335.1 g p<0.05). Lower body muscle mass did not increase in either group. Total fat mass did not alter in either group pre to post intervention. These results indicate that, overall, heat stress applied concurrently with long term RT does not improve upon performance gains.

Analyses of mitochondrial adaptations in human skeletal muscle have mostly used whole-muscle samples, where results may be confounded by the presence of a mixture of type I and II muscle fibres. Using our MS-based proteomics workflow, we provide new insights into fibre-specific mitochondrial adaptations following two types of exercise training that were very different in terms of metabolic demands and fibre recruitment patterns: moderate intensity continuous training (MICT) and sprint interval training (SIT). There was a larger number of differentially expressed proteins in each fibre type following MICT than SIT. Our novel mitochondrial normalisation strategy highlighted that most training-induced changes in mitochondrial protein abundances were stoichiometrically linked to the overall increase in mitochondrial content, except for the decreased abundance of complex IV subunits in both type I and II fibres following SIT, and the increase in proteins associated with fatty acid oxidation in type I fibres.

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